Cancer Res April 15 2017 77 (8) 1781-1782;
A kinetic modeling-based computational approach identifies effective combination therapy in B-cell lymphoma.
These findings provide a novel method to improve clinical management of patients with gliomas by providing essential information about the tumor microenvironment, thus opening new avenues for the assessment of personalized immunotherapies.
This study of the EGFR/HER2 inhibitor lapatinib shows how posttranslational modifications can trigger drug resistance in cancer.
These findings identify numerous novel metastasisassociated changes in mRNA/miRNA/lncRNA expression and epigenetic alterations in colon cancers that offer a wellspring of candidate prognostic markers and therapeutic targets.
Nerves in certain tumors provide a physical route for invasive migration, but this study suggests they can also enable oncogenic signals that drive malignant progression.
Increasing expression of the immunostimulatory cytokine LIGHT in the tumor microenvironment improves T-cell activation and infiltration in colon tumors and liver metastases.
These findings offer a mechanistic rationale to employ specific inhibitors of the PI3Kδ isoform to selectively target T regulatory cells and improve cancer immunotherapy.
These findings reveal an important mechanism by which disseminated cancer cells program an inflammatory extracellular matrix to persist and to enable brain metastasis.
These findings show how antitumor T-cell responses after vaccination can be empowered by a secondary peptide vaccination that includes coadministration of CD40 and TLR3 agonists, which strengthen the magnitude of dendritic cell responses.
These striking results show how horizontal transfer of noncoding RNA from host stromal cells to cancer cells is sufficient to promote the formation of therapy-resistant cancer stem-like cells.
Megakaryocytes, the cells that produce platelets, may suppress breast cancer metastasis despite the fact that thromboembolisms are a leading cause of death in cancer patients.
These findings define a STAT3-miR-92a-DKK1 pathway in the generation of cancer stem-like cells in ovarian tumors, with potential therapeutic applications in blocking their progression.
This study defines a novel tumor suppressor gene in gastric cancer that functions in the unfolded protein response, an important stress response that limits cancer cell growth, with clinical implications as a survival biomarker in patients.
These results establish differential interactions between the SCF-type ubiquitin ligase FBXW7 and functionally distinct isoforms of the ErbB3-binding adaptor protein EBP1, providing insights into their roles in cancer.
The focal adhesion kinase PEAK1 drives aggressive pancreatic cancer cell behaviors by activating a stem cell-like transcription factor program.
A little studied microRNA is found to inhibit tumor cell invasion and metastasis, possibly offering a general therapeutic target for the treatment of advanced cancer.
In elucidating mechanisms that link the stem-like phenotype of KRAS-mutated lung cancer cells to radiation resistance, this study identifies potential therapeutic targets to overcome this resistance.
This study describes a novel clinically validated ex vivo explant platform to predict tumor responses to anticancer drug treatments.
Degradation of a fundamental mechanism of immune escape can enhance the antitumor acitivity of CAR T cells in eradicating malignant cells in preclinical models.
Immunotherapy with oncolytic adenovirus is improved by arming the virus with a BiTE antibody that binds T cells as well as tumor cells, thereby helping productively target infiltrating T cells in tumors and improving the efficacy of oncolytic viral therapies.
These findings suggest a therapeutic strategy to combat pancreatic cancer by targeting the HSPA5-GPX4 pathway of ferroptosis, a form of regulated cell death driven by oxidative injuries, which promote lipid peroxidation.
This study introduces a novel concept in acquired resistance, namely, the role of wild-type allele-mediated resistance in response to mutation-selective inhibitors in cancer treatment.
This potentially seminal report defines a targetable ubiquitin ligase as a pivotal modifier of metastasis and immune response in aggressive breast and ovarian cancers that fail conventional therapy, with immediate implications for developing it as a broad-based drug target.
Reduced expression of a high-affinity carrier of nucleoside analogues correlates with poor event-free survival in patients receiving treatment with nucleoside analogs, with implications for treatment strategies in cancer patients receiving these drugs.
A noninvasive tactic to quantify tumor burden in a deadly pediatric brainstem tumor offers a rapid treatment monitoring option that may help improve management of this cancer.
In the intestine, Lgr5+ colonic epithelial stem cells are found to be much more radioresistant than Lgr5+ crypt base columnar stem cells, a difference based on a mechanism termed checkpoint adaptation that might generally dictate tissue radiosensitivity.
Hedgehog inhibitors in clinical trials may be useful to attack many types of cancers by blocking vital cross-talk between cancer stem cells and stromal fibroblasts needed to support tumor viability, as illustrated in this study of breast cancer.
An oncogene associated previously with myeloid leukemia development is discovered to have an important prognostic impact in aggressive triple-negative breast cancers, with possible implications for understanding its pathophysiology.
This study establishes that the vitamin D metabolizing enzyme Cyp24a1 functions as an oncogene to promote malignant progression and resistance to BRAF inhibitor treatment, offering a mechanistic rationale for targeting Cyp24a1 to improve cancer treatment.