In a recent Cancer Cell paper, researchers at St. Jude Children's Research Hospital and elsewhere report on their systematic deletions of a combination of tumor suppressor genes in a mouse model, which they found produced phenotypes with "striking similarities to subclasses of human diffuse astrocytoma." As a result of its investigations, the St. Jude-led team suggests that "there is a selective cooperativitiy among tumor suppressors" PTEN, TP53, and RB1 during glioma initiation.
Investigators in Switzerland show that URI is an "addicting" oncogene, and is amplified and overexpressed in both ovarian cancer cell lines and in human ovarian carcinomas. URI, the team writes, is "selectively required for the survival of ovarian cancer cells with increased URI copy number."
Cold Spring Harbor Laboratory's Scott Powers and his colleagues report in Cancer Cell on their oncogenomic profiling of 124 genes amplified in hepatocellular carcinoma in a mouse model, through which they "identified 18 tumor-promoting genes, including CCND1." In the team's subsequent RNAi-mediated manipulations in human hepatocellular carcinoma cells, it identified another important driver gene, FGF19 — which neighbors CCND1 on 11q13.3. "These results show that 11q13.3 amplification could be an effective biomarker for patients most likely to respond to anti-FGF19 therapy," Powers et al. write.
Finally, in a paper published online in advance in Cell, researchers at the Memorial Sloan-Kettering Cancer Center and elsewhere present a comprehensive map of double-strand breaks in yeast, which they generated by sequencing Spo11-bound oligos. From this, they found that "a hierarchical combination of factors shapes the genome-wide topography of … meiotic recombination initiation." The team says that its map "illuminates the occurrence of DSBs in repetitive DNA elements, [the] repair of which can lead to chromosomal rearrangements."