Mrinal Kanti Ghosh, Ph.D., FNASC, FAScT

Chief Scientist & Head (CBID); Professor, AcSIR, New Delhi
Cancer Biology & Inflammatory Disorder

Research Focus

Cancer has a multifaceted character which is inherent in its very origin. Diverse arrays of aberrations are required before a normal cell will defy ‘social behavior’ to fulfill its only purpose – to proliferate – at the expense of life. By then, deep down at the molecular level crucial signalling pathways would have been extensively rewired. Proteins such as p53 and PTEN which keeps scrupulous cellular growth in check are lost functionally; whereas proteins accelerating growth, such as STAT3, β-catenin and c-Myc, are up-regulated. Protein kinases like Akt and CK2 regulate these players by phosphorylation at critical residues that have important bearing upon their functions. Another class of proteins that include E3 ubiquitin ligases like CHIP and deubiquitinases like HAUSP regulate these same players by governing their half-lives. Our lab is interested and actively working on all these aspects of a tumour cell. To understand cancer and to be able to intervene in its progression we concentrate on these most basic mechanisms. An appreciation of these will probably take us one step further in the way to treating cancer.

Research Interest


Cross-regulation of Wnt/β-catenin and EGFR Signalling in Cancer: Our aim is to determine the major pathways responsible for the activation and nuclear localization of Stat3 & β-catenin in human cancer & cancer stem cells and study in particular, the involvement of EGFR & Wnt signaling for this regulation. In this context, the mechanism of nuclear accumulation of β-catenin and its subsequent trans-activation of downstream targets also plays a crucial role in cancer development. The unraveling of the potential intersections of these pathways in glioma, breast and prostate cancer may provide novel targets for drug discovery.

Deciphering cell signalling mechanism responsible for oncogenesis: The disturbance of the balance between activities of oncoproteins and tumor suppressors is primarily considered the root cause for oncogenesis. Various genetic mutations and environmental stimuli trigger such disturbances. Our focus is to investigate the cause-and-effect mechanism with respect to post-translational modifiers, transcription factors and major signalling kinases, where imbalance in their level of expression and/or their activity causes cellular transformation. Validation of the potential of these avenues is demonstrated in animal studies of glioma, breast, colorectal, lung and prostate cancer with an aim to provide novel targets for drug discovery.

 Topics of Research:

  • Signal transduction and signaling crosstalks
  • Gene regulations in cancer and cancer stem cells
  • Molecular mechanisms of oncogenesis and apoptosis
  • Post-translational regulation of oncogenes and tumor suppressors
  • Targeted delivery of nanotherapeutics across the Blood Brain Barrier (BBB)


Current Projects:

Role of DEAD Box RNA Helicases in Cancer 

RNA Helicases play crucial roles in developmental processes. Recently, it has been implied that its involvement in transcription is very important in cancer progression. In our present study we would like to study the regulation of p68/p72 through EGFR & Wnt signaling and importance in cancer progression.

Role of Ubiquitinases and Deubiquitinases in Cancer 

Ubiquitin ligases and deubiquitinases play major roles in cellular physiology by modulating half-lives of numerous proteins. Because ubiquitination and deubiquitination events can influence the time a protein spends inside the cell and the space it occupies during that time, a balance between these events is necessary for maintaining cellular homeostasis and normal functioning. Cancer cells are thought to bypass this balance towards a net increase in proliferation and growth. Therefore, understanding these key mechanisms is important for combating cancer.

          The ubiquitin proteasome system (UPS) is involved in almost every cellular physiology. The ubiquitinases and the deubiquitinases regulate their target proteins’ stability, sub-cellular localization and function, which translates to the fact that the UPS controls cell cycle, cell differentiation, epigenetic modifications, DNA damage repair, metabolism, immunity and viral infection. A malignant cell seizes the chance to shift the equilibrium between ubiquitinases and deubiquitinases in favour of promoting growth, ensuring survival, and evading apoptosis. Hence, establishing molecular pathways involving UPS components is crucial in our understanding of carcinogenesis and chemoresistance.

Role of Casein Kinase II in Modulation of Cancer Cell Signaling

Casein Kinase II/CKII is a ubiquitously expressed Ser/Thr kinase present in all cells, with known upregulated activity in Cancers (e.g. Prostate, Brain Breast etc.). Our aim is to study the various oncogenic signalings initiated and modulated by CKII, and decipher the mechanistic detail how such signaling modulation is responsible for oncogenicity of a cell. Presently among various players, we are interested to investigate the crosstalk of CKII with AKT (oncogenic kinase), PML (an important nuclear sequestering protein) and DAXX (an adapter protein).

         A Ser/Thr protein kinase that is constitutively active, CK2 phosphorylates a large number of substrates, regulates a number of signaling pathways, and is linked to a wide range of human disorders. Its function in cancer, where it controls nearly all malignant markers, is best understood. In relation to CK2 targeting in cancer, it is important to note that, in addition to kinase inhibitor monotherapy, there is high anticipation for combined therapies that simultaneously target onco-pathways, which are abnormal in a particular cancer specifically, and CK2, which more generally amplifies tumorigenic signals. Based on these considerations, CK2 is becoming a more appealing target in a number of areas of human medicine, with the benefit that there are currently a number of extremely specialized inhibitors that are highly efficient. Our goal is to understand the multiple oncogenic signalling pathways that CK2 initiates and modulates, as well as the molecular details of how this signaling modulation contributes to a cell's oncogenicity. Our current research focuses on the interactions of CK2 with AKT (an oncogenic kinase), PML (a crucial nuclear sequestering protein), and DAXX (an adaptor protein).

Drug Discovery

Targeted delivery of anti-cancer drugs using target based synthetic peptides on a nanotechnology platform.Nanotechnology has emerged as a promising platform for cancer therapy by enabling precise targeting and delivery of therapeutics to the tumor site. Nanoparticles offer a safe and efficient means of delivering drugs to the tumor region. The aim of our study is to deliver small chemicals, peptides, proteins, and nucleic acids using polymeric nanoparticles that are taken up by cancer cells and release the encapsulated drug(s) over time. We are interested in investigating significant clinical responses that can be tested for cancer therapy.

       Nanoparticles represent a highly effective approach for cancer treatment, providing unparalleled precision and efficacy. Among the variety of materials used for the fabrication of nano-system viz., Poly (lactic-co-glycolic acid) (PLGA) has gathered special attention due to its biocompatibility and biodegradability, and widely used for effective tumor targeting by efficient drug delivery to the tumor site. PLGA nanoparticles improved efficient permeability and retention effect (EPR) to the tumor cells surface for efficient diffusion. Based on our current knowledge and more than a decade of expertise we are considering the present system to deliver two or more drugs in a combinatorial approach systematically and sufficiently to the target site for effective cancer therapy.


Reviewer of several specialized journals like:

  • Cancer Research (AACR)
  • Oncogene (NPG)
  • BBA- Mol Cell Research
  • Cell Death & Disease (NPG)
  • Tumor Biology
  • FEBS Journal


Editorial Board Member: 

  • Nature Cell & Science
  • Current Molecular Pharmacology
  • Frontiers in Oncology


HOD,  Cancer Biology & Inflammatory Disorder Division


Positions & Posts Held

Position Year  Institution
Chief Scientist [Scientist - G] 20.02.2020 – till date CSIR-IICB (TRUE), Kolkata, India
Senior Principal Scientist [Scientist - F] 20.02.2015 – 19.02.2020 CSIR-IICB (TRUE), Kolkata, India
Principal Scientist [Scientist-EII]  20.02.2011 – 19.02.2015 CSIR-IICB, Kolkata, India
Senior Scientist [Scientist-EI]  20.02.2007 – 19.02.2011 CSIR-IICB, Kolkata, India
Assistant Professor 2005 – 2006 HIT, Kolkata, India
Staff-RA 2003 - 2005 Cancer Biology, Cleveland Clinic Foundation, OHIO, USA
Post-doctoral Fellow 1997 - 2003 Molecular Biology, Cleveland Clinic Foundation, OHIO, USA.
JRF/SRF 1992 - 1997 Biochemistry, University of Calcutta

Academic Qualifications   

 Degree University   Year   Subject
Ph. D University of Calcutta 1997 Science (Bio-Chemistry)
M. Sc.  University of Calcutta  1990

Bio-Chemistry [Special paper: Molecular Biology]

B. Sc. (H) University of Calcutta 1988 Chemistry (Hons.), Physics, Mathematics

Honours & Awards



Bharat Vikas Award


Merit promotion from Principal Scientist to Sr. Principal Scientist by CSIR


Fellow National Academy of Science & Technology (FNASc)


Fellow Academy of Science & Technology (FAScT)

2012 – till date

Reviewer: Oncogene, Cancer Research, Neoplasia, Tumor Biology, CDDise, BBA Mol Cell Res. etc


CSIR-EMPOWER Programme (Phase-II) approved for A+ category by DG, CSIR, (Head Quarter)


Promotion from Sr. Scientist to Principal Scientist


Outstanding (A+) performance in CSIR-EMPOWER Programme (Phase-I) by DG, CSIR, (Head Quarter)

2009 – 2010

External expert: Evaluation of Summer Project of M. Sc. Students of Biochemistry Dept., University of Calcutta.

2008 – 2012

External expert: Evaluation of Summer Project of M.Sc. students, Dept. of Biotechnology, University of Calcutta.

2007 – till date Reviewer: Evaluation of International (World Health Research & DHR, Ireland) and National (DBT, DST-SERB & CSIR) project proposals.
2007 – 2012 Member, INDO  –  US Programme Project on ‘CANCER’
2007 – 2012 Task Force Member, CSIR, Inter-agency project IAP001, IICB, Kolkata


Awarded Young Scientist fellowship, by “International Union of Biochemistry and Molecular Biology (IUBMB)”

1992 1997

Awarded JRF & SRF for Graduate Studies, DBT, Govt. of India


Awarded Graduate Aptitude Test for Engineering (GATE) [97.67 percentile]

Grants & Supports

  1. PI: CSIR FBR (Focused Basic Research): 2020 – 2023. Restoration of p53 and Rb through targeting their post-translational modifiers (PTMs) HAUSP and MDM2 in glioma and stepping towards development of novel inhibitory peptide designing from interacting interface. Total cost: Rs.113.0 Lakhs [Completed].
  2. PI: PAN-CSIR Cancer Research: 2021 – 2025.  PARP inhibitor (PARPi) treatment for effective Breast Cancer therapy: Pre-Clinical Validation & Combination Therapy with PTEN-CT Peptide. Total cost: Rs.90.0 Lakhs [Ongoing].
  3. PI: DST-SERB: 2019 – 2022. A Novel Nanotechnology based Approach of Glioma Therapy by Targeting HAUSP -MDM2 axis in combination with Temozolomide. Total cost: ~Rs.40.138 Lakhs [Completed].
  4. PI: DST-Nano Mission: 2018 – 2021. Development of a combinatorial nanovehicles assisted therapeutic system for the efficient treatment of glioma. Total cost: Rs.42.0 Lakhs (Completed).
  5. Co-PI (with CSIR-IICT): DST-SERB: 2018 – 2021. Glucocorticoid Receptor-Assisted Drug Sensitization (GRADS) in colorectal cancer therapy: Nano-therapeutic strategy towards repurposing of anti-cancer drugs. Total cost: Rs.30.67 Lakhs [Completed].
  6. Co-PI (with Bose Institute): DST-SERB: 2015 – 2018. Development of Synthetic Transcription Factors against pluripotency to Target Cancer Stem Cells. [Completed].
  7. PI: DST-Nano Mission: 2015 – 2019: Development of nano-particle based directed delivery systems for Peptide therapeutics. (Nodal of IICB: 68L). [Completed].
  8. Co-PI: Bio-Cluster, Kolkata: 2017 – 2018, Multi-dimensional Research to Enable Systems Medicine: Acceleration Using a Cluster Approach [Systems Medicine Cluster:[SyMeC], DBT, Govt. of India [Completed].
  9. PI: CSIR Task Force project: 2012 – 2017. Medicinal Chemistry for Stem Cell Biology and Regenerative Medicine (MEDCHEM). Total cost: ~Rs.24.0 Crores  [Completed]
  10. PI: CMPP-05: 2012 – 2017. Reactivation of the p53 regulatory circuit in glioblastomas bearing wild-type p53 allele by designed therapeutic peptides targeted against S100B. Total cost: ~Rs.2.07 Crores  [INDO-US] [Completed].
  11. PI: CSIR Task Force project: 2012 – 2017. Neurodegenerative diseases: Causes and corrections (miND). Total cost: ~Rs.48.0 Crores  [Completed]
  12. PI: DSR-SERB: 2012 – 2015. Crosstalk between Stat3 & B-catenin: Understanding the Mechanisms to Counteract Prostate Cancer. Total cost: Rs.48.0 Lakhs  [Completed]
  13. PI: CSIR EMPOWER project (Phase-II): 2012 – 2015. Investigation on clinical implication of CK2 and PML in Glioma samples and their role in Glioma cell lines in search of possible cure for Glioma. Total cost: ~Rs.1.52 Crores, as Individual PI  [Completed]
  14. PI: CSIR EMPOWER project (Phase-I): 2010 – 2012. Investigation on clinical implication of CK2 and PML in Glioma samples and their role in Glioma cell lines in search of possible cure for Glioma. Total cost: ~Rs.26.0 Lakhs  [Completed]
  15. PI: CSIR programme project: 2009 – 2012. System Biology Approach: Drug Discovery Against Glioma & Lung Cancer. Total cost: ~Rs.14.0 Crores  [INDO-JAPAN] [Completed].
  16. PI: DST-SERB: 2008 – 2009. Regulation of Stat: Understanding Mechanisms to Counteract Prostate Cancer.  Total cost: ~Rs.5.43 Lakhs  [Completed]
  17. PI: CSIR Task Force project: 2007 – 2012. New Insights in Cancer Biology: Identification of Novel Targets and Development of Target Based Molecular Medicine. Total cost: ~Rs.15.0 Crores  [Completed]


Patents & Publications



1.     Saha G, Roy S, Basu M and Ghosh MK* (2023). USP7 - A crucial regulator of Cancer Hallmarks. BBA – Reviews on cancer 1878, 188903. {IF=11.414; Ci=0}.

2.     Sarkar S#, Karmakar S#, Basu M, Ghosh P and Ghosh MK* (2023). Neurological damages in COVID-19 patients: mechanisms and preventive interventions. MedComm. 4: e247,1-25. {IF=9.9; Ci=3}

3.     Tabassum S, Basu M and Ghosh MK* (2023). The DEAD-box protein p68 and β-catenin: the crucial regulators of FOXM1 gene expression in arbitrating colorectal cancer. BBA - Gene Regulatory Mechanisms 1866(2) 194933. {IF=6.304; Ci=3}.

4.     Chakraborty S, Karmakar S, Basu M, Kal S and Ghosh MK * (2023). E3 Ubiquitin Ligase CHIP Drives Monoubiquitination-mediated Nuclear Import of Tumor Suppressor PTEN. J Cell Science {IF=5.235}.


5.     Basu B, Karmakar S, Basu M and Ghosh MK* (2023). USP7 imparts partial EMT state in colorectal cancer by stabilizing the RNA helicase DDX3X and augmenting Wnt/β-catenin signaling. BBA- Mol Cell Res 1870(4) 119446. {IF=5.011; Ci=0}.

6.     Ghosh MK*, Kumar S, Ganguly KK, Ghosh P, Tabassum S, Basu B, and Basu M* (2023). COVID-19 and its consequences in cancer: Insights into their association and influence on genetic and epigenetic landscape. Epigenomics 10.2217/epi-2023-0052 {IF=4.357; Ci=0}.


7.      Mukherjee S, et al., (2023). A small HDM2 antagonist peptide and a USP7 inhibitor synergistically inhibit the p53-HDM2-USP7 circuit. Chemical Biology & Drug Design 102(1). {IF=2.99; Ci=0}


8.      Saha G, Sarkar S, Mohanta PS, Kumar K, Chakraborty S, Basu M and Ghosh MK* (2022). Identification and validation of E3 ubiquitin ligase XIAP as a novel substrate of deubiquitinase USP7 (HAUSP) - Implication towards oncogenesis. Oncogene (NPG), 41:5061–5075. {IF=8.756; Ci=8}.

9.      Kumar S, Basu M*, Ghosh P, Pal U and Ghosh MK* (2022). COVID-19 therapeutics: Clinical application of repurposed drugs and futuristic strategies for target-based drug discovery. Genes & Diseases 10, 1402-1428. {IF=7.376; Ci=2}

10.   Kumar S#, Chatterjee M#, Ghosh P#, Ganguly KK#, Basu M# * and Ghosh MK# * (2022). Targeting PD-1/PD-L1 in cancer immunotherapy: an effective strategy for treatment of triple negative breast cancer (TNBC) patients. Genes & Diseases 10, 1318-1350. {IF=7.376; Ci=6}.

11.   Kumar S, Basu M*, Ghosh P, Ansari A and Ghosh MK* (2022). COVID-19: Clinical status of vaccine development to date. Br J Clinical Pharmacol, 89(1):114-149. {IF=4.335; Ci=7}.

12.   Tabassum S and Ghosh MK* (2022). DEAD-box RNA helicases with special reference to p68: Unwinding their versatility and therapeutic opportunity in cancer. Genes & Diseases 10, 1220-1241. {IF=7.376; Ci=3}.

13.   Basu B and Ghosh MK* (2022). Ubiquitination and deubiquitination in the regulation of epithelial-mesenchymal transition in cancer: Shifting gears at the molecular level. BBA- Mol Cell Res., 1869(7):119261. {IF=5.011; Ci=7}.

2020 - 2021

14.   Kumar S, Basu M and Ghosh MK* (2021). Chaperone-assisted E3 ligase CHIP: A double agent in cancer. Genes & Diseases 9(6):1513-1547. {IF=7.243; Ci=14}.

15.   Kal S, Chakraborty S, Karmakar S and Ghosh MK* (2021). Wnt/β-catenin signaling and p68 conjointly regulate CHIP in colorectal carcinoma. BBA - Mol Cell Res. 1869(3):119185. {IF=5.011; Ci=9}

16.   Datta N, Chakraborty S, Basu M, Ghosh MK* (2021). Tumor suppressors having oncogenic functions: the double agents. Cells, 10(1):46. {IF=7.666; Ci=41}.


17.   Ghosh MK* Chakraborty D, Sarkar S, Bhowmik A and Basu M (2019). The interrelationship between cerebral ischemic stroke and glioma: A comprehensive study on recent reports. Signal Transduction & Targeted Therapy (NPG), 4:42:1-13. {IF=13.493; Ci=38}

18.   Khare V, Tabassum S, Chatterjee U, Chatterjee S and Ghosh MK* (2019). RNA helicase p68 deploys β-catenin in regulating RelA/p65 gene expression: Implications in Colon cancer. J Expt. & Clinic Can Res., 38:330:1-19. {IF=7.068; Ci=26}

19.   Datta N, Islam S, Chatterjee U, Chatterjee S, Panda CK, and Ghosh MK* (2019). Promyelocytic Leukemia (PML) Gene Regulation: Implication towards curbing oncogenesis. Cell Death Dis. (NPG), 10:656:1-18. {IF=6.304; Ci=11}

20.   Basu B and Ghosh MK* (2019). Extracellular vesicles in Glioma: From Diagnosis to Therapy. BioEssays, 41:1800245:1-9. {IF=4.62; Ci=61}

21.   Sarkar S, Chakraborty D, Bhowmik A and Ghosh MK* (2019). Cerebral ischemic stroke: cellular fate and therapeutic opportunities. Frontiers in Bioscience, Landmark, 24:435-450. {IF=4.009; Ci=57}

2017 - 2018

22.   Bhattacharya S, Chakraborty D, Basu M and Ghosh MK* (2018). Emerging insights into HAUSP (USP7) in physiology, cancer and other diseases. Signal Transduction & Targeted Therapy (NPG), 3:17:1-12. {IF=5.873; Ci=115}

23.   Bhowmik A, Chakravarti S, Ghosh A, Shaw R, Bhandari S, Bhattacharyya S, Sen PC and Ghosh MK* (2017). Anti-SSTR2 Peptide based targeted delivery of potent PLGA encapsulated 3,3´-diindolylmethane nanoparticles through blood brain barrier prevents glioma progression. Oncotarget (NPG), 8:65339-65358. {IF=5.168; Ci=32}

24.   Bhowmik A, Basu M, Ghosh MK* (2017). Design, synthesis and use of peptoids in the diagnosis and treatment of cancer. Frontiers in Bioscience, Elite Ed. 9:101-108. (Invited) {IF=1.94; Ci=7}.

25.   Bhandary S et al., (2017). Targeting IL-6/IL-6R Signaling Axis in Triple-Negative Breast Cancer by a Novel Nifetepimine-Loaded Cascade Ph Responsive Mesoporous Silica Based Nanoplatform. Global Journal of Nanomedicine 3(1).


26.   Sarkar M, Khare V and Ghosh MK* (2016). The DEAD box protein p68: a novel coactivator of Stat3 in mediating oncogenesis. Oncogene (NPG), 36(22):3080-3093.  {IF=7.519; Ci=26}

27.   Ghosh A et al., (2016). Formulation and antitumorigenic activities of nanoencapsulated nifetepimine: A promising approach in treating triple negative breast carcinoma. Nanomedicine-NBM, 12:1973–1985. {IF=6.155; Ci=6}

28.   Das N, Datta N, Chatterjee U and Ghosh MK* (2016). ERα transcriptionally activates CK2α: a pivotal regulator of PML and AKT in oncogenesis. Cell Signal, 28:675-687.  {IF=4.3; Ci=16}

29.   Sarkar M and Ghosh MK* (2016). DEAD box RNA helicases: crucial regulators of gene expression and oncogenesis. Frontiers in Bioscience, Landmark, 21:225-250.  {IF=4.725; Ci=47}

30.   Paul I, Basu M and Ghosh MK* (2016). Chaperones and Glioma Immunotherapy. J. Cancer Sci Ther, 8:069-070. {IF=3.2; Ci=4} (Invited)


31.   Ahmed SF, Das N, Sarkar M, Chatterjee U, Chatterjee S, and Ghosh MK* (2015). Exosome-mediated delivery of the intrinsic C-terminus domain of PTEN protects it from proteasomal degradation and ablates tumorigenesis. Mol Ther. (NPG), 23:255–269.   {IF=8.986; Ci=41}

32.   Paul I and Ghosh MK* (2015). A CHIPotle in physiology and disease. Int J Biochem Cell Biol 58:37–52.  {IF=5.085; Ci=48} (Invited)

33.   Bhattacharya S and Ghosh MK* (2015). HAUSP regulates cMyc via deubiquitination of TRRAP. Cell Oncol 38(4):265-77.  {IF=6.730; Ci=30}

34.   Bhowmik A, Khan R and Ghosh MK* (2015). Blood brain barrier: A challenge for effectual therapy of brain tumors. BioMed Res Int. Article ID 320941. {IF=2.583; Ci=235}


35.   Sarkar M, Khare V, Guturi KKN, Das N and Ghosh MK* (2014). The DEAD box protein p68: a crucial regulator of AKT/FOXO3a signaling axis in oncogenesis. Oncogene 34: 5843–5856. {IF=8.459; Ci=58}

36.   Guturi KK, Sarkar M, Bhowmik A#, Das N# and Ghosh MK* (2014). DEAD-box protein p68 is regulated by β-catenin/transcription factor 4 to maintain a positive feedback loop in control of breast cancer progression. Breast Cancer Res., 16:496.  {IF=6.345; Ci=52}

37.   Mandal T, Bhowmik A, Chatterjee A, Chatterjee U, Chatterjee S and Ghosh MK* (2014). Reduced phosphorylation of Stat3 at Ser-727 mediated by casein kinase 2 - protein phosphatase 2A enhances Stat3 Tyr-705 induced tumorigenic potential of glioma cells. Cell Signal 26:1725-1734.  {IF=4.3; Ci=67}

38.   Bhattacharya S and Ghosh MK* (2014). HAUSP, a novel deubiquitinase for Rb – MDM2 the critical regulator. FEBS Journal 281:3061–3078.  {IF=5.542; Ci=65}

39.   Paul I and Ghosh MK* (2014). The E3 ligase CHIP: insights into its structure and regulation. BioMed Res Int. Article ID 918183.  {IF=2.583; Ci=79}

40.   Bhattacharya S and Ghosh MK* (2014). Cell Death and Deubiquitinases: Perspectives in Cancer. BioMed Res Int. Article ID 435197.     {IF=2.583; Ci=42}

41.   Dhar A et al., (2014). Simultaneous inhibition of key growth pathways in melanoma cells and tumor regression by a designed bidentate constrained helical peptide. Biopolymers 101:344-58.  {IF=2.25; Ci=13}


42.   Paul I, Ahmed F, Bhowmik A, Deb S and Ghosh MK* (2013). The Ubiquitin Ligase CHIP Regulates c-Myc Stability and Transcriptional Activity. Oncogene 32(10):1284-95.  {IF=8.559; Ci=141}

43.   Chatterjee A, Chatterjee U and Ghosh MK* (2013) Activation of protein kinase CK2 attenuates FOXO3a functioning in a PML-dependent manner: implications in human Prostate Cancer. Cell Death Dis. (NPG) 4:e543. {IF=6.044; Ci=49}

44.   Bhowmik A, Das N, Pal U, Mandal M, Bhattacharya B, Sarkar M, Jaisankar P, Maiti NC,  Ghosh MK* (2013). 2,2'-diphenyl-3,3'-diindolylmethane: a potent compound induces apoptosis in breast cancer cells by inhibiting EGFR pathway. PLoS One 8(3):e59798. {IF=3.534; Ci=44}

45.   Paul I, Bhattacharya S, Chatterjee A and Ghosh MK* (2013). Current understanding on EGFR and Wnt/β-catenin signaling in glioma and their possible crosstalk. Genes & cancer 4(11-12):427-446. {IF=5.656; Ci=172}


46.   Ahmed F, Deb S, Paul I, Mandal T, Chatterjee A and Ghosh MK* (2012). The chaperone-assisted E3 ligase C terminus of Hsc70-interacting protein (CHIP) targets PTEN for proteasomal degradation. J Biol Chem. 287(19):15996–16006. {IF=4.651; Ci=150}

47.   Naidu GKK, Mandal T, Chatterjee A, Sarkar M, Bhattacharya S, Chatterjee U and Ghosh MK* (2012). Mechanism of β-catenin-mediated transcriptional regulation of epidermal growth factor receptor expression in glycogen synthase kinase 3 β-inactivated prostate cancer cells. J Biol Chem.  287(22):18287-96.  {IF=4.651; Ci=79}

48.   Mondal S et al., (2012) . Natural products: Promising resources for cancer drug discovery. Anti-Cancer Agents Med Chem. 12:49-75.  {IF=2.87; Ci=204}. (Invited)

49.   De K, et al., (2012) Synthesis, radiolabeling and preclinical evaluation of a new octreotide analogue for somatostatin receptor positive tumour scintigraphy. J Pept Sci. 18:720–730.  {IF=2.1; Ci=23}

1995 - 2011

50.   Dazard JE, et al., (2011). The dynamics of E1A in regulating networks and canonical pathways in quiescent cells. BMC Res Notes 26;4:160.  {IF=2.5; Ci=4}

51.   Sha J, Ghosh MK, Zhang K and Harter ML (2010). E1A interacts with two divergent pathways to induce quiescent cells into S phase. J Virol 84: 4050-59. {IF=5.189; Ci=35}

52.   Ghosh MK, Sharma P, Harbor PC, Rahaman SO and Haque SJ (2005). PI3K-AKT pathway negatively controls EGFR-dependent DNA-binding activity of Stat3 in glioblastoma multiforme cells. Oncogene (NPG), 24:7290-300.  {IF=7.59; Ci=72}

53.   Ghosh MK, Rahaman SO and Haque SJ (2004). AKT attenuates EGFR-dependent DNA-binding activity of Stat3 in glioblastoma multiforime cells. NEURO-ONCOLOGY, 6 (4):316-317.  {IF=5.3}

54.   Ghosh MK and Harter ML (2003). A viral mechanism for remodeling chromatin structure in Go cells. Molecular Cell 12:255-260.   {IF=19.328; Ci=82}

55.   Ghosh MK, Arun R, Chattopadhyay DJ and Chatterjee IB (2003). Cytochrome P450-mediated oxidative damage of nuclear membrane proteins and its prevention by vitamin C. Ind J Biochem Boiphys, 40:309-314. {IF=0.958}

56.   Mal A, Sturniolo M, Schiltz RL, Ghosh MK and Harter ML (2001). A role for histone deacetylase HDAC1 in modulating the transcriptional activity of MyoD: Inhibition of the myogenic program. EMBO J 20:1739-1753.  {IF=12.286; Ci=297}

57.   Chattopadhyay D, Ghosh MK, Mal A and Harter ML (2001). Inactivation of p21 by E1A leads to the induction of apoptosis in DNA-damaged cells. J Virology 75:9844-9856.  {IF=5.59; Ci=74}

58.   Mal A, Chattopadhyay D, Ghosh MK, Poon RYC and Harter ML (2000). p21 and retinoblastoma protein control the absence of DNA replication in terminally differentiated muscle cells. J Cell Biology. 149:281-292.  {IF=13.323; Ci=92}

59.   Panda K, Chatterjee R, Ghosh MK, Chattopadhyay DJ and Chatterjee IB (1999). Vitamin C prevents cigarette smoke induced oxidative damage of proteins and increased proteolysis. Free Radic Biol Med. 27:1064-1079. {IF=7.376; Ci=128}

60.   Ghosh MK, Mukhopadhyay M and Chatterjee IB (1997). NADPH-initiated cytochrome P450-dependent free iron-independent microsomal lipid peroxidation: Specific prevention by ascorbic acid. Mol. Cell. Biochem., 166:35-44. {IF=2.613; Ci=50}

61.   Nandi A, Mukhopadhyay CK, Ghosh MK, Chattopadhyay DJ and Chattergee IB (1997). Evolutionary significance of vitamin C biosynthesis in terrestrial vertebrates. Free Radic Biol Med. 22:1047-54.  {IF=7.376; Ci=116}

62.   Ghosh MK, Chattophadhyay DJ and Chatterjee IB (1996). Vitamin C prevents oxidative damage. Free Radic Res., 25: 173-179.  {IF=4.148; Ci=52}

63.   Mukhopadhyay CK, Ghosh MK and Chatterjee IB (1995). Ascorbic acid prevents lipid peroxidation and oxidative damage of proteins in guinea pig extrahepatic tissue microsomes. Mol Cell Biochem., 142:71-78.  {IF=2.613; Ci=23}

64.   Chatterjee IB, Mukhopadhyay CK and Ghosh MK (1995). Vitamin C: A potential saviour against free radical induced oxidative damage. Current Science, 69:747-751.  {Ci=31}

# / † authors contributed equally & * Corresponding author.



1.   Sarkar S, Basu M and Ghosh MK* (2022). ROS induced cancers with special interest in glioma: targeting ROS in a combinatorial approach for successful chemotherapy. Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Published by Springer (Invited). 

2.   Ghosh P, Ghosh MK* (2020). 2019-nCoV: Strategy to Combat the Ongoing Outbreak and Future Perspectives. Acta Scientific Cancer Biology 4(6):06-07. (Invited)

3.   Molecular diagnostics & therapeutics: Conference Report (2019). Indian Journal of Biochemistry & Biophysics, 56:333-335 (Invited).

4.   Basu M and Ghosh MK* (2019). Helicobacter Pylori Infection Leads to Colorectal Cancer Development: A Major Scientific Debate. Acta Scientific Cancer Biology 3(5):22-23 (Invited).

5.   Basu B, Saha G, Ghatak Choudhury S and Ghosh MK (2018). Cellular Homeostasis or Tumorigenesis: USP7 Playing the Double Agent. Cancer Cell & Microenvironment 4:e1624 (Invited).

6.   Ghosh MK* (2018). The Emerging Roles of the DEAD Box RNA Helicase p68 in Oncogenesis. Acta Scientific Cancer Biology 3(1):10-11 (invited).

7.   Paul I, Basu M and Ghosh MK* (2018). CHIP (Carboxy Terminus of HSC70 Interacting Protein). Encyclopedia of Signaling Molecules, 2nd Edition, 1083-91 (Invited).

8.   Basu B, Bhattacharya S, Saha G and Ghosh MK* (2018). USP7 (Ubiquitin Specific Protease 7). Encyclopedia of Signaling Molecules, 2nd Edition, 5848-54 (Invited).

9.   Ahmed SF and Ghosh MK* (2013). Chapter 2: Post-Translational Regulation of PTEN and its Implication in Cancer. in "PTEN: Structure, Mechanism-of-Action, Role in Cell Signaling and Regulation". Protein Science and Engineering. Published by Nova Biomedical, Nova Science Publishers, Inc., New York, USA. Pg:51-77.