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Cancer Research - Science topic

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Breast cancer continues to pose a significant global challenge to women's health. Fortunately, with the continuous progress in science and technology, our understanding of the disease and treatment methods has been deepening. As a dedicated cancer research journal, Oncology Research is committed to disseminating the latest advancements in breast cancer research. Our goal is to empower patients, physicians, and researchers with the knowledge necessary to better understand and respond to this serious disease.
Over the past two years, we have proudly published a series of pivotal breast cancer research papers, showcasing exceptional work from renowned scientists worldwide. With rigorous screening, our team has curated a selection of significant papers on breast cancer published between 2022 and 2023. These articles encompass a wide range of aspects, including early diagnosis, personalized treatment, immunotherapy, and more. By delving into these innovative studies, we aim to provide valuable insights into breast cancer development, novel treatment approaches, and preventive strategies.
Join us in exploring these cutting-edge research findings, enabling us to collectively advance our knowledge and make meaningful progress in combating breast cancer.
01.Has_circ_0000069 expression in breast cancer and its influences on prognosis and cellular activities
GANG WANG, MINGPING QIAN, WEI JIAN, JUHANG CHU, YIXIANG HUANG*
02.An inflammatory-related genes signature based model for prognosis prediction in breast cancer
JINGYUE FU, RUI CHEN, ZHIZHENG ZHANG, JIANYI ZHAO, TIANSONG XIA*
03.Targeting triple-negative breast cancer: A clinical perspective
LAZAR S. POPOVIC*, GORANA MATOVINA-BRKO, MAJA POPOVIC, KEVIN PUNIE, ANA CVETANOVIC, MATTEO LAMBERTINI
04.Senescent mesenchymal stem/stromal cells in pre-metastatic bone marrow of untreated advanced breast cancer patients
FRANCISCO RAÚL BORZONE*, MARÍA BELÉN GIORELLO, LEANDRO MARCELO MARTINEZ, MARÍA CECILIA SANMARTIN, LEONARDO FELDMAN, FEDERICO DIMASE, EMILIO BATAGELJ, GUSTAVO YANNARELLI, NORMA ALEJANDRA CHASSEING*
05.The role of AFAP1-AS1 in mitotic catastrophe and metastasis of triple-negative breast cancer cells by activating the PLK1 signaling pathway
SHUIZHONG CEN, XIAOJIE PENG, JIANWEN DENG, HAIYUN JIN, ZHINAN DENG, XIAOHUA LIN, DI ZHU, MING JIN6, YANWEN ZHU, PUSHENG ZHANG, YUNFENG LUO, HONGYAN HUANG*
06.Integrative multiomics analysis identifies a metastasis-related gene signature and the potential oncogenic role of EZR in breast cancer
GUODONG XIAO, FENG CHENG1, JING YUAN1, WEIPING LU1, PEILI WANG2, HUIJIE FAN1*
07.circRNAs in drug resistance of breast cancer
SEMA MISIR*, SERAP OZER YAMAN, NINA PETROVIĆ, CEREN SUMER, CEYLAN HEPOKUR, YUKSEL ALIYAZICIOGLU
08.The Implication of microRNAs as non-invasive biomarkers in 179 Egyptian breast cancer female patients
NADIA Z. SHAABAN, NASHWA K. IBRAHIM, HELEN N. SAADA, FATMA H. EL-RASHIDY, HEBATALLAH M. SHAABAN, NERMEEN M. ELBAKARY*, AHMAD S. KODOUS*
Thank you for your time.
Sincerely,
Oncology Research Editorial
Contact Us:
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Henderson, Nevada, 89052, US
Tel: +1 702 673 0457
Fax: +1 844 635 2598
Office Hours: 9:00-17:00 (UTC -8:00)
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Vishwas Chavan Sun Sheng Thanks for sharing.
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Dear Colleagues and friends,
as Co-Chairman, I would like to invite you to join us and present your work at the VII INTERNATIONAL CANCER IMMUNOTHERAPY CONFERENCE (CICON23) – TRANSLATING SCIENCE INTO SURVIVAL, which will be held in Milan from September 20th to 23rd, 2023.
Launched in 2015, under the patronage of the Cancer Research Institute (CRI), the American Association for Cancer Research (AACR), and the European Network for Cancer Immunotherapy (ENCI), the Conference continues to provide groundbreaking discoveries, being the ideal place to promote the fast- moving field of immunology and immunotherapy.
We have assembled a line-up of outstanding speakers, including the Nobel Laureate Jim Allison together with Arlene Sharpe, Tony Ribas, Lisa Coussens, Nir Hacohen, Padmanee Sharma, Ozlem Tureci, Laurance Zitvogel, and Shannon Turley just to name a few. At the same time, we dedicated slots for talks selected from the best abstracts, opportunities for short oral posters presentations, and ample time to discuss the data.
Our goal is to provide an exciting and unique opportunity for all attendees, students, postdocs and PIs, to meet top scientists and talk with colleagues in an informal environment.
Some additional information about the Scientific and Social Program could be found on the site, http://www.cancerimmunotherapyconference.org/program-of-events
You can submit your abstracts here: http://www.cancerimmunotherapyconference.org/abstracts, till the 15th of June, 2023, so, please, use your chance and submit your abstract now!
We particularly encourage students and postdocs to attend the conference and, in order to facilitate their presence, we offer special registration rates and travel bursaries, which can be applied for during the abstract submission., so, get your ticket now for the early bird price!
If you have any questions or need further information, please do not hesitate to contact me.
I look forward welcome you at the COCON23!
Best regards
Dr. Pier Francesco Ferrucci
Chair CICON23,
President of the Italian Network Tumor Bio-immunotherapy (NIBIT),
Scientific Director Grazia Focacci Foundation,
SEMM Faculty,
Director of Tumor Biotherapy Unit,
IEO - Istituto Europeo di Oncologia - IRCCS
Via Ripamonti 435 - 20141 Milano, Italia
If this message does not display properly, please click here to view it online in your browser
ABSTRACT SUBMISSION DEADLINE JUNE 15, 2023
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I will be pleased to attend this congress. Thanks a lot.
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Anyone knows name of a journal for cancer research where I can publish freee of cost or low cost.
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Indian Journal of medical and Paediatric Oncology
Journal of Cancer Research and Therapeutics
South Asian Journal of Cancer
Journal of Cancer Research and Practice
Clinical Cancer Investigation Journal
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Dear Colleagues and friends,
as Co-Chairman, I would like to invite you to join us and present your work at the VII INTERNATIONAL CANCER IMMUNOTHERAPY CONFERENCE (CICON23) – TRANSLATING SCIENCE INTO SURVIVAL, which will be held in Milan from September 20th to 23rd, 2023.
Launched in 2015, under the patronage of the Cancer Research Institute (CRI), the American Association for Cancer Research (AACR), and the European Network for Cancer Immunotherapy (ENCI), the Conference continues to provide groundbreaking discoveries, being the ideal place to promote the fast- moving field of immunology and immunotherapy.
We have assembled a line-up of outstanding speakers, including the Nobel Laureate Jim Allison together with Arlene Sharpe, Tony Ribas, Lisa Coussens, Nir Hacohen, Padmanee Sharma, Ozlem Tureci, Laurance Zitvogel, and Shannon Turley just to name a few. At the same time, we dedicated slots for talks selected from the best abstracts, opportunities for short oral posters presentations, and ample time to discuss the data.
Our goal is to provide an exciting and unique opportunity for all attendees, students, postdocs and PIs, to meet top scientists and talk with colleagues in an informal environment.
Some additional information about the Scientific and Social Program could be found on the site, http://www.cancerimmunotherapyconference.org/program-of-events
You can submit your abstracts here: http://www.cancerimmunotherapyconference.org/abstracts, till the 15th of June, 2023, so, please, use your chance and submit your abstract now!
For registration please go to: http://www.cancerimmunotherapyconference.org/registration.
We particularly encourage students and postdocs to attend the conference and, in order to facilitate their presence, we offer special registration rates and travel bursaries, which can be applied for during the abstract submission., so, get your ticket now for the early bird price!
If you have any questions or need further information, please do not hesitate to contact me.
I look forward welcome you at the COCON23!
Best regards
Dr. Pier Francesco Ferrucci
Chair CICON23,
President of the Italian Network Tumor Bio-immunotherapy (NIBIT),
Scientific Director Grazia Focacci Foundation,
SEMM Faculty,
Director of Tumor Biotherapy Unit,
IEO - Istituto Europeo di Oncologia - IRCCS
Via Ripamonti 435 - 20141 Milano, Italia
ABSTRACT SUBMISSION DEADLINE JUNE 15, 2023
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I am really interested to participate but I have no fund for registration and accommodation
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Hi,
I have been having difficulties in monitoring CAF activation because the lung fibroblasts Wi-38 that I am using seem to already have high levels of expression of a-SMA, FAP and PDGFRb, according to my Western Blot. I am not sure if it has to do with the origin of the cells or the cell culture conditions that are activating them. Any guidance will be greatly appreciated!
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Monitoring cancer-associated fibroblast (CAF) activation can be challenging, especially when using fibroblasts derived from different sources. In general, it is believed that CAFs are primarily derived from activated resident fibroblasts in the tumor microenvironment, although some evidence suggests that they can also be derived from bone marrow-derived cells or other cell types.
When it comes to choosing between adult fibroblasts and fetal fibroblasts for monitoring CAF activation, it really depends on the type of cancer and the stage of tumor development being studied. CAFs have been shown to exhibit different phenotypes and molecular markers depending on the tumor type and stage, which can affect the choice of cell type for monitoring CAF activation.
For example, CAFs derived from adult lung fibroblasts may be more relevant for studying lung cancer, while fetal fibroblasts may be more relevant for studying embryonic or pediatric tumors. However, it's important to note that fetal fibroblasts may not accurately represent the CAFs that are present in the tumor microenvironment of adult patients.
Regarding your issue with high levels of a-SMA, FAP, and PDGFRb expression in the Wi-38 cells you are using, it's possible that the culture conditions are contributing to the activation of these cells. Fibroblasts can become activated in response to various stimuli, including growth factors, extracellular matrix components, and mechanical stress. Therefore, it may be helpful to review the culture conditions you are using and adjust them as needed to minimize the activation of your cells.
In addition to Western blot analysis, there are other techniques available for monitoring CAF activation, including immunofluorescence staining, qPCR, and functional assays such as migration and invasion assays. It may be helpful to use a combination of these techniques to gain a more complete understanding of CAF activation in your experimental system.
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I have been culturing 293T cells since last 2 years and never had this issue. They develop multiple vesicles seeding after 2-3 days, fail to grow and degenerate. I have tried changing media with fresh cells, but with same results. Are they infected or some other deficiency ? Kindly refer to the attached pics. 
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I am facing the exact problem on my 293t as well. probably it’s because of the culture medium since I have ready brought it for over half a year. Going to try the addition of sodium pyruvate and glutamate in my culture medium
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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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I've used a drug that I am suspecting increases cell migration. I've got data of area at 0 hour and 24h of a scratch assay. I've got many replicates but can't seem to figure out the best strategy for statistical analysis. Any suggestion with some brief explanation?
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Dear Hammad
First, record the number of migrated cells in every replicate for treated and untreated samples using image analysis tools (e.g. ImageJ and the like), Then you can utilize unpaired t-test to make a statistical comparison. However, if you have employed more than one concentration of the drug of interest, you must use one-way ANOVA (followed by tukey's post-test) to compare the performance of different concentrations (including zero concentration=untreated group). I suggest to use GraphPad Prism as a simple and straightforward statistical software.
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Hello PCa research community,
I am searching for an appropriate prostate epithelial cell line to use as a non-cancerous, non-tumorigenic, control for my PCa experiments. I came across the RWPE-1 cell line as a commonly used control in my literature reviews. I cannot seem to find it being sold on any of the well known vendors (ATCC, Sigma, etc). Does anyone who works with this cell line know of where I can reliably purchase a vial?
Alternatively, ff anyone is willing to share a vial with our research group, we'd also be incredibly grateful!
All the best,
Isaac
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Hi Isaac
In my group we actually use the cell line PNT-2, which is also an immortalized prostate tissue cell line. It's available from sigma
Hope it suits you
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I got an invitation through email to attend this conference. Exaggerated statements like "The entire World Cancer 2023 team is enthusiastic about your work" made me suspicious of this conference and if it is another spam. Anyone has an experience can tell us about this conference?
@bobkeller
Thanks
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Although Frankfurt is a beautiful city especially the historical “Altstadt” is worthwhile visiting, I would not attend the conference. The organization behind all this is “Innovinc” https://innovinc.org/Current-Conference click on current conference and you end up here https://cancercongress.org There are numerous red flags:
-Contact info 5201 Great America Pkwy #320, Santa Clara, CA 95054, United States is at best a virtual office (in other words why hide where you are originate from)
-As mentioned in the above link the “130 seats left” looks fake, looking at the photo’s no more than a dozen people attend their conference(s)
Personally I would avoid this one.
Best regards.
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I am using propidium iodide (Hi-media Product) but i want to know how much Concentration of propidium iodide is required to stain in 100 cells
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Can anyone suggest me that how much number of cells are required for flow cytometry and what is stock concentration and incubation time of Propidium Iodide?
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A few years ago I moved from my job as a biologist in a research institute to a private research manager.
Right now I'm looking for ideas on how to collaborate with other researchers in academic institutions.
I have experience in lateral flow, immunology and cancer research.
Currently my main asset is my experience and I eager to do research again.
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1. Develop an Area of Expertise: Develop a specific area of expertise related to your research interests. This can be done by reading relevant books, journal articles, and other resources in your chosen field.
2. Network: Networking is important for any researcher. Reach out to colleagues, professors, and other experts in the field for advice and to stay abreast of the latest developments.
3. Attend Conferences: Attend conferences related to your research interests to stay current on the latest developments and to meet other researchers in the field.
4. Join Professional Organizations: Joining professional organizations related to your research interests can help you stay current on the latest developments, as well as provide you with access to valuable resources.
5. Develop Collaborative Relationships: Connect with other researchers for collaboration opportunities. This can help you develop new ideas, gain new perspectives, and learn from one another.
6. Utilize Online Resources: Take advantage of the wealth of information available on the Internet. Use search engines, databases, and other resources to stay up to date on the latest developments and research findings.
7. Publish Your Work: Publishing your work is a great way to make a name for yourself in the
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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 was doing a cancer research and also became interested in stem cell these days. But since I don't know much things about stem cell, I wanna study about the relationship between stem cell and cancer.
I think I heard that there are quite much relationship between them but don't know what are they.
Can someone tell me about it or recommend some papers related to this?:)
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cancer stem cells (CSCs) :are cancer cells with high capacity for self-renewal, multi-differentiation activity, and the ability to initiate tumorigenesis, found in primary tumors.CSCs are considered as the source from which cancer cells arise, and they are therapy resistant and responsible for metastatic dissemination, thereby CSC-targeted therapy would be an important challenge in cancer research.
here some reviews that may help you
good luck
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I'm passionate in oncology research. I did bachelor in Zoology and now pursuing MPhil Molecular Biology and Biotechnology and working on cancer genetics. I am greatly interested to do PhD in cancer research from a world renowned institute but I think with this profile I would get a position in top ranked institute for PhD. Should I go for another master from a renowned foreign institute with major in oncology?
Thanks
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I am also at a similar position as you are in. I have completed my MSc. in Genomic Medicine from the University of Birmingham. I am planning to learn Bioinformatics, maybe I will do that from 6months courses and then try to gain some experience in this field.
I think gaining some practical experience is quite necessary at the moment for you as well. After that you can always opt for PhD.
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Hi friends,
So I'm new to cell culturing research and synthetic biology and I'm working with MDA-MB-231 cells. Fairly regularly I have to at least split plates in order to maintain the cells, but I am also passaging cells for other things. Normally on a 10cm petri dish I'd plan to seed ~5.0E5 cells/mL for regular splitting and in a 96 well plate I'd seed ~4.5E4 cells/mL for my experiments. One thing I'm confused on still is using the hemocytometer to calculate cell density because I'm not entirely sure what my dilution factor should be.
Normally, I'll remove the old media, wash with PBS then trypsinize cells, after incubating for 5mins I add a bit more media until the total volume is 10mL, then I spin everything down. After that, I aspirate out the supernatant and am left with a small pellet of cells that I then break up and dilute with ~2-6mL of fresh media before using the hemocytometer to count the number of cells in 10uL.
My question is since I'm removing all the old media after centrifugation but then am adding new (different amount) media prior to counting, how does that impact the overall dilution factor?
Here's an example of what I was taught to do to find the amount of cells in 1mL, I just wanted to confirm that I'm on the right track. I was told if I resuspended my pellet in 3mL of media and then counted 75 cells I'd have:
75 cells/10E-4mL media
75 E4 cells/1mL media
7.5E5 cells/1mL media --> multiply this by 3 since you used 3mL to dilute before counting to get total number of cells (is this what accounts for the dilution factor?)
Total of 2.25E-6 cells that could be split however you see fit? Sometimes determining how many plates to get out can feel like a guessing game. Let me know if you see any issues with my method or suggestions that might be helpful, I welcome them. Please do try to be kind as I'm still learning and figuring things out. Thank you.
Kylie
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Alternatively, for adherent cells, you could seed the cells as calls/cm2 instead of cells/mL.
You already know how many cells/mL you seed in 96well plates or on culture dishes, and in which volume. (e.g.: if you seed ~4.5E4 cells/mL for experiments in96 well plates, in 100 uL volume, that is ~4.5E3 cells/well. usually, a 96well plate well is ~1/3 cm2 --> you seed approx. (4.5E3 * 3 =) 13.5E4 cells/cm2)
This way, you could also think about the following aspects of cell culture:
* keeping the seeding density similar across culture vessels
* keeping the amount of medium constant across culture vessels
for me, it gave me better confidence/understanding of when the cells are "happy", and some guesstimate if there is something wrong with their growth, or maybe they just need new medium or were seeded too dense/diluted.
As a rough value, usually around 20,000 cells/cm2 was a good start for most cells that I worked with (rodent liver, human bronchial, human neural stem cells), and one of the first experiments I usually did was a cell titration curve to have an idea how they grow (i.e., what is the critically low concentration when they would not grow, or how long it takes until they reach confluence. I'd usually start from ~100,000 or 150,000 cells/mL in 2-fold dilution steps in a 96 well plate). This is great for planning experiments and keeping the culture healthy e.g. over the weekend.
For estimating the number of cells from the hemocytometer: your calculation looks fine to me :-)
from the total number of cells you can work out how to split the cells. Alternatively, the formula recommended by Sebastian Lungu-Mitea works well.
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Researchers have discovered that breast cancer cells are more likely to jump into the blood when people are resting. The revelation is relevant because cancer is at its deadliest when a tumour’s cells worm their way into the bloodstream and travel to a new location in the body to set up shop — a process called metastasis. It doesn’t mean that people with breast cancer should avoid sleep — that’s bad for you. But it does give clinicians a better understanding of how to track these rogue cells. “The first lesson for me is that the time of day you take a blood sample can give you misleading information”, says cancer biologist Chi Van Dang...
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I am analysing several drugs on tumour cell lines. I need a quick way to calculate IC50 based on data generated.
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Dear researcher
Sigma plot software is recommended.
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Could you please provide any tips or ideas you have for creating the finest meta analysis review on cancer? Rather than writing a review article, I'd like to begin working on a meta analysis.
regards
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I totally agree with Timo Van Canegem that the word by itself "cancer" is such a broad term and I would narrow down to a particular sub-type and/or treatment. My best suggestion for this would be if you are uncertain as to which type to focus on to look at what type or types are treated or investigated in your organisation. For example, where I work currently, they are particularly interested in lung cancers and where I was working before has a special focus on bowel and breast cancers.
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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 should use the BCH for inhibition experiment for LAT1. I saw that BCH is soluble in 1M NH4OH but I cannot use this solution with cells.
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The following attachment may be relevant to this query
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in cancer therapy, sometimes you have to target multi-targets to understand the molecular pathway of the specific protein. CHyMErA can target multi targets but it is not safe and has a high risk of extra mutation!
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thank you dear Dr Muralimohana Rao Singuru
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Is there a chance for cancer research fields, such as exponential growth of infected blood cells methodology, to be related to COVID-19 research generally?
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Have a look at this useful RG link.
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This seminal paper by Paul Mischel rediscovered the relationship between extrachromosal DNA (ecDNA) and cancer:
1. How much would it cost to replicate the part of the experiment that generated subcutaneous tumors from seeds containing 200/2000/20000 cells of FACS-sorted EGFRvIII High/EGFRvIII Low subpopulations?
2. How much would it cost to sequence these tumor cells?
Thanks for your help!
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Shalini Sanyal Thanks for your answe.
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Hi
I'm trying to design a simple cube-shaped DNA origami with specific dimensions from just single stranded DNA oligos. 
Since there is no specific scaffold the origami is based on, cadnano is difficult to use...
I understand you can use Nupack... but I'm not sure how to create 3d objects using Nupack. 
Would there be a better program fit for this or what would be the ways doing so in nupack?
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Hi, I hope you already found an answer to this, but I think for cubes and other structures with specific dimensions ADENITA is a good option. Adenita SAMSON edition is a SAMSON (https://www.samson-connect.net/) plugin. you only need to add the app in the shop. You can use freeware option of SAMSON and it works quite nice.
De Llano, E.; Miao, H.; Ahmadi, Y.; Wilson, A.J.; Beeby, M.; Viola, I.; Barisic, I. Adenita: interactive 3D modelling and visualization of DNA nanostructures. Nucleic Acids Res. 2020, 48, 8269–8275, doi:10.1093/nar/gkaa593.
Best
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Permissible limit of arsenic in drinking water was 50 μg/l by WHO which was later reduced to 10 μg/l. Currently many countries like Bangladesh and China have not updated their own Permissible limits. However, this is been observed that on the event of long term exposure of arsenic at low concentration that is less then 10 μg/l in drinking water, health complication arises.
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I made a stock solution (25mM) of Pioglitazone hydrochloride (Tocris) in DMSO. It has dissolved finely. Then I treated the cells maintained in serum free DMEM with a final concentration of 100 micromoler of Pioglitazone. Here it forms crystals, precipitates in the culture vessel, but I am not getting the desired effect of it on the cells. Please suggest how to achieve the proper effect of Pioglitazone treatment?
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I don't have a solution, bur we also see hair-like crystals forming in our culture media when pioglitazone concentration ≥10µM.
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Cell culture.
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It is about 6-12 hours, it grows really fast. For me, A flask is fully confluent after 48 hours, even it is splitted at 1-5.
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I want DNA microarray cancer data sets with features and samples to form a gene expression matrix for applying intelligence techniques (such as basiayan neural network algorithm) to classify cancer data sets. Please help me.
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There is an increasing amount of research on the ketogenic diet in cancer therapy. However, I can't find much about this diet in those guidelines produced by governmental cancer research institutes such as American Institute for Cancer Research (AICR). As a matter of fact it seems like the word ketogenic is totally missing from the databases.
Am I missing something?
Sincerely Yours,
Christer Sundqvist
PhD Helsinki
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Thanks for the answers here
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Gene expression in the liver is zonated , is during aging a shift in zonation possible of the expressed genes?
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I think it is...
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The main ‘party trick’ of cancer stem cell (CSC) seem to be that it provide another explanation for tumour heterogeneity (i.e. cell divide asymmetrically give rise to progeny cells that are different). Secondly, asymmetric cell division is what makes this model ‘useful’ (i.e. clinically relevant): CSC model refer to a subpopulation of cells that must be targeted for effective thematic outcome. But if asymmetric cell division does not take place (i.e. if all cells divide symmetrically) than any therapy that kill cancer is in fact targeting the CSC (i.e. there is no point in identifying CSC- each cell would be one under symmetric cell division).
So, is asymmetric cell division a hallmark of CSC model? Any good literature on this?
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Hi!
I am trying to find a good immunocompetent mouse model to study triple negative breast cancer (TNBC). The 4T1-BALB/c model is perhaps not ideal for studies on immunosuppression and as 4T1 is derived from BALB/c mice, it cannot be transplanted in the C57BL/6 strain. Can someone suggest a good animal model to study TNBC-induced immunosuppression?
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Suhnrita Chaudhuri E0771 in C57BL/6 mice is, but still controversial as a pure TNBC model
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I'm using the BrdU antibody of the roche kit but i can't see any signal.
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In this case, it might be better to use another proliferation marker such as EDU because BrdU staining is mainly depending on denaturation by Hcl or you could try heating instead of Hcl treatment.
Good
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I had a contaminated cell culture I suspected several things, including the media. I put the media (only) in a T-25 flask and used 2 agar plates to check bacterial contamination (one opened in the laminar air flow the other in the CO2 incubator) and left them is in the CO2 incubator at 37 oC (after I cleaned it),
two days later I didn't find any thing on the agar plates and no changes in color or clarity of the media in flask however I examined the flask under the microscope and found these things .. What could it be?
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I understand that this can be very frustrating. The other answers are excellent responses for your problem. It is interesting that you had no contamination in your T-25 or agar plates.
I have found that without a cell layer to guide you, it is quite difficult to locate the media in a flask. Are you absolutely sure that you were looking at the media and not the bottom of the flask - the patterns in your picture resemble scratches and divots on the outside of the flask.
In any case, to help prevent contamination in your media, you can aliquot into 50 ml tubes and use those instead of an entire bottle at the same time.
Hope this helps!
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I am working with rectal swab samples in the field of colorectal cancer research. Does anyone have experience (or can point towards any relevant literature) of specifically working with proteins (extraction, characterization, or anything even remotely connected to protein work) in rectal swab samples (or any mucosal swab samples).
Thank you!
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Hi Colleague
Find the paper at the following URL may help you:
Regards...
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I just asking cancer expertise to suggestions the best books can read by MSc students before start their PhD program in cancer research
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Hallmarks of Cancer: The next generation
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I'm fairly new to cancer research and there's a host of articles on Sunitinib being administered via oral gavage in mice models but I'm unable to find any information on studies that have explored directly injecting tumors with Sunitinib. Just curious.
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Hi Paul
The name of the article is as follows:
Injecting activator of a powerful tumor suppressor directly into the cancer increases tumor destruction, decreases toxicity. Science Daily May 23, 2017.
Regards.
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Hello Everyone,
I've been writing a review article (almost done) on cancer research. Is anyone interested in collaborative writing and publication? Please let me know. We can share our ideas on extending the content of the paper and get it published mutually.
Professionals with an interest in cancer research are most welcome.
Thanks,
Dr. Ranbir
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I am now writing the article on the relationship between susceptibility genes and dysbiosis.
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I currently doing a research for anticancer drugs and have a plan to use CA 15-3 as tumor marker to measure the effectivity. Some reference tell that CA 15-3 and MUC 1 are synonym, but i also found some reference that stated CA 15-3 and MUC are different. My question is "Could I use ELISA kit for MUC 1 to measure the CA 15-3?" because my local supplier can't find the ELISA kit for CA 15-3 in affordable price.
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In principle yes, but with slight modification on the recommended protocol
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I read many papers about exosome isolation from fresh blood or frozen plasma, but not for frozen whole blood. I am wondering whether can I get exosomes from cryopreserved whole blood? One of my workmate told me the blood cells were broken if crypreserved and would affect the isolation of exosomes? What I need is the exosomes and their surface biomarkers. Could anyone give me your prescious advices? thank you so much.
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yes that can be done because DMSO has helped maintain the cells intact without any physiological disruption.
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when i was working in hood for cell culture, i forget to turn off the UV light .
1.is the UV light within less than 30 minutes leads cell damage for example SKBR3, or MCF10A ?
2. is the medium also affected with this situations? thank you
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I know this question is old, but I will post an answer in case someone searches this question now (as I did). Two of my undergraduates were responsible for feeding mammary epithelial cells from a slaughter (they are from tissue so there are fibroblasts mixed in too) and they accidently left the UV light on when feeding. Not sure how that's possible, but it happened.
Anyway, I saw some points that people were making about if the UV light is old/doesn't get cleaned often it won't work as well, so I had a lot of hope prior to looking at the cells because our UV light hasn't been changed in about 2 years.
It is important to note that the plates/flasks were not in the hood for more than 5-10 minutes. We had a combination of plates and flasks.
Results: After 24 hours cells were peeling off very obviously on the plates. Flasks were not bad at all. Seemed like well protected. Conclusion from day 1: cells were definitely damaged from only 5-10 minutes of UV light in the hood (we have normal hood UV lights that are built into the hood) and the plastic from T flasks will protect cells as Daniel stated.
I will provide more updates as they happen.
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Could anybody please tell me what are the different types of cells that originate from HNSCC patient samples. What are the type of studies that it can be used for?
I understand there are epithelial, fibroblasts, and keratinocytes that can be derived from HNSCC tumor samples. Can immunological studies be done using these type of cells?
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It really depends on what type of immunological studies you intend to run. Going back to the lymphocyte example I might do it in a deferent way .. by bringing lymphocyte form a different source and incubate the lymphocyte with the HNSCC and look for a response.
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I am looking for a scientifically oriented internet site providing new research in the category of cancer treatments.
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Thanks
Timothé Ménard
!
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I isolated a large amount (I hope) of exosomes and I need to quantify the membrane proteins with a Bradford assay before doing a WB.  I started off with 70 ml of conditioned medium which I managed to concentrate to about 1 ml before ultracentrifugation. After ultracentrifugation I added 200 ul PBS to my samples. My expectation is that the concentration of exosomes is quite high. So now I need to do a Bradford assay and  I would like to know how to dilute my samples.
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I'd like to kindly confirm from your response if the appropriate assay type for exosomal protein quantification with nanodrop is 1A/cm = 1 mg/ml.
I understand this is a general reference setting for protein solution, but I'd like to ask if IgG assay type is also relevant considering the lower detection limit which is about 0.06mg/ml compared to 0.08mg/ml for 1A/cm = 1 mg/ml assay type.
Thanks!
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Hello,
I am new to cancer research and I am trying to optimize my small cell lung cancer cell protocol.
I purchased a cell line from ATCC (H1105) and I have been growing the cells in RPMI 1640 media (10% FBS + penicillin/streptomycin.
I am looking for anyone who was worked with these cells in the past and who can let me know if these cells look normal?
I noticed the cells grow very slowly and form spheres.
Am I using the right media? How can I get the cells to grow faster? Can someone refer me to a good SCLC cell culture protocol? Thank you.
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Simple mechanical mixing is fine especially since your cells haven't formed confluent clusters yet.
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I need to confirm a knockdown of HER2 in SKBR3 and BT474 cells, have had problems blotting for HER2 in the past so any advice with regards to the protocol or antobody choice is much appreciated, thanks
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Thank you for all your amazing work! All the best!
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For my cancer research, I am doing cell culture with HPNE and MIA PACA. So, I would like to know the answer.
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Thank you
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I am studying on cancer research and ı used bcl 2 antibody to understand there is apoptosis or not. I got good band ı tested with ponceu red. Finally I got this result.ı used uvp chemi doc it2 imager to preview membrane.I tried a lot of times what do you think about this result?
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Hi Berna,
As Dr Mohammed comments, we need more details to understand the problem and think about how to help you. For example, may you show us the SDS-PAGE before blotting in order to analysis if the amount of protein loaded is adequated or to much, as it appears? The acrylamida percentage? Molecular weight of your target proteins? Previous treatments of the proteins? And finally, it is neccessary add a lane with molecular weight markers.
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MDA-MB-231, thawing
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From my personal experience, it seems like there are three issues that might have been contributing to your problem:
1- Not diluting the DMSO after thawing. You can fix this by adding about 5X the volume of cells of cell culture media (if you have about 2 mls of cells, add it to 10 mls of media). Then, you should centrifuge to pallet your cells and aspirate as much of the DMSO+media mix as possible after centrifugation. Finally, you can add more media and transfer the cells to a cell culture dish. This should get rid of almost all of the DMSO and give the cells a "happy" environment.
2 - Trying to change the media too soon. Cells can take quite some time to attach, especially after the stress of freeze/thaw. Six hours does not seem like enough time to change the media. Moreover, they might secrete factors in the media that will aid their growth and proliferation, and by changing the media too soon you get rid of those factors. Wait 24 h before changing the media: you will probably see a lot of (dead) cells floating, which is normal. Just aspirate the media and add more. After this, you should see some cells happily attached. Do not change the media or split cells before they are about 60% confluent (which can take 5-7 days for MDA-MB-231, depending on how many survive thawing), unless there are a lot of dead cells floating.
3- Contamination? If you are worried about contamination, it might be worth adding some antibiotic to your media, just to be sure. 1 % Penstrep should do the trick.
Best of luck! =)
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Tumor suppressor genes (such as Rb, APCPTEN and the ever famous p53) are often downregulated in cancer cells, if not completely lost or dysfunctional.
I'd like to know if there are any tumor suppressor genes that are upregulated in metastatic cancer cell lines/models? If so, could you link to articles/publications/studies of such genes? Are these genes bi-modal? Or have people figured out the molecular mechanism behind these genes?
I'd appreciate any and all help provided.
Thank you.
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Hi ,, Here you can find some example ...
SRPX, PRSS8, PTCH1, and finally P53 are TSG upregulated in cancer and promote cancer survival and spread.
You can easily find article connecting this Up-regulated TSG with invasive cancer.
Ref:
1. Exploiting the p53 Pathway for the Diagnosis and Therapy of Human Cancer.
2. The serine protease prostasin (PRSS8) is a potential biomarker for early detection of ovarian cancer
3. SRPX and HMCN1 regulate cancer‑associated fibroblasts to promote the invasiveness of ovarian carcinoma.
4. Targeting the Multidrug Transporter Ptch1 Potentiates Chemotherapy Efficiency.
Hope this info helps.. My wishes to your research ..
Regards
Suresh
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Many thanks.
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Interesting question
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Hi everyone
I am planning to use the Qiagen RT2 Profiler PCR array for signaling pathways. Is it really necessary to use the RT2 SYBR Green Mastermixes and the RT2 First Strand Kit with the profiler array? Can I use Applied Biosystems SYBR Green PCR mastermix instead (Cat no. 4309155) as well as my already synthesized cDNAs? The platform is Roche Light Cycler 480.
Looking forward for some help. Many thanks.
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u should use rt2 first strand kit, otherwise, the controls will not work. controls are required for data analsis.
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Dear friends and colleagues,
there is a very important resource on the web that is "Atlas of Genetics and Cytogenetics in Oncology and Haematology". The Atlas is a peer reviewed on-line journal / encyclopedia / database established in 1997 that collects data about cancer genes, solid tumors, leukaemia and other resources. It is in open free access for readers and there are no fees for the authors.
I'm searching volunteers and collaborators that would to write with me reviews about single genes involved in cancer.
I have published several papers so far and I believe that Atlas is a very valuable tool for us researchers, scientists and scholars.
I invite you to visit the Atlas website at http://atlasgeneticsoncology.org/index.html for more information. Here is my latest article published http://atlasgeneticsoncology.org//Genes/GC_EEF1B2.html to show you my working method. Anyone wishing to collaborate with me to write a specific review on a gene can tell me as well.
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I have research and interests in medical genetics on a less laboratory research results level. I rely on the scientific research in Atlas of Genetics and Cytogenetics in Oncology and Haematology nonetheless. Congratulations on your ambitious and important research project! Best regards.
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Which colorectal cell lines that has c-Met overexpression or amplification, dose anyone has any related literature please send me
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H820
MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib
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recently I am working on a project about the effect of bio-luminescence in cancer research. It would be my honor and pleasure to help me on this way
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First, you have to check whether the transcriptomic data available for the organism you study. based on transcriptomic data you will be able to isolate genes related to luminescent activities by PCR. After cloning with a protein expression vector, you will be able to isolate the proteins.
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Vitamins are useful against various diseases.
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Tretinoin / Retinoic Acid (RA) is a differentiation-inducing agent. Tretinoin for APL drives leukemic promyelocytes to differentiate into mature granulocytes but some of the leukemia-initiating cells (LICs) remain, albeit in lower numbers. Combining RA with arsenic trioxide (AS) leads to better survival of APL patients because AS induces APL cell apoptosis and RA+AS synergize to eradicate LICs via PML-RARα degradation.
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The event of death by metastasis or recurrence is very common, many researchers have linked the tendency of some tumors to re-appear to the presence of occult or dormant cancer cells that may have a phenotype that allows them to remain "hidden" from the immune response. However, the understanding of these cells and the mechanisms that they use to achieve evasion remain mostly unknown. It is critical to understand these cells better and to be able to detect their presence for they are of great therapeutic importance.
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Hi
LGR5 is the best biomarker for detection of cancer stem cells in colorectal patients .
u can browse our my profile and see our paper about that
Regards
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Cancer is very dangerous disease and allopathy drugs are unable to treat. Phyto-constituents of Lady's finger may act against this. 
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CML model is suitable for cancer research?
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TARGET THERAPY AND MONITORING OF CHRONIC MYELOID LEUKEMIA
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There are a lot of published data that showed association between vitD deficiency and many disorders e.g. diabetes, metabolic syndrome, CVD, cancer,...
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Please see the following PDF attachment.
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I am looking for information concerning the effect of publications regarding 5-year survival of diseases, like cancer, on the feelings of the patient. As the statistics are frequently published, and available on many websites with information on serious diseases, I was wondering whether psychological research was done as to the impact these statistics have on patients, dealing with diseases. I have tried to find such research myself, but the overwhelming majority of research I have found deals solely with diagnostic importance of these analysis. I will be most thankful for any advice and references on this issue.
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A high survival rate cultivate hope among patients with specific disease like cancer. If you tell a person that the five year survival is 90%, his hope of being one of the 90 who survived will be high and justifiable. If someone knows that the survival of lung cancer is very low, in most instances they will surrender to their fate
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several old studies says no, more recent studies says yes. Robert Bell in 1870 used raw salad to increase amygdalin in cancer patients and used saliva to detect the presence. Several sources say amygdaline converts to cyanide in an acidic enviroment and when gets in contact with acid lactic of cancer masses convert to cyanide and kill them (sort of selective killing). To be absorbed as amygdaline and avoid convertion into cyanide in the gut it should be taken from food rather administered directly. There are some roman texts about incresing lifespan of cancer patients with regular intake of 2-3 bitter almonds (rich on amygdaline) a day. Anyone has experience on it? Are research on amygdaline extensive and satisfactory? What is your opinion?
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Role of amygdalin (laetrile or vitamin B17) in cancer treatment is not yet scientifically proven. Please go through the following RG links.
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An exogenous RNA molecule is involved in the pathogenesis of cancer and transfered cancer among animals. It is living organism.
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In addition to viruses, certain kinds of bacteria can cause some cancers. The most prominent example is the link between chronic infection of the wall of the stomach with Helicobacter pylori and gastric cancer.
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Can anyone suggest me the precise and new anti-cancer target for docking of peptide type compounds. As per literature reports the chemical class of the above peptides are mitotic inhibitors. The BAX and BID along with Caspase 3 were highly expressed with peptides while in cytotoxicity studies. When the above genes are over expressing (Biomarkers) is an indication of apoptosis. Can I choose Caspase 3 as druggable target for these compounds and go for docking ?
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If an article suggests the intracellular protein inhibition for the induction apoptosis in cancer would it be feasible to inhibit the pathway by inhibiting the membrane proteins or receptor tyrosine kinase, as the peptide based drugs are more of surface acting molecules
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Cancer research has developed precise biomarkers to use a proper cure for different kind of cancers. Why there is no proper biomarker to find the precise treatment in autoimmune desease, such as psoriatic arthritis?
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I Know. Thanks anyway for aswering me.
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Since humanized and SCID mice are very expensive to procure and maintain. I was wondering to develop a cost and effective approach to develop an in vivo model for cancer research. Thymectomy is well established method to cause immunosuppression. I was wondering what will happen if we try to develop PDX model in thymectomized alone or in combination with immunosuppressants in C57bl/6 or Balb/c mice. Will tumor model be developed ?
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I DONT KONW
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I woul like to submit a Review article in the Journal of Cancer Research and Clinical Oncology. Are there publication fees for this Journal?
Thank you in advance!!
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Thank you to everybody! Is it the same for Current Hematologic Malignancy Reports Journal?No publication fees?
Thank you
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Hello everyone,
I have just started using Olympus fluoview for confocal microscopy and I don't know much about microscopy. I plate my cells (HeLa) in 4 welled Chambers slide. Stain the cells with Mito tracker dye, fix it with 4% PFA, wash, add mounting media and do the microscopy. The first time everything was fine. The second time I was trying to optimize the dye concentration, but something went wrong. The microscope kept on showing 'The focus position not found in scanned containers'. I had two slides and both of them had the same problem. When I tried with my old slide, it was fine. I have no clue what is wrong with my slide. All the chemicals and reagents that I have used is same as before except for PFA. The second time I diluted 8% PFA with sodium phosphate buffer to get 4% PFA. Can PFA cause problem finding focus?
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Apparently I went back to my old protocol and it worked fine. I don't remember the detail since it has been a while.
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We are trying to test some formulations of PD1 antibody on cancer models and would like to have a robust in vitro technique for future in vivo assessments.
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If you want to measure the effect on cytotoxicity you can just use it in a standard coincubation cytotoxicity assay using overnight activated PBMCs for example.
You can then compare killing rates between treated and untreated samples.
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Most studies on CAR-T cells use NSG mice (B/T cell deficient) based on the papers I found. Only a few use nude mice (T cell deficient, B cell present), which is what we are hoping to do. Does anyone have experience with using nude mice tumor model in CAR-T cell studies? What are the problems with using nude mice for CAR-T cell studies (since B cell is APC), and what are the potential solutions? Thanks a lot for any responses!  
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Hi Shirley,
Thanks for your rely^^.
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In my job, I transient transfected Active-wnt3a construct into Hek293T and Hek293 for expression , I collected three batch(fresh medium 5ml in 10cm dish for 24hr)
conditioned medium and concentrated in 500 µl ,but it didnt have any effect when it treatment 20µl for TopFlash repoter assay!!!!
Can any one tell me what can i do?
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In support of Svitlana’s answer, i can add my personal observations. I did a secretion assay on 293T cells expressing Wnt3a and found barely detectable Wnt even after concentrating the conditioned medium 30 times. Wnt3a was robustly expressed (as evidenced by western blot on whole cell lysate) but curiously i could not detect the higher mass (glycosylated) form of Wnt3a. Svitlana, do you know if Wnt1 is secreted by 293T cells?
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I have submitted a manuscript to clinical cancer research and the status changed to "decision pending" on the same day "under review". And I wonder whether it is not good news, how long will I receive the email from the editor?
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It is anybody's guess. It is likely that the journal has disclosed its review procedure policy at its website. If the preliminary review by the editor is a prerequisite for review by reviewers, it is likely that a "decision" to review the manuscript or not to review is "pending" . Therefore, it can be interpreted both ways.
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We are looking for highly motivated candidates to join our lab. More info available in the link below:
Any help with spreading the word about them will be highly appreciated.
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Thanks for sharing this info.
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