Breaking Advances
Cancer Res July 15 2017 77 (14) 3723-3724;
RAS-responding effector genes that control cell-cycle transit rely upon coordinate upregulation of a long non-coding RNA, implicating it as a possible therapeutic target in RAS-driven cancers.
This study offers a useful in vivo model of human sporadic forms of BRAF-mutant GIST to help unravel its pathogenesis and therapeutic response to novel experimental agents.
These findings illuminate a metastasis pathway in the common pediatric brain tumor medulloblastoma, which offers possible theranostic opportunities.
By defining miRNAs that sustain stem cells in the crypts of normal colon tissue, this study illuminates a pivotal mechanism through which cancer stem-like cells may be created to seed colorectal cancers.
This important paper describes the discovery of a positive feedback mechanism that sustains PI3K/Akt signaling in tumor cells that lack PI3K/Akt mutations, illuminating the nearly universal role this pathway has in tumor cell survival.
These findings challenge the notion of the detrimental role of estrogen plus progesterone in breast cancer, revealing a signaling cascade that upregulates the tumor suppressor protein PML in response to both hormones.
This deep sequencing study of stage I-III colon cancer specimens identifies novel oncogenic gene fusions in colorectal cancer that may drive malignant progression and offer new targets for personalized therapy.
By refuting the prevailing view that cells lacking Mdm2 can survive if p53 is also absent, this important study provides a therapeutic rationale for targeting Mdm2 to eliminate p53-null lymphomas and sarcomas.
This potentially seminal study offers preclinical proof of concept for combining CDK7 and BCL-2/BCL-XL inhibitors as a mechanism-based therapeutic strategy to improve the management of aggressive triple-negative breast cancers, which still lack effective biomarkers and precision treatment approaches.
Two extracellular vesicle-derived microRNAs are found to drive liposarcoma progression by stimulating the secretion of proinflammatory IL6 from tumor-associated macrophages, offering new theranostic opportunities in this cancer setting.
Targeting a second enzyme involved in NAD+ biosynthesis overcomes the resistance to NAMPT inhibitors observed in clinical trials, offering a path toward new therapies.
These findings demonstrate potent antitumor activity of targeting CHK1 in chemosensitive and chemoresistant models of small cell lung cancer, especially those with MYC amplification or overexpression.
Combining the BCL-2 inhibitor venetoclax with radioimmunotherapy yields a synergistic therapeutic response in preclinical models of three lymphoma subtypes, with optimal dosing curing all mice with no detectable toxicity.
Combining an oncolytic virus with an immune checkpoint drug creates an in situ autologous vaccine effect, establishing a tumor-specific treatment that is both efficacious and durable.
In seeking to improve responses to combination therapy, a model that incorporates parameters for cancer evolution suggests variations in dosing regimens that can safely increase therapeutic efficacy, with immediate clinical implications.
The findings of this important study add to the understanding of the biological basis for tumor phenotypes, which can be quantified by medical imaging.
A companion diagnostic PET imaging agent can enable clinicians to rapidly identify small cell lung cancer patients most likely to benefit from treatment with a Notch ligand-targeting therapy, despite low levels of ligand expression on the surface of the cancer cells.
These findings present the design, development, and clinical testing of a cancer detection system of nearly perfect accuracy that can improve surgical resections while in the operating room.
These findings show significant differences in the associations between circulating androgen concentrations and invasive ovarian cancer risk by subtype, underscoring the importance of examining etiologic differences by subtype.