Showing papers in "Cancer Cell in 2014"

TL;DR: Although myofibroblast-depleted tumors did not respond to gemcitabine, anti-CTLA4 immunotherapy reversed disease acceleration and prolonged animal survival, and underscores the need for caution in targeting carcinoma-associated fibroblasts in PDAC.

TL;DR: De deleting Shh in a well-defined mouse model of PDAC demonstrated that some components of the tumor stroma can act to restrain tumor growth, and administration of VEGFR blocking antibody selectively improved survival of Shh-deficient tumors.

TL;DR: Findings suggest that lncRNA-ATB, a mediator of TGF-β signaling, could predispose HCC patients to metastases and may serve as a potential target for antimetastatic therapies.

TL;DR: P53-like MIBCs were consistently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53- like phenotype after therapy.

TL;DR: It is reported that breast cancer associated exosomes contain microRNAs (miRNAs) associated with the RISC-Loading Complex (RLC) and display cell-independent capacity to process precursor micro RNAs (pre-miRNas) into mature miRNAs.

TL;DR: There is growing evidence that these mutant p53s have both lost wild-type p53 tumor suppressor activity and gained functions that help to contribute to malignant progression.

TL;DR: It is shown that miR-105, which is characteristically expressed and secreted by metastatic breast cancer cells, is a potent regulator of migration through targeting the tight junction protein ZO-1.

TL;DR: In this paper, the authors summarize lessons learned from preclinical and clinical studies over the past decade and propose strategies for improving antiangiogenic therapy outcomes for malignant and nonmalignant diseases.

TL;DR: Administration of RG7155 to patients led to striking reductions of CSF-1R(+)CD163(+) macrophages in tumor tissues, which translated into clinical objective responses in diffuse-type giant cell tumor (Dt-GCT) patients.

TL;DR: It is shown that 5-aza-2'-deoxycytidine treatment not only reactivates genes but decreases the overexpression of genes, many of which are involved in metabolic processes regulated by c-MYC.

TL;DR: This article performed massively parallel sequencing of paired tumor/normal samples from 203 multiple myeloma (MM) patients and identified significantly mutated genes and copy number alterations and discovered putative tumor suppressor genes by determining homozygous deletions and loss of heterozygosity.

TL;DR: Across multiple mouse tumor models and human tumor biopsies, the intratumoral dendritic cell (DC) populations are delineated as distinct from macrophage populations, and CD103(+) DCs are extremely sparse and yet remarkably capable CTL stimulators.

TL;DR: A key role is defined for TIGIT in inhibiting chronic CD8(+) T cell-dependent responses to tumor formation and chronic immune responses to chronic viral infection.

TL;DR: Current paradigms of targeting ERBB receptors with cancer therapeutics and the understanding of mechanisms of action and resistance to these drugs are discussed.

TL;DR: A better understanding of Ras biology and biochemistry, coupled with new ways of targeting undruggable proteins, is likely to lead to new Ways of defeating Ras-driven cancers.

TL;DR: Interleukin (IL)-10 expression by macrophages is identified as the critical mediator of this phenotype and expression of IL12A and cytotoxic effector molecules were predictive of pathological complete response rates to paclitaxel in human breast cancer.

TL;DR: Genomic rearrangements lead to recurrent structural breakpoints within TERT promoter region, which correlates with highly elevated TERT expression and manifestation of kataegis, representing a mechanism of TERT upregulation in cancer distinct from previously observed amplifications and point mutations.

TL;DR: Functional assays in different SHH-MB xenograft models demonstrated that SHh-MBs harboring a PTCH1 mutation were responsive to SMO inhibition, whereas tumors harboring an SUFU mutation or MYCN amplification were primarily resistant.

TL;DR: It is shown that mesenchymal-like breast cancer cells activate macrophages to a TAM-like phenotype by GM-CSF, which suggests that a positive feedback loop between GM- CSF and CCL18 is important in breast cancer metastasis.

TL;DR: A mouse model recapitulating key features of human metabolic syndrome, NASH, and HCC by long-term feeding of a choline-deficient high-fat diet is developed, demonstrating that distinct molecular mechanisms determine NASH and H CC development.

TL;DR: It is found that VGLL4 directly competes with YAP for binding TEADs and this finding suggests that disruption of YAP-TEADs interaction by aVGLL4-mimicking peptide may be a promising therapeutic strategy against Yap-driven human cancers.

TL;DR: It is found that many drug-treated "oncogene-addicted" cancer cells engage a positive feedback loop leading to Stat3 activation, consequently promoting cell survival and limiting overall drug response, and inhibition of a Stat3 feedback loop may augment the response to a broad spectrum of drugs that target pathways of oncogene addiction.

TL;DR: It is found that Gαq stimulates YAP through a Trio-Rho/Rac signaling circuitry promoting actin polymerization, independently of phospholipase Cβ and the canonical Hippo pathway, thereby identifying YAP as a suitable therapeutic target in uveal melanoma, a GNAQ/GNA11-initiated human malignancy.

TL;DR: The evidence implicating endoplasmic reticulum dysfunction in the pathology of cancer is examined and how recent findings may help to identify novel therapeutic targets is discussed.

TL;DR: The study indicates that the interaction with BRD4 is critical for the oncogenic function of Twist in BLBC, and Pharmacologic inhibition of the Twist-BRD4 association reduced WNT5A expression and suppressed invasion, cancer stem cell (CSC)-like properties, and tumorigenicity of BLBC cells.

TL;DR: Both NASH and HCC development were dependent on TNF produced by inflammatory macrophages that accumulate in the MUP-uPA liver in response to hepatocyte ER stress.

TL;DR: It is proposed that downregulation of super-enhancer-associated transcription factor genes contributes, in part, to SCLC sensitivity to transcriptional inhibitors and that THZ1 represents a prototype drug for tailored SclC therapy.

TL;DR: The combination of PI3K and CDK 4/6 inhibitors overcomes intrinsic and adaptive resistance leading to tumor regressions in PIK3CA mutant xenografts.

TL;DR: AML cells with the R882H mutation have severely reduced de novo methyltransferase activity and focal hypomethylation at specific CpGs throughout AML cell genomes.

TL;DR: An essential role of the Hippo-YAP pathway in Gq/11-induced tumorigenesis is revealed and YAP is suggested as a potential drug target for UM patients carrying mutations in GNAQ or GNA11.