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I am a biomedical engineer with experience in deep learning applications for classifying and predicting various diseases. Recently, I have been working on projects involving disease classification and prediction through deep learning, with a particular focus on CNNs and advanced image processing techniques. Currently, I am preparing for a master’s degree in data science to deepen my expertise in this field. I am open to collaborating on research articles and can assist as an editor or peer reviewer for relevant journals. Additionally, I am available to work as a volunteer researcher at universities, contributing my skills in biomedical engineering, bioprinting, and microbiology.
If you are interested in collaboration or if I can assist with your research, please feel free to contact me at biomedical.emr@gmail.com.
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Dear Emir Öncü,
I am looking for collaboration with microbiologist globally.
If you interested we can do it.
With regards.
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I encountered an unusual observation while constructing a nomogram using the rms package with the Cox proportional hazards model. Specifically, when Karnofsky Performance Status (KPS) is used as a alone predictor, the nomogram points for KPS decrease from high to low. However, when KPS is combined with other variables in a multivariable model, the points for KPS increase from low to high. Additionally, I've noticed that the total points vary from low to high for all variables, while the 1-year survival probability shifts from high to low.
Could anyone help clarify why this directional shift in points occurs? Are there known factors, such as interactions, scaling differences, or confounding effects, that might explain this pattern?
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Thank you
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Using A375 to stimulate NK cells to release CD107a and IFN - γ in a 1:1 ratio, but the experimental results show that NK cells have a lower ability to release CD107a and IFN-γ under A375 stimulation. How should I change the ratio of NK cells co cultured with A375 cells to evaluate the expression of CD107a and IFN-γ in NK cells? Should more target cells be inserted? In what proportion?
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To increase CD107a and IFN-γ release, set the E ratio to 5:1 or 10:1, resulting in more NK cells per A375 target. Higher E ratios often increase NK cell activation and cytokine release.
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As it is a crucial part of my project and me being an undergraduate student, I am interested in learning better and cost efficient method for analysing Anti-Cancer property of my desired phytochemical.
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Hello Ajay,
You may use in vitro assays to identify anticancer properties of the phytochemical in cultured murine or human tumor cell lines. However, there are cell-free systems as well, which you may use that include assays which measure enzyme inhibition, receptor binding, protein–small molecule interactions, or interference with components of important signal transduction pathways.
If you have a cell culture facility, then the simplest and commonly used in vitro cell-based assay would be the cytotoxicity assay such as the MTT assay.
You would need a cancer cell line (preferably derived from the tumor
tissue of the cancer of your interest. For instance, if you are aware that your phytochemical is effective against breast cancer, you may use breast cancer cell line such as MDA-MB-231 or MCF-7 cell line) to test various concentrations of the phytochemical on the cells.
You may follow the MTT protocol as provided below.
1. Plate the cancer cells of interest in a 96-well plate format at a desired cell density such that they are 80% confluent on the day of readout. If cells are overconfluent on the final day of the assay, you may end up with inaccurate results.
2. After 24 hours, when the cells have attached to the substratum, treat the cells with the phytochemical by changing the media with the treatment media at various concentration ranging from 5ug/ml to 500ug/ml (at least 5 concentrations).
3. Incubate the cells with the treatment media for 24, 48 and 72 hours.
4. After the treatment period, aspirate the treatment media and add MTT reagent to a final concentration of 0.2 to 0.5mg/ml and incubate in the dark for 1 to 4 hours for the formation of formazan crystals.
5. After incubation, solubilize the crystals into a colored solution with the solubilizing solution which may include either dimethyl
sulfoxide or acidified isopropanol solution, or a solution of 10% SDSin 0.01M hydrochloric acid.
6. Measure the absorbance at a wavelength of 570 nm.
7. IC50 value may be calculated from the graph constructed by plotting cell survival versus extract concentration.
Please note that IC50 stands for half-maximal inhibitory concentration, and it's a measure of how much of a drug or herbal extract is needed to inhibit a biological process by half. It's a widely used and informative way to measure a drug's efficacy and potency.
Good Luck!
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Cure of cancer?, respectfully to whom it may concern:
If I found a cure of cancer, I’m wondering what I should do with it? I’m just coming out of a 40 days fast of only drinking maple syrup and pure lemon juice plus a little cinnamon powder and nothing else since I had unimaginable pain in my colon end. I figured out that although we humans can last for weeks on this diet /fast, cancer has no food on that and just goes away and the pain is gone too. I received this prescription by tuning in into the HeilstrOm and I figured out that it also enhances the reception of the HeilstrOm greatly, which brings great happiness too, as I describe in my book
Best regards, hope this helps someone
Chris K. Frueh
Independent Researcher
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@Seraphina Anderson good point
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I am using knockout MIAPaCa-2 and ASPC-1 pancreatic cancer cell lines and intend to develop an in vivo tumor model. However, my study involves CD8 T-cell expression analysis, so I cannot use nude mice.
Additionally, if I inject the knockout cell lines directly, will the resulting tumor maintain the knockout status of the cells, and what would the efficiency be in terms of tumor formation and maintaining the gene knockout in vivo?
Any recommendations for the best variant of mice to evaluate both tumor growth and immune response.
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Lisa Smith
Thanks. My work involves studying the expression of CD8 T cells after cancer induction. Is immunodeficient mice a good option for this?
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Hello everyone. I am addressing the cancer researchers here who have worked on oral cancer cells or cell culture using OSCC cell lines. Which cell viability assay do you recommend for drug assays on OSCC cells? What are the benefits and limitations of your chosen assays?
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I personally received Mtt assay
if you are interested in learning about the basic Of this assay you can read this article
(( Proinsulin C-Peptide Enhances Cell Survival and Protects against Simvastatin-Induced Myotoxicity in L6 Rat Myoblasts))
Best Wishes.
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Hello everyone
i plan to do atovaquone oral dose in mice . I plan to use castor oil as diluent. Does anyone have experience in working with atovaquone or how to prepare one ?
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With atovaquone you're out there on the bleeding edge. Good luck!
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I am now taking a course in the SEER database. I want to know how to get ideas to work on. If anyone with relative experience tell me.
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Can you please share the link and is it good?
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I have no idea why my orthotopic mouse models have failed.
I have used gastric cancer cell lines, and I injected the cells into a mouse stomach.
Here is my procedure and a result photo as a failed example.
1. Detach gastric cancer cells with 0.25% trypsin, then wash the cells with PBS
2. Centrifuge for 3 min, 1200 rpm at room temperature
3. Suction the trypsin and PBS, then put 1 mL of PBS
4. Get 1 x 10^8 cells in 1 mL of PBS, which is an example, counted by a cell counter
5. Transfer 100 uL of cell suspension to get 5 x 10^6 cells for 2 mice
4. Centrifuge for 0.5 min
5. Remove the PBS and put 15 uL of Matrigel and 15 uL of PBS
6. Suspend the 30 uL of gastric cancer cells and put it into a 0.5 mL insulin syringe
7. Keep the cells in the ice
8. Anesthetize a syngeneic mouse (4-6 weeks old) with 2% Isoflurane
9. Open the abdominal cavity
10. Take out the stomach then inject the cells, and try to inject them into the serosa; however, I sometimes inject the cells into the muscle layer.
11. If bleeding occurs after cell injection, the injection has failed
12. Suture the peritoneal cavity
13. Remove the stomach after a month, and dissect the stomach
Mice have never died, and they do not have any cancer organs even if I injected gastric cancer cell lines in their stomach.
Metastasis has also never been discovered.
This experiment has been conducted with the naked eye without a microscope.
I have been frustrated. What is my problem? Would you do me a favor, please?
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Hello, I prefer to resuspend with a micropipette.
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Hi guys,
I'm working on the tumor mouse model. In general, I prepared tumor cells and injected cells into the flank of mice subcutaneously.
After around 3 weeks, I found, in the same group, there's a variation in the tumor weight. For instance, some tumor were around 1.2g, some 0.6g.
Could you give me some suggections or tips about how do tumor inejction?
Which type of needle do you need for injection? or How to prepare tumor cells suspension? or whatever something you think is important to do that successfully
Many thanks :)
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Thank you so much for your suggestions! I didn't think about the position of syringe before, and I think your suggestion would help me a lot!
Do you think that different gauge needles could make a difference? Why do you choose 26G?
We don't have matrix gel, so the cells were resuspended in the PBS.
When I took out the tumor, I found there were more like fat tissue in the tumor, and in some tumors, there's a lot of blood, eventhough I injected the same cells.
Best wishes,
Tingting
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I have cultured PBMC and some RBC contaminant for 2 weeks in suspension and low attachment plate. From the very first day, I noticed that there are many cells that have already turned all black-ish or grey-ish color. I don't know why and I keep continuing my culture process because the sample is very limited and I don't want to waste any samples. This is very confusing as because I will do viability assay using trypan blue, but the cells were already black. So I can't see the blue-ish color that supposed to appear. For additional information, my medium is DMEM F12, EGF, FGF, CoCl2, ITS, Penstrep, and Amphotericin.
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Hello Rafli, your micrograph does appear to illustrate apoptosis in your cultures. I can's see any serum in your DMEM usulaly ~10%FBS? I would also suggest that you remove the amphotericin and titrate the cobalt, as I would anticipate both reagent are stressing/killing the cultures.
best wishes
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How can personalized lifestyle modifications, including diet, exercise, stress management, and sleep hygiene, be integrated into conventional medical treatments to optimize health outcomes and potentially reverse or manage chronic diseases or any other diseases in the past, present or in the future?
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We can no longer rely on the philosophy of determinism (control) of classical science.They only apply to invariant properties of physics; not to society/biology/ecology.The models of classical science become deadly if used on medicine (health care).
Our participation in creation operates in our body, as human AND humanity. Science is incapable to describe that; the same is the case for any religion. But we can all experience it in our body: it is based on this uniVersal dynamic.
Integral Health Care makes use of all the healing arts of the whole Earth. East & West, Far-East & Far-West therein logically complement each other. Together they define and form Integral Health Care.
Together they can prevent, early-detect/correct, cure and palliate.
The essence is simple:
  • The West created an anatomic (“somatic”) structural understanding of our body.This bases itself on the Classical models of deterministic science.
  • The East (Ayurveda) focused on supporting the physiological processes of our body.This calls for a Relativistic type of thinking.
  • The Far-East (Acupuncture) designed an approach to recalibrate the regulatory system of our body.This requires a Probabilistic approach.
  • The Far-West (Spiritual Healing) works primarily with the Information Integration system of the body.This calls for a universal integral/unified Field description.
  • The principles and method for integration of these forms of healing is found in our living body. Our body is not a mechanical object: it is an information processor which interacts with its context. In our living being, information integrates with matter, with the essence of life: Freedom of Choice. Our body is our best example on the way objective reality is based on subjective realisation. Realise that the scientific model of reality changed from Determinism to Relativity to Probability to Creativity. Our participation in creation means that our reality is based on our realisation. Especially for health care this means a change from Objectivity to Subjectivity: “what you think matters”.
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Hello everyone, I need help to understand how I can "co-cultivate" human platelets (derived from whole blood) with cancer cells. I have specific questions:
-How can I avoid platelets from clumping?
-How can I avoid platelets from stick to the bottom of the transwell plates I am using fot this co-culture system?
-Have someone worked already with apheresis platelets?
Thank you for your help!!
Giulia
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Maybe use an anticoagulant in you culture medium like heparin?
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If you are interested in this topic, you might wish to investigate the International Association for Near Death Studies (IANDS.org). or delve into Consciousness Studies.
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I am interested in analyzing the correlation between the expression of a set of genes and transposable elements (TEs) in cancer. However, despite there are multiple online databases for gene expression in cancer, including TCGA, they do not include repetitive elements. Despite I've found some papers analyzing transposable elements and quantifying their expression in different cancer using TCGA data, supplemental tables only provide the fold change end p-values for differentially expressed TEs. Also, to identify and quantify TEs, the raw sequencing data, which have controlled access, would be necessary. Therefore, I was wondering if there is some database or published resource where I could find information regarding TE expression per sample in TCGA database. Does someone know something like that? Alternatively, if someone have analyzed this type of data and have some worksheet with pre-processed data that could be shared, I would be deeply grateful.
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Hi Glauco,
Are you aware of the Xena browser (https://xenabrowser.net/)? There are at least gene expression, mutation and methylation data per patient for the TCGA cohorts. Unfortunately I am not sure about the TE data, since I am not working with that but I think that Xena would be your best bet.
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I am not entirely sure if there are standard practices for tumour immunohistochemical preparation seeing as tumours aren't usually the most organized structures, but I may be wrong.
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Received glass slide mounted tumors tissues form OT
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Does anyone know an institute/research facility in Europe running research in the field of cancer therapy and willing to accept a student of Micro- and Nanotechnoligies in Biophysics for Erasmus+ holiday traineeship?
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ips institute upm university Malaysia
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Relationship between exercise, the gut microbiome, and cancer is complex and multifaceted. Factors such as the type and intensity of exercise, individual differences in gut microbiota, and genetic factors all play a role. What your views? Do share specific researches for the same.
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As you have stated gut microbiome and cancer relations are maybe the most complex issue of all medicine as within the scope of gastrointestinal oncology. The secrets of this utmost complex issue with so many unsolved neoplastic mechanisms are hidden as if rooted in darkest unknown ocean deeps. I recommend you to read the links below...
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Dear scientists, clinicians, and researchers on the ResearchGate platform,
I am planning to assess the molecular mechanisms of developing drug resistance in cancer cells. However, I lack knowledge regarding the bystander effect. Can you kindly assist me with the following questions:
1. What is the fundamental understanding of the bystander effect in the development of drug resistance in cells?
2. Why is it important to measure gene mutations that cause drug resistance, whether through direct or bystander effects?
3. What is the most effective in vitro setting to demonstrate this bystander effect and resistance development?
4. How can we measure the direct and bystander effects of gene mutations causing chemotherapy resistance in cancer cell lines? What parameters should we assess?
5. Lastly, what are the clinical implications of measuring this bystander effect?
Thank you very much for your assistance.
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I am NOT a doctor but my research with an AI tool provided following info:
1. In the context of drug resistance, the bystander effect suggests that the presence of mutated cells can influence the surrounding non-mutated cells, leading to the development of resistance mechanisms. This can occur through the transfer of signaling molecules, genetic material, or other factors that mediate cellular communication.
2. A few reasons. Firstly, understanding the specific mutations responsible for resistance helps in the development of targeted therapies that can overcome or prevent resistance mechanisms. Secondly, monitoring these mutations allows for the early detection of emerging resistance, enabling timely treatment adjustments to improve patient outcomes. Lastly, studying gene mutations and their effects contributes to a deeper understanding of the underlying mechanisms of drug resistance, aiding in the development of more effective treatment strategies.
3. The most effective in vitro setting to demonstrate the bystander effect and resistance development depends on the specific research question and the cell type being studied. Co-culture experiments, where mutated and non-mutated cells are cultured together, can mimic the cellular interactions that occur in vivo and provide insights into the bystander effect. Additionally, organoid models or three-dimensional cell cultures that closely resemble the tumor microenvironment may offer more physiologically relevant settings to investigate the bystander effect.
4. To measure the direct and bystander effects of gene mutations causing chemotherapy resistance in cancer cell lines, several parameters can be assessed. These include:
- Cell viability and proliferation assays: Assessing the growth and survival of cancer cells in the presence of chemotherapy drugs can provide insights into their sensitivity or resistance.
- Gene expression analysis: Comparing gene expression patterns between drug-sensitive and drug-resistant cell lines can identify key genes or pathways involved in resistance development.
- Protein expression and activity: Analyzing protein levels and activities associated with drug resistance mechanisms, such as drug efflux pumps or DNA repair enzymes, can shed light on their contribution to resistance.
- Signaling pathway analysis: Investigating signaling pathways involved in resistance development, such as those related to cell survival or apoptosis, can provide mechanistic insights.
- Transfer experiments: Conducting experiments where media or conditioned media from drug-resistant cells are transferred to drug-sensitive cells can help assess the transferability of resistance and the bystander effect.
5. The clinical implications of measuring the bystander effect in drug resistance are significant. By understanding the mechanisms underlying resistance development, clinicians can make informed decisions regarding treatment strategies. This knowledge can guide the selection of appropriate therapies, the optimization of treatment regimens, and the identification of potential combination therapies to overcome drug resistance. Additionally, measuring the bystander effect can aid in the development of predictive biomarkers for resistance, allowing for personalized medicine approaches and improved patient outcomes.
Hope it helps
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A very Emergency case, The Mother of my best friend, the results of her MRI said that she had nodular peritoneal thickening that suggested peritoneal serosal carcinoma, and ovarian cancer, also she has ascites, what is the source of ascites in case of high CA-125? We are suggesting a surgery to remove the ovarian, peritoneal biopsy and taking different samples to histology laboratory for culture and characterization, Any Informations would be helpful and well Appreciated, Many Thanks
Ali
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I am NOT a doctor but as compter science professional, little more AI provided detail:
In cases where there is nodular peritoneal thickening, ovarian cancer, and ascites, the source of ascites can be the result of various factors, including the presence of cancer cells in the peritoneal cavity.
CA-125 is a tumor marker that is often elevated in cases of ovarian cancer, although it can also be elevated in other conditions. The presence of high CA-125 levels, along with the imaging findings of nodular peritoneal thickening, suggests the possibility of peritoneal serosal carcinoma, which is a type of cancer that affects the lining of the abdominal cavity (peritoneum). Ovarian cancer can sometimes spread to the peritoneum, leading to peritoneal serosal carcinoma.
Ascites refers to the accumulation of fluid in the abdominal cavity. In the context of ovarian cancer, ascites can occur due to several reasons, including:
1. Peritoneal involvement: Cancer cells can spread to the peritoneum, leading to inflammation and the production of fluid.
2. Impaired lymphatic drainage: The presence of cancer can disrupt the normal flow of lymphatic fluid, leading to its accumulation in the abdomen.
3. Liver involvement: Advanced ovarian cancer can involve the liver, leading to impaired liver function and fluid accumulation.
Surgery, as you mentioned, is often a crucial component of the treatment plan for ovarian cancer. The specific surgical procedures performed can vary depending on the individual case, but they may include removal of the ovaries (oophorectomy), peritoneal biopsy, and collection of various samples for histological examination. These procedures aim to obtain a definitive diagnosis, determine the extent of the disease, and guide further treatment decisions.
Please consult qualified healthcare professionals who can provide personalized advice and guidance based on the specific details of your best friend's mother's case. They will be able to provide the most accurate information and help determine the most appropriate course of action.
Hope it helps
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A study by Peeters et al. (2017) suggests that sugar traps cancer in a 'vicious cycle' which make it more aggressive and harder to treat (1). On the question-and-answer site Quora, Ray Schilling, MD, concludes: "there is a connection between the consumption of sugar and starchy foods and various cancers in man. Animal experiments are useful in suggesting these connections, but many clinical trials including the Women’s Health Initiative have shown that these findings are also true in humans. It is insulin resistance due to sugar and starch overconsumption that is causing cancer" (2).
References
1. Peeters K, Van Leemputte F, Fischer B, Bonini BM, Quezada H, Tsytlonok M, Haesen D, Vanthienen W, Bernardes N, Gonzalez-Blas CB, Janssens V, Tompa P, Versées W, Thevelein JM. Fructose-1,6-bisphosphate couples glycolytic flux to activation of Ras. Nat Commun 2017; 8: 922. doi: 10.1038/s41467-017-01019-z. https://www.nature.com/articles/s41467-017-01019-z.pdf
2. Schilling R. Why isn't sugar portrayed as bad like cigarettes? https://www.quora.com/Why-isnt-sugar-portrayed-as-bad-like-cigarettes
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Although sugar is not directly labeled a carcinogen, recent research has unveiled the link between sugar consumption and cancer risk. Sugar, primarily sucrose and high-fructose corn syrup is commonly found in processed foods, sugary beverages, and sweet treats. Excessive sugar intake has long been associated with various health issues, such as obesity, diabetes, and heart disease. However, the emerging connection between sugar and cancer has garnered recent attention. High sugar consumption can lead to chronic inflammation, insulin resistance, and the promotion of obesity, creating an environment conducive to certain types of cancer. While sugar itself does not directly induce cancer, it can contribute by fueling the rapid division and growth of cancer cells, particularly in breast and lung cancer cases. Some research suggests that reducing sugar intake could be an effective strategy for cancer prevention and improving the outcomes of cancer treatments. It is crucial to note that the relationship between sugar and cancer is complex and not entirely understood. Several factors, including genetics and overall diet, contribute to an individual's cancer risk. Therefore, the main message is not to demonize sugar but to stress the importance of moderation and a well-balanced diet. Simultaneously, sugar is not classified as a direct carcinogen, but a growing body of evidence indicates that excessive sugar consumption can contribute to the risk of developing cancer. Maintaining a healthy, well-balanced diet with limited sugar intake is advisable for overall health and potentially reduces cancer risk.
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This generalizable immunotherapy approach to cancer seems compelling:
Unlike many other immunotherapies, this one does not require pre-defining antigens.
Based on research from the Levy lab at Stanford, this method introduces a non-specific technique to attack cancers by injecting immunoenhancing agents (TLR9 and OX40) locally into the tumor site. In mouse models, these agents activated a robust, targeted anti-tumoral response.
Clinical trials were launched in 2019/2020.
What's the best way to track the clinical trials and see how this therapy work on humans?
Thanks!
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Because older adults are under-represented in clinical trials, doctors can’t be certain that approved cancer drugs will work as intended in this age group. In the absence of high-quality evidence, researchers are looking for ways to improve medical decision-making and better predict outcomes based on age...
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Q1. What is the difference between the HeLa-derived new strain cell line and the HeLa cell cross-contamination cell line?
Most contaminating cell lines are discarded, but occasionally contaminating cells acquire new properties (e.g., by mutation or viral transfection, e.g., by the HeLa derivative Det98) and eventually constitute a new line and are therefore not discarded. Thus In the case of KB (CVCL_0372) cells, I would like to know which type of cell line it is.
Q2. HeLa cell derivative KB cells are described as 'oral carcinoma' or 'cervical carcinoma' in some research.
Currently, I am conducting an anti-cancer experiment using KB cells. I wonder if there is any problem in writing a thesis by treating KB cells as cervical cancer and accurately defining them as HeLa derivatives.
:
Related reference
1) Vaughan, L., Glänzel, W., Korch, C., & Capes-Davis, A. (2017). Widespread Use of Misidentified Cell Line KB (HeLa): Incorrect Attribution and Its Impact Revealed through Mining the Scientific LiteratureWidespread Use of Misidentified Cell Lines. Cancer research, 77(11), 2784-2788. https://doi.org/10.1158/0008-5472.CAN-16-2258
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Q1. The KB cell line (CVCL_0372) is derived from a cell line called HeLa, but it is not considered a HeLa cross-contamination cell line. Instead, KB cells are classified as HeLa derivatives. The term "HeLa derivative" refers to cell lines that have been derived from the original HeLa cell line through various means, such as mutation or viral transfection. These derivatives can acquire different characteristics and properties while still retaining some similarities to the parent HeLa cells.
Q2. KB cells are commonly described as an oral carcinoma cell line, rather than a cervical carcinoma cell line. While both oral carcinoma and cervical carcinoma are types of cancer, it is important to accurately define the cell line being used in your research. In this case, KB cells are derived from HeLa cells, which are originally derived from cervical cancer cells.
When writing your thesis, it is crucial to provide accurate and specific information about the cell line you are using. You can mention that KB cells are derived from HeLa cells, which were derived from cervical cancer cells. However, it is generally recommended to refer to KB cells as an oral carcinoma cell line, as that is the most commonly accepted designation for this specific cell line.
All the best
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Currently, I am looking for a solution to develop chemotherapeutic drug resistance in a primary cancer cell line. But after a quick look at the literature, it is indicated that the management of acquirement of drug resistance takes plenty of time, more than eight months! Is there any convenient method to subculture chemoresistant cell lines in a short time? Or any other suggestions rather than eight months interval with an increasing dose of chemotherapeutic agent?
Best regards.
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Hi..Rather than establishing the resistance cell line,I've found some published articles compared the resistance of various cell lines (from the same cancer type) following drug treatment. Cells with greater survival rate following drug treatment were selected as a resistance model
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Drugs Informations
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Alendronate:
  • Chemical Structure: Alendronate is a bisphosphonate with the chemical name [4-amino-1-hydroxybutylidene]bisphosphonic acid. Its chemical formula is C4H13NO7P2 and its molecular weight is 249.1 g/mol.
  • Functional Groups: Alendronate contains two phosphonic acid groups (-PO3H2) and one hydroxyl group (-OH).
  • Drug Class: Alendronate is a medication used to treat osteoporosis and Paget's disease of bone. It is classified as a bisphosphonate drug.
Paclitaxel:
  • Chemical Structure: Paclitaxel is a natural product with the chemical name (2aR,4S,4aS,6R,9S,11S,12S,12aR,12bS)-12b-(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,6,11-trihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca[3,4]benz[1,2-b]oxet-9-yl (2R,3S)-3-(tert-butoxycarbonylamino)-2-hydroxy-3-phenylpropanoate. Its chemical formula is C47H51NO14 and its molecular weight is 853.9 g/mol.
  • Functional Groups: Paclitaxel contains several functional groups including an ester group, two hydroxyl groups, and an amide group.
  • Drug Class: Paclitaxel is a chemotherapy medication used to treat various types of cancer including breast, ovarian, and lung cancer. It is classified as a taxane drug.
Thiophene:
Thiophene can be dissolved in various solvents including ethanol, ether, benzene, and toluene. The solubility of thiophene in water is very low (0.052 g/L at room temperature) and it is generally not recommended to dissolve it in water. To dissolve thiophene, it can be added to the solvent slowly with stirring and heating may also be necessary to increase solubility. It is important to handle thiophene with care as it is flammable and toxic.
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I want to isolate the macrophage cell membrane and then coated it on nanoparticles. There are many protocols for the isolation of cell membrane vesicles, but I want to separate the macrophage cell membrane and next prepare cell membrane cracks. In addition, protocols suggest different hypotonic lysis buffers for macrophage cell membrane isolation (20 mM Tris-HCl, 10 mM KCl, 2 mM MgCl2, and 1 EDTA-free mini protease inhibitor tablet or 1 mmol L −1 NaHCO3, 0.2 mmol L −1 EDTA and 1 mmol L −1 PMSF or Tris-magnesium buffer (TM buffer, pH 7.4, 0.01 M Tris and 0.001 M MgCl2), which I don’t know the best one. After cell lysis, the protocols are followed by sucrose gradient or differential centrifugation, or sonication. I am worried about confirming the cell membrane after isolation and the best protocol for membrane isolation and saving them besides coating the nanoparticles with macrophage cell membrane cracks.
Any help is appreciated!
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Following two papers should be helpful:
Wang, F., Deng, Y., Yu, L., Zhou, A., Wang, J., Jia, J., ... & Lin, X. (2022). A Macrophage Membrane–Polymer Hybrid Biomimetic Nanoplatform for Therapeutic Delivery of Somatostatin Peptide to Chronic Pancreatitis. Pharmaceutics, 14(11), 2341.
Zhu, S., Li, Z., Zheng, D., Yu, Y., Xiang, J., Ma, X., ... & Ren, Q. (2023). A cancer cell membrane coated, doxorubicin and microRNA co-encapsulated nanoplatform for colorectal cancer theranostics. Molecular Therapy-Oncolytics, 28, 182-196.
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Hi All, I am working with A549 cell line and trying to culture spheroids using low attachment 96 well plates. So far I have attempted some different seeding densities from 2000 to 10,000 cells and can either form very large spheroids (700-900um), which are more compact and have a spherical defined shape, or alternatively smaller spheroids (still fairly big though around 500um) are less compact and not completely spherical. However for my experiment where I wish to add drug compounds (2D IC50 approx 1uM) I am not observing significant size/morphology change on the larger spheroids despite at least a 10uM concentration for 1 week. I am thinking possibly I can try to treat smaller spheroids for a more obvious visual change. Does anyone know how i might successfully make small compact spheroids (less than 500um) which are reproducible with this cell line? Thanks in advance for any help someone may be able to provide.
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Of course, time is a significant factor for spheroids' size and viability of cells, due to when you seed the cells to the generation of spheroids after the cells are in the proliferative stage. More time (days) can lead to the big size of spheroids, in addition, the cells located in the core zone are suffered from nutrients, oxygen, and ...
I suggest you set up the best time to achieve reliable results too
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Other than "The Cancer Proteome Atlas (TCPA)" (https://tcpaportal.org/tcpa/index.html), which other cancer-based databases/tools can be used to associate a list of genes to identify different types of cancer.
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Antonis Tsintarakis thank you for your reply! I will look into the BEST tool you have suggested.
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Please spread the word: Folding at Home (https://foldingathome.org/) is an extremely powerful supercomputer composed of thousands of home computers around the world. It tries to simulate protein folding to Fight diseases. We can increase its power even further by simply running its small program on our computers and donating the spare (already unused and wasted) capacity of our computers to their supercomputation.
After all, a great part of our work (which is surfing the web, writing texts and stuff, communicating, etc.) never needs more than a tiny percent of the huge capacity of our modern CPUs and GPUs. So it would be very helpful if we could donate the rest of their capacity [that is currently going to waste] to such "distributed supercomputer" projects and help find cures for diseases.
The program runs at a very low priority in the background and uses some of the capacity of our computers. By default, it is set to use the least amount of EXCESS (already wasted) computational power. It is very easy to use. But if someone is interested in tweaking it, it can be configured too via both simple and advanced modes. For example, the program can be set to run only when the computer is idle (as the default mode) or even while working. It can be configured to work intensively or very mildly (as the default mode). The CPU or GPU can each be disabled or set to work only when the operating system is idle, independent of the other.
Please spread the word; for example, start by sharing this very post with your contacts.
Also give them feedback and suggestions to improve their software. Or directly contribute to their project.
Folding at Home's Forum: https://foldingforum.org/index.php
Folding at Home's GitHub: https://github.com/FoldingAtHome
Additionally, see other distributed supercomputers used for fighting disease:
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Vahid Rakhshan I will definitely spread the word about this amazing initiative. It's great to know that we can contribute to such a noble cause by simply utilizing our excess computer power. Thank you for bringing this opportunity to my attention. Let's join hands in making a difference in the fight against diseases.
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Anyone who has C26 tumor cells (cachexia-inducing, NOT the related Ct26) or knows where to buy/get them?
I want to induce cachexia in C57 mice with a tumor cell line that is not LLC but can´t find anywhere to buy the C26, everyone seem to have got it is as a gift from somewhere.
If someone has them, I would be very happy if you would share it with us and I will of course pay any shipping expences.
Thank you
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Hi,
C26 cells are from Balb/c background.
If you want to study cachexia in C57 background. You can use KPC model (intraspleenic or intrapancreatic models).
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I'm trying to write a java programme that will solve the system of ordinary differential equations using the Runge-Kutta fourth-order (RK4) technique. I need to solve a system of five equations. Those are not linear.
And determining all of the equilibrium solutions to this system of differential equations also requires.
Can someone help me? Thank you in advance.
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Hereby attached is a system of three Ordinary Differential Equations (ODE). We have to use numerical methods such as RK4 and Euler to obtain the results using Java. I think RK4 is better for this kind of problem. In this thread, Dudley J Benton has already mentioned C programming for this. It is really amazing.
For the parameter values, you can use your own values for your convenience.
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I am curious about the average quality of PhD research proposals, especially those with cancer research as a focus. Any suggestions, guidance, tricks, or words of wisdom?
Thank you.
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You should make sure that your research proposal in cancer is created meticulously, if you have to make it more appealing to prospective professors. The panel of experts should get convinced with regards to the significance of your research. The research proposal that you put forward should clearly project that you will be able to justify your research and that you will execute it as per the required standards.
In your introduction you should exemplify your problem which you will be attempting to resolve and emphasize its significance. You should prove to the panel of experts that you have a command on research in your field by providing them with an extensive review of existing literature. The research methodology should be chosen carefully, and you should justify why have you made such a choice so that the reader is convinced.
Effective management of time plays a crucial role, and therefore you should provide a realistic timeframe and the resources that you would require to complete your research. The research question should be very much clear to the panel of experts.
So, before you begin writing the PhD research proposal in cancer you need to have a detailed meeting with your guide to select the topic of research and the research methodology, both of which are of utmost importance. Plan your proposal and create a proper outline before you start writing. Extensive work must be done in reviewing the literature in your domain of research to understand the current gaps. This will help you to choose a unique topic, and you will not end up with a topic that has already being researched.
Good Luck!
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Hello, I am a new researcher working on an anticancer drug discovery.
I've been reading some papers that cytotoxicity assay is using IC50 as it results to measure the effectiveness of a compound in inhibiting biological/biochemical function.
but my senior colleague asked me to consider using LC50 for the results as well.
should I use the IC50 or the LC50? or both?
or you could give me some advice about the research I conduct at the moment.
Thank you
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IC50 and LC50, both are similar in relation to their measurement.
If you are planning to study the anti-cancer activity of the candidate compound on mammalian cells (invitro study), then you need to consider IC50. IC50 gives the informative measure of a drug's efficacy. It indicates how much drug is needed to inhibit a biological process by half, thus providing a measure of potency.
On the other hand, LC stands for lethal concentration usually referring to the concentration of a chemical which is used in environmental studies that involves groups of animals exposed to a concentration (or a series of concentrations) for a period of time (usually 4 hours). The animals are then clinically observed for up to 14 days.
The concentration of the chemical that kills 50% of the test animals during the observation period is the LC50 value. When an LC50 value is reported, it should also state the kind of test animal studied and the duration of exposure. For instance, LC50 (mouse) 5mg/m^3/2hr.
The killing effect of the candidate drug has a sigmoidal relationship with drug concentration, and this sigmoidal model would be a proper way to measure the effectiveness of a compound in inhibiting biological/biochemical function.
So, use IC50 for the cytotoxicity assay.
Best.
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This question is spurred by the different effects of BRCA1/2 vs. PARP.
Thanks in advance for insights.
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DNA repair pathways are involved in maintaining genetic stability and, in this respect, repair factors are to be considered as tumor suppressors. This applies to the BRCA1/2 genes, for which inherited mutations in one allele predispose to cancer. There is no paradox in the fact that PARP inactivation leads to the death of BRCA-deficient tumor cells. In this case where homologous recombination is impaired, cell survival relies on PARP-dependent backup repair processes. Apparently, here, PARP promotes tumor development but even in non-tumor HR-deficient cells, survival would depend on PARP. We just take advantage of this synthetic lethality phenomenon due to HR deficiency to kill cancer cells.
Anyway PARP functions are not restricted to DNA repair and it is possible that in some peculiar circumstances PARP may rather promote tumorigenesis.
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Evidence?
That possibility is raised in:
Monikaben Padariya, Mia-Lyn Jooste, Ted Hupp, Robin Fåhraeus, Borek Vojtesek, Fritz Vollrath, Umesh Kalathiya, Konstantinos Karakostis, The Elephant Evolved p53 Isoforms that Escape MDM2-Mediated Repression and Cancer, Molecular Biology and Evolution, Volume 39, Issue 7, July 2022, msac149, https://doi.org/10.1093/molbev/msac149
That would, if it were true, help explain Peto’s Paradox in relation to elephants.
On the other hand: resolution of Peto’s paradox would require co-evolution of genes species by species that impede cancers. Is that likely? Isn’t it more likely that there is a universal mechanism? For example:
What are your views?
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Dear Good people,
Which is better for publishing? To test the anti-cancer activity for a drug on a few proteins from two signaling pathways(one or two proteins by maximum for each pathway) or just multiply proteins from the same pathway(two or three proteins by maximum for each pathway)!...
I wish for sure to be able financially to target more in the future. Thanks in advance
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Try the STITCH protein network and KEGG to get a better decision. Let me collaborate with you computationally.
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Globally, there is a rising incidence of cancer, largely attributed to increased life expectancy. A Lancet paper emphasizes that disruptions in cancer screening, diagnosis, and treatment during the COVID-19 pandemic may lead to excess cancer deaths, potentially reversing the declining mortality trend for certain cancers.
Harvard Medical School researchers note that COVID-19 poses unique challenges for cancer patients, particularly due to weakened immune systems resulting from cancer or its treatments. This susceptibility increases the severity of COVID-19. Are cancer rates on the rise globally after COVID-19?
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It is increased due to alter body immune system by virus and drugs taken during infection
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Dear all,
I am working on EMT-invasion of cancer cells. I have observed changes in the expression level of ECM-associated genes. Upon submission of a manuscript, one reviewer suggested: " to investigate possible changes to the organization of cell-culture ECM and its ability to support cell migration or invasion".
Can anyone help me to understand this comment? How exactly (specific experiments) can we proceed? What is it that the reviewers want?
Thanks in advance,
Swarnali
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It's only one.
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Hi Everyone, I have query regarding the DFI event value (i.e., 1 or o). I know DFI event indicates recurrence event. But, I am getting confused whether DFI event 1 indicates recurrence or 0 indicates recurrence in the sample. my confusion arises because of DFS definition and in general survival event value meaning (where, 1 indicates dead while 0 indicate alive). It would be great help if someone can share some publication where it clearly indicated.
Thank You
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Good question . I thought it is 1. I hope following article will help you
Information regarding OS, DFI, DSS and PFI and their time ...
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Brain Tumor Imaging Protocol will reduce variability and increase accuracy in determining progression and response of investigational therapies.
In the pictures below, with the FFT and DFT methods and the PCA phase recovery, which is common in optical microscopes, I obtained the magnetic resonance imaging (MRI) phase of the human brain tumor and the phase obtained.
Can the process be performed on MRI without prescribing Jumpstarting Drugs (JBTDDC)?
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سلام عقیل عزیز
ایمیل بنده در قسمت نام کاربری موجود است
آرزوی موفقیت
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Dear Good People
Is it possible to study the effect of a compound on the activity of a certain signaling pathway but you only have antibodies for the total protein/nonphosphorylated form involved in that pathway! or it would be a waste of time and money?
"P.S."... No abs for the phosphorylated forms are available📷
Thanks in advance!
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Dear Doaa Yamani,
you could try to do immunoprecipitation experiments with, e.g., anti-phospho-Y or anti-phospho-S antibodies, to pull down all phosphorylated proteins in your samples. Then do western blotting and use your antibodies for the nonphosphorylated proteins to detect any enrichment after compound treatment of your cells.
There are several commercial kits available, but in principle it comes down to incubate your cell lysate with the first antibody that will bind to all phopsphorylated proteins in your sample (PY-20 detects phosphorylated tyrosine). Then you capture that complex with, e.g., Immunoglobulin binding Protein A or G coupled to either beads or agarose. After washing the pellet, resuspend your sample in sample buffer for western blotting, the bound proteins are released and loaded on the SDS gel. Detection is done with your antibodies for the nonphosphorylated proteins you mentioned in your question.
You have to be careful though during the detection step, since the Immunoglobulins (the heavy and light chains) used for the pull-down experiment can cause problems during the second detection step (check the species your antibodies are derived from to minimize cross-reactivity!).
Good luck with your experiments,
Christian
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The Boyden chamber protocol requires a high budget for us. We want to try modifying this test instead. Can we combine it with a protocol like the filter diffusion protocol?
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First of all, thank you for your reply. I'm going to do research on that. It took me so long to respond because of some health issues. Thanks for helping. Yuning Hou
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Hello,
I am conducting an experiment on testing the cytotoxicity of a drug on brain tumor cells. I am using Thermo Fishers alamarBlue reagent and measuring absorbance at 570nm/600nm to measure cytotoxicity. I have two questions:
-I have attached a photo of the equation that Thermo told me to use when calculating the % reduction. What does this equation mean?
-One of my supervisors is doing the same experiment but with different cells, she calculates percentage by merely averaging the blank values (Media + alamarBlue reagent) at 600nm and subtracting that from 570nm readings.
when it comes to calculating the IC50 value, which method is more accurate? because bot methods give totally different values.
I have attached the protocol from Thermo and the photo of the equation given by Thermo
Any help will be very much appreciated!
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If you use the absorbance differences (the absorbance of the sample minus the absorbance of the control) at each wavelength, you would require a different equation to calculate the % reduced. The equation you showed earlier includes the control absorbances, so you should enter them into the equation.
As for the protocol used by your supervisor, I don't think any calculation of % reduced is involved. It simply uses the change in the absorbance measurement at 570 nm (minus the background from the culture medium, measured at 600 nm) to represent the degree of reduction. The extinction coefficient at 570 nm of reduced Alamar Blue is higher than that of oxidized Alamar Blue by almost 2-fold, so the more reduction occurs, the more the absorbance at 570 nm increases. To be honest, I don't understand why the background from the culture medium measured at 570 nm instead of 600 nm isn't subtracted in this method.
If you want to, it would actually be pretty easy to derive equations for the concentrations of oxidized and reduced Alamar Blue from absorbance measurements at 570 and 600 nm and the provided extinction coefficients if you first subtract the background from the culture medium at each wavelength (in other words the ∆absorbances.) It just involves a pair of equations and high school algebra for dealing with simultaneous equations.
∆A570 = (E570,ox)Cox + (E570,red)Cred
∆A600 = (E600,ox)Cox + (E600,red)Cred
where C stands for concentration and E stands for extinction coefficient.
To solve for Cred, for example:
Cox = [∆A570 - (E570,red)Cred]/(E570,ox)
Cox = [∆A600 - (E600,red)Cred]/(E600,ox)
[∆A570 - (E570,red)Cred]/(E570,ox) = [∆A600 - (E600,red)Cred]/(E600,ox)
Cred = [∆A570(E600,ox) - ∆A600(E570,ox)]/[(E570,red)(E600,ox) - (E570,ox)(E600,red)]
The denominator is a constant, with the value 1.706 x 1010 in whatever units the given extinction coefficients are in, presumably M-1cm-1. Putting in all the constants gives:
Cred = (6.896 x 10-6)∆A570 - (4.739 x 10-6)∆A600
Convert from molar to micromolar to get rid of the 10-6s, and
Cred = (6.896)∆A570 - (4.739)∆A600.
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Hi
Is there anyone who has experience of culturing resected cancer tissue?
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You may refer to the article attached below wherein the investigators presented an ex vivo culture system for precision-cut slices of human pancreatic cancer. They have tried to establish conditions that allow successful culturing of pancreatic ductal adenocarcinoma with good tissue viability in a reproducible manner.
Best.
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Because in my experiments even by adding adhesive molecules such as collagen, gelatin, fibronectin I always get cell aggregates and not adhesion as in the plate. Could the stiffness of the gel have something to do with it? Or is it difficult to see stretched cells on the gel?
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Antony Ieva When you add your cells to a hydrogel, the 3D internal structure will provide multiple points of contact for the cell to adhere unlike a 2D monolayer where the cell is stretched out and has contact with the one side of the TC plate.
If your cell density is low, initially the cells will appear as spheres similar to cells when they are trypsinised and in suspension. To visualize cells stretching out into their original shape, you will have to culture them for long time for example, 2-3 weeks. The cells will form clusters (high cell density) or remain in spherical form (low to medium cell density) in the first week.
Another consideration in the stiffness of your gel. Since A549 are lung epithelial cells, you may find references to native lung tissue ECM stiffness (compression modulus) and make your gels in a similar stiffness range.
As long as your cells do not die and not crawl out of your gel, they are fine and have adhered to the gel. if your gels are translucent enough, you can stain your cells with Rhodamin-phalloidin/DAPI and perform confocal /multiphoton imaging (after 2 weeks) to check the actual cytoskeleton to give you better understanding.
Hope this helps
All the best.
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Please take a look at the attached file.
I irradiated cells using a fractionation regime of 3 x 1 Gy after exposure to a substance in different concentrations.
I made an XY table with the determined SFs and plotted a graph using the LQ-model.
The equation I used was Y=exp(-3*(A*3*X + B*3*X^2)). Its an edition of the provided equation Y=exp(-1*(A*X + B*X^2)) in regard to the fractionation regime.
To determine the AUC I used the standard analyzing tool that Graphpad provided.
Could someone tell me, if this is right or if I mistaken somewhere?
Tank you very much in advance!
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There are two, very different, ways to model an LQ model. The first assumes that the fractionated curve continues along the single dose curve. The second assumes that there is full recovery from each fraction and therefore the initial curve is repeated from the previous dose SF. The area between these curves is called the "envelope of additivity". See G.G. Steel or Peckham and Steel for more on this addition of survival curves for multifractionated doses. Interestingly, ionizing radiations (with shouldered survival curves) tend to repeat the initial portion of the curve (so-called repair of sublethal damage, but actually split-dose recovery), while some alkalizing agents, such as Bleomycin, have their curve continue along the single-dose curve (no split-dose recovery).
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I have been finding the proof that this epitope called NLVPMVATV does not induce cytokine storm for days, but in vain. Could anyone please help me? I really need a reference paper to support this or else my project will be in a great trouble.
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Hi,
Check the references below:
HCMV UL83/pp65 (NLVPMVATV)
CMV pp65 peptide NLVPMVATV (HLA-A*0201) is a single peptide for stimulation of T cells. The peptide from human cytomegalovirus (CMV) phosphoprotein (pp65) is synthesized as it is presented by the MHC class I HLA-A*0201 allele and can be used for targeted in vitro generation and expansion of antigen-specific CD8+ T cells.
Reference:
"Although the anti-pp65 antibodies and the pp65 antigens are detected in immune-depressed patients with active viral infection [16], the antibody response to the pp65 antigen in normal infected individuals is not always detectable by immunoblotting [17]. It has been reported that the pp65 antigen is targeted by a cell-mediated immune response and that its vaccination can induce a pp65-specific CTL response"
Reference:
Hope it helps,
Best regards
Tomasz
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I saw many papers are introducing or immunizing mice with ovalbumin (OVA), will this induce a cytokine storm? Is there any paper suggesting that OVA doesn't induce cytokine storm? I've been searching this for days, please help.
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No, there are essentially 3 major types of immune response to infection: an antiviral response which illicits interferon, a pro inflammatory response that makes il1, il6, tnfalpha etc wich is normally directed against bacterial and fungal infections ( and can lead to cytokine storm) and then the allergic response directed against allergens like ova that generates il4, il10, il13.
In mouse models, balb/c mice are typically used to study allergic responses as thy are inherently more allergic and c57bl/6 are used to study proinflammatory responses and diseases because they are inherently more prone to this type of immune reaction.
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As I know, smoking can cause lung cancer and body cells turn into cancer cells due to mutations. However, what is the name of the carcinogenic substance in cigarettes and how can it make body cells mutate?
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Benzo[a]pyrene (BP) is one of several ring-shaped chemicals called polycyclic aromatic hydrocarbons that are produced when organic matter, such as a tobacco leaf, is burnt. When it enters the body, BP becomes a powerful DNA disruptor, producing mutations that can lead to cancer.
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Hey everyone,
I am looking for a way to show truncating mutations in BRCA1/2 via IHC. The idea is to use two slides per sample for each of BRCA1/2, respectively. In theory, samples that have a truncating mutation should show expression on the N-, but not C-terminal IHC slide.
I also found the following publication (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799150/) by Watson et al. (2009), where they developed a IHC antibody that specifically targets the BRCA2-C terminal region, and showed that this method worked for them.
Unfortunately, the paper is a couple years old - and I cannot find this antibody anywhere - or any other BRCA2-C antibody. There are some that use aa 2400 as the immunogen, but I am looking for something more in the region of aa 3000 to really include all truncations.
Has anyone implemented a similar assay to allow for quick and easy IHC of FFPE samples to check for truncating BRCA1/2 mutations?
Thank you for your help!
Sincerely,
Marcel
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Fortis Life Sciences (Bethyl Labs antibodies) has Rabbit pAb anti-BRCA2 where they describe the immunogen as "between 3350 and C-term": http://www.fortislife.com/p/A300-005A
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We need your expertise & opinion!
Please fill in this questionnaire:
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Is best to prevention also to treatment.
The best test option for screening of CRC is FIT test and consecutively colonoscopy.
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Dear fellow researchers,
I wanted to know if I should use basal media for preparing working concentrations of paclitaxel, cisplatin and 5 fu. Are these drugs sensitive to FBS in media? How much percent FBS is allowed to be added along with drugs in basal media. Thanks in advance!
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In some previous work I did with paclitaxel, we dissolved it in DMSO (5 mg/mL). Dissolving drugs directly into media is the most ideal method as you have less controls to deal with. However, if you choose to use a solvent like DMSO or ethanol which provide better solubility for many drugs, just be sure to include a control that contains the same percentage of DMSO/ethanol dissolved directly into media alone (without drug) to account for any background noise when running plates, etc. Yes, you will eventually have to dilute your working stock solution in media in order to actually treat the cells. Hope that clarifies things. All the best!
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I want to know:
  1. if microbes play any role in increasing cancer stemness and metastasis.
  2. do they increase cross-talk in the tumor microenviroment
  3. any other way microbes increases lethality of cancer
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Microbiota influence many aspects of our health including our cancer risk. Since both microbes and cancer cells rely on incoming resources for their survival and replication, excess energy and nutrient input from the host can play a role in cancer initiation and progression.
Metastasis, in this view, is a secondary disease that affects the initial tumor cell. The original cell's cell cycle is disrupted, yet it has no desire to leave its source. According to the fusion theory, a healthy migratory leukocyte merges with a primary tumor cell, resulting in the acquisition of a metastatic phenotype. The resulting hybrid, like the original cancer cell, has the ability to travel across the body of a white blood cell while dividing uncontrollably
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More women in the U.S. are choosing to have their breasts removed for early cancers instead of breast-conserving procedures that deliver equal results, according to a new study.
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Hello Researchers,
What is the most appropriate way to analyze the IC50 and Percent Inhibition of the MTT test by the GraphPad Prism in 2022?
With kind regards,
José.
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Hello Jose,
I usually use Graphpad prism 6, however, I hope the latest version does not vary that much.
I used to calculate the % of viability by using an excel template first, then I paste the viability% values in prism.
Please find the steps below from my lab book that may help you how to plot the dose-response curve and how to calculate IC50.
gOOD lUCK
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Could someone kindly clarify why aerobic glycolysis is required for cancer cells? That is, if tumor cells used OXPHOS, would they be unable to grow and metastasize as well?
The most commonly cited benefit of aerobic glycolysis seems to be accelerated glucose uptake, but why is this required for long-term growth as opposed to short-term spurts? The timeline for cancer progression is normally months or years, not hours or days.
Moreover, despite consuming glucose faster, total ATP production from aerobic glycolysis is lower. That is, during the time OXPHOS consumes 1 glucose molecule, aerobic glycolysis may consume 13 glucose molecules -- yet this yields fewer ATP molecules.
If correct, total energy production inadequately explains the relationship between cancer cells and aerobic glycolysis.
Is the timing of ATP essential? Perhaps cancer cells need fewer shots of ATP molecules but at a higher frequency rather than wait for one large batch from OXPHOS?
Or what are the other benefits of aerobic glycolysis over OXPHOS?
Ultimately, why would cancer cells be less successful with OXPHOS?
Thanks in advance for your help.
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Entire models ogf glycolysis and TCA cycle are created by figment of imagination of lactate production and ATP are the products of glucose catbolism. The models were initially developed by Canbridge school of thought on lactic acid and CO2 production, later Usurped by Warburg. Ironically protagonists and antagonists of lactic acid theory of energy and lactate production became prisoner's of this misguided notion. The models were based on the assumption that stress induced phosphate uptake promotes glycolysis and fermentation, a misinterpretation of his own experiments by Harden. Neither glucose, nor glucose polymers are the source of alcohol production. Th errors were was extrapolated by Warburg's discover of DPN and TPN as thermostable cofactors. It's the fructose which is the source of alcohol. Harden's work was also taken as model for glycolysis, both by experimental scientists and mathematical modellers. These models assumed that glucose is the energy source, and devided glucose catabolism into two blocks: Sugar ---(Block 1)---- FbisP ---( Block 2)----CO2 by Meyerhof, hill, Cories, and Warburg in experimental models, and Fell and Martin Brand and co-workers in Mathematical models. (See Keith manchester's article in TIBS 25 – FEBRUARY 2000). In the name of refining the unanswered qustions in Harden's work, they created a simplistic view of metabolism and created irrepairable confusions in basic science of cell metabolism.In fact, Fructose, Phosphate and Lipolysis (autophagy) devide the glycogen resrves into four blocks, which converge on alcohol priduction on one hand, and Glyceraldehyde-3phosphate on the other. Somatic cells activate RNA synthesis to remodel metabolism to incorporate nutrient metabolites into biomass. Inhibition of Nucleic acid synthesis promotes, gluconeogenesis, lipogenesis, and protein synthesis, which promotes cell differentiation and homeostasis. The puzzles of Covid Vaccines and the delta variant and O-micron variants emerge, as ROS generated are likely to induce alterations in viral genome during RNA synthesis, which manifests in altered viral capid phenotype!
Although Meyerhof, Hill and Cori couple altered their opinions on the role of aldolase, and pyruvate kinase, cancer Biologists are still struggling with "understanding Warburg effect"," reversible Warburg effect". and "Hall marks of cancer still emerging". These workers generate extensive data try to look to their results through Warburg lens not through their own eys and Brain. Unless this attitude is altered, the basic science will be on a wrong path, we face more tortuous Pandemics in future, with aggressive markets chasing for alibies to .make money
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What are the limitations and disadvantages of Real-Time PCR (RT-PCR)?
What is a more specific and sensitive technique that can be used in the laboratory instead, particularly in cancer diagnosis?
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The limitations of Real-Time PCR are as follows:
1. High false-negative due to presence of amplification inhibitors. This holds true for pathogen detection particularly, for new emerging or highly variable pathogen.
2. The multiplexing is still limited in Real-time PCR.
3. The variation increases with the number of cycles.
4. The overlap of emission spectra.
5. The occurrence of non-specific binding particularly, when carrying out SYBR green analysis.
6. The PCR product increases exponentially but one cannot monitor the amplicon size.
7. Kits are not available for all kinds of genes and disorders.
8. It needs specialized laboratories, operated by highly trained technicians for developing novel qPCR assays, which makes it too costly and difficult to scale up.
You could use other techniques that could be performed in the laboratory.
1) Fluorescence In Situ Hybridization (FISH), also known as molecular cytogenetic testing, is a way to visualize and document the location of genetic material, including specific genes or DNA sequences within genes. FISH is used to look for the presence, absence, relative positioning, and/or number of specific DNA segments under a fluorescence microscope. FISH is particularly helpful in identifying copy number variations, especially translocation and amplifications.
2) Comparative genomic hybridization (CGH) is a special FISH technique (dual probes) which is applied for detecting all genomic imbalances. CGH is used to determine copy number alterations of genome in cancer and those cells whose karyotype is hard or impossible to prepare or analyze.
3) Single Strand Conformational Polymorphism (SSCP) is one of the simplest screening techniques used for detecting unknown mutations (microlesions) such as unknown single-base substitutions, small deletions, small insertions, or micro inversions. A DNA variation causes alterations in the conformation of denatured DNA fragments during migration within gel electrophoresis. The logic is comparison of the altered migration of denatured wild-type and mutant fragments during gel electrophoresis.
4) Heteroduplex analysis in which a mixture of wild-type and mutant DNA molecules is denatured and renatured to produce heteroduplices. Homoduplices and heteroduplices show different electrophoretic mobilities through nondenaturing polyacrylamide gels.
5) Denaturing Gradient Gel Electrophoresis (DGGE) has been used for screening of unknown point mutations. It is based on differences in the melting behavior of small DNA fragments (200-700 bp); even a single base substitution can cause such a difference.
6) DNA microarrays can detect thousands of genes at once. DNA “chips” or microarrays can be used to test for multiple mutations. In this technology, single DNA strands including sequences of different targets are fixed to a solid support in an array format. On the other hand, the sample DNA or cDNA labeled with fluorescent dyes is hybridized to the chip. Then using a laser system, the presence of fluorescence is checked; the sequences and their quantities in the sample are determined.
7) Use of Next Generation Sequencing (NGS) allows comprehensive description of germ-line DNA, analysis of somatic mutations and RNA profiles in naturally occurring tumors, systematic analysis of microbiomes, etc. The resulting data can help in the identification of novel hereditary syndromes, molecular targets for cancer therapy, tumor-specific diagnostic markers, etc. But this technique would be expensive to work with.
Best Wishes.
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Hello, I am trying to apply vcftools --diff in order to extract the different variants between two VCF files.
vcftools --vcf marked_I_tumor-pe.vcf --diff marked_I_normal-pe.vcf --diff-site --out t_v_n
I am getting this as result :
VCFtools - 0.1.16 (C) Adam Auton and Anthony Marcketta 2009 Parameters as interpreted: --vcf marked_I_tumor-pe.vcf --out out.diff.sites --diff marked_I_normal-pe.vcf --diff-site Comparing sites in VCF files... Found 75584 sites common to both files. Found 419593 sites only in main file. Found 84102 sites only in second file. Found 2908 non-matching overlapping sites. After filtering, kept 498085 out of a possible 498085 Sites Run Time = 6.00 seconds 0
I want to extract these 419593 sites which only belong to the main file (the first file) do you know if there is a way to do that? Can these sites that I want to extract be in a new vcf file? If you could help me, I would be more than thankful!
Thanks
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Run the vcf-isec command along with the -c option. For example, to get the variants present only within your tumour samples, try inputting "vcf-isec -c marked_I_tumor-pe.vcf marked_I_normal-pe.vcf > tumor_only_variants.vcf", and for normal variants only, just swap the order of the input vcf files. Hope the above helps.
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I have two vcf files corresponding to the results of healthy tissue and tumor tissue. I want to compare these vcf files and remove their similarities. More specific I want to remove the information of the healthy tissue from the tumor one. Have you any suggestions on which tool I should use or any way that I can do my analysis?
Thanks in advance.
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Hello everyone,
I am fairly new to cell culturing. For my experiments, I plate cells in 35 mm dishes. A crucial step in data analysis is cell-segmentation using the Stardist plug-in on ImageJ. However, I am struggling to obtain proper segmentation because all my cells tend to grow in clusters, making the segmentation processes highly unprecise.
To overcome this, when plating cells, I'd like to obtain single cells (similar to the image I attached.)
Does anybody have any suggestion on how this can be done?
I usually work with OVCAR cells.
Thank you in advance,
Giammarco
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Wash the cells with PBS without Ca2+/Mg2+ at the time of trypsinization and preferably use trypsin with EDTA. Clumps form because of the presence of free DNA in cell suspension which are released from dead cells. Free DNA attracts cells which bind altogether forming clusters.
You can use DNase I at concentrations from 20-100µg/ml to avoid formation of clusters. For each cell type, the working concentration must be determined individually.
Hope this is helpful.
Best.
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Some drugs/ carcinogen cause mutation in DNA, Which carcinogen causes highest mutation in genome?
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Hi Amrit,
The most commonly mutated gene in people with cancer is p53 or TP53. More than 50% of cancers involve a missing or damaged p53 gene. Most p53 gene mutations are acquired. Among most active carcinogenic mutagens the championship title belongs to polycyclic aromatic hydrocarbons (PAHs). These are the most abundant indirect-acting carcinogens to which humans are exposed to on a daily basis. Exposure has been associated with the development of breast, skin or lung cancer. Bioactivation of PAHs is required in order for these agents to exhibit mutagenic properties, which is primarily mediated by cytochrome P450 enzymes (among many others, our data on this subject - in http://www.xenobiovir.com/). Bioactivated metabolites target multiple genomic sites, including guanine and adenine bases via PAH diol epoxides. This results in the generation of bulky BPdG chemical DNA adducts; examples include quinone-mediated cross-linking of N7 position of guanine and N3 of adenine.
All the best,
Ilya
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I am planning a study where I want to select a few potential miRNAs that are responsible for inhibiting protein translation from a particular gene.
I am new in this area so it would be helpful for me if I get some guidance on how to select the miRNAs for a specific gene and if there is a way to determine miRNA and mRNA interactions with any bioinformatics tool before moving forward.
I have selected a few miRNAs for my gene from TargetScan, Mirdb, and Mirtarbase but I want some other opinions.
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One paper that I can recommend on this particular study is this one:
Especially, the molecular simulation part. You can try it
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I am updating my earlier review on the role of Fluoride doped Hydroxyapatite in Cancer and my current focus is on Psammoma Bodies which have been found, and identifed as high risk, in a very wide range of Cancers. These include Cancers of the Bone, Spine, Brain, Choroid Plexus, Dura Mater, Gliofibroma, Medulloblastoma, Meningioma, Cervix and Endometrium, Ovary, Kidney, Lung, Mesothelioma, Pancreas, Skin, Hemangioendothelioma, Olfactory Neuroblastoma, Duodenal Somatostatinoma, Stomach and Thyroid. Early studies did not have the benefit of advanced analytical techniques, or did not even consider the Fluoride content or composition of the mineralization. Can anyone help by supplying analytical data based on Raman spectroscopy, neutron activation, x-ray or wet analysis?
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Hello, Dear Geoff.
We continue to work on the subject you mentioned. There are methods that can analyze this.
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We want to know if one protein can be used as a breast cancer biomarker or not. So we'll have to compare normal and patients, and our question is whether we can get samples from patients who received chemotherapy before?
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thank you for answring my quesion dear Dr Erum Zafar
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I am working with differentially expressed miRNAs where I only have the name of the mir itself without further details, for example mir-204.
Now for target prediction analysis using databases, there is mir-204-3p and mir-204-5p based on the 3p/5p strand position (forward or reverse). Regarding the functionality of both strands, it seems that both could be biologically functional, yet I read somewhere (https://www.biostars.org/p/150526/) that the 5p is the original arrangement and therefore it is more likely to be the active option. Is it reasonable to conclude that I should always take the 5p strand, or should I maybe take both into consideration?
Would appreciate your insight on this matter!
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If you got your miRNA of interest based on data from a previous study, and want to know if it corresponds to 5p/3p in the current miRBase relase, you can do the following: first, lookup the old miRNA ID in older miRBase releases and retrieve its sequence; then, do a search in miRBase using the retrieved sequence, and see to which mature miRNA it corresponds to.
In your case, mir-204 (from e.g. miRBase v.17) corresponds to mir-204-5p (miRBase v.22).
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perhaps the most useful aspect of epigenetic processes is that they are readily reversible. Unlike genetic effects that also play a role in cancer and aging, epigenetic aberrations can be relatively easily corrected. One of the most widespread approaches to epigenetic alterations in cancer and ageing is dietary control. now, I would like to know more about the types and mechanisms of that nutrition that have a positive impact on epigenetic alteration during cancer???
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thank you, dear Shin Murakami for your sugession
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Dear Community,
we transplant (stem) cells to the mouse brain and would like to exclude that these transplants may cause a tumor. What are straightforward methods to assess/exclude tumor formation in the mouse brain?
The tissue is 4% PFA fixed and cut in 40um coronal sections.
Thank you for your help!
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With time, tumor growth produces major tissue disruption that hematoxylin/eosin or trichrome staining will show clearly in comparison with controls and non-tumor implanted samples. 40 um sections may be a bit too thick for high mag, high resolution imaging, however. The attached paper reference shows examples of the disruption.
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MMR - Immunostaining shows loss of MLH1 and PMS2 in the invasive carcinoma. There is positive nuclear staining with MSH2 and MSH6. CDX2 is negative.
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A mismatch repair deficiency in an advanced tumor does not necessarily mean a Lynch syndrome. It can just be a late mutation. Some authors consider this under the name of mutator mutations. As a Karolin Heinze says above you need to test the patient for germline mutations.
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crRNA is responsible for recognizing and binding the sequences next to protospacer-adjacent motif (PAM), NGG, on the target DNA, whereas tracrRNA is essential to maintain cas9 nuclease activity. and most of the miRNA does not contain the PAM sequence (5’-NGG-3) 4. so how can you target them by using CRISPR Cas system?
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