Discrete tissue niches are emerging as essential prerequisites enabling cell communication and function in both homeostasis and disease. In a recent Cell paper, Di Pilato et al. identify a unique dendritic cell-cytotoxic T cell crosstalk within the perivascular space that facilitates T cell survival and proliferation and drives anti-tumor activity. [ABSTRACT FROM AUTHOR]
The non-receptor tyrosine kinase Src is inactivated by the C-terminal Src kinase Csk. In a recent paper in Developmental Cell, Vidal et al. show that loss of Drosophila Csk (dCsk) in a large field of cells results in cell proliferation and disorganization of tissue architecture. In contrast, local inactivation of dCsk in a small field of cells results in loss of cells that are adjacent to normal tissue. This loss occurs by basal migration and death by apoptosis. These findings may shed light on mechanisms that restrain tumor initiation. [Copyright &y& Elsevier]
*CELL proliferation, *COCARCINOGENESIS, *LIVER cancer
Abstract
c-Jun, a component of transcription factor AP-1, has been known to play an important role in the control of cell proliferation. It was also suspected to be a critical mediator of tumor promotion. In a recent paper in Cell, Eferl et al. have now provided conclusive evidence that c-Jun expression is critical for induction of liver cancer by a classical protocol of tumor initiation—tumor promotion. [Copyright &y& Elsevier]
The c-Myc proto-oncogene is an essential activator of cell proliferation and one of the genes most commonly deregulated in cancer. Although these activities of c-Myc are thought to result from its function as a transcription factor, the scientific literature contains hints that this is not the whole story. A new paper in Nature by Dominguez-Sola et al. reports the surprising observation that c-Myc promotes DNA replication via a nontranscriptional mechanism, and that c-Myc deregulation causes DNA damage predominately during S phase. These results identify c-Myc as a new DNA replication factor and suggest an alternative model for its role in cell growth and tumorigenesis. [Copyright &y& Elsevier]
Niacinamide, Vascular Endothelial Growth Factor A, Sorafenib, endocrine system, Cancer Research, Carcinoma, Hepatocellular, Stromal cell, Antineoplastic Agents, Biology, Article, Mice, 03 medical and health sciences, Paracrine signalling, 0302 clinical medicine, medicine, Carcinoma, Animals, Humans, neoplasms, Cell Proliferation, 030304 developmental biology, 0303 health sciences, Hepatocyte Growth Factor, Macrophages, Phenylurea Compounds, Liver Neoplasms, Gene Amplification, Cell Biology, medicine.disease, digestive system diseases, 3. Good health, Vascular endothelial growth factor A, Treatment Outcome, Oncology, Drug Resistance, Neoplasm, Tumor progression, 030220 oncology & carcinogenesis, Hepatocellular carcinoma, Disease Progression, Cancer research, Hepatocyte growth factor, medicine.drug
Abstract
Focal amplifications in 6p21 containing the VEGFA locus occur in 7%–10% of hepatocellular carcinoma (HCC). A recent paper describes how VEGF-A stimulates paracrine secretion of hepatocyte growth factor by stromal cells, which induces tumor progression. HCC patients with VEGFA amplification are distinctly sensitive to sorafenib.
Published
2014
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