Questions related to Molecular Oncology
I need the most common methods and procedures to screen a phytochemical having anticancer activity both in vivo (animal model) in vitro and in computational systems.
Does anyone have experience with DSS colitis model?
I want to discuss about the scoring system of DAI, for example, to score the bleeding: I want to score as follow (no bleeding=0, mild-moderate blood pellet = 1, dark red pellet=3, gross bleeding =4 ). However, I couldn't find paper using such system. so is it ok to use my own scoring system or any one have reference for such scoring system?
Thanks in advance.
can somebody explain me, why there is a borderline in many studies that patients in neoadjuvant BRCA1-cohorts have to be younger than 50 years of age? Is there some literature which explains it?
i have treated a tumor cell line using a plant extract and terminated the treatment at different times (eg: 1 hour, 2 hours, 4 hrs and so on) and estimated some enzyme activities and observed that the enzymes decreased up to a certain time, increased again and then decreased again.... how do i interpret this and what exactly is happening??
I am looking for information regarding extravasation of chemotherapeutic agents from capillaries to tissues. If you could share your information, that would be very helpful.
In the majority of studies, it is written that compound X exhibited cytotoxic activity or antiproliferative activity, which sometimes becomes confusing to get across. Therefore, a clear cut picture outlining the major difference between two terminologies will be acknowledged.
I am studying novel immuno therapeutic strategies in cancer and have had trouble in establishing a reliable system to study combination therapy with PD-1 blockade. I am wondering if anyone has had success with such a model. I have tried B16 tumors and EL4 tumors. Thank you.
Does anyone know or read the paper about the gene, which has opposite effects on tumor growth in vitro and in vivo? I want to get some clue. If you know some or have related paper, please let me know. Thank you in advance.
miRNAs are epigentic regulators and altered expression is reported in cancer. How to find out mutations in miRNA genes and their relevance in cancer? or are the mutaions in miRNA genes or its altered expression relevant in cancer?
There is a Co(III) mustard based prodrug which reduced in hypoxia environment and toxic to the cancer cells. if this complex reduced in cancer cell environment then why not other Co(III) complexes reduced to co(II)? if so what is criteria ? which type of coordinating ligand will facilitate the dissociation of inert Co(III) to labile Co(II)?
what are all the simple method to determine the stability cobalt(III) in biological environment? kindly give some relevant article.
I'm growing 4T1 cells in mice. I'm implanting two contralateral tumors per mouse. I'm having a hard time getting the tumors to grow symmetrically. I understand they won't all be perfect, but I'm getting a lot of shapes that are difficult to caliper, or I'll have tumors with small satellite tumors right next to them. With 2 tumors on 1 mouse, its hard to get enough mice to enroll in study.
I'm implanting 1 x 10^5 cells in 100 uL volumes. I draw the cells up into the syringe in an 18 g needle, and I implant the cells using a 25 g needle. I slowly inject the tumors on the flank and slowly remove the syringe. The cells are being implanted using serum free media.
Should I use a smaller gauge (27g) needle to implant? Should I move my implant site up to the shoulder? Should I switch to PBS instead of media?
The Polycomb Repressor Complexes (PRC1 and PRC2) are crucial to keep stem cells in a pluripotent state, by silencing all genes that would be involved in premature differentiation or cell fate determination. PRC2 is involved in H3 trimethylation and PRC1 in methylation of CpG islands. Regulation of both PRC1 and PRC2 is mainly on the level of post-translational modification of the PRC components (such as EZH1/2, PCL1-3, RING1A-B ...) and target specifity is speculated to be governed by non-coding RNAs. There are also many observations that suggest illegitimate PRC2 activation plays a role in carcinogenesis, tumor progression and development of therapy resistant sub-clones. I am wondering if there is a (or a set of) reliable gene-expression markers which represent a good indicator for the activity of PRC1 or PRC2.
I would be grateful for any suggestions, Michael
We all have experiences that more and more mutations are found in tumors. A few of them are recurrence (driver mutations) but most of them are not. The problem is how to determine a mutation actually a driver mutation for a specific tumor? What standard we should follow and what should be the rule? Many of the mutations may be merely passenger mutations caused by the genetic instability after carcinogenesis process.
KRAS,NRAS,BRAF wild type colorectal cancer can response the anti-EGFR therapy using cetuximab or panitumumab. However, in some cases such as Her2 or MET amplification there will be an resistant to anti EGFR therapy although tumor has KRAS,NRAS and BRAF wild type genotype. If there is a polysomy in chromosome 17(Her2:CEP17 ratio 1, however there is a increasing number of chromosome 17 such as 3:3,4:4), using FOLFIRI+Cetuximab+Herceptin can overcome EGFR resistant in metastatic colorectal cancer?
I need to find an antibody to detect high risk HPV types in one go using western blot. could you kindly let me know if there is any company can provide this antibody?
I need the murine cancer cell line. But the problem i am facing is whether cancer cell lines from C57/BL6 mice can be used to study in Balb/c mice or not. Another problem is that, I found some Balb/c mice cancer cell line but mostly in old articles.
I was getting good results before, but all of a sudden when I repeated the procedure with the same cell line, same drug, and same drug concentrations, it went wrong. Please find attached before and after pictures.
I was wondering if anyone could share how to identify osteoblastic niche for quiescent hematopoietic stem cells in bone marrow by doing IHC staining
Although the malignant tumors at the initial stage from the stemness starts as a Monoclonal origin, upon the further proliferation, a secondary clonal population of cancer cells are generated. This further continues to go and change the clonality.
Hence, do the malignant tumors need to be addressed as a monoclonal or polyclonal?
This project is in a rare type of lymphoid cancer. Due to this rarity, there are only 3 cell lines available for the disease, which I have in the lab. They are drug-sensitive cell lines (drug disclosed only if you are interested in collaboration) and I also have their 3 drug-resistant clones, which were developed in the lab (so total sample n=6). Unfortunately, I do not have any patient samples. I wish to conduct RNA-seq to examine changes at the mRNA level as well as SNV's in these cells. The goal is to identify changes that characterize drug-resistant cells vs. their drug-sensitive WT counterparts. Please tell me if this type of an analysis is possible with such low sample numbers? If so, please let me know if you are interested in collaborating to analyze the resultant RNA-Seq data?
I am looking for specific markers for arterioles, capillaries and venues for doing immunohistochemial staining by which I can distinguish them properly when I visualize the section under the microscope.
Cytokeratins are generally considered as diagnostic marker for epithelial tissues. In molecular classification different sub-types of cytokeratins are used. CK 5/6 specifically stains the basal epithelial cells, whereas, CK 8/18 stains the luminal epithelial cells. On basis of reactivity of these sub-types of cytokeratins, the human and canine mammary tumours are classified into basal and luminal types and basal subtypes atre associated with poor prognosis as compared to luminal tumours. So, in a way cytokeratins can be used as prognostic markers to access prognosis of mammary tumours.
Does a primary tumor contain specific cancer cells that can leave the tumor and cause metastasis? Or are these changes triggered by the tumor microenvironment after the cancer cell has left the tumor?
Some cells seem to produce cancers more frequently than others. There are > 200 distinct human cell types; do all of these produce cancers under some circumstances? If not what is special about cells that never produce cancer? Why do some cells produce cancer relatively frequently while others do not? How well is this predisposition toward or against cancer development understood?
In measurement of A549 reversal of phenotype/ differentiation using ATRA, how many A549 cells can you seed to produce the required CEA amounts in the medium?
I am trying to build a new mathematical model of glioblastoma, starting with the most up to date molecular biology, I cannot find a clear answer to why motile cells invade. Hypothetically they are undergoing haptotaxis toward a gradient of nutrient of extracellular matrix, but I lack the details at this point.
Submissions are invited for experienced and ambitious International researchers working on aspects related to Molecular Oncology for a thematic issue "ADVANCES IN MOLECULAR ONCOLOGY". Please note that for submission of "review articles" you are requested to submit your proposal and a list of PUBMED indexed publication list. The deadline is 15th of October, 2013.
I need advice here. Anyone has any good/detailed protocols on developing drug-resistant cancer cell lines? I am interested in creating such cell lines using sub-toxic drug doses at incremental levels.
Some time ago a got an idea. Most of the modern therapies against cancer are low in effect because many cancer cells skills allow survival by adopting specific escape and survival systems. Now I think this strategy is wrong because there is no drug (carried by a monoclonal antibody or a nano-particle) capable of destroy 'tout court' a cancer mass. So any exogenous pressure we promote will be transformed in a darwinian cell selection . And what about if we use cancer cells against cancer cells? You know, cancer cells have some obscure mechanisms permitting them to recognize other tumor cells: they don't kill each other, they responsed in chorus to a stimulus and even metastasize together. So if we might create a tumor cell clone capable of detect and destroy selectively the other tumor cells it will be highly beneficial. It is using an army against an army of equal power. At the end of the battle the result would be the death of both of them. I know this is just an idea because we still don't know the ways through which cancer cells promote their own survival messages and produced combined attacks to the organism, but I mean the strategy to use cancer cells as weapon is not so bad. I'd like to know your opinions and if my suggestion might be technically applicable.
I'd like to know if melanoma patients with the BRAF K601E mutation are sensitive to the vemurafenib/dabrafenib treatment.