Breaking Advances
Cancer Res January 15 2012 72 (2) 377-378;
A gene overexpressed in many cancers that promotes cell survival in stressed tumor microenvironments is found to also exert a major role in suppressing a central pathway of cellular senescence.
This seminal study provides direct clinical evidence that the survival of a cancer patient is prolonged by antiangiogenic therapy if the therapy achieves increased tumor blood perfusion, in support of the vascular normalization hypothesis for cancer treatment.
This study offers compelling evidence that genetic polymorphisms in oxidative stress–related genes in the host affect chemosensitivity, such that host gene status must be considered to optimize personalized chemotherapy beyond variations in simply the tumor cells themselves.
This study of cancer susceptibility and progression in mice lacking IL-10 challenges the generally held view that this immune inhibitory cytokine supports cancer, instead offering powerful evidence that endogenous IL-10 actually suppresses cancer by impeding the development of 2 key cellular mechanisms of immune escape.
One use of the recently approved immune activating drug ipilumimab may be to enhance the benefits of tumor cryoablation, a simple older treatment strategy being explored anew in breast and prostate cancers, where it might be very effectively combined with immunotherapy to enhance cure rates in patients with localized tumors.
This important paper elucidates a fascinating mechanism of immune escape from NK cells in which platelets function to shield cancer cells and promote their metastatic spread.
Findings define a role for a circulating regulator of multidirectional trafficking of tumor cells between tumors, blood, and normal tissues, with general implications for metastasis formation and tumor progression.
The perspective that tumor suppressor functions often manifest as immune responses against tumor cells is quickly widening with broader investigations in more valid immunocompetent models of cancer.
This study offers in vivo evidence that the JNK stress kinases have a tumor suppressor function in the setting of mammary carcinogenesis, a role that likely extends to many other settings of epithelial carcinogenesis.
This study offers a sound preclinical rationale for immediate clinical repositioning of arsenic trioxide, an approved treatment for acute promyelocytic leukemias, as a radiosensitizer for any solid tumor.
This provocative study suggests that lactic acidosis occuring in the microenvironment of many solid tumors can abolish canonical responses to hypoxia, suggesting that many models used for development of cancer-selective therapeutics against tumor hypoxia may be deeply flawed.
This large UK-based case–control study suggests potentially important associations of circulating IGF-II, IGFBP-2, and IGFBP-3 in prostate cancers that are detected by the PSA test.
Matrix metalloproteases regulated by the Rb-E2F pathway may serve as its major connection to invasion and metastasis control, with implications for therapeutic intervention such as through targeting the Rb-Raf-1 interaction as illustrated in this study.
Findings argue that androgen-deprivation therapy, used widely in prostate cancer treatment, can trigger epithelial-mesenchymal transition, a foreboding event that may detract from the response to other treatments.
Findings define a mechanism used by cancer stem cells to produce an extracellular matrix glycosaminoglycan that may help seed a metastatic niche in foreign organ microenvironments, with major implications for antimetastatic therapy.
This study reveals insights into the mechanism by which clinical resistance and metastatic progression occur with aromatase inhibitors, a first-line treatment for endocrine-sensitive breast cancers.
This study reveals how p53 controls the Warburg effect, a universal property of cancer cells in which glycolysis is driven powerfully despite aerobic conditions that should otherwise favor oxidative phosphorylation.