Breaking Advances
Cancer Res March 1 2011 71 (5) 1509-1510;
Findings provide a preclinical rationale for clinical targeting of a Notch receptor ligand to improve treatment of colon cancers with oncogenic KRAS mutations, which are refractory to existing treatments.
This study reports a rapid, simple and inexpensive assay to detect cancer cells in blood, offering a potentially important tool for clinical management of cancer and cancer relapse.
A single nucleotide polymorphism identified in a key immune regulatory transcription factor associates with elevated risk of the most common types of skin cancer.
Depleting platelets in tumor-bearing mice preferentially increases the leakiness of the tumor vasculature, leveraging the efficacy of administered chemotherapies without worsening toxic side-effects.
Cellular exchange of microRNAs is emerging as a fascinating new mechanism by which tumor stromal cells can influence the tumor cell pathophysiology
Findings offer preclinical evidence that breast cancer metastasis can be blocked by targeting an important oxidase in the tumor microenvironment.
Small molecule inhibitors now in clinical development to block both mTORC kinases can leverage the anti-angiogenic actions of VEGF inhibitors.
This interesting mouse model study suggests that tumor suppressor alterations in stromal tissue may be sufficient to drive progression of some types of cancer
Findings highlight a novel immunotherapeutic target that is tractable for small molecule inhibition and that could be broadly relevant to many types of human cancer.
Toll receptors that control innate immune response are not only expressed by immune cells but also by many human cancer cells, which might be targeted directly by Toll receptor agonists in certain disease settings.
Findings reveal a novel mechanism by which STAT3 modulates immunosurveillance by NK immune cells, by repressing the expression of a key NK cell recognition molecule on cancer cells.
“Findings suggest that the established role of arachadonic acid biosynthesis in colon tumorigenesis may be driven to a large degree from mast cells that support myeloid- derived suppressor cells, an important component of the tumor microenvironment thought to drive immune escape.”
This study defines a tumor-derived inducer of inflammation that provides an important mechanistic link between chronic inflammation and prostate carcinogenesis.
Findings reveal a regulatory cycle that can act synergistically to favor cancer cell proliferation in hypoxic tumor microenvironments.
Results shed light on a potentially important mechanism involved in estrogen mimicry at the estrogen receptor-alpha, with implications for understanding breast cancer risk and the development of novel therapeutics for treatment of endocrine independent breast cancer.
In patients with ulcerative coliitis, cell senescence acts as a tumor suppressor mechanism that is abrogated during the transition from low-grade to high-grade dysplasia.
Findings describe an microRNA-based mechanism constituting a double feedback loop for control of a pivotal chromatin remodeling factor in cancer cells.
Results identify a new function of cyclin D1 that could help explain its important pathophysiological roles in lymphomas and solid tumors.
“A single-hit mutation in Keap1, a key regulator of the important cytoprotective gene Nrf2, is sufficient to generate a selective advantage in the cancer microenvironment.”
Findings reveal the mechanisms of cancer-induced cardiac atrophy, which are distinct from skeletal muscle and exhibit sex differences.
This study reveals an important mechanistic linkage in metastasis of liver cancers, with potential therapeutic implications.
Findings define an Abl-related tyrosine kinase in a mechanism of breast cancer invasion that is mediated by invadopodia maturation and function.
Findings suggest a mechanism through which a transcriptional coactivator can promote invasive progression in breast cancers, where it has been implicated as a marker of poor prognosis.
Combination therapy targeting PI3K/AKT signaling and DNA methylation can effectively reactivate epigenetically silenced genes and slow tumor progression.
In this large prospective study, long-term use of cholesterol-lowering drugs was associated with lower risk of melanoma, endometrial cancer, and non-Hodgkin lymphoma.
Findings suggest strategies for therapeutic targeting of a stem-like phenotype in a relevant cohort of cancer patients.
Findings show how an cellular efflux transporter can circumvent a major pathway to activate therapeutic nucleoside mimetic drugs.
Findings prompt clinical study of a tractable therapy for thyroid cancer based on disruption of a functionally critical cell surface receptor signaling complex
Findings describe the use of macrophages to target an oncolytic adenovirus to hypoxic areas of prostate tumors, to improve viral inhibition of primary and secondary tumour growth.
Combinatorial profiling of double-strand DNA break repair machinery yields peptides capable of modulating DNA repair phenotypes and sensitizing tumor cells to genotoxic therapy.
Findings suggest an effective strategy to defeat chemoresistance in human pancreatic cancers, which remains a primary clinical challenge.
A kinase originally linked to Parkinson's disease may offer a potential therapeutic target in treatment of cancers characterized by a specific deficiency in DNA repair.
Findings offer initial preclinical proof-of-concept for small molecule blockade of a important translational regulator as a tractable cancer therapeutic approach.
Determining the chromosome instability (CIN) status of patient tumors may provide useful information on the clinical response to many cytotoxic agents and small molecules.
Findings suggest that the dimeric state of an oncogenic receptor in cancer cells may impact their therapeutic response to anti-receptor antibodies.
This study rationalizes anticancer combinations that not only synergize but also overcome drug resistance, a primary challenge in cancer care.
This incisive and important preclinical study shows how using histone deacetylase inhibtors to restore ER expression in ER-negative tumors can be used to sensitize them to the therapeutic effects of aromatase inhibitors.
“This study reveals a vital mechanistic connection between the widely employed cancer drug 6-thioguanine and its effects on DNA hypomethylation, with implications for understanding therapeutic efficacy.”
A calcium-binding molecule that is prognostic in several cancers is found to be critical to maintain stemness properties, with implications for new cancer targeting strategies.
This study establishes the root causal relationships between Myc and E2F, two key transcription factors involved in virtually all human cancers.
Findings define an important transcriptional target of BRCA1 that may provide insight into the pathogenesis of basal-like breast cancers, an aggressive but poorly understood disease.
Insights into how oncogenic addiction is maintained to the MET kinase, which drives a powerful program of invasive growth in cancer cells, suggests strategies to strengthen cancer therapies based on MET inhibition.
A comprehensive survery defines a set of microRNAs that are important regulators of androgen receptor levels and prostate cancer cell proliferation.
Findings prompt a rethinking of CDC25B regulation and function and how its impaired expression in cancer may affect susceptibility and chemotherapeutic response.
Findings prompt new insights into how androgen signaling might be selectively blocked in prostate cancer cells while sparing normal androgen-dependent processes.
Infectious complications during colon cancer surgery may contribute to liver metastasis, suggesting benefits to inhibiting these complications during the peri-operative period.
Findings suggest a strategy to render AML cells sensitive to proteosome inhibitory drugs, which are presently ineffective in this disease.
A key regulator of the Hippo tumor suppressor pathway functions as a potent oncogene