Nature Communications: New research could help predict who is more likely to develop cancer

Everyone is exposed to low levels of carcinogens (substances or radiation that promote cancer formation).
one of the most common is benzodiameal, a common chemical pollutant found in smoke, exhaust gases and grilled meat and fish from stoves such as wood-burning stoves.
an active , BPDE, directly destroys DNA sequences, forming compounds that in turn promote cancer-causing mutations.
that while existing models show how BPDE causes these mutations, some of these pathways remain unclear.
it is now thought that BPDE compounds cause mutations in DNA synthesis because they activate a process known as translation synthesis, in which cells copy DNA.
, however, there is evidence that another process, called congenital recombination (HR), is involved, working by copying other undetested parts of the genome.
HR proteins repair complex DNA damage, such as broken DNA strands and interchains, and protect and restore stopped or interrupted replication forks.
new study uses BPDE to treat human cell line before using molecular biology methods, such as microscopes, to detail the congenital recombination pathways.
results provide new insights into how HR can be activated through an unusual mechanism in BPDE compounds and processes, even without stagnating or folding replication forks: it is activated at single-stranded gaps in DNA that are caused by the Reboot activity of the PrimPol gene.
's findings also address long-standing problems, suggesting that in large DNA additions, the exchange between sister chromosomal monosomes (the same copies of chromosome DNA replication) has traditionally been associated with the replication fork collapse and the DSB repair-related gap between HR products and repairing the post-replication gap.
, these replicated gaps are created by PrimPol, which reveals PrimPol's role in DNA damage tolerance.
massive DNA addition induces the formation of RAD51 lesions without the replication fork stopping or crashing.
Eva Petermann, co-author of the study from the Institute of Cancer and Genomic Sciences at the University of Birmingham, said: "Our study reveals the effects of benzeneexposure in cells, which is important for understanding the environmental causes of cancer and the general development of cancer.
understanding of this mechanism can help better predict and detect the negative effects of pollution and help to better explain cancer genomics.
E.g., genetic variants of the HR gene BRCA2 and RAD52 are considered susceptible to lung cancer, which means that understanding how HR helps cells process benzene sto help us predict who may be more susceptible to lung cancer"" In the future, it will be important to study the effects of such gene variants on HR in ssDNA gaps.
a PRIMPOL variant is also thought to play a potential role in cancer.
also helps predict who is more sensitive to carcinogen exposure.
" References: Ann Liza Piberger, Akhil Bowry, Richard D. W. Kelly, Alexandra K. Walker, Daniel González-Acosta, Laura J. Bailey, Aidan J. Doherty, Juan Méndez, Joanna R. Morris, Helen E. Bryant, Eva Petermann. PrimPol-dependent single-stranded gap formation mediates homologous recombination at bulky DNA adducts. Nature Communications, 2020; 11 (1) DOI: 10.1038/s41467-020-19570-7MedSci Original Source: MedSci Original Copyright Notice: All noted on this website "Source : The text, images and audio and video materials of Metz Medicine or Source: MedSci Originals are owned by Metz Medicine and may not be reproduced by any media, website or individual without authorization, and shall be reproduced with the words "Source: Mets Medicine".
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