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Myriad Genetics

CompanyMunich, Germany
About: Myriad Genetics is a company organization based out in Munich, Germany. It is known for research contribution in the topics: Cancer & Breast cancer. The organization has 562 authors who have published 586 publications receiving 56046 citations. The organization is also known as: Myriad Genetics, Inc..


Papers
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Journal ArticleDOI
TL;DR: Results provide direct evidence that COX‐2 is an important mediator of wear debris‐induced osteolysis and suggests that COx‐2 inhibitors are potential therapeutic agents for the prevention of wearbris‐induced fractures.
Abstract: Aseptic loosening is a major complication of prosthetic joint surgery and is manifested as chronic inflammation, pain, and osteolysis at the bone implant interface. The osteolysis is believed to be driven by a host inflammatory response to wear debris generated from the implant. In our current study, we use a selective inhibitor (celecoxib) of cyclo-oxygenase 2 (COX-2) and mice that lack either COX-1 (COX-1-/-) or COX-2 (COX-2-/-) to show that COX-2, but not COX-1, plays an important role in wear debris-induced osteolysis. Titanium (Ti) wear debris was implanted surgically onto the calvaria of the mice. An intense inflammatory reaction and extensive bone resorption, which closely resembles that observed in patients with aseptic loosening, developed within 10 days of implantation in wild-type and COX-1-/- mice. COX-2 and prostaglandin E2 (PGE2) production increased in the calvaria and inflammatory tissue overlying it after Ti implantation. Celecoxib (25 mg/kg per day) significantly reduced the inflammation, the local PGE2 production, and osteolysis. In comparison with wild-type and COX-1-/- mice, COX-2-/- mice implanted with Ti had a significantly reduced calvarial bone resorption response, independent of the inflammatory response, and significantly fewer osteoclasts were formed from cultures of their bone marrow cells. These results provide direct evidence that COX-2 is an important mediator of wear debris-induced osteolysis and suggests that COX-2 inhibitors are potential therapeutic agents for the prevention of wear debris-induced osteolysis.

104 citations

Journal ArticleDOI
TL;DR: Tissue-specific and time-dependent expression of COX-2 appears necessary for normal postnatal renal development and the maintenance of normal renal architecture and function in adult mice.

102 citations

Journal ArticleDOI
TL;DR: BRCA mutations occurred more frequently in platinum-sensitive EOC than platinum-resistant disease, and the high overall frequency of BRCA deficiency in EOC underscores the importance of tumor profiling.

102 citations

Journal ArticleDOI
TL;DR: Multiple susceptibility gene testing in PDAC patients with family history of pancreatic cancer is warranted regardless of FPC status and will inform genetic risk counseling for families.

102 citations

Journal ArticleDOI
TL;DR: This preliminary molecular analysis suggests that serous borderline tumors have some molecular features usually associated with malignancy but are unlikely to represent a precursor of invasive serous carcinoma, and mucinous borderline tumors may represents a precursor or variant of mucinous carcinoma of the ovary.
Abstract: Ovarian tumors of low malignant potential ("borderline tumors") have been proposed variably to represent a distinctive type of malignancy, precursors of frank ovarian malignancy, or a nonmalignant process. We analyzed 81 malignant and 39 borderline ovarian tumors for p53 immunoreactivity and alterat

102 citations


Authors

Showing all 562 results

NameH-indexPapersCitations
Richard D. Smith140118079758
Rosalind A. Eeles10654445058
David E. Goldgar10341950450
Mark H. Pollack8946426511
Jacques Simard8340928493
Julian R. Sampson7121222192
Johanna M. Rommens7120242630
David A. Frank6820117557
Sean V. Tavtigian6519435641
Mark H. Skolnick6421130548
Lisa A. Cannon-Albright6232728945
Alexander Gutin5416717705
Dominic P. Williams491346665
Nelleke A. Gruis4915913080
Nicola J. Camp462137772
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20221
202139
202043
201930
201827
201724