Breaking Advances
Cancer Res April 1 2014 74 (7) 1883-1884;
This study describes the functional consequences of the most frequent DNA polymerase variant linked to colorectal and endometrial cancer, challenging the recently forwarded idea that hypermutated human cancers must result from loss of exonucleolytic proofreading.
This article highlights the superior qualities of a novel noninvasive imaging method to monitor tumor development and therapeutic response in preclinical models.
This preclinical study reports a method to quantify antibody accumulation and pharmacodynamics in brain tumors, where delivery after systemic administration is often difficult to assess, offering a holistic in vivo approach to assess CNS-targeting drugs.
Therapeutic inactivation of CTLA-4–related molecules like VISTA may have enormous potential for generalized immunotherapy of cancer.
This study offers a preclinical proof-of-concept to evaluate the efficacy and mechanisms of action of a VISTA-targeting antibody in multiple tumor models.
This study offers a preclinical proof-of-concept for an antimetastasis vaccine targeting Twist, a transcription factor that promotes metastasis and drug resistance in many tumor types.
This study describes a preclinical model for dormant metastases controlled by the immune system, an understanding of which may lead to new insights into how to extend survival by blocking relapses of metastatic cancer.
These findings offer new insights into how the proinflammatory cytokine IL-17A influences tumor immunity, with potential implications for the development of tumor immunotherapy.
ICAT inhibition reduces the mesenchymal amoeboid transition involved in invasive cancer cell motility, limiting metastasis formation.
This study provides a mechanistic rationale to immediately reposition the use of Src inhibitors currently in clinical trials for the treatment of malignancies associated with mutation of the tumor suppressor gene TSC2.
As a candidate therapeutic target, overexpressed cyclin E1 is a driving force of hormone-independent growth, genetic instability, and progression of “triple-negative” breast cancers and other aggressive cancers.
This study shows how the nuclear receptor LRH-1 modulates the sensitivity of breast cancer cells to antiestrogen therapy, suggesting new insights into how resistance may emerge to limit treatment effectiveness.
These findings identify a therapeutic target for treatment of Kaposi sarcoma, a cancer best known for its association with AIDS patients at highest risk of this herpesvirus-driven disease.
This study describes a myeloid cell–carcinoma signaling network that links the tumor microenvironment in new ways with tumor growth, highlighting opportunities to target tumors where this network is active.
These results suggest new insights into prostate cancer etiology, establishing a central role for histone modification and providing a rationale for clinical evaluation of epigenetic-targeted therapy in prostate cancer patients.
These findings define an EGF-related signaling pathway that mediates the oncogenic effects of secondary bile acids in gastrointestinal cancers, the targeting of which may enhance therapeutic responses.
More rapid visualization of HPV-positive oral tumor growth will assist the development of chemotherapeutic and radiotherapeutic strategies to stem this rapidly growing disease.
These findings describe an important regulatory feedback on a key tumor suppressor pathway that may have a pivotal role in epithelial tumors.
These findings define miR-126 as a therapeutic focus to specifically eradicate stem-like cells in acute myeloid leukemias that tend to relapse in patients despite early positive responses to chemotherapy.
These findings point to a specific inhibition of NOTCH2/3, rather than NOTCH1, as a strategy for attacking cancer stem-like cells in metastatic colon cancer.
These results identify a novel target to improve treatment of HER2-positive breast cancer through leveraging existing anti-HER2 therapy.