Editorial
George C. Prendergast
Cancer Res January 1 2010 70 (1) 1-3; DOI:10.1158/0008-5472.CAN-09-4246
AMP kinase, a master regulator of cellular energy metabolism, may provide a key link between obesity-associated inflammation and increased breast cancer risk.
NAMPT has properties of a positive biological modifier of NAD-dependent inflammation and cell growth that prompt interest in it as a pharmacological target for cancer treatment.
This meeting report summarizes discussions among systems biologists concerning how to achieve greater integration of approaches in the field with the mainstream of cancer research.
Study describes a creative new biological approach to image and treat metastatic disease.
Decreased Endothelin receptor B signals facilitate de novo melanomas that do not arise from nevi.
Eradication of H. pylori infections in stomach has been associated with an increased incidence of upper GI cancers, perhaps as a result of a greater incidence of gastric inflammation normally reduced by an H. pylori-induced extracellular protease.
Improving the ability to predict relapse of localized lung adenocarcinoma after surgical resection, through the miRNA expression profiling methods reported in this study, may alter therapeutic decisions and improve patient outcomes.
Therapies that are less effective against cancer stem cells may quicken tumor evolution, increasing tumor heterogeneity and speeding the development of tumor progression and drug resistance.
To facilitate liver metastasis, IGF-1 must act beyond the tumor cell to provide an essential support to obesity-associated inflammatory processes in the tumor microenvironment.
MDSC promote tumor formation by suppressing T cell activity through multiple mechanisms, including by blocking their essential need for cysteine.
Imaging a central marker of the unfolded protein response identifies regions of tumor growth.
Metabolic aberrations in tumors affect not only tumor cells but other cell types in the tumor, including immune cells whose antigen presenting capacity becomes subverted.
Findings define a tractable approach to degrade two important cellular mechanisms of immune suppression that are erected by advanced tumors and that inhibit the efficacy of immune stimulatory therapies.
Chemokine attack may offer an effective way to degrade immune escape by tumors, heightening the antitumor response to vaccines.
A straightforward tactic to increase the effective immunogenicity of anti-cancer DNA vaccines is demonstrated.
IFNγ, which is critical to the antitumor activity of IL-12, is also responsible for inducing the feedback inhibitory mechanisms that regulate post-IL-12 immune responses. Specifically, IFNg induces the enzyme indoleamine 2,3 dioxygenase (IDO), which in turn promotes the expansion of CD4+ CD25+ Foxp3+ T-suppressor cells, short-circuiting post-therapy antitumor T-effector activity.
Findings define a subnuclear targeting mechanism by which the function of the NF-κB factor RelA can be switched to promote either apoptosis or survival, addressing long-standing questions about this dual nature of NF-κB in different settings, including different cancers.
Results rationalize the clinical evaluation of bortezimib (Velcade) to treat imatinib-resistant GIST tumors.
A chromosomal region commonly deleted in osteosarcoma contains a novel group of cooperatively acting tumor suppressors, possibly with significance in other tumors as well.
SNPs in 2 of 142 genes in the p53 network may predict clinical responses in chemotherapy of soft tissue sarcomas.
Findings define the developmental transcription factor OTX2 as a central oncogenic driver in medulloblastoma.
Transcriptional repressor ZBRK1 upregulated by BRCA1 has properties that may offer new insights into metastasis susceptibility in cervical carcinomas.
Attenuations in the expression of a novel LEF/TCF pathway effector in hemtopoeitic cells might contribute to the development of chronic lymphocytic leukemia (CLL).
Receptors that are well known to bind and respond to environmental toxins may also exert important unrelated functions in tumor suppression.
Groundbreaking findings identify a similar fundamental risk factor underlying sporadic and familial forms of ovarian cancer.
Functional alterations in RNA splicing that may occur widely in cancer are known to have significance for certain oncogenes and tumor suppressor genes, but the molecular basis for these alterations is only recently emerging as addressed in this study of cyclin D1 in prostate cancer.
Metastatic prostate cancer is sustained by a possible ErbB3 signaling pathway leading through FoxA to the developmental gene AGR2, offering a new realm for therapeutic explorations against this deadly disease.
Molecular diagnostics that could improve primary screening and triage of cervical lesions are described.
Vanadate is commonly employed as an inhibitor of protein tyrosine phosphatases but it is also a potent inhibitor of p53 mediated apoptosis.
New strategies to treat a common and deadly pediatric brain tumor are suggested by findings that PI3K/Akt signaling is needed to support β-catenin pathways that are known to mediate tumor cell proliferation and survival.
Study of a negative modifier complex that appears to affect an important signaling pathway in brain tumors may offer a new therapeutic direction.
Small molecule inhibitors of the mTOR complexes represent a recent refinement of strategies to disrupt a fundamental cell growth and survival pathway for the purpose of cancer treatment.
Resistance to the HER2 antibody trastuzumab, used widely in breast cancer treatment, may arise partly as a result of its ability to elevate expression of a receptor tyrosine kinase that can promote trastuzumab resistance.
New prognostic markers predicting metastatic spread of cancers to the liver cancer might be found among 12 vascular proteins identified in a mouse model of liver metastasis.
Personalized therapy with estrogen-lowering drugs may be advanced with findings of pharmacogenomic markers that can predict how efficiently specific patients may respond to treatment.
Novel gold compounds with cytotoxic activity based may act by altering an important class of chromatin regulators.
The reliance of lung cancer stem cells on c-Kit signaling suggests a possible opportunity to reposition imatinib (Gleevec) as an adjuvant to cytotoxic chemotherapy for improving lung cancer treatment.
A class of cell surface receptors upregulated with the acquisition of androgen independence in prostate cancer may be useful as targeting tools.
Findings suggest novel targets in the HIF pathway of hypoxia response that may sensitize glioblastomas to therapeutic attack.
FOXO1 targeting by microRNAs may mediate an important step in endometrial tumorigenesis, suggesting new tactics to restore FOXO1 expression and attack established tumors.
Study findings confirm the importance of mucins in metastasis and offer proof of concept for use of miR-145 as a novel anti-metastatic therapy.
Cancer stem cell theory postulates that more effective therapies will emerge only with better characterization of tumor-propagating cells that may be relatively rare in tumors, yet vital to their growth and evolution, as studied here in new models of melanoma.
The capability to directly clone patient antibodies through human hybridoma technology offers a strategy to identify novel 'theranostic' markers in cancer that occur naturally during human tumorigenesis.
Findings rationalize an evaluation of patients whose tumors harbor mutations in BRCA2 for treatment with a combination of temozolomide and inhibitors of DNA polymerase β.
A tractable target for drug development acting downstream of Notch may yield new treatments for deadly glioblastomas.