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Aklank Jain

Researcher at Central University of Punjab

Publications -  75
Citations -  2673

Aklank Jain is an academic researcher from Central University of Punjab. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 22, co-authored 55 publications receiving 1664 citations. Previous affiliations of Aklank Jain include University of Texas at Austin & University of Texas MD Anderson Cancer Center.

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Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements.

TL;DR: The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously.
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DNA triple helices: biological consequences and therapeutic potential.

TL;DR: The biological consequences and therapeutic potential of triple helical DNA structures are discussed and it is anticipated that the information provided will stimulate further investigations aimed toward improving DNA triplex-related gene targeting strategies for biotechnological and potential clinical applications.
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Molecular Mechanisms of Action of Genistein in Cancer: Recent Advances

TL;DR: Various molecular interactions of genistein with various cellular targets in cancer models covers various molecular mechanisms prevention, treatment, in vivo, in vitro, and clinical studies to help the scientific community understand genisteIn and cancer biology and will provoke them to design novel therapeutic strategies.
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SNHG12: An LncRNA as a Potential Therapeutic Target and Biomarker for Human Cancer.

TL;DR: It is proposed that small nucleolar RNA host gene 12 (SNHG12), a lncRNA, may serve as both a biomarker and a druggable therapeutic target with promising clinical potential.
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Mismatch repair and nucleotide excision repair proteins cooperate in the recognition of DNA interstrand crosslinks.

TL;DR: Electrophoretic mobility-shift assays and chromatin immunoprecipitation analysis of MutSβ and NER proteins with Tdp-ICLs suggest that proteins from the MMR and N ER pathways interact in the recognition of ICLs, and provide a mechanistic link by which proteins from multiple repair pathways contribute to ICL repair.