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Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
A possible mechanism involved in cancer protection may be p16, a tumor suppressor protein, that in humans is encoded by the CDKN2A gene and plays an important role in cell cycle regulation. It prevents cell division once individual cells come into contact (known as “contact inhibition”). The cells of most mammals, including naked mole-rats, undergo contact inhibition via the gene p27, which prevents cellular reproduction at high cell densities. The combination of p16 and p27 in naked mole rat cells is a double barrier to uncontrolled cell proliferation,209 one of the hallmarks of cancer and is known to be implicated in the prevention of several cancers, notably melanoma.
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Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
A possible mechanism involved in cancer protection may be p16, a tumor suppressor protein, that in humans is encoded by the CDKN2A gene and plays an important role in cell cycle regulation. It prevents cell division once individual cells come into contact (known as “contact inhibition”). The cells of most mammals, including naked mole-rats, undergo contact inhibition via the gene p27, which prevents cellular reproduction at high cell densities. The combination of p16 and p27 in naked mole rat cells is a double barrier to uncontrolled cell proliferation,209 one of the hallmarks of cancer and is known to be implicated in the prevention of several cancers, notably melanoma.
MicroRNAs diagnostic and prognostic value as predictive markers for malignant mesothelioma
Published in Archives of Environmental & Occupational Health, 2020
Elena Sturchio, Maria Grazia Berardinelli, Priscilla Boccia, Miriam Zanellato, Silvia Gioiosa
MM is generally resistant to conventional chemotherapy and radiation cancer treatments, and the tumor is diagnosed 20-40 years following first exposure. The long latency period between exposure to asbestos fibers and the development of malignant mesothelioma suggests that more events are needed at both genetic and epigenetic level for the transformation of mesothelial cells into tumor cells, some of which may be directly or indirectly caused by asbestos fibers. To date, the genetic basis of disease is unknown but appears to involve multiple types of chromosomal abnormalities, such as alterations of chromosome number and structure, translocations and gains or losses of genetic material. Karyotype analysis revealed that loss of genetic material is more common than gain, and include chromosomes 9p, 3p and 22q in regions containing main tumor suppressor gene altered in MPM (CDKN2A, BAP1 and NF2).3