MedicalResearch.com Interview with:
Paola Scaffidi, PhD
Cancer Epigenetics Laboratory
The Francis Crick Institute
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: Every cancer is different, but even within the same tumor cells are highly diverse, and only some of them are truly immortal and drive tumor growth. This is quite surprising if we think that cancer arises from one cell that keeps replicating itself. So why are some cancer cells more dangerous than others? And why do some cells “get tired” along the way and, at some point, stop dividing?
In our study we describe one cellular mechanism that provides some answers to these questions. We have found that to be able to divide indefinitely, cancer cells have to strongly reduce the levels of a nuclear protein called histone H1.0. This is needed to allow activation of many genes important for cancer cell proliferation, which otherwise would be somehow “hidden” within the cell nucleus. Importantly, though, while tumors grow, some cells raise back the levels of H1.0, which hides these genes again and makes the cells stop proliferating. So the end result is that within the same tumor we have a mix of cells, some which keep these important genes on, while others switch them off and, as a consequence, lose their ability to divide, and differentiate into a more mature state.
MedicalResearch.com: What should readers take away from your report?
Response: One important implication of our findings is that they show this process through which cancer cells “tire out” and differentiate happens spontaneously while tumors grow. This happens more or less efficiently, hitting sometimes only a few cells, sometime most of them, but the good news is that it does happen and it happens naturally, indicating that what is needed to do this is in place. So if we can find a way to make this process more efficient, and make all cancer cells differentiate, this could be an effective way to neutralize their malignant features and possibly convert a malignant tumor into a benign one.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Response: We have shown the effects induced by H1.0 in cancer cells using genetic approaches. Future efforts should focus on developing pharmacological approaches to increase H1.0 levels within tumors. Furthermore, characterization of other cellular mechanisms that revert cancer cells’ immortality and force them to differentiate could open new avenues for cancer treatment.
MedicalResearch.com: Is there anything else you would like to add?
Response: Additional explanation about the study can be found at this link http://scienceblog.cancerresearchuk.org/2016/09/29/flicking-the-switch-on-cancers-immaturity/
MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.
C. M. Torres, A. Biran, M. J. Burney, H. Patel, T. Henser-Brownhill, A.-H. S. Cohen, Y. Li, R. Ben-Hamo, E. Nye, B. Spencer-Dene, P. Chakravarty, S. Efroni, N. Matthews, T. Misteli, E. Meshorer, P. Scaffidi. The linker histone H1.0 generates epigenetic and functional intratumor heterogeneity. Science, 2016; 353 (6307): aaf1644 DOI:10.1126/science.aaf1644
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