In This Issue
Cancer Discov September 1 2020 10 (9) 1241-1244; DOI:10.1158/2159-8290.CD-ITI10-9
Aged dermal fibroblasts secreted altered levels of several lipids, which entered melanoma cells via the fatty acid transporter FATP2, the inhibition of which synergized with targeted therapy in aged mice.
Loss of function of the tumor-suppressor gene Fbxw7 conferred resistance to PD-1 blockade by decreasing expression of dsRNA sensors, leading to an altered tumor immune microenvironment.
Taxane-resistant triple-negative breast cancer cells had altered methionine metabolism, leading to epigenetic changes at transposable elements and creating a therapeutic vulnerability to EZH2 inhibitors.
An immunosuppressive subtype of cancer-associated fibroblast was heterogeneous, with only certain subsets modulating immune-cell infiltration in the tumor microenvironment and immunotherapy response.
The serine-synthesis enzyme PHGDH was necessary and sufficient for metastasis to the brain, where amino acid availability is limited, and PHGDH inhibition suppressed brain metastasis.
The tumor suppressor CHD1 increased IL6 expression to recruit myeloid-derived suppressor cells to Pten-null prostate tumors, and CHD1 depletion or IL6 inhibition enhanced the efficacy of immune checkpoint blockade.
Increased exon skipping, particularly affecting proteasome-related transcripts, was mediated by elevated serine/arginine-rich splicing factor 6 (SRSF6) levels in T-cell acute lymphoblastic leukemia.
A new analytic method identified RBMS1, which acted as a posttranscriptional regulator that bound and stabilized the 3′ untranslated region of target mRNAs, as a suppressor of metastasis in colorectal cancer.