scispace - formally typeset
P

Paul J. Williams

Researcher at University of Texas Health Science Center at San Antonio

Publications -  43
Citations -  4104

Paul J. Williams is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Bone metastasis & Bone resorption. The author has an hindex of 25, co-authored 40 publications receiving 3840 citations. Previous affiliations of Paul J. Williams include University of Texas at San Antonio & Osaka University.

Papers
More filters
Journal ArticleDOI

Comparative Preclinical and Clinical Pharmacokinetics of a Cremophor-Free, Nanoparticle Albumin-Bound Paclitaxel (ABI-007) and Paclitaxel Formulated in Cremophor (Taxol)

TL;DR: The volume of distribution at steady state and clearance for paclitaxel formulated as Cremophor-free nanoparticle ABI-007 were significantly greater than those for paclitexel formulated with Cremophileor (Taxol) in rats, consistent with the absence of pac litaxel-sequestering Cremphor micelles after administration of A BI-007.
Journal ArticleDOI

A bone-seeking clone exhibits different biological properties from the MDA-MB-231 parental human breast cancer cells and a brain-seeking clone in vivo and in vitro.

TL;DR: The data suggest that phenotypic changes allow breast cancer cells to promote osteoclastic bone resorption, survive, and proliferate in bone, which consequently leads to the establishment of bone metastases.
Journal Article

The Bisphosphonate Ibandronate Promotes Apoptosis in MDA-MB-231 Human Breast Cancer Cells in Bone Metastases

TL;DR: The results suggest that BP suppresses bone metastases through promotion of apoptosis in metastatic cancer cells as well as in osteoclasts, and it still remains open whether BP has direct anticancer actions in vivo.
Journal ArticleDOI

Zoledronic Acid Inhibits Visceral Metastases in the 4T1/luc Mouse Breast Cancer Model

TL;DR: The results of this study are consistent with the notion that ZOL affects breast cancer metastasis to visceral organs as well as bone, and may be attributable to inhibition of migration and invasion of breast cancer cells.
Journal ArticleDOI

Cell–cell contact between marrow stromal cells and myeloma cells via VCAM-1 and α4β1-integrin enhances production of osteoclast-stimulating activity

TL;DR: Data suggest that myeloma cells are responsible for producing osteoclastogenic activity and that establishment of direct contact with marrow stromal cells via α 4 β 1 -integrin/VCAM-1 increases the production of this activity by myel cancer cells.