Dr Santosh Kumar

@ggu.ac.in

Associate Professor, Dept of Biotechnology
Guru Ghasidas Vishwavidyalaya, Bilaspur

Dr Santosh  Kumar
Dr. Santosh Kumar is an Associate Professor of Biotechnology at Guru Ghasidas Vishwavidyalaya, India, and a cancer biologist with over a decade of international research experience spanning premier institutions in India and the United States. His research program focuses on uncovering fundamental mechanisms of cancer progression, with particular emphasis on mitochondrial biology, metabolic reprogramming, therapy resistance, and cancer stem cell dynamics.
Dr. Kumar obtained his Ph.D. from the National Centre for Cell Science (NCCS), Pune, and subsequently trained at globally renowned institutions including MD Anderson Cancer Center, Baylor College of Medicine, University of Houston, and the University of Mississippi Medical Center. His work across these institutions has provided critical insights into oncogenic signaling, mitochondrial–nuclear crosstalk, SUMOylation, and inflammation-driven tumor progression.
As a recipient of the prestigious DST Ramanujan Fellowship, Dr. Kumar establ

EDUCATION

Ph.D. Biotechnology, National centre for cell science, Pune, 2009

RESEARCH, TEACHING, or OTHER INTERESTS

Cancer Research, Biotechnology, Molecular Biology, Endocrinology
24

Scopus Publications

1727

Scholar Citations

21

Scholar h-index

22

Scholar i10-index

Scopus Publications

  • Green Tea's EGCG: Brewing Hope in the Battle against Breast Cancer
    Manoj Kumar, Roop Lal, Amit Sehgal, Suman Rawat, Ankit Kumar, Santosh Kumar, Sunil Kumar Dhatwalia
    Natural Products Journal, 2026
    Breast cancer, a pervasive global malignancy, is anticipated to undergo a significant increase by 2040. Despite the conventional armamentarium of treatments including chemotherapy, radiation therapy, and surgery, the intricate landscape of breast cancer, characterized by its multifaceted surface receptors and signalling pathways, presents formidable challenges to treatment efficacy. Epigallocatechin-3-gallate (EGCG), extracted from Camellia sinensis, has emerged as a subject of interest due to its robust antioxidative properties stemming from its chemical structure. EGCG exerts its effects on pivotal stages of tumour growth and proliferation by modulating key signalling pathways such as MAPK, PI3K, NFkB, and ERK1/2 influencing apoptosis and cell cycle regulation. Clinical trials have provided insights into EGCG's potential impact on breast cancer such as mammographic density and pharmacokinetics, indicating its potential as a potent therapeutic agent. Moreover, when administered with conventional chemotherapy, EGCG demonstrates synergistic effects, enhancing therapeutic outcomes. Nevertheless, further research is warranted to validate the safety and efficacy of EGCG in breast cancer prevention and treatment.
  • Synthesis, Characterization, and Comparative Analysis of Zinc Oxide Nanoparticles using Calendula Officinalis Flower Extract and its Antibacterial Activity
    Letters in Applied Nanobioscience, 2025
  • Antioxidants ameliorates glucose/glucose oxidase-induced myocardial damage through mitochondrial and MAPK pathway
    Santosh Kumar, Prachi Agrawal, Prachi Mendhey, Sunil Kumar Dhatwalia, Sandhya L. Sitasawad
    3 Biotech, 2025
  • Introduction to microbiomes in health and diseases
    Prachi Agrawal, Prachi Mendhey, Robins Kumar, Subham Patel, Prakash Kumar Kaushik, Abhishek Dadsena, Santosh Kumar
    International Review of Cell and Molecular Biology, 2025
  • Imidazo[1,2-a]Quinoxaline-2-Carbonitrile Derivative (RA-22) Inhibits Self-Renewal and Growth of Cancer Stem and Cancer Cells via Downregulating AKT Pathway
    Pramit Kumar, Umesh Prasad Yadav, Gaurav Joshi, Sahil Arora, Manvendra Kumar, Joydeep Chatterjee, Vikas Chandra, Sandeep Singh, Raj Kumar, Santosh Kumar
    Chemistryselect, 2024
    EGFR activation in colorectal and breast cancer stimulates downstream pathways like Ras/Raf/MEK/ERK and PI3 K/Akt, fostering cell proliferation, invasion, metastasis, and therapy resistance, underscoring its significance as a therapeutic target in both cancers. In the present work, we rationally designed ( E )‐4‐methyl‐1‐((3‐oxo‐1‐phenylbutyl)amino)‐4‐styryl‐4,5‐dihydroimidazo[1,2‐a]quinoxaline‐2‐carbonitrile ( RA‐22 ) as EGFR inhibitor. Our research investigates the role of RA‐22 as a target molecule for EGFR, exploring its anticancer potential and mechanism of action across breast cancer and colorectal cancer cell lines. The in‐vitro studies showed its cytotoxic response towards MDA‐MB‐231 and HCT‐116 and its inhibitory effect on cancer stem cells in mammosphere/spheroid culture. The compound downregulates the oncogenic signalling proteins like STAT‐3, AKT, PAN‐AKT, and ERK and also reduces the expression of the anti‐apoptotic protein Bcl‐2 and increases the apoptotic proteins like Cleaved‐PARP, Cleaved‐Caspase‐3, and Cleaved‐Caspase‐9.
  • Natural Compound-Based Nanoparticles to Target Free Radicals in Cancer
    Umesh Prasad Yadav, M. Rhuthuparna, Kanika Vasudeva, Prabhat Suman, Anjana Munshi, Santosh Kumar, Sandeep Singh
    Handbook of Oxidative Stress in Cancer Therapeutic Aspects Volume 1, 2022
    Cell proliferation and malignant transformation are enabled by genetic and epigenetic changes. During the malignancy process, malignant cells acquire distinguishing characteristics. Cancer cells have acquired the ability to generate more reactive oxygen species (ROS), resulting in high oxidative stress. ROS-mediated signaling is needed for cancer cell physiology, and high levels of ROS cause oxidative stress-induced cytotoxicity in cancer cells. To avoid ROS-mediated cytotoxicity, cancer cells modulate their redox state through various antioxidant mechanisms and keep their ROS levels below the threshold. Cancer treatment that targets oxidative stress is an appealing option. Many natural oxidative stress modulators and bioactive compounds have been used in the treatment of cancer. Conventional uptake of bioactive molecule is associated with lower bioavailability, solubility, unlikely biodistribution, and side effects. Traditional drug uptake is improved by nanoformulation, making it easier to overcome side effects, improve biodistribution, and extend drug duration time. Natural prooxidant-loaded nanoparticles efficiently carry prooxidant to the tumor site and selectively and efficiently induce oxidative stress-mediated cell death in cancer cells.
  • Design, synthesis and anticancer activity of 2-arylimidazo[1,2-a]pyridinyl-3-amines
    Umesh Prasad Yadav, Arshad J. Ansari, Sahil Arora, Gaurav Joshi, Tashvinder Singh, Harsimrat Kaur, Nilambra Dogra, Raj Kumar, Santosh Kumar, Devesh M. Sawant, Sandeep Singh
    Bioorganic Chemistry, 2022
  • Let-7a induces metabolic reprogramming in breast cancer cells via targeting mitochondrial encoded ND4
    Praveen Sharma, Vibhuti Sharma, Tarunveer Singh Ahluwalia, Nilambra Dogra, Santosh Kumar, Sandeep Singh
    Cancer Cell International, 2021
    Background and objectives MicroRNA (miRNA) that translocate from the nucleus to mitochondria are referred to as mitochondrial microRNA (mitomiR). Albeit mitomiRs have been shown to modulate gene expression, their functional impact within mitochondria is unknown. The main objective of this study is to investigate whether the mitochondrial genome is regulated by miR present inside the mitochondria. Methods and results Here, we report mitomiR let-7a regulates mitochondrial transcription in breast cancer cells and reprogram the metabolism accordingly. These effects were mediated through the interaction of let-7a with mtDNA, as studied by RNA pull-down assays, altering the activity of Complex I in a cell line-specific manner. Our study, for the first time, identifies the role of mitomiR (let-7a) in regulating the mitochondrial genome by transcriptional repression and its contribution to regulating mitochondrial metabolism of breast cancer cells. Conclusion These findings uncover a novel mechanism by which mitomiR regulates mitochondrial transcription.
  • Metabolic Adaptations in Cancer Stem Cells
    Umesh Prasad Yadav, Tashvinder Singh, Pramit Kumar, Praveen Sharma, Harsimrat Kaur, Sadhana Sharma, Sandeep Singh, Santosh Kumar, Kapil Mehta
    Frontiers in Oncology, 2020
    Cancer stem cells (CSCs) are a small and elusive subpopulation of self-renewing cancer cells with remarkable ability to initiate, propagate, and spread the malignant disease. In addition, they exhibit increased resistance to anticancer therapies, thereby contributing to disease relapse. CSCs are reported to be present in many tumor types such as melanoma, sarcoma, mammary tumors, colon cancer and other solid tumors. These cells from different tumors show unique energetic and metabolic pathways. For example, CSCs from one type of tumor may predominantly use aerobic glycolysis, while from another tumor type may utilize oxidative phosphorylation. Most commonly these cells use fatty acid oxidation and ketone bodies as the main source of energy production. CSCs have a remarkable ability to reprogram their metabolism in order to survive under adverse conditions such as hypoxia, acidosis, and starvation. There is increasing interest to identify molecular targets that can be utilized to kill CSCs and to control their growth. In this review, we discuss how an understanding of the unique metabolism of CSCs from different tumors can offer promising strategies for targeting CSCs and hence to prevent disease relapse and to treat the metastatic disease.
  • CAR T cell therapy: newer approaches to counter resistance and cost
    Rajesh Kumar Yadav, Asgar Ali, Santosh Kumar, Alpana Sharma, Basab Baghchi, Pritanjali Singh, Sushmita Das, Chandramani Singh, Sadhana Sharma
    Heliyon, 2020
    The genetically engineered Chimeric Antigen Receptor bearing T-cell (CAR T cell) therapy has been emerged as the new paradigm of cancer immunotherapy. However, recent studies have reported an increase in the number of relapsed haematological malignancies. This review provides newer insights into how the efficacy of CAR T cells might be increased by the application of new genome editing technologies, monitoring the complexity of tumor types and T cells sub-types. Next, tumor mutation burden along with tumormicroenvironment and epigenetic mechanisms of CAR T cell as well as tumor cell may play a vital role to tackle the cancer resistance mechanisms. These studies highlight the need to consider traditional cancer therapy in conjunction with CAR T cell therapy for relapsed or cases unresponsive to treatment. Of note, this therapy is highly expensive and requires multi-skill for successful implementation, which results in reduction of its accessibility/affordability to the patients. Here, we also propose a model for cost minimization of CAR T cell therapy by a collaboration of academia, hospitals and industry.
  • E-pharmacophore guided discovery of pyrazolo[1,5-c]quinazolines as dual inhibitors of topoisomerase-I and histone deacetylase
    Gaurav Joshi, Sourav Kalra, Umesh Prasad Yadav, Praveen Sharma, Pankaj Kumar Singh, Suyog Amrutkar, Arshad J. Ansari, Santosh Kumar, Ashoke Sharon, Sadhana Sharma, Devesh M. Sawant, Uttam C. Banerjee, Sandeep Singh, Raj Kumar
    Bioorganic Chemistry, 2020
  • Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia
    Parash Parajuli, Santosh Kumar, Audrey Loumaye, Purba Singh, Sailaja Eragamreddy, Thien Ly Nguyen, Seval Ozkan, Mohammed S. Razzaque, Céline Prunier, Jean-Paul Thissen, Azeddine Atfi
    Developmental Cell, 2018
  • Novel SUMO-Protease SENP7S Regulates β-catenin Signaling and Mammary Epithelial Cell Transformation
    Samaneh Karami, Feng-Ming Lin, Santosh Kumar, Shaymaa Bahnassy, Hariprasad Thangavel, Maram Quttina, Yue Li, Jing Ren, Tasneem Bawa-Khalfe
    Scientific Reports, 2017
  • SUMOylation of HP1α supports association with ncRNA to define responsiveness of breast cancer cells to chemotherapy
    Feng-Ming Lin, Santosh Kumar, Jing Ren, Samaneh Karami, Shaymaa Bahnassy, Yue Li, Xiaofeng Zheng, Jing Wang, Tasneem Bawa-Khalfe
    Oncotarget, 2016
  • Fatty Acid Oxidation-Driven Src Links Mitochondrial Energy Reprogramming and Oncogenic Properties in Triple-Negative Breast Cancer
    Jun Hyoung Park, Sajna Vithayathil, Santosh Kumar, Pi-Lin Sung, Lacey Elizabeth Dobrolecki, Vasanta Putluri, Vadiraja B. Bhat, Salil Kumar Bhowmik, Vineet Gupta, Kavisha Arora, Danli Wu, Efrosini Tsouko, Yiqun Zhang, Suman Maity, Taraka R. Donti, Brett H. Graham, Daniel E. Frigo, Cristian Coarfa, Patricia Yotnda, Nagireddy Putluri, Arun Sreekumar, Michael T. Lewis, Chad J. Creighton, Lee-Jun C. Wong, Benny Abraham Kaipparettu
    Cell Reports, 2016
  • Functional characterization of a WWP1/Tiul1 tumor-derived mutant reveals a paradigm of its constitutive activation in human cancer
    Thomas Courivaud, Nathalie Ferrand, Abdelouahid Elkhattouti, Santosh Kumar, Laurence Levy, Olivier Ferrigno, Azeddine Atfi, Céline Prunier
    Journal of Biological Chemistry, 2015
  • Disruption of the PHRF1 Tumor Suppressor Network by PML-RARα Drives Acute Promyelocytic Leukemia Pathogenesis
    Céline Prunier, Ming-Zhu Zhang, Santosh Kumar, Laurence Levy, Olivier Ferrigno, Guri Tzivion, Azeddine Atfi
    Cell Reports, 2015
  • TG2: Player That Dictates the Rules in Cancer Progression
    Kapil Mehta, Santosh Kumar
    Multi Targeted Approach to Treatment of Cancer, 2015
  • Transglutaminase 2 reprogramming of glucose metabolism in mammary epithelial cells via activation of inflammatory signaling pathways
    Santosh Kumar, Taraka R. Donti, Navneet Agnihotri, Kapil Mehta
    International Journal of Cancer, 2014
  • Tissue transglutaminase expression promotes castration-resistant phenotype and transcriptional repression of androgen receptor
    Amy Lee Han, Santosh Kumar, Jansina Y. Fok, Amit K. Tyagi, Kapil Mehta
    European Journal of Cancer, 2014
  • Tissue transglutaminase, inflammation, and cancer: How intimate is the relationship?
    Santosh Kumar, Kapil Mehta
    Amino Acids, 2013
  • Tissue Transglutaminase Constitutively Activates HIF-1α Promoter and Nuclear Factor-κB via a Non-Canonical Pathway
    Santosh Kumar, Kapil Mehta
    Plos One, 2012
  • Tissue transglutaminase as a central mediator in inflammation-induced progression of breast cancer
    Navneet Agnihotri, Santosh Kumar, Kapil Mehta
    Breast Cancer Research, 2012
  • Evidence that GTP-binding domain but not catalytic domain of transglutaminase 2 is essential for epithelial-to-mesenchymal transition in mammary epithelial cells
    Anupam Kumar, Jia Xu, Bokyung Sung, Santosh Kumar, Dihua Yu, Bharat B Aggarwal, Kapil Mehta
    Breast Cancer Research, 2012

RECENT SCHOLAR PUBLICATIONS

  • Intercellular Mitochondrial Trafficking as a Master Regulator of Tumor Progression and Cancer Stem Cell Plasticity
    P Agrawal, S Tiwari, P Mendhey, P Jampala, H Rajak, N Kurrey, N Ahmed, ...
    Onco 6 (2) , 2026
    2026
  • Antioxidants ameliorates glucose/glucose oxidase-induced myocardial damage through mitochondrial and MAPK pathway
    S Kumar, P Agrawal, P Mendhey, SK Dhatwalia, SL Sitasawad
    3 Biotech 15 (9), 323 , 2025
    2025
  • Green Tea's EGCG: Brewing Hope in the Battle against Breast Cancer
    M Kumar, R Lal, A Sehgal, S Rawat, A Kumar, S Kumar, SK Dhatwalia
    The Natural Products Journal , 2025
    2025
    Citations: 1
  • Introduction to microbiomes in health and diseases
    P Agrawal, P Mendhey, R Kumar, S Patel, PK Kaushik, A Dadsena, ...
    International Review of Cell and Molecular Biology 394, 1-42 , 2025
    2025
    Citations: 3
  • Synthesis, Characterization, and Comparative Analysis of Zinc Oxide Nanoparticles using Calendula Officinalis Flower Extract and its Antibacterial Activity
    L Radhakrishnan, SA Sathar, S Jamal, S Kumar, N Ahmed
    2025
    Citations: 1
  • Imidazo[1,2‐ a ]Quinoxaline‐2‐Carbonitrile Derivative (RA‐22) Inhibits Self‐Renewal and Growth of Cancer Stem and Cancer Cells via Downregulating AKT Pathway
    P Kumar, U Prasad Yadav, G Joshi, S Arora, M Kumar, J Chatterjee, ...
    ChemistrySelect 9 (23), e202400223 , 2024
    2024
    Citations: 3
  • Natural compound-based nanoparticles to target free radicals in cancer
    UP Yadav, M Rhuthuparna, K Vasudev, P Suman, A Munshi, S Kumar, ...
    Handbook of Oxidative Stress in Cancer: Therapeutic Aspects, 1-14 , 2022
    2022
    Citations: 2
  • Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Book Chapter-Natural Compound-Based Nanoparticles to Target Free Radicals in Cancer.
    SS Yadav UP, Rhuthuparna M, Vasudev K, Suman P, Munshi A, Santosh Kumar
    2022
  • Design, synthesis and anticancer activity of 2-arylimidazo [1, 2-a] pyridinyl-3-amines
    UP Yadav, AJ Ansari, S Arora, G Joshi, T Singh, H Kaur, N Dogra, ...
    Bioorganic Chemistry 118, 105464 , 2022
    2022
    Citations: 26
  • Let-7a induces metabolic reprogramming in breast cancer cells via targeting mitochondrial encoded ND4
    P Sharma, V Sharma, TS Ahluwalia, N Dogra, S Kumar, S Singh
    Cancer cell international 21 (1), 629 , 2021
    2021
    Citations: 29
  • Metabolic adaptations in cancer stem cells
    UP Yadav, T Singh, P Kumar, P Sharma, H Kaur, S Sharma, S Singh, ...
    Frontiers in oncology 10, 1010 , 2020
    2020
    Citations: 151
  • CAR T cell therapy: newer approaches to counter resistance and cost
    RK Yadav, A Ali, S Kumar, A Sharma, B Baghchi, P Singh, S Das, C Singh, ...
    Heliyon 6 (4) , 2020
    2020
    Citations: 34
  • E-pharmacophore guided discovery of pyrazolo [1, 5-c] quinazolines as dual inhibitors of topoisomerase-I and histone deacetylase
    G Joshi, S Kalra, UP Yadav, P Sharma, PK Singh, S Amrutkar, AJ Ansari, ...
    Bioorganic Chemistry 94, 103409 , 2020
    2020
    Citations: 41
  • Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia
    AA Santosh Kumar, Parash Parajuli, Audrey Loumaye, Purba Singh, Sailaja ...
    Developmental Cell 45, 712–725 , 2018
    2018
    Citations: 63
  • Abstract A38: Twist1-driven fatty pancreas formation facilitates pancreatitis and pancreatic ductal adenocarcinoma progression
    TL Nguyen, P Singh, P Parajuli, L Li, C Prunier, S Kumar, S Eragmerdi, ...
    Cancer Research 78 (10_Supplement), A38-A38 , 2018
    2018
  • Twist1 activation in muscle progenitor cells during development or adulthood causes severe muscle loss reminiscent of human cancer cachexia.
    P Parajuli, S Kumar, A Loumaye, P Singh, S Eragamreddy, TL Nguyen, ...
    CANCER RESEARCH 78 (10), 49-50 , 2018
    2018
  • Twist1-driven fatty pancreas formation facilitates pancreatitis and pancreatic ductal adenocarcinoma progression.
    TL Nguyen, P Singh, P Parajuli, L Li, C Prunier, S Kumar, S Eragmerdi, ...
    CANCER RESEARCH 78 (10), 49-49 , 2018
    2018
  • Abstract A40: Twist1 activation in muscle progenitor cells during development or adulthood causes severe muscle loss reminiscent of human cancer cachexia
    AA Parash Parajuli, Santosh Kumar, Audrey Loumaye, Purba Singh, Sailaja ...
    Cancer Research 78 (10), A40 , 2018
    2018
  • Abstract A38: Twist1-driven fatty pancreas formation facilitates pancreatitis and pancreatic ductal adenocarcinoma progression
    AA Thien Ly Nguyen, Purba Singh, Parash Parajuli, Lianna Li, Celine Prunier ...
    Cancer research 10 (78), A38 , 2018
    2018
  • Abstract B33: Tgif inactivation defines a synthetic lethal interaction among oncogenic Kras and Twist1 in pancreatic ductal adenocarcinoma
    P Parajuli, P Singh, Z Wang, S Kumar, L Li, S Eragamreddi, TL Nguyen, ...
    Molecular Cancer Therapeutics 16 (10_Supplement), B33-B33 , 2017
    2017

MOST CITED SCHOLAR PUBLICATIONS

  • Fatty acid oxidation-driven Src links mitochondrial energy reprogramming and oncogenic properties in triple-negative breast cancer
    JH Park, S Vithayathil, S Kumar, PL Sung, LE Dobrolecki, V Putluri, ...
    Cell reports 14 (9), 2154-2165 , 2016
    2016
    Citations: 359
  • Metabolic adaptations in cancer stem cells
    UP Yadav, T Singh, P Kumar, P Sharma, H Kaur, S Sharma, S Singh, ...
    Frontiers in oncology 10, 1010 , 2020
    2020
    Citations: 151
  • Tissue transglutaminase constitutively activates HIF-1α promoter and nuclear factor-κB via a non-canonical pathway
    S Kumar, K Mehta
    Plos One 7 (11), e49321 , 2012
    2012
    Citations: 137
  • Tissue transglutaminase as a central mediator in inflammation-induced progression of breast cancer
    N Agnihotri, S Kumar, K Mehta
    Breast Cancer Research 15 (1), 202 , 2013
    2013
    Citations: 128
  • N-Acetyl Cysteine prevents glucose/glucose oxidase-induced oxidative stress, mitochondrial damage and apoptosis in H9c2 cells.
    SKSL Sitasawad
    Life Science 84 (11-12), 328-336 , 2009
    2009
    Citations: 123
  • Multiple antioxidants improve cardiac complications and inhibit cardiac cell death in streptozotocin-induced diabetic rats
    SPSLS Santosh Kumar
    PLoS One 8 (7), e67009 , 2013
    2013
    Citations: 90
  • Cadmium induced mitochondrial injury and apoptosis in Vero cells: Protective effect of diallyl tetrasulfide from garlic.
    KS Murugavel P, Pari L, Sitasawad SL, Kumar S
    Int J Biochem Cell Biol. 39 (1), 161-170 , 2007
    2007
    Citations: 90
  • Evidence that GTP-binding domain but not catalytic domain of transglutaminase 2 is essential for epithelial-to-mesenchymal transition in mammary epithelial cells
    A Kumar, J Xu, B Sung, S Kumar, D Yu, BB Aggarwal, K Mehta
    Breast Cancer Research 14 (1), 1-15 , 2012
    2012
    Citations: 81
  • Transglutaminase 2 reprogramming of glucose metabolism in mammary epithelial cells via activation of inflammatory signaling pathways
    S Kumar, TR Donti, N Agnihotri, K Mehta
    International journal of cancer 134 (12), 2798-2807 , 2014
    2014
    Citations: 73
  • Twist1 Activation in Muscle Progenitor Cells Causes Muscle Loss Akin to Cancer Cachexia
    AA Santosh Kumar, Parash Parajuli, Audrey Loumaye, Purba Singh, Sailaja ...
    Developmental Cell 45, 712–725 , 2018
    2018
    Citations: 63
  • Tissue transglutaminase, inflammation, and cancer: how intimate is the relationship?
    S Kumar, K Mehta
    Amino acids 44 (1), 81-88 , 2013
    2013
    Citations: 62
  • A Novel Triterpenoid Isolated from the Root Bark of Ailanthus excelsa Roxb (Tree of Heaven), AECHL-1 as a Potential Anti-Cancer Agent
    MS Lavhale, S Kumar, SH Mishra, SL Sitasawad
    PLoS One 4 (4), e5365 , 2009
    2009
    Citations: 57
  • E-pharmacophore guided discovery of pyrazolo [1, 5-c] quinazolines as dual inhibitors of topoisomerase-I and histone deacetylase
    G Joshi, S Kalra, UP Yadav, P Sharma, PK Singh, S Amrutkar, AJ Ansari, ...
    Bioorganic Chemistry 94, 103409 , 2020
    2020
    Citations: 41
  • Tissue transglutaminase expression promotes castration-resistant phenotype and transcriptional repression of androgen receptor
    AKTKM Amy Han, Santosh Kumar, Jansina Y. Fok
    Eur J Cancer 50 (9), 1685-96 , 2014
    2014
    Citations: 40
  • CAR T cell therapy: newer approaches to counter resistance and cost
    RK Yadav, A Ali, S Kumar, A Sharma, B Baghchi, P Singh, S Das, C Singh, ...
    Heliyon 6 (4) , 2020
    2020
    Citations: 34
  • Novel SUMO-Protease SENP7S Regulates β-catenin Signaling and Mammary Epithelial Cell Transformation.
    BKT Karami S, Lin FM, Kumar S, Bahnassy S, Thangavel H, Quttina M, Li Y, Ren J
    Scientific Reports 7 (46477) , 2017
    2017
    Citations: 32
  • Let-7a induces metabolic reprogramming in breast cancer cells via targeting mitochondrial encoded ND4
    P Sharma, V Sharma, TS Ahluwalia, N Dogra, S Kumar, S Singh
    Cancer cell international 21 (1), 629 , 2021
    2021
    Citations: 29
  • Disruption of the PHRF1 tumor suppressor network by PML-RARα drives acute promyelocytic leukemia pathogenesis
    C Prunier, MZ Zhang, S Kumar, L Levy, O Ferrigno, G Tzivion, A Atfi
    Cell reports 10 (6), 883-890 , 2015
    2015
    Citations: 27
  • Steroids up-regulate p66Shc longevity protein in growth regulation by inhibiting its ubiquitination
    S Kumar, S Kumar, M Rajendran, SM Alam, FF Lin, PW Cheng, MF Lin
    PLoS One 6 (1), e15942 , 2011
    2011
    Citations: 27
  • Design, synthesis and anticancer activity of 2-arylimidazo [1, 2-a] pyridinyl-3-amines
    UP Yadav, AJ Ansari, S Arora, G Joshi, T Singh, H Kaur, N Dogra, ...
    Bioorganic Chemistry 118, 105464 , 2022
    2022
    Citations: 26