Cancer Res February 15 2017 77 (4) 813-814;
An AML executable signaling model with cell-specific context switches can enable personalized tailoring of drug combinations to increase sensitivity and overcome drug resistance.
These findings suggest that the poor efficacy of anti-PD-1 as an immune checkpoint therapy for many patients could be accentuated greatly by adjuvant radiotherapy, thereby broadening its useful application against cancers, where robust but relatively infrequent responses have been documented.
Identification in lung tumors of a particular subset of T lymphocytes at their earliest phase of functional differentiation will provide a useful biomarker to monitor the earliest stages of development of adaptive tumor immunity.
These findings in a Drosophila model system illuminate a mechanism by which the human SMARB1/hSNF5 gene gives rise to malignant rhabodoid tumors during early childhood.
The ETS family transcription factor ESE3 binds and upregulates expression of the E-cadherin gene, a determinant of epithelial function and an inhibitor of invasion and metastasis in pancreatic cancer cells.
A new mouse knockout model for the tumor suppressor gene Maspin resolves questions surrounding its specific functions in cancer and its therapeutic potential for cancer diagnosis and treatment.
A novel mouse model for alveolar soft part sarcoma (ASPS) demonstrates induction of hemangiopericytes by ASPS cells as well as intravasation of tumor cells mediated by GPNMB, providing novel mechanisms of ASPS development, angiogenesis, and hematogenous metastasis.
The new mouse model reported in this study will accelerate research on radiotherapy for gastrointestinal malignancies and speed drug development to protect normal tissues in this setting.
These findings support the hypothesis that estrogen carcinogenicity relates mainly to the mitogenicity of a specific pathway of estrogen metabolism (16-pathway metabolites).
These findings highlight a recently discovered natural product as a potent bioactive inhibitor of thioredoxin-1, a critical regulator of thiol homeostasis in cancer cells, and a candidate anticancer modality with potentially broad use in many types of cancer.
These findings provide a rationale for continued development of a structural framework for the generation of potent and selective MTHFD2 inhibitors for cancer treatment.
These findings reveal that the therapeutic efficacy of mda-7/IL-24 treatment in multiple cancer types is dependent upon downregulation of miR-221.
Glioblastomas upregulate the isocitrate dehydrogenase IDH1 to help meet their demands for the reductant NADPH and this study shows how inhibiting this metabolic adaptation can improve the efficacy of radiotherapy in this disease.
These findings define an 18-gene signature with prognostic utility in several cancers, where Myc activation occurs commonly, even in the absence of Myc gene amplification.
Extending the functional impact of RB loss in cancer, this study shows how this event promotes metastasis via expression of the cell migration receptor RHAMM, with potential implications for a broadly applicable therapeutic strategy in advanced cancers.
This milestone study establishes the noncanonical WNT family member Wnt5a as a master regulator of brain invasion in glioblastoma and offers a rationale for its therapeutic targeting in glioblastoma patients.
These findings suggest candidate diagnostic markers of innate or acquired resistance to antiangiogenic resistance, with implications for personalized care with antiangiogenic tyrosine kinase inhibitors.
A newly identified miRNA-regulated pathway influences prostate cancer metastasis and serves as a potential therapeutic target.
These findings uncover a link between nucleolar ARF expression and adverse drug response, suggesting that patients with upregulated ARF may benefit from a combination of chemotherapy and modulator of protein translation.