نتایج جستجو برای: kras

تعداد نتایج: 7276  

2018
Marzia Del Re Eleonora Rofi Giuliana Restante Stefania Crucitta Elena Arrigoni Stefano Fogli Massimo Di Maio Iacopo Petrini Romano Danesi

Rationale KRAS is the most common and, simultaneously, the most ambiguous oncogene implicated in human cancer. Despite KRAS mutations were identified in Non Small Cell Lung Cancers (NSCLCs) more than 20 years ago, selective and specific inhibitors aimed at directly abrogating KRAS activity are not yet available. Nevertheless, many therapeutic approaches have been developed potentially useful to...

Journal: :gastroenterology and hepatology from bed to bench 0
atena irani shemirani mahdi montazer haghighi phd saman milanizadeh mohammad yaghoob taleghani seyed reza fatemi behzad damavand

aim : the aim of the current investigation was to examine the profile of kras mutations accompanied with msi (microsattelite instability) status in polyps and colorectal carcinoma tissues in an iranian population. background : kras mutations in colorectal cancer cause resistance to anti-epidermal growth factor receptor (egfr). so it can be considered as a true indicator of egfr pathway activati...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2017
Haiwei Mou Jill Moore Sunil K Malonia Yingxiang Li Deniz M Ozata Soren Hough Chun-Qing Song Jordan L Smith Andrew Fischer Zhiping Weng Michael R Green Wen Xue

Genetic lesions that activate KRAS account for ∼30% of the 1.6 million annual cases of lung cancer. Despite clinical need, KRAS is still undruggable using traditional small-molecule drugs/inhibitors. When oncogenic Kras is suppressed by RNA interference, tumors initially regress but eventually recur and proliferate despite suppression of Kras Here, we show that tumor cells can survive knockout ...

Journal: :gastroenterology and hepatology from bed to bench 0
ehsan nazemalhosseini mojarad roya kishani farahani mahdi montazer haghighi hamid asadzadeh aghdaei peter jk kuppen mohammad reza zali

knowledge about the clinical significance of v-raf murine sarcoma viral oncogene homolog b1 ( braf ) mutations in colorectal cancer (crc) is growing. braf encodes a protein kinase involved with intracellular signaling and cell division. the gene product is a downstream effector of kirsten ras 1( kras ) within the ras/raf/mapk cellular signaling pathway. evidence suggests that braf mutations, li...

2017
Yijun Jia Tao Jiang Xuefei Li Chao Zhao Limin Zhang Sha Zhao Xiaozhen Liu Meng Qiao Jiawei Luo Jinpeng Shi Hui Yang Yan Wang Lei Xi Shijia Zhang Guanghui Gao Chunxia Su Shengxiang Ren Caicun Zhou

We performed this retrospective study to investigate whether the KRAS mutation status and its subtypes could predict the effect of first-line platinum-based chemotherapy in Chinese patients with non-small cell lung cancer (NSCLC). Patients received who had KRAS mutations were enrolled. Correlations between KRAS mutations, specific mutant subtypes and responses to chemotherapy were analyzed usin...

2015
Sara Alves Lisandra Castro Maria Sofia Fernandes Rita Francisco Paula Castro Muriel Priault Susana Rodrigues Chaves Mary Pat Moyer Carla Oliveira Raquel Seruca Manuela Côrte-Real Maria João Sousa Ana Preto

The recent interest to modulate autophagy in cancer therapy has been hampered by the dual roles of this conserved catabolic process in cancer, highlighting the need for tailored approaches. Since RAS isoforms have been implicated in autophagy regulation and mutation of the KRAS oncogene is highly frequent in colorectal cancer (CRC), we questioned whether/how mutant KRAS alleles regulate autopha...

2011
Saleh Al-Ghamdi Abdulkader Albasri Julien Cachat Salih Ibrahem Belal A. Muhammad Darryl Jackson Abdolrahman S. Nateri Karin B. Kindle Mohammad Ilyas

CTEN/TNS4 is an oncogene in colorectal cancer (CRC) which enhances cell motility although the mechanism of Cten regulation is unknown. We found an association between high Cten expression and KRAS/BRAF mutation in a series of CRC cell lines (p = 0.03) and hypothesised that Kras may regulate Cten. To test this, Kras was knocked-down (using small interfering (si)RNA) in CRC cell lines SW620 and D...

Journal: :PloS one 2015
Nibedita Chattopadhyay Allison J Berger Erik Koenig Bret Bannerman James Garnsey Hugues Bernard Paul Hales Angel Maldonado Lopez Yu Yang Jill Donelan Kristen Jordan Stephen Tirrell Bradley Stringer Cindy Xia Greg Hather Katherine Galvin Mark Manfredi Nelson Rhodes Ben Amidon

In non-clinical studies, the proteasome inhibitor ixazomib inhibits cell growth in a broad panel of solid tumor cell lines in vitro. In contrast, antitumor activity in xenograft tumors is model-dependent, with some solid tumors showing no response to ixazomib. In this study we examined factors responsible for ixazomib sensitivity or resistance using mouse xenograft models. A survey of 14 non-sm...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2015
Pierre Laurent-Puig Deniz Pekin Corinne Normand Steve K Kotsopoulos Philippe Nizard Karla Perez-Toralla Rachel Rowell Jeff Olson Preethi Srinivasan Delphine Le Corre Thevy Hor Zakaria El Harrak Xinyu Li Darren R Link Olivier Bouché Jean-François Emile Bruno Landi Valérie Boige J Brian Hutchison Valerie Taly

PURPOSE KRAS mutations are predictive of nonresponse to anti-EGFR therapies in metastatic colorectal cancer (mCRC). However, only 50% of nonmutated patients benefit from them. KRAS-mutated subclonal populations nondetectable by conventional methods have been suggested as the cause of early progression. Molecular analysis technology with high sensitivity and precision is required to test this hy...

2017
Adrian Vallejo Naiara Perurena Elisabet Guruceaga Pawel K Mazur Susana Martinez-Canarias Carolina Zandueta Karmele Valencia Andrea Arricibita Dana Gwinn Leanne C Sayles Chen-Hua Chuang Laura Guembe Peter Bailey David K Chang Andrew Biankin Mariano Ponz-Sarvise Jesper B Andersen Purvesh Khatri Aline Bozec E Alejandro Sweet-Cordero Julien Sage Fernando Lecanda Silve Vicent

KRAS mutated tumours represent a large fraction of human cancers, but the vast majority remains refractory to current clinical therapies. Thus, a deeper understanding of the molecular mechanisms triggered by KRAS oncogene may yield alternative therapeutic strategies. Here we report the identification of a common transcriptional signature across mutant KRAS cancers of distinct tissue origin that...

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