Breaking Advances
Cancer Res July 15 2015 75 (14) 2763-2764;
This study describes a mechanism through which an aggressive breast cancer activates pDC to promote a regulatory Th2 response, with implications for therapeutic targeting of a tumor-immune axis of growing recognition in its significance to malignancy.
NOS inhibition has long been studied in cancer to limited impact, but these new preclinical results show how inhibiting NOS in patients after they undergo radiotherapy can relieve immune escape in the tumor microenvironment and greatly improve treatment responses.
This report identifies a stromal cell population expressing the fibroblast activation protein (FAP), which is required for the desmoplastic response seen in many human carcinomas, also showing how FAP-expressing cells promote tumor growth via immune suppression and immune-independent remodeling of the stromal microenvironment.
This work describes a novel and clinically feasible strategy to facilitate the safe delivery of systemic viral anticancer therapies by using clinically available β3 integrin inhibitors to control the problematic inflammatory side effects induced by these effective anticancer agents.
These findings show how prostaglandin signaling in neutrophils and cancer-associated fibroblasts in the colorectal tumor microenvironment shape its inflammatory character, providing a mechanistic rationale to use EP2 antagonists as an alternative to aspirin for chemoprevention.
Results show how mutations in a leukemia-associated gene act epigenetically by influencing the DNA methylation of hematopoietic-specific enhancers that affect leukemia development.
The use of mtDNA copy number measured in blood samples prior to diagnosis is associated with elevated risk of developing breast cancer.
These results suggest that to drive malignant cell growth K-Ras requires the activity of the Met receptor kinase, a therapeutic target already being explored in the clinic, with implications in addressing the long-standing challenge of how to attack K-Ras–driven human tumors.
Inhibition of a vacuolar ATPase that functions as an ion pump in maintaining cellular pathophysiology in cancer appears to selectively disturb iron metabolic pathways, thereby blocking tumor growth.
This study describes a new method for in vivo miRNA precipitation (miRIP), which can identify target-specific miRNAs for an mRNA not otherwise identified by current in silico methods.
These findings offer a preclinical validation of the antiangiogenic uses for a novel mycotoxin in the generalized treatment of solid tumors.
These findings define a mechanistic basis and a biomarker to predict the sensitivity of ovarian cancer cells to a cytotoxic DNA methyltransferase inhibitor, with potentially generalizable applications.
These findings offer a preclinical rationale for repositioning the well-established drug azathioprine to inhibit metastasis of deadly pancreatic cancers.
This important study shows how kinase upregulation in cancer cells can foster resistance to a kinase inhibitory drug, but that this upregulation also sensitizes cells to kinase-mediated toxicities that can be exploited by altering the drug dosing schedule, as a strategy to defeat the drug resistance.
PD-L1 expression in tumors is important for PD-1/PD-L1–based therapeutics and can be monitored noninvasively using SPECT/CT imaging, which may more readily enable patient selection for trials of this type of antibody-based immune checkpoint therapy.
By focusing on recurrent 3p21 deletions in head and neck cancers, this study identifies a novel metastasis suppressor gene that offers an appealing prognostic biomarker and therapeutic target in this setting.
This important study shows how the serine protease TMPRSS2 promotes the growth, invasion, and metastasis of prostate cancer cells via activation of the matrix protease matriptase, with implications that targeting these two proteases may offer new options to treat advanced prostate cancer.