What is it about?
The genetics behind why ovarian tumors form remain unknown. Only a few familial cancer genes are known. In this paper, the authors establish of the first time that a cellular recycling gene, BECN1, is directly responsible for allowing tumors to form when the gene becomes suppressed. This surpasses previous literature which showed association with tumor formation, and was the first to show a causal relationship in ovarian cancer.
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Why is it important?
While many families know that their BRCA1 or BRCA2 mutation predisposes them to breast and ovarian cancer, some families do not know why they have family history of particular cancer types. BECN1 is not often mutated like BRCA1 or BRCA2 is. However, one of the first things that happens in cancer development is chromosome instability. In this paper, BECN1 suppression mimicking a loss of a chromosome was shown to be sufficient to yield higher predisposition to cancer, which helps us understand how cancers, particularly ovarian cancers, develop.
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This page is a summary of: Autophagy gene haploinsufficiency drives chromosome instability, increases migration, and promotes early ovarian tumors, PLoS Genetics, January 2020, PLOS, DOI: 10.1371/journal.pgen.1008558.
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Encyclopedia of chromosome alterations important in cancer
Haploinsufficiency drives Darwinian evolution. Siblings, while alike in many aspects, differ due to monoallelic differences inherited from each parent. In cancer, solid tumors exhibit aneuploid genetics resulting in hundreds to thousands of monoallelic gene-level copy-number alterations (CNAs) in each tumor. Aneuploidy patterns are heterogeneous, posing a challenge to identify drivers in this high-noise genetic environment. Here, we developed Shifted Weighted Annotation Network (SWAN) analysis to assess biology impacted by cumulative monoallelic changes. An atlas of CNA pathways altered in each cancer type is released. These CNA network shifts highlight new, attractive targets to exploit in solid tumors.
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