Breaking Advances
Cancer Res January 15 2011 71 (2) 291-292;
Findings define a novel immune escape mechanism supporting breast cancer growth which is mediated by a heat shock chaperone protein.
This study defines a co-stimulatory signal for tumor-infiltrating T cells that is required along with T-cell receptor engagement to trigger cytolytic granule lysis of cancer cell targets.
A novel transgenic mouse model may offer an ideal system to study the pathogenesis of human multiple myeloma, an aggressive disease that remains relatively poorly managed.
Introduction of HMGA2 overexpression in ovarian surface epithelial cells is sufficient for a tumor transformation both in vitro and in vivo through regulation of epithelial to mesenchymal transition.
Findings reveal a mechanism through which the pro-tumorigenic gastrointestinal hormone gastrin acts to promote invadopodia formation and invasive motility of colorectal carcinoma cells.
Restricting membrane translocation of AKT from the cytoplasm may have important implications for endocrine cancers and possibly other cancers where AKT dysregulation often occurs.
Findings offer a mechanistic rationale based on modulation of alternate RNA splicing for testing of a common anti-hypertensive drug as an adjuvant therapy in leukemia.
Findings define a new function for histone H2AX, a marker of DNA damage response and repair, that may inform the role of its phosphorylation in oncogenesis.
Findings establish a key pathway of clinical pathogenicity and aggressiveness in neuroblastoma, suggesting the use of HDAC inhibitors and nerve growth factor to treat MYCN-amplified tumors with the poorest prognosis.
Findings offer mechanstic evidence for calcium and vitamin D3 as chemopreventive agents against colorectal neoplasms, suggesting several modifiable, pre-neoplastic risk biomarkers for colorectal neoplasms.
Pathogenic effects of soluble receptor IL-6Rα in ovarian cancer might be specifically antagonized to enhance chemotherapeutic efficacy in ovarian cancer.
Findings suggest tactics to circumvent acquired resistance to a Hedgehog pathway inhibitor that is currently in clinical development as an anticancer treatment.
Findings describe a drug therapy that can attack tumors with K-ras mutations that are resistant to existing EGFR specific therapies.
This study offers new insights into how epigenetic therapy may affect different tumor cell populations and impact cell differentiation through activation of polycomb marked genes and pathways implicated in development.
While encouraging the concept of combining CHK2 inhibition with genotxic anti-cancer drugs, this study also strongly supports the use of CHK2 inhibitors to potentiate the anticancer effects of PARP inhibitors, an exciting new modality for cancer treatment.
Findings offer preclinical proof-of-concept that small molecule inhibitors of a glycoprotein modifying enzyme could offer a widely applicable strategy to treat advanced cancers.
Lead compounds offer proof- of- concept for aptamer peptides that can exert immunogenic anti-tumor effects based on blockade of the central protein-folding chaperone molecule Hsp70.
A mechanistically unique microtubule inhibitor in Phase III trials induces an irreversible mitotic block that contributes to its in vivo antitumor efficacy under intermittent dosing conditions.
An important pro-apoptotic drug currently in human clinical trials is found to activate gene transcription, heighten DNA damage, and trigger senescence in cancer cells that are not susceptible to death induced by this agent, potentially expanding its effective use as a cancer therapy.
Findings describe a novel, chimeric bio-nanoparticle based vaccine that induces auto-antibodies directed against the native conformation of a pan-cancer target and demonstrating cytocidal and tumoricidal effector functions.
This study describes a pathogenic growth regulatory pathway in prostate cancer that suggests important novel targets for therapy.
Drugs that can defeat resistance mechanisms to TRAIL may improve opportunities to exploit the anti-cancer properties of this cytokine.
MicroRNA signatures that can be detected in blood serum may allow definition of different risk-stratified patients with prostate cancer.
Results elucidate a DNA repair mechanism that is critical to maintain chromosome stability in cells, a deficiency which greatly increases cancer risk.
Findings strongly reinforce the concept that therapeutics which target Akt signaling are likely to be effective in blocking the growth of metastatic prostate cancer cells.
Findings reveal an interesting microRNA-regulated extracellular tumor suppressor pathway that is critical to support androgen-independent prostate cancers and amenable to therapeutic disruption.
A novel non-transcriptional function of CDX2 plays a key role in tumor suppression through stabilization of p27Kip1.
Findings describe a potentially important mechanism of resistance to endocrine therapies used widely in nearly all ER+ breast cancer patients, with implications on how to bypass this resistance mechanism.
Strategies aimed at interfering with the proposed cytokine loops may provide a means of targeting the cancer stem cell population.