Say, if you thought its a tumor suppressor gene, but found it induces quiescence. Is it better not to invest much time on it?
Isn't it important to study the 'steady' state of the cell? To see what it is doing and get a baseline, maybe cancerous vs healthy cells? Maybe these states are altered between the two? I would find it interesting to study.
I don't understand the question. Are you talking about in vitro induction of quiescence. And do you mean with quiescence that you suppress growth and proliferation a lot?
"but found it induces quiescence.": that is an interesting finding depending on how you define quiescence on the molecular level, in vitro and in vivo.
There are examples form completely other fields which struggle with strange questions (http://www.r-bloggers.com/three-tips-for-posting-good-questions-to-r-help-and-stack-overflow/) and to be able to answer a question requires a certain amount of information, of common rules and language.
Could you refine your question?
Thanks Melissa and Professor Andl.
@ Professor Andl, I am not talking about induction of quiescence through serum starvation, contact inhibition or other means. Say, a particular gene has some antitumor activity which was confirmed by several groups in vitro and in vivo experiment. But when I overexpress it in my cell, it arrests cells at Go/G1, keeps the cells at this stage for long time and this process is reversible. Those cells are almost negative in Ki67 staining and doesn`t incorporate BrdU. In microarray, stem cell quiescence gene signature is enriched. (This is how I thought about quiescence). They don`t show clonogenicity but induce cancer stem cell markers.
Now, with this outcome, I received some discouraging criticism from my colleague. They said, gene that keeps the cells at Go, doesn`t have much impact and we should not invest too much time on it. Rather, G2/M arrest is more interesting. What do you think about their comment?
I disagree G/o could be very important. If it is held at G/o then it cannot be reproducing more cancerous cells. Maybe a great way to stop or slow the overactive growth of some cells. I find that many only study what they want to happen rather than looking at the whole picture, What one sees as utter failure or waste of time could hold many answers.
Thanks Melissa, I was thinking on the other side. Although cells in Go state can suppress tumorigenesis, there is a chance for those cells to start proliferating again. So, they can strike back again after many years when both patient and doctor believe that the cancer is eradicated. This happens in case of metastatic dormancy.
Thanks ruhul for the update. Your project sounds interesting. Of course there are several ways to look at this. My point if view is simple. If the quality of the research meets certain criteria then it does not matter what the topic is. It is all interesting. However, science is maintained generally by governmental funding and is limited. Here in the USA much focuses on human disease. This makes sense. But we can't do much research in humans and have to use lots of mouse models, kind of an national institute of mouse health, nimh.
But to put the mouse data in context to humans, it would be nice how representative the mouse is. And again, we are back to your question: is it worth? Money, fame, fortune, insight, publications? In a more perfect world this would not play a role, in reality it does.
Your results sound interesting enough to me for the real world. One can twist your approach towards cancer stem cells (in case such cells really exist) or the cell population in a tumor that is resistance to treatment.
Thank you very much Professor Andl for your input. I just have one more question. Do you think-i might have some insights if I consider my approach towards tumor dormancy or cancer stem cell hypothesis or there are some other ways to look at it?
Sure, tumor dormancy is a hotly debated issue with little clear data and concepts. Some groups performed label-retaining experiments in humans and generally failed to show their existence in human premalignant and malignant lesions. However, there are limitations of this approach since the success depends on how long the labeling period is and how often the "dormant" cells divide. If the labeling is too short and the dormancy prolonged, one will not label many dormant cancer stem cells. Checking human tumor tissues for your marker may help. Checking established slow cycling cell populations for your marker may help. These cells may be pretty rare in tumors...
Many many thanks, Professor Andl. It seems difficult to retrieve concrete result. I will try to do according to your suggestions.
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