نتایج جستجو برای: ژن pik3ca

تعداد نتایج: 18195  

2015
Maria Schwaederle Sheryl K Elkin Brett N Tomson Jennifer Levin Carter Razelle Kurzrock

In order to gain a better understanding of the underlying biology of squamous cell carcinoma (SCC), we tested the hypothesis that SCC originating from different organs may possess common molecular alterations. SCC samples (N = 361) were examined using clinical-grade targeted next-generation sequencing (NGS). The most frequent SCC tumor types were head and neck, lung, cutaneous, gastrointestinal...

2013
Grace M. Wang Hong Yuen Wong Hiroyuki Konishi Brian G. Blair Abde M. Abukhdeir John P. Gustin D. Marc Rosen Samuel Ray Denmeade Zeshaan Rasheed William Matsui Joseph P. Garay Morassa Mohseni Michaela J. Higgins Justin Cidado Danijela Jelovac Sarah Croessmann Rory L. Cochran Sivasundaram Karnan Yuko Konishi Akinobu Ota Yoshitaka Hosokawa Pedram Argani Josh Lauring Ben Ho Park

The selective pressures leading to cancers withmutations in bothKRAS and PIK3CA are unclear. Here, we show that somatic cell knockin of both KRAS G12V and oncogenic PIK3CAmutations in human breast epithelial cells results in cooperative activation of the phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways in vitro, and leads to tumor formation in immunocompromi...

Journal: :Molecular cancer therapeutics 2014
Christine Fritsch Alan Huang Christian Chatenay-Rivauday Christian Schnell Anupama Reddy Manway Liu Audrey Kauffmann Daniel Guthy Dirk Erdmann Alain De Pover Pascal Furet Hui Gao Stephane Ferretti Youzhen Wang Joerg Trappe Saskia M Brachmann Sauveur-Michel Maira Christopher Wilson Markus Boehm Carlos Garcia-Echeverria Patrick Chene Marion Wiesmann Robert Cozens Joseph Lehar Robert Schlegel Giorgio Caravatti Francesco Hofmann William R Sellers

Somatic PIK3CA mutations are frequently found in solid tumors, raising the hypothesis that selective inhibition of PI3Kα may have robust efficacy in PIK3CA-mutant cancers while sparing patients the side-effects associated with broader inhibition of the class I phosphoinositide 3-kinase (PI3K) family. Here, we report the biologic properties of the 2-aminothiazole derivative NVP-BYL719, a selecti...

2004
Daniel K. Broderick Chunhui Di Timothy J. Parrett Yardena R. Samuels Jordan M. Cummins Roger E. McLendon Daniel W. Fults Victor E. Velculescu Darell D. Bigner Hai Yan

The phosphatidylinositol 3 -kinase pathway is activated in multiple advanced cancers, including glioblastomas, through inactivation of the PTEN tumor suppressor gene. Recently, mutations in PIK3CA, a member of the family of phosphatidylinositol 3 -kinase catalytic subunits, were identified in a significant fraction (25–30%) of colorectal cancers, gastric cancers, and glioblastomas and in a smal...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2005
Douglas A Levine Faina Bogomolniy Cindy J Yee Alex Lash Richard R Barakat Patrick I Borgen Jeff Boyd

PURPOSE Activation of the phosphatidylinositol 3-kinase (PI3K)-AKT pathway, resulting in increased cell proliferation, survival, and motility, is believed to play an oncogenic role in many cancer types. The PIK3CA gene encodes the p110alpha catalytic subunit of PI3K, and is amplified in some ovarian cancers, whereas the AKT2 gene is amplified in some ovarian, breast, and pancreatic cancers. Rec...

2016
Meagan B. Myers Malathi Banda Karen L. McKim Yiying Wang Michael J. Powell Barbara L. Parsons

Mutant cancer subpopulations have the potential to derail durable patient responses to molecularly targeted cancer therapeutics, yet the prevalence and size of such subpopulations are largely unexplored. We employed the sensitive and quantitative Allele-specific Competitive Blocker PCR approach to characterize mutant cancer subpopulations in ductal carcinomas (DCs), examining five specific hots...

Journal: :Clinical chemistry 2008
Ruth E Board Nicola J Thelwell Paul F Ravetto Stephen Little Malcolm Ranson Caroline Dive Andrew Hughes David Whitcombe

BACKGROUND Mutations in the PIK3CA gene (phosphoinositide-3-kinase, catalytic, alpha polypeptide) have recently been described in a number of cancers, and their detection is currently limited because of the low sensitivity of conventional sequencing techniques. METHODS We combined Amplification Refractory Mutation System (ARMS; AstraZeneca) allele-specific PCR and Scorpions (DxS) to develop a...

2013
Sun Tian Iris Simon Victor Moreno Paul Roepman Josep Tabernero Mireille Snel Laura van't Veer Ramon Salazar Rene Bernards Gabriel Capella

OBJECTIVE To develop gene expression profiles that characterise KRAS-, BRAF- or PIK3CA-activated- tumours, and to explore whether these profiles might be helpful in predicting the response to the epidermal growth factor receptor (EGFR) pathway inhibitors better than mutation status alone. DESIGN Fresh frozen tumour samples from 381 colorectal cancer (CRC) patients were collected and mutations...

2018
Hye Jin Chang Hee Sung Shin Tae Hoon Kim Jung-Yoon Yoo Hanna E Teasley Jean J Zhao Un-Hwan Ha Jae-Wook Jeong

The PI3K/AKT signaling pathway plays a critical role in the maintenance of equilibrium between cell survival and apoptosis. The Pik3ca gene is mutated in a range of human cancers. It has been found to be oncogenic, and mutations lead to constitutive activation of the PI3K/AKT pathway. The expression patterns of PIK3CA proteins in the uterus of mice during early pregnancy indicate that it may pl...

2017
Ju Sun Kim Jung Eun Kim Kyung Kim Jeeyun Lee Joon Oh Park Ho Yeong Lim Young Suk Park Won Ki Kang Seung Tae Kim

Background: Anti-EGFR therapies have been recommended for advanced colorectal cancer (CRC) with wild-type RAS and PIK3CA mutation. However, PIK3CA mutations are a poor prognostic marker and a negative predictor of response to anti-EGFR therapies in RAS wild-type CRC. Therefore, new and advanced treatment strategies are needed for personalized medical treatment of patients with wild-type RAS and...

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