World's Best Scientists 2026 revealed!

D-Index & Metrics

Medicine

D-Index
86
Citations
23039
World Ranking
14280
National Ranking
7218

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Cancer
  • Internal medicine

Ravi Bhatia mainly focuses on Cancer research, Chronic myelogenous leukemia, Leukemia, Stem cell and Imatinib mesylate. The various areas that Ravi Bhatia examines in his Cancer research study include Haematopoiesis, Progenitor cell, Tyrosine kinase, Kinase activity and Bone marrow. His Chronic myelogenous leukemia research is multidisciplinary, incorporating elements of K562 cells and Philadelphia chromosome.

His research integrates issues of Myeloid, Myeloid leukemia and Transplantation in his study of Leukemia. He does research in Stem cell, focusing on Cancer stem cell specifically. His Imatinib mesylate study integrates concerns from other disciplines, such as breakpoint cluster region and ABL.

His most cited work include:

  • Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome–positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance (638 citations)
  • Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment. (492 citations)
  • miR-328 Functions as an RNA Decoy to Modulate hnRNP E2 Regulation of mRNA Translation in Leukemic Blasts (422 citations)

What are the main themes of his work throughout his whole career to date?

His primary areas of study are Cancer research, Stem cell, Progenitor cell, Immunology and Leukemia. The concepts of his Cancer research study are interwoven with issues in Chronic myelogenous leukemia and Tyrosine kinase, ABL. His work investigates the relationship between Chronic myelogenous leukemia and topics such as Integrin that intersect with problems in Cell adhesion and Cell adhesion molecule.

His Stem cell study combines topics in areas such as Myeloid and Bone marrow. His biological study spans a wide range of topics, including Cancer cell, Molecular biology, Apoptosis and CD38. His Leukemia study is related to the wider topic of Internal medicine.

He most often published in these fields:

  • Cancer research (47.45%)
  • Stem cell (34.18%)
  • Progenitor cell (32.14%)

What were the highlights of his more recent work (between 2015-2021)?

  • Cancer research (47.45%)
  • Stem cell (34.18%)
  • Internal medicine (21.17%)

In recent papers he was focusing on the following fields of study:

Ravi Bhatia mostly deals with Cancer research, Stem cell, Internal medicine, Leukemia and Myeloid leukemia. His research integrates issues of Cell growth, Progenitor cell, Tyrosine kinase, ABL and Chronic myelogenous leukemia in his study of Cancer research. His research in Stem cell intersects with topics in Immunology and Bone marrow.

His work in Internal medicine tackles topics such as Oncology which are related to areas like Philadelphia chromosome, Discontinuation, Polycythemia vera, Risk stratification and Essential thrombocythemia. His study in the field of Myelogenous also crosses realms of PARP1. His Myeloid leukemia study combines topics from a wide range of disciplines, such as Hematopoietic stem cell transplantation, DNA methylation, CXCR4, CD33 and Drug resistance.

Between 2015 and 2021, his most popular works were:

  • High Frequency and Poor Outcome of Philadelphia Chromosome-Like Acute Lymphoblastic Leukemia in Adults. (172 citations)
  • Clonal Hematopoiesis Associated With Adverse Outcomes After Autologous Stem-Cell Transplantation for Lymphoma (162 citations)
  • Chronic myeloid leukemia, version 1.2019 (137 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Cancer
  • Internal medicine

Leukemia, Cancer research, Stem cell, Myeloid leukemia and Internal medicine are his primary areas of study. His study with Leukemia involves better knowledge in Immunology. The Cancer research study combines topics in areas such as Haematopoiesis, Bone marrow, Tyrosine-kinase inhibitor and DNA repair.

His study in Stem cell is interdisciplinary in nature, drawing from both Chronic myelogenous leukemia and Tyrosine kinase, Nilotinib. His Internal medicine research incorporates themes from Philadelphia chromosome and Oncology. Ravi Bhatia studied Hematopoietic stem cell and breakpoint cluster region that intersect with ABL.

Best Publications

  • Nilotinib (formerly AMN107), a highly selective BCR-ABL tyrosine kinase inhibitor, is effective in patients with Philadelphia chromosome–positive chronic myelogenous leukemia in chronic phase following imatinib resistance and intolerance

    Hagop M. Kantarjian;Francis Giles;Norbert Gattermann;Kapil Bhalla

  • Persistence of malignant hematopoietic progenitors in chronic myelogenous leukemia patients in complete cytogenetic remission following imatinib mesylate treatment.

    Ravi Bhatia;Melissa Holtz;Ning Niu;Rachel Gray

  • miR-328 Functions as an RNA Decoy to Modulate hnRNP E2 Regulation of mRNA Translation in Leukemic Blasts

    Anna M. Eiring;Jason G. Harb;Paolo Neviani;Christopher Garton

  • Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival

    Ashley Hamilton;G. Vignir Helgason;Mirle Schemionek;Bin Zhang

  • PAX5 -driven subtypes of B-progenitor acute lymphoblastic leukemia

    Zhaohui Gu;Michelle L. Churchman;Kathryn G. Roberts;Ian Moore

  • Activation of p53 by SIRT1 inhibition enhances elimination of CML leukemia stem cells in combination with imatinib

    Ling Li;Lisheng Wang;Liang Li;Zhiqiang Wang

  • High Frequency and Poor Outcome of Philadelphia Chromosome-Like Acute Lymphoblastic Leukemia in Adults.

    Kathryn G. Roberts;Zhaohui Gu;Debbie Payne-Turner;Kelly McCastlain

  • T cells expressing CD123-specific chimeric antigen receptors exhibit specific cytolytic effector functions and antitumor effects against human acute myeloid leukemia

    Armen Mardiros;Cedric Dos Santos;Tinisha McDonald;Christine E. Brown

  • Clonal Hematopoiesis Associated With Adverse Outcomes After Autologous Stem-Cell Transplantation for Lymphoma

    Christopher J Gibson;R Coleman Lindsley;Vatche Tchekmedyian;Brenton G Mar

  • Altered Microenvironmental Regulation of Leukemic and Normal Stem Cells in Chronic Myelogenous Leukemia

    Bin Zhang;Yin Wei Ho;Qin Huang;Takahiro Maeda

  • Acute myeloid leukemia transforms the bone marrow niche into a leukemia-permissive microenvironment through exosome secretion

    B. Kumar;M. Garcia;L. Weng;X. Jung

  • Solid Cancers After Bone Marrow Transplantation

    Smita Bhatia;Andrew D. Louie;Ravi Bhatia;Margaret R. O’Donnell

  • Stem cell quiescence.

    Ling Li;Ravi Bhatia

  • Predictors of therapy-related leukemia and myelodysplasia following autologous transplantation for lymphoma: an assessment of risk factors.

    Amrita Krishnan;Smita Bhatia;Marilyn L. Slovak;Daniel A. Arber

  • Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferation.

    Melissa S. Holtz;Marilyn L. Slovak;Feiyu Zhang;Charles L. Sawyers

  • Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment

    Su Chu;Helen Xu;Helen Xu;Neil P. Shah;Neil P. Shah;David S. Snyder;David S. Snyder

  • Effective Targeting of Quiescent Chronic Myelogenous Leukemia Stem Cells by Histone Deacetylase Inhibitors in Combination with Imatinib Mesylate

    Bin Zhang;Adam C. Strauss;Su Chu;Min Li

  • Microenvironmental protection of CML stem and progenitor cells from tyrosine kinase inhibitors through N-cadherin and Wnt–β-catenin signaling

    Bin Zhang;Min Li;Tinisha McDonald;Tessa L. Holyoake

  • Persistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatment.

    Su Chu;Tinisha McDonald;Allen Lin;Sujata Chakraborty

  • BCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance. Commentary

    Ravi Bhatia;Mateusz Koptyra;Rafal Falinski;Michal O. Nowicki

Frequent Co-Authors

Stephen J. Forman
Stephen J. Forman City Of Hope National Medical Center
Smita Bhatia
Smita Bhatia University of Alabama at Birmingham
Tessa L. Holyoake
Tessa L. Holyoake University of Glasgow
Jerald P. Radich
Jerald P. Radich Fred Hutchinson Cancer Research Center
Jorge E. Cortes
Jorge E. Cortes Augusta University
Philip B. McGlave
Philip B. McGlave University of Minnesota
Daniel J. Weisdorf
Daniel J. Weisdorf University of Minnesota
Arturo Molina
Arturo Molina Sutro Biopharma
Hagop M. Kantarjian
Hagop M. Kantarjian The University of Texas MD Anderson Cancer Center

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