Questions related to Chemoresistance
Currently, I am looking for a solution to develop chemotherapeutic drug resistance in a primary cancer cell line. But after a quick look at the literature, it is indicated that the management of acquirement of drug resistance takes plenty of time, more than eight months! Is there any convenient method to subculture chemoresistant cell lines in a short time? Or any other suggestions rather than eight months interval with an increasing dose of chemotherapeutic agent?
Dear scientists, clinicians, and researchers on the ResearchGate platform,
I am planning to assess the molecular mechanisms of developing drug resistance in cancer cells. However, I lack knowledge regarding the bystander effect. Can you kindly assist me with the following questions:
1. What is the fundamental understanding of the bystander effect in the development of drug resistance in cells?
2. Why is it important to measure gene mutations that cause drug resistance, whether through direct or bystander effects?
3. What is the most effective in vitro setting to demonstrate this bystander effect and resistance development?
4. How can we measure the direct and bystander effects of gene mutations causing chemotherapy resistance in cancer cell lines? What parameters should we assess?
5. Lastly, what are the clinical implications of measuring this bystander effect?
Thank you very much for your assistance.
I work on VEGFA / VEGFR-2 cytokine/receptor in AML and I will inhibit it to see if the signaling pathway has a role or not in AML chemoresistence
I will test the inhibition by detection of phosphorylation, but there are a lot of phosphorylation sites, how can I choose the accurate site for my experiment
TGF-β and BMP signaling are present in the cancerous cell show almost the same function of chemoresistivity, enhanced proliferation, higher EMT transition. Then why would cells have both mechanisms? Also, what is the major difference between both of them?
Hi, I am designing my proposal on gene which cause chemoresistance in cancer. From literature review I have come up with a gene COL11A1 which has previously been identified as a chemoresistance biomarker. I want to know that what if I do not receive any positive result of staining then what measure will I do to atleast get guarantee that something to work on?
Hi , I want to know that if I hypothesize that Gene A promoting chemoresistance in PDAC but what to do if I do not get any positive staining in my sample? What measure will I have to take which will guarantee me to get atleast something to work on?
I have analyzed 20 clinical samples, 10 which are chemosensitive and 10 which are chemoresistant, using TMT labelling and high-resolution mass spectrometry. I am really stuck at how to analyse the results. I've used MaxQuant and am hoping to use Perseus to interpret the data but I'm not sure how to do this. There are many missing values, can I impute data even with no replicates? Do I have to normalize my data? Any links to guides or help would be greatly appreciated! Thank you!
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
Hi all, I was wondering how to go about obtaining highthroughput seq data from databanks. We are interested in the expression of a few genes we believe might regulate acquired chemoresistance. I'm not quite sure where to start. I have searched TCGA and NCI's GDC data portal but I was wondering if there are other databanks I could request information from. What about tissue samples? Our group would like to work with patient samples and data to validate a few findings and aren't quite sure where to start. Any help would be greatly appreciated.
I am working on chemoresistance of human squamous cell carcinoma (SCC12) in the context of tumor microenvrionment, CAFs specifically.
I have already done experiments with different concentrations of each drug (cisplatin, docetaxel and 5-FU) ranging from 0-120uM for cisplatin, 0-100uM for docetaxel and 0-500uM for 5-FU.
I am wondering does anybody have experience with these drugs to tell me what are the physiological concentrations in patients? I have checked for concentration in plasma but I could not find a consistent answer.
I would like my results to reflect the conditions in patients.
CHEK2-related breast cancers are very chemoresistant. Can somebody explain me, why they are so chemoresistant? Anthracyclines are not working here compared to BRCA1-carriers.
In many cancer, ALDH1A1 found to be associated with chemoresistance. Does anyone has comprehensive understanding on the molecular mechanism of ALDH1A1 mediated chemoresistance? I just found an article showing ABCB1 modulation through ALDH1A1-NEK2 pathway. Are there any more gene/protein that directly linked with ABC transporters as well as ALDH1A1? Any suggestion will be appreciable.
This is a question that will be raised by most oncologists. The corollary of this question is: Will this method raise glutathione in cancer cells as well, leading to their chemoresistance to chemotherapy? The literature suggests that when using actual glutathione precursors (like available cysteine/cystine) will lead to what has been termed "selective modulation" of glutathione. This is a situation where cancer cells down-regulate GSH (negative feedback inhibition) but healthy cells increase their GSH levels. This has the potential of potentiating the effect of the chemo on tumor calls while decreasing chemotherapy side-effects. See http://www.ncbi.nlm.nih.gov/pubmed/18158761
I would like to use a comet assay to test the effect of my protein-of-interest on DNA damage response, double strand breaks and chemoresistance in cancer cells.
There are several types of comet assays. Which type is most suitable for my analysis. Any why?