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Amit Dutt

Researcher at Homi Bhabha National Institute

Publications -  97
Citations -  8258

Amit Dutt is an academic researcher from Homi Bhabha National Institute. The author has contributed to research in topics: Cancer & Lung cancer. The author has an hindex of 27, co-authored 84 publications receiving 7430 citations. Previous affiliations of Amit Dutt include University of Zurich & Brigham and Women's Hospital.

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Somatic mutations affect key pathways in lung adenocarcinoma

Li Ding, +96 more
- 23 Oct 2008 - 
TL;DR: Somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B are found.
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High-throughput oncogene mutation profiling in human cancer

TL;DR: High-throughput genotyping is adapted to query 238 known oncogene mutations across 1,000 human tumor samples and established robust mutation distributions spanning 17 cancer types, offering a new dimension in tumor genetics, where mutations involving multiple cancer genes may be interrogated simultaneously and in 'real time'.
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SOX2 is an amplified lineage-survival oncogene in lung and esophageal squamous cell carcinomas

TL;DR: A peak of genomic amplification on chromosome 3q26.33 found in squamous cell carcinomas of the lung and esophagus contains the transcription factor gene SOX2, which is necessary for normal esophageal squamous development, promotes differentiation and proliferation of basal tracheal cells and cooperates in induction of pluripotent stem cells.
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Mutations in the DDR2 Kinase Gene Identify a Novel Therapeutic Target in Squamous Cell Lung Cancer

TL;DR: Findings suggest that gain-of-function mutations in DDR2 are important oncogenic events and are amenable to therapy with dasatinib, and provide a rationale for designing clinical trials with the FDA-approved drug d asatinib in patients with lung SCCs.
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Inhibitor-Sensitive FGFR1 Amplification in Human Non-Small Cell Lung Cancer

TL;DR: It is demonstrated that a non-small cell lung carcinoma cell line harboring focal amplification of FGFR1 is dependent onFGFR1 activity for cell growth, as treatment of this cell line either with FG FR1-specific shRNAs or with FGFR small molecule enzymatic inhibitors leads to cell growth inhibition.