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Journal ArticleDOI

Modulation of cell death in the tumor microenvironment.

TLDR
It is suggested that stable microregions of hypoxia may play a positive role in tumor growth and that targeting the biological responses to Hypoxia and the pathways leading toHypoxia tolerance may also be attractive therapeutic strategies.
About
This article is published in Seminars in Radiation Oncology.The article was published on 2003-01-01. It has received 67 citations till now. The article focuses on the topics: HIF1A & Hypoxia (medical).

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Citations
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Journal ArticleDOI

Activating transcription factor 4 is translationally regulated by hypoxic stress.

TL;DR: It is shown that a subset of transcripts are preferentially translated during hypoxia, including activating transcription factor 4 (ATF4), an important mediator of the unfolded protein response, and an important integrated response between ER signaling and the cellular adaptation to hypoxic stress.
Journal ArticleDOI

Molecular basis of angiogenesis and cancer.

TL;DR: The molecular basis of angiogenesis during tumor growth is discussed and some of the molecules that are involved in this angiogenic switch are illustrated.
Journal ArticleDOI

Nanodrug delivery in reversing multidrug resistance in cancer cells.

TL;DR: Current review highlights various nanodrug delivery systems to overcome mechanism of MDR by neutralizing, evading, or exploiting the drug efflux pumps and those independent ofdrug efflux pump mechanism by silencing Bcl-2 and HIF1α gene expressions by siRNA and miRNA, modulating ceramide levels and targeting NF-κB.
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Autocrine laminin-5 ligates α6β4 integrin and activates RAC and NFκB to mediate anchorage-independent survival of mammary tumors

TL;DR: It is shown that autocrine LM-5 mediates anchorage-independent survival in breast tumors through ligation of a wild-type, but not a cytoplasmic tail–truncated α6β4 integrin, which is necessary for basal and epidermal growth factor–induced RAC activity and RAC mediates tumor survival.
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The tumor microenvironment in the post-PAGET era.

TL;DR: The conclusion is that the tumor microenvironment, by exerting regulatory functions and selective pressures drives cancer cells into one of several molecular evolution pathways thereby determining and shaping their malignancy phenotype.
References
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Journal ArticleDOI

Tumor Angiogenesis: Therapeutic Implications

TL;DR: This new capillary growth is even more vigorous and continuous than a similar outgrowth of capillary sprouts observed in 2016 and is likely to be accompanied by neovascularization.
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Targeting of HIF-alpha to the von Hippel-Lindau Ubiquitylation Complex by O2-Regulated Prolyl Hydroxylation

TL;DR: It is shown that the interaction between human pVHL and a specific domain of the HIF-1α subunit is regulated through hydroxylation of a proline residue by an enzyme the authors have termed Hif-α prolyl-hydroxylase (HIF-PH).
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The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

TL;DR: It is indicated that the interaction between HIF-1 and pVHL is iron dependent, and that it is necessary for the oxygen-dependent degradation of HIF α-subunits, which may underlie the angiogenic phenotype of VHL-associated tumours.
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Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis.

TL;DR: It is shown that vascular endothelial growth factor (VEGF) probably functions as a hypoxia-inducible angiogenic factor and is specifically induced in a subset of glioblastoma cells distinguished by their immediate proximity to necrotic foci and the clustering of capillaries alongside VEGF-producing cells.
Journal ArticleDOI

Endostatin: an endogenous inhibitor of angiogenesis and tumor growth.

TL;DR: This work has identified endostatin, an angiogenesis inhibitor produced by hemangioendothelioma, a 20 kDa C-terminal fragment of collagen XVIII that specifically inhibits endothelial proliferation and potently inhibitsAngiogenesis and tumor growth.
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