Questions related to Cancer Cell Biology
I have been working on Fluourescence in situ hybridization with HeLa cells. I hope to see noncoding RNA in HeLa cell. For negative control, I designed control set pretreated with RNase A(degrading all RNAs), and treated with specific probe. Before that, Samples were fixed with 4% paraformadehyde and permeablized. I wonder that RNase A is good working even at fixed sample?
Logistics seeks both to address real-world problems and research questions and to unite terminological, conceptual and methodological research aspects. In the last 20 years, biological research has developed extremely powerful methods and tools for fundamental and applied research. There is furthermore an increasing desire to build integrative research platforms that combine interdisciplinary and multi-level data to the structural complexity of biological systems. How much attention do you give to logistics for your research plans? Do you think logistics supports research methods, innovation, quality, value, and impact as well as training and participation opportunities for students as well as for practitioners? If so how and if not why not.
Just need to know if they grow (percentage of graft success, assuming one million cells in matrigel or similar conditions, orthotopic), and how long does it take, in order to plan some experiments.
What exactly is the role of HSP-90 in extracellular environment of the cell? I am wondering whether hsp90 is involved in the translocation of the client protein from outside to inside of the cell. If somebody is having some references please share with me. I am very curious about this molecule.
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.
I'm preparing pancreatic cancer cells spheroids. Which concentration of collagenase can be used to dissociate them?
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!
Hi, I am a beginner in the field of cancer genomics. I am reading gene expression profiling papers in which researchers classify the cancer samples into two groups based on expression of group of genes. for example "High group" "Low group" and do survival analysis, then they associate these groups with other molecular and clinical parameters for example serum B2M levels, serum creatinine levels for 17p del, trisomy of 3. Some researchers classify the cancer samples into 10 groups. Now if I am proposing a cancer classification schemes and presenting a survival model based on 2 groups or 10 groups, How should I assess the predictive power of my proposed classification model and simultaneously how do i compare predictive power of mine with other survival models? Thanks you in advance.
I have attempted to perform a double-thymidine block on my cells using a 24h first inc.-9h release-16 second inc. and 16-9-16 incubation periods in FUCCI DLD-1 cells. I haven't seen any synchronization. Does anyone have any recommendations or tips?
I tried staining MCF7 and MB231 for Vimentin and Cytokeratin antibodies, and surprisingly, I saw both cell lines showed both markers. According to the literature, MB231 is a mesenchymal type cell and MCF7 is luminal, so shouldn't it be that MB231 shows more cells positive for Vimentin as compared to MCF7?
I am already aware that HepG2 and Hep3B are both HCC cell lines, but due to site-permission issues I am not able to access most literature. I need an etiological as well as characteristic differences between the two. Can anyone help?
My research is to analyse the estrogenic activity of possible substances that migrate from plastics using the E-screen test based on the ability of MCF-7 cells to proliferate in the presence of oestrogens. However, so far I have not been able to validate the assay since I have failed to see significant differences between the effects caused by my positive control (17β oestradiol at almost any concentration) and my negative control. There is one paper that suggest that different "sublines" of MCF 7 cells show different sensitivities to oestrogen. So, I was wondering if you have been able to see differences between the proliferation in the presence of E2 and in presence of the negative control. and where did you get your mother stock of MCF-7
Does anyone have an IHC protocol for detection of a his-tagged protein in mouse tumor tissue (cryo, not paraffin)?
I'm trying to stain for a protein that contains a 6His tag and accumulates in tumor tissue (human tumor xenograft grown in mice). I used the M.O.M. blocking kit from Vector Labs to block endogenous mouse IgG, then incubated with the mouse penta-his primary antibody. The secondary antibody used was the Vector Labs Impress HRP-anti-mouse antibody. The problem is I get really high background signal, even in the negative control (no primary antibody). It seems the only species of penta his antibody is mouse derived, so maybe someone knows a source of rabbit, goat, or donkey penta his antibody?
Hi I am trying to see which Rab5 isoform would be ideal to track E-Cadherin exocytic vesicles. Does anyone have experience with this?
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).
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
I want to use the amplex red assay to quantify H2O2 levels in different cellular clones. Many protocols I found online or previous answers on RG contradict each other.
The major debate is about performing the assay:
- on cultured cells directly
- on culture media removed from cell cultures
What's best in your opinion ?
Someone also said that phenol red could interfere with the assay.
Thanks for the help you can provide !
I am working on mechanism study of some anticancer compounds using A549 and H460 NSCLC cell lines. I want to check if my compounds are non-toxic to normal cell or not. Some researcher use human normal lung fibroblasts HEL-299 and MRC-5 cells while others use normal cell lines that don't belong to lung tissue. I want to use only normal lung cell, not from other tissue. Can anyone suggest me which one is the best normal lung cell line model?
I know rapamycin is generally used as an immunosuppresive agent in the treatment of organ transplantation (kidney transplantation) and works through inhibiting the mTORC1 complex. Additionally, due to the inhibition of mTORC1, rapamycin also produce some anticancer effect. So, my question is, if the immunity get suppressed because of rapamycin effect how it will provide anti-cancer effect? As cancer cells could proliferate more due to the low immunity of the body. Looking forward to hearing from the experts. Thanks in advance.
Aneuploidy, an imbalanced complement of chromosomes, was identified as a distinct feature of cancer cells more than a century ago. Indeed, ~90% of solid tumors are aneuploidy. The random gain and loss of complete chromosomes has many favorable properties as a mechanism for phenotypic switching, both in the context of a preemptive bet-hedging strategy as well as a rapid means for coping with unfamiliar environmental stresses. Aneuploidy might be a useful bet-hedging strategy for responding to environmental perturbations that are not frequently encountered. As aneuploidy perturbs hundreds of genes simultaneously, it has the potential to affect larger numbers of genes and processes per event relative to a spontaneous mutation. Importantly, unlike a spontaneous mutation, aneuploidy and any associated growth defects can also revert at a high frequency (cancer reversion).
So, aneuploidy may be the proof of “cancer is adaptation mechanism”
I would like to label Human Serum Albumin for my experiments.
My supervisor suggested NHS and 6-Aminofluorescein as working agents.
Can anybody please suggest a working protocol?
Any suggestions on storing? Can I freeze the labelled protein in a solution?
If you have any other suggestions I would be very grateful!
In my experiment, I need to use ascorbic acid to treat cancer cells. As we all know ascorbic acid is very unstable in aqueous solution because of its oxidizing behavior, can anyone please tell me if I want to do treatment with ascorbic acid to cell lines then how could I prepare it? Should I adjust ascorbic acid to PH 7?
I want to know the experimental and technical differences between the breast cancer cell lines SUM159 and MDA-MB-231 cells. I wonder, do they have efficiency in sphere-formation( Stemness).
please help me with this.
The given IC-50 concentration in the data sheet of inhibitor 10 micro molars, to look at the inhibition of IL-8. The concentrations above the IC-50 seem to be giving considerable results for eg. the concentration of 20 micro molars. The methodology used for the detection is IL-8 Indirect ELISA. Kindly suggest.
I have some questions related to a drug called Cobalt 2 chloride hexahydrate.
I am currently preparing an experiment related to Hypoxia. I bought a drug called " Cobalt 2 chloride hexahydrate" (from Sigma Aldrich) with the molecular weight of 237.9 g/mol and the total weight is 5g.
I want to know what is the best stock concentration should we make for this drug? Plus, how much H20 should we add to the drug ? and the optimal condition to store this stock concentration?
Furthermore, can you recommend me the best final concentration of this drug to mimic the Hypoxia environment? any ideas?
We have mice injected w/ specific cancer cell lines. The cancer cell lines failed to pick up the luciferase bioluminescent tag. We have a rubric of categories to measure the mice, but I was curious to see if there were any other variables that we could measure that would give proxy measurement for changes in tumor size.
I would like to study development mechanism of colon cancer, could anyone give some advice about the advantage or feature of each of FHC and CCD 841 CoN?
I wanted to know if we can store frozen cells in -80 C refrigerator. These cells are stored in liquid nitrogen tank (-200 C) as of now. But as liquid nitrogen vaporizes, we need to keep refilling the tank every two months. Since, the university is going to be under lockdown due to COVID-19, we will not be allowed to enter labs or be able to order new liquid nitrogen. So will it be feasible to store these frozen cells at -80 C for the coming 3-4 months?
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.
Oncology is a branch of medicine that deals with the prevention, diagnosis, and treatment of cancer. A medical professional who practices oncology is an oncologist. The name's etymological origin is the Greek word ὄγκος (óngkos), meaning 1. "burden, volume, mass" and 2. "barb", and the Greek word λόγος (logos), meaning "study".
Cancer survival has improved due to three main components: improved prevention efforts to reduce exposure to risk factors (e.g., tobacco smoking and alcohol consumption), improved screening of several cancers (allowing for earlier diagnosis), and improvements in treatment.
Metformin's anti-cancerous properties have been demonstrated in various cancer cells in vitro, such as lung, pancreatic, colon, ovarian, breast, prostate, renal cancer cells, melanoma, and even in acute lymphoblastic leukemia cells.
It was suggested that the tumoral microenvironment is associated with long-term outcome in primary and metastatic tumors.Metformin reduces inflammatory microenvironment Is regulated microenvironment with metformin reprogramme malignant cancer Cells toward a benign phenotype.
I guess I'm not understanding the concept well. If I treated cells (5000/well) with a range of doses from 6nM to 92nM (and this is an MTT assay and I've used Prism8), why is the IC50 only .9nM? I guess I'm not reconciling what I'm putting into the assay and what prism spits out. Are the values from Prism in the same units as my initial concentration? I also log transformed the values so Idk if that has anything to do with it.
In the body, when one develops a tumor, the microenvironment is very important. How do the cell cultures of cancer cells grow in the flasks without that micro-environment and only with the media and the serum?
Any suggested readings?
Is it because we are trying to target these cells before they have a chance to divide??? I guess I don't understand the logic behind this.
I'm focusing on the Ras/Raf/MapK/Erk pathway and I'm expecting to see both when I treat with a MEK inhibitor in pancreatic cell cancer line. While I dramatically reduced levels of pERK, there's VERY little cell death. Does this mean that apoptotic pathways aren't necessarily rescued in this case or it is a technical issue where I should leave my cells in the treatment for longer than my current timepoint?
I am trying to grow cancer cells and do MTT assay for drug screening. Are there any alternatives to FBS? I know that FBS and FCS are widely used for cell culturing, but I am looking for other options.
I found one online and got it ordered:
But the cells are not growing properly in this.
Any suggestions in this regard?
Is there any portal or application that accepts Seurat objects as input and lets me see genes’ expression across the clusters? Of course, my lab’s service provider can help using Seurat itself, but I need to come to them several times when I have a request. I am learning Seurat, but it would be nice to have a tool that supports it upfront without command lines.
I am looking for a simple and low-cost method of monitoring the cholesterol content in the cell membranes. My initial idea was to stain them with cholera toxin (anti-GM1 ganglioside) to get information about lipid rafts, so indirectly about the cholesterol content.
Do you have any better ideas?
i want to knoe in details hoe to calcule the cut off value for roc curve and hoe to make this rock curve and the calculation formula for sensistivity and specificity
I have two questions, please shed some light on this. I am new to in vivo studies and some may find my questions are trivial. TIA.
My first question is,
I wanted to develop the MCF7 mouse xenografts. I did a search and came to know that the injection of estradiol is recommended to develop tumours prior to injecting the MCF7 cells. Also, I have seen some papers without estradiol. Can you tell me the role of estradiol in tumour formation? Can the mice form tumour without estradiol?
Once the tumour reaches a definite volume, I wanted to inject my compound of interest. Here is the question, which is a simple way to inject? I have found the following ways related to my studies.
2. Microosmotic pump
4. Oral gavage
Please recommend me a simple way to introduce my compound to the mice. If you have a better option also welcome.
Many thanks in advance,
autophagic activity suppression by Rubicon is a signature of aging.
how many time it takes in the suppression of autophagic activity by Rubicon?
When Rubicon functions in neurons?
How Rubicon functions in neurons?
I want to know whether tumor cells share their information by time passing. I were wondering if anybody could answer my question and introduce some good resources in this regard?
I like to know the possible markers of metabolism in cancer cells such as in monitoring glycolytic, extracellular acidification and oxygen consumption rates, effected by treatment with an extract.
I have overall 2 years of Research experience including my Master thesis project. I have co authored 2 publication in international journal. One poster in international conference. I have cleared IELTS exam with 6.5 band in 2018.
I am looking for PhD admission.
My area of expertise and interest are: oncology, reproductive biology and developmental biology.
any help and guidance, I will highly appreciate.
Thanks in advance.
Kindly feel free to comment or inbox me.
I am studying gene expression profile through analyses of proteins expressed upon treatment of cancer stem cell line with a novel herbal substance (in the extract) to predict gene function in the mechanism of reaction. I would, therefore, need to know the best method to determine/screen proteins expressed solely consequent upon this treatment in achieving this considering;
1. Model of the study (cancer stem cell line)
2. Testing molecules (drug candidate from herb)
3. Analyses involved.
I am currently looking for academic professional that can accept my studentship for PhD program in any of the following research area:
1. Antimalarial or anticancer novel compound synthesis and biochemical evaluation.
2. Structural biology of uncharacterized enzyme target for malarial or cancer therapy.
3. And other related research topics.
These studies will involve the use of bioinformatics/computational and biochemical/biophysical techniques.
Country of interest: Brazil, USA, Germany and other available countries.
Kindly let me know your willingness
I will be graduating soon with an MSc in cancer pharmacology from the UK. I want to know what job titles/description should I apply to in Singapore. my practical experience is mainly in cell culture. I also have a BSc in Pharmacy.
Any help is appreciated.
I am attempting to stain cells in my colony forming assay and would like to find a protocol, specificaly one that does not involve formaldehyde or buffered formalin.
Im co-culturing the caco2, Ht29-MTX cell lines (ratio 1:10) on a silicon porous membrane by the pore sizes of 6um (center-center 50um). Actually I dont use the SERUM-FREE media and I do not know why do they use it in litreture for caco2 cell lines cultivate.
The result is that I see the cells in the holes but they are almost stoped to pass to the other side. And on the top surface of membrane, there are only clusters of cells instead of the cell monolayer.
I want to use data analysis to figure out how to predict the factors affecting the incidence of brain and bone cancer, but my challenge is the reliability of the data provided on the kaggle.com website. Is it possible to trust the data?
I have several microarray gene expression datasets, but they use different naming systems for the probes. What are some simple ways to convert all the probes to the same type (e.g. Affymetrix)? Thanks.
Hi, I am currently design a assay for testing the cytotoxicity of primary T cells against tumor cell lines. Here is the design:
Cryo-preserved PBMCs were retrieved and cultured with 9ug/mL PHA, 20%FBS RPMI1640 medium for 48 hours. Then the PBMCs were stained with CD3 antibody and were sorted for CD3+ T cells. The adherent tumor cell lines A549 were seeded the day before add T cells in 96 well plate (3000 cells/well). Tumor cells were stained with LIVE/DEAD® Viability/Cytotoxicity Kit (Themo Fisher: L3224). After T cell purification and tumor cell staining, we add T cells to tumor cells in 200 ul medium. Finally, the cytotoxicity were observed in In-Cell-Analyzer 2200 (GE) for 6 hours by real-time imaging and count for red signal of dead tumor cells. The RNA of T cells were collected after recording of images, and cytotoxicity genes expression, like IFNG, PRF1, GZMB, will be run on real-time qPCR. CD3 will be used as housekeeping gene.
I know the PHA will activate T cells and stimulate them proliferating via CD2 and calcium influx pathway. And I do observe obvious cytotoxicity in the preliminary experiments. Could anybody give me some advices to improve this method? .
I am working on Bioinformatics and Computational Biology. I am using Cytoscape tool for network visualization or analysis. Now I am working on lung cancer-related genes. In this work, I want to add some clustering methods to analyze for a better outcome. Please suggest me which one is better than any other plugin?
I already use the clusterOne plugin but want something more such like as MCL, k-medoid clustering.
Thanks for advance.
for example, I have used POPE cell membrane in my research work (molecular dynamics), but according to the paper that I attached below, this membrane is a kind of normal membrane.
if there is somebody who knows how to modify this membrane as a cancerous membrane, please recommend me.
I tested 25 ug/ml and 40ug/ml of Fluorescently labeled transferrin in melanome cells during different times of observation, but no fluorescent signal was detected inside the cells.
Is there anyone here who has had the same problem?
The plant is already known as anti-cancerous, but the biochemical study has not been done. However the active compound, from the plant has been researched already to find anti-cancerous activity in various in-silico studies, however no wet-lab is done. How should the road map of the studies can be carried out ?
I am working on Epithelial to Mesenchymal Transition (EMT) in A549 cell line by treating positive inducers such as EGF to up-regulate the mesenchymal markers like vimentin. I'm doing western blot to detect the changes of vimentin expression level over treatment time of the inducers. I could detect the protein band of vimentin at the position of its proper size, but the change of protein expression level flutuate too much.
For example, I expected increase of the vimentin expression level by the treatment of EGF at least in early timepoints right after the treatment, but it wasn't. Neither at longer imepoints. Sometimes the level of vimentin was completely disappear, sometimes increased, or just remained in the same level. I always confirmed the expression level of beta-actin or GAPDH as a loading control, and it was consistent.
I tried same kind of expreriments using mesenchymal cell line like MDA-MB-231, and in this case, the degree of the fluctuation was decreased but it doesn't completely disappear.
The passage of the cell lines are all around 10, which is I think low enough, and I grow my cells in complete medium RPMI 1640 (10% FBS, 1% Penicillin/Streptomycin) and I treated the EMT inducers after 16 hours serum starvation.
I doubt that the A549 cells that I prepared for the experiments were not in good condition, so this can be the reason of the fluctuation. Do you think that the health of the cell can affect to the level of vimentin much? If so, how can I troubleshoot my problem? Any suggestion or advices can help me a lot. Thanks in advance.
I would like to know the viscosity of Matrigel (Corning) as function of temperature. I already know that it solidifies at 37° and its liquid at 4°, but i would like to know what's the transition form, and what happens with different Matrigel concentrations.
Thanks in advance,
Mack et al studied subtypes of three ependymoma(same histopathology) brain tumors and found that one subtype carries an intrachromosomal translocation that creates a new tumor-driving gene, another lacks tumor-driving mutations but has aberrant epigenetic modifications, and a third shows neither gene mutations nor epigenetic aberrations. There were three genotype but one cancer phenotype. Similarly Martincorena and colleagues found thousands of mutations in cancer-relevant genes, including cancer-driver genes, in normal eyelid epidermis .(multiple cancer genotypes but no cancer phenotype).
In disparate classes of biological systems, there are more genotypes than phenotypes. Where sufficient information exists to enumerate these phenotypes, there are exponentially more genotypes than phenotypes, as a function of the number of system parts. This means that any one phenotype typically has many genotypes that form it.
In a brief, cancer is the decision of the cell to choose the innovative/adaptive phenotype and understanding the genotype does not mean understanding cancer.
1. Mack, S. C., Witt, H., Piro, R. M., Gu, L., Zuyderduyn, S., Stütz, A. M., et al. (2014). Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 506, 445–450.
2. Martincorena, I., Roshan, A., Gerstung, M., Ellis, P., Van Loo, P., McLaren, S., et al. (2015). High burden and pervasive positive selection of somatic mutations in normal human skin. Science 348, 880–886.
I am doing a pilot study to assess the cytotoxic abilities of different T lymphocyte populations when cocultured with B16 Ova In Vitro. I have seen different articles labeling their effector/cytotoxic T Cells with a target dye to gate them out and look at Annexin and PI positive cells. But I do not have any target dye to label my cells. Instead can harvest my cocultured tumor + T cells and first do a CD4 CD8 surface staining with antibodies and then follow Annexin PI staining protocol? I understand the 2 stainings are different but will that affect my apoptosis results in any way? Has anyone done this before and has had luck with it? Please help me to understand better. Thanks
During routine microscopic observation of Cancer Associated Fibroblasts (CAFs), my colleague Pedro Barcellos and I came across these odd geometric "dark" structures inside the cells. We haven't been able to determine what this would be. This was not evident in all cells, but in a fair share of them. And also present in different biological replicates.
We would love to know what these structures represent or to have any hints about what they might be.
In collaboration with Frontiers in Oncology (latest Clarivate Analytics' impact factor: 4.416), "Cancer Metabolism" section, and together with Professors Athanassios Vassilopoulos and Lucia Altucci, we are bringing together a selected group of international experts to contribute to an open-access article collection titled "Sirtuinome Rewiring to Hijack Cancer Cell Behavior and Hamper Resistance to Anticancer Intervention". Frontiers provides a free and immediate Gold Open Access-based online access to the scholarly literature for anyone in the world to read, distribute and reuse. In this regard, we are pleased to inform that a 25% discount will be granted for accepted manuscripts. For more detailed informations, please go to https://www.frontiersin.org/research-topics/10447, and remember that submission deadline is November 2nd, 2019. ------------------------------------------------------------------------------------------------------------- Call for Papers Extensive reprogramming of energy metabolism and detoxification processes are increasingly seen as critical factors involved in metastatic progression and in development of chemo- and radio-resistance. Mammal sirtuins (SIRT1-7) are a family of conserved NAD+-dependent protein deac(et)ylases and/or mono-[ADP-ribosyl]transferases with varied cellular distribution. Their role as crucial regulators in energy metabolism and adaptation to cellular stress is currently under extensive investigation worldwide, not only in physiological processes (e.g. in aging) but also in the pathogenesis of cardiovascular and neurodegenerative diseases, diabetes and cancer. In particular, sirtuin-dependent signaling is suspected to play a dual role in cell biology, on one hand protecting DNA from genomic instability and limiting the replicative potential, on the other hand inhibiting senescence and promoting survival and growth advantage. Interestingly, SIRT3-5 localize to mitochondria and regulate targets involved in a diverse array of biomolecular pathways, many of which govern energy metabolism and apoptotic death. Such characteristics confer a great importance to sirtuins, in terms of preventive medicine and therapeutic potential. Unfortunately, despite the rapidly increasing interest in the field, results are still insufficient to draw definitive conclusions. More importantly, the question as to whether sirtuins can be considered as tumor suppressors or oncogenic proteins remains unanswered. In this Research Topic we welcome Original Research and Review articles focused on clarifying the mechanisms underlying sirtuin-driven responses to endogenous and exogenous stressors in tumor and malignant cells, in terms of metabolic rewiring, antioxidant protection and cell cycle control. In addition, researchers are also invited to provide data and opinion regarding strategies aimed at controlling the expression and activity of sirtuin-responsive cellular systems, with particular attention to pharmacological and nutraceutical approaches. Finally, studies focused on sirtuin-dependent pathways leading to malignant progression and/or development of chemo- and radio-resistance in cancer cells are also welcome. Potential topics include but are not strictly limited to the following: 1) In vitro or in vivo studies focused on sirtuin-dependent regulation of redox-based responses to stressors in tumor and malignant cells, with particular attention to metabolic reprogramming, DNA damage repairing capacity, antioxidative potential, and proliferation; 2) In vitro or in vivo researches on the mechanisms underlying the action of synthetic and natural compounds on the expression and activity of sirtuins and downstream cellular pathways in tumor and malignant cells; 3) In vitro or in vivo studies investigating the role of sirtuin-dependent intracellular and extracellular signaling associated with cancer progression and/or development of resistance towards chemo- and/or radio-therapies. Stefano Falone, Ph.D. (Department of Clinical Medicine, Public Health, Life Sciences and Environment Sciences, University of L'Aquila, L’Aquila, Italy) Athanassios Vassilopoulos, Ph.D. (Northwestern University, Chicago, IL, USA) Lucia Altucci, Ph.D. (University "Luigi Vanvitelli", Naples, Italy) Topic Editors, Cancer Metabolism Section, Frontiers in Oncology
It is confusing concept in the literature that some papers use the term "HER2 positive" and some "HER2 overexpression". You may refer to the definition in the specific paper, but sometimes they even dont mention what they mean with "HER2 positive" cell.
Any clarification would highly appreciated.
I'm a Research associate at 57357 hospital , Egypt , I would like to ask about two cell lines : RD , RH30 ( Rahbdomyosarcoma ) we couldn't find them in Egypt and we are committed to certain budget , deadlines and masters thesis based on this project , anyone know a trusted source or a lab in any country usually uses them to give as aliquot ? Thank you in advance !
Has any serum protein been associated with the induction of EMT/MET of solid tumor cell?
I found this interesting device (https://darwin-microfluidics.com/collections/microfluidic-organ-on-a-chip/products/ddi-chip-distance-dependent-interaction-chip-pack-of-3). Have you any experience in the use of microfluidics to study cell cross-talking and signaling?