Hilary Kenny

Ovarian follicle development requires Smad3.

Follicle size class contributes to distinct secretion patterns of inhibin isoforms during the rat estrous cycle.

c-Met overexpression is a prognostic factor in ovarian cancer and an effective target for inhibition of peritoneal dissemination and invasion.

Use of a novel 3D culture model to elucidate the role of mesothelial cells, fibroblasts and extra-cellular matrices on adhesion and invasion of ovarian cancer cells to the omentum.

Thrombin induces tumor invasion through the induction and association of matrix metalloproteinase-9 and beta1-integrin on the cell surface.

The initial steps of ovarian cancer cell metastasis are mediated by MMP-2 cleavage of vitronectin and fibronectin.

Loss of E-cadherin promotes ovarian cancer metastasis via alpha 5-integrin, which is a therapeutic target.

MMP-2 functions as an early response protein in ovarian cancer metastasis.

Organotypic models of metastasis: A three-dimensional culture mimicking the human peritoneum and omentum for the study of the early steps of ovarian cancer metastasis.

{beta}3-integrin expression on tumor cells inhibits tumor progression, reduces metastasis, and is associated with a favorable prognosis in patients with ovarian cancer.

Targeting the urokinase plasminogen activator receptor inhibits ovarian cancer metastasis.

The first line of intra-abdominal metastatic attack: breaching the mesothelial cell layer.

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

Urokinase plasminogen activator system-targeted delivery of nanobins as a novel ovarian cancer therapy.

Three-dimensional modeling of ovarian cancer.

Mesothelial cells promote early ovarian cancer metastasis through fibronectin secretion.

Quantitative high throughput screening using a primary human three-dimensional organotypic culture predicts in vivo efficacy.

Molecular pathways: trafficking of metabolic resources in the tumor microenvironment.