Postdoctoral researcher in cancer biology with expertise in redox signaling, tumor progression, and therapeutic resistance, particularly in breast cancer. My work focuses on molecular mechanisms of oncogenic signaling, tumor microenvironment interactions, and identification of novel therapeutic targets in triple-negative breast cancer and hormone receptor signaling pathways.
EDUCATION
Ph.D. in Biotechnology (Cancer Biology) from National Centre for Cell Science, Pune, 2022
M.Sc. in Biotechnology from Gulbarga University, 2009
B.Sc. in Biotechnology from Gulbarga University, 2007
8
Scopus Publications
126
Scholar Citations
4
Scholar h-index
2
Scholar i10-index
Scopus Publications
EC359 Enhances Trametinib Efficacy in Ras/Raf-Driven Ovarian Cancer by Suppressing LIFR Signaling William C. Arnold, Durga Meenakshi Panneerdoss, Baskaran Subramani, Megharani Mahajan, Behnam Ebrahimi, Paulina Ramirez, Bindu Santhamma, Suryavathi Viswanadhapalli, Edward R. Kost, Yidong Chen, Zhao Lai, Hareesh B. Nair, Ratna K. Vadlamudi, Yasmin A. Lyons Biomolecules, 2025 Ovarian cancer (OCa) remains the most lethal gynecologic malignancy in the United States, with low-grade serous and mucinous subtypes frequently driven by KRAS mutations. These mutations activate downstream MAPK and PI3K/AKT signaling pathways, contributing to tumor progression and resistance to therapy. Although the MEK inhibitor trametinib is used to target these pathways, its efficacy is limited in KRAS-mutant OCa due to compensatory activation of the leukemia inhibitory factor (LIF)/LIF receptor (LIFR) axis. In this study, we evaluated the therapeutic potential of combining trametinib with EC359, a selective LIFR inhibitor, in Ras/Raf-driven OCa models. EC359 significantly reduced cell viability, clonogenic survival, and induced cell death via ferroptosis in vitro. Mechanistic studies revealed that EC359 suppressed trametinib-induced activation of LIFR downstream signaling. RNA-seq analysis showed that combination therapy downregulated mitochondrial translation and MYC target genes while upregulating apoptosis-related genes. In vivo, EC359 and trametinib co-treatment significantly reduced tumor growth in xenograft and PDX models without inducing toxicity. Our studies identify LIFR signaling as a critical vulnerability in Ras/Raf-mutant and low grade serous OCa. Further, it provides strong preclinical rationale for EC359 and trametinib combination therapy as a new therapeutic strategy for treating Ras/Raf-driven OCa and low-grade serous OCa.
The Discovery and Characterization of HBS-101, a Novel Inhibitor of Midkine, as a Therapeutic Agent for the Treatment of Triple-Negative Breast Cancer Megharani Mahajan, Alondra L. Rodriguez Sanchez, Sridharan Jayamohan, Dileep K. Vijayan, Jessica D. Johnson, Huan Xie, Yang Wang, Dong Liang, John R. Sanchez, Panneerdoss Subbarayalu, Manjeet K. Rao, Ratna K. Vadlamudi, Gangadhara R. Sareddy, Hareesh B. Nair, Suryavathi Viswanadhapalli Molecular Cancer Therapeutics, 2025 Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with a poor clinical outcome. There is a dire need for the development of new targeted therapies for TNBC. Midkine (MDK), a multifunctional cytokine/growth factor, functions as an oncoprotein, and its expression is elevated in various cancers. The absence of small-molecule inhibitors targeting MDK represents a significant knowledge gap for translation. In this study, we identified HBS-101 as a potent MDK inhibitor with high specificity. Our modeling studies revealed that the interaction of HBS-101 with MDK is primarily driven by hydrophobic forces, and this interaction disrupted MDK’s binding to its endogenous receptors. Microscale thermophoresis, cellular thermal shift assay, and biotin pull-down studies confirmed the direct interaction of HBS-101 with MDK. Therapeutically, HBS-101 treatment significantly reduced cell viability (IC50 0.3–2.8 µmol/L), clonogenic survival, invasiveness, and increased apoptosis. The underlying mechanism of HBS-101 involves suppression of the Akt/mTOR, STAT3, and NF-κB pathways. Importantly, HBS-101 exhibits distinct pharmacologic advantages, including oral bioavailability, blood-brain barrier penetration, and in vivo stability. Histologically, doses of up to 10 mg/kg showed no observable organ toxicity and had no effect on the mice’s body weight. Dose range studies identified 5 mg/kg as the minimal effective dose, achieving more than a 50% tumor reduction. HBS-101 treatment led to a significant reduction in the growth of xenograft tumors derived from patients with TNBC in vivo and markedly reduced TNBC brain metastatic tumor growth and prolonged mice survival. Collectively, our studies identified a first-in-class MDK inhibitor, HBS-101, that can be used to treat MDK-driven cancers.
Targeting the Leukemia Inhibitory Factor/Leukemia Inhibitory Factor Receptor Axis Reduces the Growth of Inflammatory Breast Cancer by Promoting Ferroptosis Bianca Romo, Zenaida Fuentes, Lois Randolph, Megharani Mahajan, Emily J. Aller, Behnam Ebrahimi, Bindu Santhamma, Uday P. Pratap, Panneerdoss Subbarayalu, Harika Nagandla, Christoforos Thomas, Hareesh B. Nair, Ratna K. Vadlamudi, Suryavathi Viswanadhapalli Cancers, 2025 Background: Inflammatory breast cancer (IBC) is a rare subtype of breast cancer accounting for 7% of breast cancer-related fatalities. There is an urgent need to develop new targeted treatments for IBC. The progression of IBC has been associated with alterations in growth factor and cytokine signaling; however, the function of the LIF (leukemia inhibitory factor)/LIFR (leukemia inhibitory factor receptor) cytokine pathway in the progression of IBC remains unknown. This study evaluated the role of LIFR signaling and tested the efficacy of the LIFR inhibitor EC359 in treating IBC. Methods: The utility of using LIFR inhibition as a treatment strategy in IBC was tested using cell survival, apoptosis, colony formation, invasion, and pre-clinical KPL4 xenografts. Western blotting, siRNA, RT-qPCR, and lipid peroxidation assays were used to establish the mechanism of EC359 therapy. Results: The reduction in LIFR levels using siRNA markedly decreased growth in colony formation assays and reduced the invasion of IBC cells. Pharmacological inhibition of LIFR with EC359 effectively reduced cell survival and the clonogenic capacity of IBC cells. RT-qPCR assays revealed that EC359 markedly decreased the expression of the LIFR target genes. Western blot analyses confirmed that EC359 treatment suppressed downstream LIF/LIFR signaling pathways and promoted apoptosis. Treatment of cells with the ferroptosis inhibitor Fer-1 negated the capacity of EC359 to induce apoptosis. Mechanistic investigations demonstrated that EC359 predominantly triggered ferroptosis by inhibiting the glutathione antioxidant defense system through the downregulation of Glutathione peroxidase 4 (GPX4) levels. EC359 (5 mg/kg/day) was effective in reducing the growth of the IBC KPL4 xenograft tumors. Conclusion: These findings demonstrates that LIFR inhibition promote ferroptosis-mediated cell death in IBC and that EC359 represent novel therapeutic for IBC treatment.
PELP1 Is a Novel Therapeutic Target in Hepatocellular Carcinoma Khaled Mohamed Nassar, Xue Yang, Adriana Baker, Rahul Gopalam, William C. Arnold, Timilehin T. Adeniran, Marian H. Hernandez Fernandez, Megharani Mahajan, Zhao Lai, Yidong Chen, Gangadhara R. Sareddy, Suryavathi Viswanadhapalli, Lu-Zhe Sun, Ratna K. Vadlamudi, Uday P. Pratap Cancer Research Communications, 2024 Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths in the United States, with a median survival period of approximately 10 months. There is an urgent need for the development of effective targeted therapies for the treatment of HCC. Proline-, glutamic acid–, and leucine-rich protein 1 (PELP1) signaling is implicated in the progression of many cancers, although its specific contribution to the progression of HCC is not yet well understood. Analysis of The Cancer Genome Atlas HCC gene expression data sets and IHC analysis of HCC tissue microarray revealed that HCC tumors had elevated expression of PELP1 compared with normal tissues, and high expression of PELP1 is associated with unfavorable survival outcomes. Suppression of PELP1 expression using short hairpin RNA significantly reduced the cell viability, clonogenicity, and invasion of HCC cells. Importantly, SMIP34, a first-in-class small-molecule inhibitor targeting PELP1, effectively decreased the cell viability, clonogenic survival, and invasiveness of HCC cells. Gene expression analysis using RNA sequencing revealed that PELP1 knockdown cells exhibited a decrease in c-Myc, E2F, and other oncogenic pathways related to HCC. Mechanistic studies showed that SMIP34 treatment impaired the Rix complex, a critical component of ribosomal biogenesis, in HCC cells. Furthermore, the knockdown or pharmacologic inhibition of PELP1 significantly decelerated the HCC tumor growth in xenograft models. In summary, our study findings indicate that PELP1 could serve as a promising target for therapeutic intervention in HCC. Significance: HCC is one of the leading causes of cancer fatalities in the United States. Effective targeted therapeutics for HCC are urgently needed. In this study, we show that PELP1 proto-oncogene is crucial to HCC progression and that PELP1 inhibition reduced HCC cell proliferation in vitro and in vivo. Our results imply that PELP1-targeted drugs like SMIP34 may be useful as new therapeutic agents for HCC treatment.
Novel LIPA-Targeted Therapy for Treating Ovarian Cancer Alexia B. Collier, Suryavathi Viswanadhapalli, Rahul Gopalam, Tae-Kyung Lee, Kara Kassees, Karla Parra, Gaurav Sharma, Tanner C. Reese, Xihui Liu, Xue Yang, Behnam Ebrahimi, Uday P. Pratap, Megharani Mahajan, William C. Arnold, Adriana Baker, Chia-Yuan Chen, Scott Terry Elmore, Panneerdoss Subbarayalu, Gangadhara R. Sareddy, Philip T. Valente, Edward R. Kost, Jung-Mo Ahn, Ratna K. Vadlamudi Cancers, 2024 Ovarian cancer (OCa) is the most lethal form of gynecologic cancer, and the tumor heterogeneities at the molecular, cellular, and tissue levels fuel tumor resistance to standard therapies and pose a substantial clinical challenge. Here, we tested the hypothesis that the heightened basal endoplasmic reticulum stress (ERS) observed in OCa represents an exploitable vulnerability and may overcome tumor heterogeneity. Our recent studies identified LIPA as a novel target to induce ERS in cancer cells using the small molecule ERX-41. However, the role of LIPA and theutility of ERX-41 to treat OCa remain unknown. Expression analysis using the TNMplot web tool, TCGA data sets, and immunohistochemistry analysis using a tumor tissue array showed that LIPA is highly expressed in OCa tissues, compared to normal tissues. ERX-41 treatment significantly reduced the cell viability and colony formation ability and promoted the apoptosis of OCa cells. Mechanistic studies revealed a robust and consistent induction of ERS markers, including CHOP, elF2α, PERK, and ATF4, upon ERX-41 treatment. In xenograft and PDX studies, ERX-41 treatment resulted in a significant reduction in tumor growth. Collectively, our results suggest that ERX-41 is a novel therapeutic agent that targets the LIPA with a unique mechanism of ERS induction, which could be exploited to treat heterogeneity in OCa.
miR-140-5p regulates the hypoxia-mediated oxidative stress through Nrf2 Megharani MAHAJAN, Sandhya SİTASAWAD Journal of Cellular Neuroscience and Oxidative Stress, 2023 Rapid and uncontrollable cell proliferation, altered metabolism, and abnormal vasculature of cancer cells make them hypoxic and result in the generation of reactive oxygen species (ROS), causing oxidative stress. Hypoxia-mediated oxidative stress represents a significant barrier to effective cancer treatment. miRNAs are emerging as a potential regulator of hypoxia-responsive genes and hypoxia-mediated oxidative stress. Based on the role of miR-140-5p in regulating a hypoxia-responsive gene, this study is aimed at understanding the miR-140-5p role in regulating hypoxia-mediated oxidative stress under breast tumor hypoxia. We found that the miR-140-5p might control the hypoxia-mediated ROS generation by regulating the Nrf2 expression. Knowing the significance of miR-140-5p in regulating hypoxia-mediated oxidative stress and breast tumor progression, targeting miR-140-5p might represent a promising strategy for anti-breast cancer therapy.
Mir-140-5p attenuates hypoxia-induced breast cancer progression by targeting nrf2/ho-1 axis in a keap1-independent mechanism Megharani Mahajan, Sandhya Sitasawad Cells, 2022 Hypoxia and oxidative stress significantly contribute to breast cancer (BC) progression. Although hypoxia-inducible factor 1α (Hif-1α) is considered a key effector of the cellular response to hypoxia, nuclear factor erythroid 2–related factor 2 (Nrf2), a master antioxidant transcription factor, is a crucial factor essential for Hif-1α-mediated hypoxic responses. Hence, targeting Nrf2 could provide new treatment strategies for cancer therapy. miRNAs are potential regulators of hypoxia-responsive genes. In a quest to identify novel hypoxia-regulated miRNAs involved in the regulation of Nrf2, we found that miR-140-5p significantly affects the expression of Nrf2 under hypoxia. In our study, miR-140-5p expression is downregulated in BC cells under hypoxic conditions. We have identified Nrf2 as a direct target of miR-140-5p, as confirmed by the luciferase assay. Knockdown of miR-140-5p under normoxic conditions significantly enhanced Nrf2/HO-1 signaling and tumor growth, angiogenesis, migration, and invasion in BC. In contrast, overexpression of miR-140-5p under hypoxic conditions revealed opposite results. Further silencing Nrf2 expression mimicked the miR-140-5p-induced anti-tumor effects. Consistent with the knockdown of miR-140-5p in vitro, mice injected with miR-140-5p-KD cells exhibited dramatically reduced miR-140-5p levels, increased Nrf2 levels, and increased tumor growth. In contrast, tumor growth is potently suppressed in mice injected with miR-140-5p-OE cells. Collectively, the above results demonstrate the importance of the Nrf2/HO-1 axis in cancer progression and, thus, targeting Nrf2 by miR-140-5p could be a better strategy for the treatment of Nrf2-driven breast cancer progression.
KEAP1-NRF2 pathway regulates aldh and contributes to radioresistance in breast cancer stem cells Dinisha Kamble, Megharani Mahajan, Rohini Dhat, Sandhya Sitasawad Cells, 2021 Tumor recurrence after radiotherapy due to the presence of breast cancer stem cells (BCSCs) is a clinical challenge, and the mechanism remains unclear. Low levels of ROS and enhanced antioxidant defenses are shown to contribute to increasing radioresistance. However, the role of Nrf2-Keap1-Bach1 signaling in the radioresistance of BCSCs remains elusive. Fractionated radiation increased the percentage of the ALDH-expressing subpopulation and their sphere formation ability, promoted mesenchymal-to-epithelial transition and enhanced radioresistance in BCSCs. Radiation activated Nrf2 via Keap1 silencing and enhanced the tumor-initiating capability of BCSCs. Furthermore, knockdown of Nrf2 suppressed ALDH+ population and stem cell markers, reduced radioresistance by decreasing clonogenicity and blocked the tumorigenic ability in immunocompromised mice. An underlying mechanism of Keap1 silencing could be via miR200a, as we observed a significant increase in its expression, and the promoter methylation of Keap1 or GSK-3β did not change. Our data demonstrate that ALDH+ BCSC population contributes to breast tumor radioresistance via the Nrf2-Keap1 pathway, and targeting this cell population with miR200a could be beneficial but warrants detailed studies. Our results support the notion that Nrf2-Keap1 signaling controls mesenchymal–epithelial plasticity, regulates tumor-initiating ability and promotes the radioresistance of BCSCs.
RECENT SCHOLAR PUBLICATIONS
Targeting midkine with HBS-101 enhances chemotherapy and immunotherapy response in TNBC via immune activation and oncogenic pathway suppression B Subramani, M Mahajan, P Subbarayalu, Z Xu, N Mukherjee, ... Cancer Research 86 (7_Supplement), 3796-3796 , 2026 2026
454 A novel MDK targeted therapy for the treatment of endometrial cancer E Aller, ALR Sanchez, M Mahajan, X Yang, P Ramirez, P Subbarayalu, ... Journal of Clinical and Translational Science 10 (s1), 144-144 , 2026 2026
Pelp1 inhibition disrupts dna repair and enhances topoisomerase inhibitor efficacy in triple negative breast cancer K Nassar, J Sanchez, D Panneerdoss, E Behnam, X Yang, U Pratap, ... CLINICAL CANCER RESEARCH 32 , 2026 2026
Epigenetic Reactivation of estrogen receptor beta Enhances Antitumor Activity of a Novel estrogen receptor beta agonist CIDD-0149897 in Triple-Negative Breast Cancer U Pratap, M Mahajan, K Nassar, T Adeniran, N Karinel, G Sareddy, ... CLINICAL CANCER RESEARCH 32 , 2026 2026
Abstract PS4-07-16: Epigenetic Reactivation of estrogen receptor beta Enhances Antitumor Activity of a Novel estrogen receptor beta agonist CIDD-0149897 in Triple-Negative … U Pratap, M Mahajan, K Nassar, T Adeniran, N Karinel, G Sareddy, ... Clinical Cancer Research 32 (4_Supplement), PS4-07-16-PS4-07-16 , 2026 2026
Abstract PS4-04-23: Pelp1 inhibition disrupts dna repair and enhances topoisomerase inhibitor efficacy in triple negative breast cancer K Nassar, J Sanchez, D Panneerdoss, E Behnam, X Yang, U Pratap, ... Clinical Cancer Research 32 (4_Supplement), PS4-04-23-PS4-04-23 , 2026 2026
EC359 Enhances Trametinib Efficacy in Ras / Raf -Driven Ovarian Cancer by Suppressing LIFR Signaling WC Arnold, DM Panneerdoss, B Subramani, M Mahajan, B Ebrahimi, ... Biomolecules 15 (10), 1396 , 2025 2025
The discovery and characterization of HBS-101, a novel inhibitor of midkine, as a therapeutic agent for the treatment of triple-negative breast cancer M Mahajan, AL Rodriguez Sanchez, S Jayamohan, DK Vijayan, ... Molecular cancer therapeutics 24 (9), 1308-1319 , 2025 2025 Citations: 7
Abstract LB435: Novel MDK targeted therapy for treating triple negative breast cancer M Mahajan, AL Rodriguez Sanchez, S Jayamohan, JD Johnson, ... Cancer Research 85 (8_Supplement_2), LB435-LB435 , 2025 2025
Targeting the LIF/LIFR axis reduces the progression of inflammatory breast cancer by promoting ferroptosis BA Romo, Z Fuentes, L Randolph, M Mahajan, EJ Aller, B Ebrahimi, ... Cancer Research 85 (8_Supplement_1), 1630-1630 , 2025 2025
Inhibiting PELP1 signaling enhances the therapeutic effectiveness of topoisomerase inhibitors in triple-negative breast cancer KM Nassar, JR Sanchez, DM Panneerdoss, B Ebrahimi, X Yang, ... Cancer Research 85 (8_Supplement_1), 4194-4194 , 2025 2025
Investigating the potential of EC359 in inducing ferroptosis for the treatment of type I and type II endometrial cancers EJ Aller, X Yang, MR Mahajan, B Ebrahimi, P Ramirez, HB Nair, E Kost, ... Cancer Research 85 (8_Supplement_1), 5989-5989 , 2025 2025
Targeting the leukemia inhibitory factor/leukemia inhibitory factor receptor Axis reduces the growth of inflammatory breast cancer by promoting ferroptosis B Romo, Z Fuentes, L Randolph, M Mahajan, EJ Aller, B Ebrahimi, ... Cancers 17 (5), 790 , 2025 2025 Citations: 2
PELP1 is a novel therapeutic target in hepatocellular carcinoma KM Nassar, X Yang, A Baker, R Gopalam, WC Arnold, TT Adeniran, ... Cancer Research Communications 4 (10), 2610-2620 , 2024 2024 Citations: 3
Novel LIPA-Targeted Therapy for Treating Ovarian Cancer AB Collier, S Viswanadhapalli, R Gopalam, TK Lee, K Kassees, K Parra, ... Cancers 16 (3), 500 , 2024 2024 Citations: 6
An overview of hypoxia-induced oxidative stress and NRF2 role in breast cancer progression M Mahajan DYSONA–Life Science 4 (2), 50-65 , 2023 2023
Mir-140-5p attenuates hypoxia-induced breast cancer progression by targeting nrf2/ho-1 axis in a keap1-independent mechanism M Mahajan, S Sitasawad Cells 11 (1), 12 , 2021 2021 Citations: 35
Keap1-Nrf2 pathway regulates ALDH and contributes to radioresistance in breast cancer stem cells D Kamble, M Mahajan, R Dhat, S Sitasawad Cells 10 (1), 83 , 2021 2021 Citations: 71
miR-140-5p Attenuates Hypoxia-Induced Breast Cancer Progression by Targeting Nrf2/HO-1 Axis in a Keap1-Independent Mechanism. Cells 2022, 11, 12 M Mahajan, S Sitasawad s Note: MDPI stays neutral with regard to jurisdictional claims in published … , 2021 2021
Keap1-Nrf2 Pathway Regulates ALDH and Contributes to Radioresistance in Breast Cancer Stem Cells. Cells. 2021; 10: 83 D Kamble, M Mahajan, R Dhat, S Sitasawad s Note: MDPI stays neu-tral with regard to jurisdictional clai-ms in … , 2021 2021 Citations: 2
MOST CITED SCHOLAR PUBLICATIONS
Keap1-Nrf2 pathway regulates ALDH and contributes to radioresistance in breast cancer stem cells D Kamble, M Mahajan, R Dhat, S Sitasawad Cells 10 (1), 83 , 2021 2021 Citations: 71
Mir-140-5p attenuates hypoxia-induced breast cancer progression by targeting nrf2/ho-1 axis in a keap1-independent mechanism M Mahajan, S Sitasawad Cells 11 (1), 12 , 2021 2021 Citations: 35
The discovery and characterization of HBS-101, a novel inhibitor of midkine, as a therapeutic agent for the treatment of triple-negative breast cancer M Mahajan, AL Rodriguez Sanchez, S Jayamohan, DK Vijayan, ... Molecular cancer therapeutics 24 (9), 1308-1319 , 2025 2025 Citations: 7
Novel LIPA-Targeted Therapy for Treating Ovarian Cancer AB Collier, S Viswanadhapalli, R Gopalam, TK Lee, K Kassees, K Parra, ... Cancers 16 (3), 500 , 2024 2024 Citations: 6
PELP1 is a novel therapeutic target in hepatocellular carcinoma KM Nassar, X Yang, A Baker, R Gopalam, WC Arnold, TT Adeniran, ... Cancer Research Communications 4 (10), 2610-2620 , 2024 2024 Citations: 3
Targeting the leukemia inhibitory factor/leukemia inhibitory factor receptor Axis reduces the growth of inflammatory breast cancer by promoting ferroptosis B Romo, Z Fuentes, L Randolph, M Mahajan, EJ Aller, B Ebrahimi, ... Cancers 17 (5), 790 , 2025 2025 Citations: 2
Keap1-Nrf2 Pathway Regulates ALDH and Contributes to Radioresistance in Breast Cancer Stem Cells. Cells. 2021; 10: 83 D Kamble, M Mahajan, R Dhat, S Sitasawad s Note: MDPI stays neu-tral with regard to jurisdictional clai-ms in … , 2021 2021 Citations: 2
Targeting midkine with HBS-101 enhances chemotherapy and immunotherapy response in TNBC via immune activation and oncogenic pathway suppression B Subramani, M Mahajan, P Subbarayalu, Z Xu, N Mukherjee, ... Cancer Research 86 (7_Supplement), 3796-3796 , 2026 2026
454 A novel MDK targeted therapy for the treatment of endometrial cancer E Aller, ALR Sanchez, M Mahajan, X Yang, P Ramirez, P Subbarayalu, ... Journal of Clinical and Translational Science 10 (s1), 144-144 , 2026 2026
Pelp1 inhibition disrupts dna repair and enhances topoisomerase inhibitor efficacy in triple negative breast cancer K Nassar, J Sanchez, D Panneerdoss, E Behnam, X Yang, U Pratap, ... CLINICAL CANCER RESEARCH 32 , 2026 2026
Epigenetic Reactivation of estrogen receptor beta Enhances Antitumor Activity of a Novel estrogen receptor beta agonist CIDD-0149897 in Triple-Negative Breast Cancer U Pratap, M Mahajan, K Nassar, T Adeniran, N Karinel, G Sareddy, ... CLINICAL CANCER RESEARCH 32 , 2026 2026
Abstract PS4-07-16: Epigenetic Reactivation of estrogen receptor beta Enhances Antitumor Activity of a Novel estrogen receptor beta agonist CIDD-0149897 in Triple-Negative … U Pratap, M Mahajan, K Nassar, T Adeniran, N Karinel, G Sareddy, ... Clinical Cancer Research 32 (4_Supplement), PS4-07-16-PS4-07-16 , 2026 2026
Abstract PS4-04-23: Pelp1 inhibition disrupts dna repair and enhances topoisomerase inhibitor efficacy in triple negative breast cancer K Nassar, J Sanchez, D Panneerdoss, E Behnam, X Yang, U Pratap, ... Clinical Cancer Research 32 (4_Supplement), PS4-04-23-PS4-04-23 , 2026 2026
EC359 Enhances Trametinib Efficacy in Ras / Raf -Driven Ovarian Cancer by Suppressing LIFR Signaling WC Arnold, DM Panneerdoss, B Subramani, M Mahajan, B Ebrahimi, ... Biomolecules 15 (10), 1396 , 2025 2025
Abstract LB435: Novel MDK targeted therapy for treating triple negative breast cancer M Mahajan, AL Rodriguez Sanchez, S Jayamohan, JD Johnson, ... Cancer Research 85 (8_Supplement_2), LB435-LB435 , 2025 2025
Targeting the LIF/LIFR axis reduces the progression of inflammatory breast cancer by promoting ferroptosis BA Romo, Z Fuentes, L Randolph, M Mahajan, EJ Aller, B Ebrahimi, ... Cancer Research 85 (8_Supplement_1), 1630-1630 , 2025 2025
Inhibiting PELP1 signaling enhances the therapeutic effectiveness of topoisomerase inhibitors in triple-negative breast cancer KM Nassar, JR Sanchez, DM Panneerdoss, B Ebrahimi, X Yang, ... Cancer Research 85 (8_Supplement_1), 4194-4194 , 2025 2025
Investigating the potential of EC359 in inducing ferroptosis for the treatment of type I and type II endometrial cancers EJ Aller, X Yang, MR Mahajan, B Ebrahimi, P Ramirez, HB Nair, E Kost, ... Cancer Research 85 (8_Supplement_1), 5989-5989 , 2025 2025
An overview of hypoxia-induced oxidative stress and NRF2 role in breast cancer progression M Mahajan DYSONA–Life Science 4 (2), 50-65 , 2023 2023
miR-140-5p Attenuates Hypoxia-Induced Breast Cancer Progression by Targeting Nrf2/HO-1 Axis in a Keap1-Independent Mechanism. Cells 2022, 11, 12 M Mahajan, S Sitasawad s Note: MDPI stays neutral with regard to jurisdictional claims in published … , 2021 2021
