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Hilary A. Kenny

Researcher at University of Chicago

Publications -  44
Citations -  5349

Hilary A. Kenny is an academic researcher from University of Chicago. The author has contributed to research in topics: Ovarian cancer & Metastasis. The author has an hindex of 24, co-authored 43 publications receiving 4275 citations. Previous affiliations of Hilary A. Kenny include Northwestern University.

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Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth

TL;DR: It is shown that primary human omental adipocytes promote homing, migration and invasion of ovarian cancer cells, and that adipokines including interleukin-8 (IL-8) mediate these activities, and adipocytes provide fatty acids for rapid tumor growth.
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Loss of E-Cadherin Promotes Ovarian Cancer Metastasis via α5-Integrin, which Is a Therapeutic Target

TL;DR: It is shown here that inhibition of E-cadherin in ovarian cancer cells causes up-regulation of alpha(5)-integrin protein expression and transcription, providing an explanation for how E- cadher in loss increases metastasis.
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The initial steps of ovarian cancer cell metastasis are mediated by MMP-2 cleavage of vitronectin and fibronectin

TL;DR: It is shown that MMP-2 expression was upregulated in OvCa cells upon attachment to their microenvironment, and this indicates that M MP-2 expressed by metastatic Ov Ca cells functionally regulates their attachment to peritoneal surfaces.
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Adipocyte-induced CD36 expression drives ovarian cancer progression and metastasis.

TL;DR: Results suggest that omental adipocytes reprogram tumour metabolism through the upregulation of CD36 in OvCa cells and targeting the stromal-tumour metabolic interface via CD36 inhibition may prove to be an effective treatment strategy against OvCa metastasis.
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c-Met Overexpression Is a Prognostic Factor in Ovarian Cancer and an Effective Target for Inhibition of Peritoneal Dissemination and Invasion

TL;DR: It is suggested that c-Met overexpression is a prognostic factor in ovarian cancer and that targeting c- met in vivo inhibits peritoneal dissemination and invasion through an alpha(5)beta(1) integrin-dependent mechanism.