About

Professor Jayshree Mishra is associated with the Texas A&M Irma Lerma Rangel College of Pharmacy. The provided page text does not include specific details about her research focus, academic background, or key contributions. The content primarily discusses the college's initiatives for first-generation students and shares personal stories of first-generation students and faculty, including Professor Indra K. Reddy. Therefore, there is no detailed professional biography available for Professor Jayshree Mishra in the provided text.

Research topics

• Immunology
• Medicine
• Bioinformatics
• Biology
• Internal medicine
• Pharmacology
• Intensive care medicine

Selected publications

• Abstract 6132: Linking metabolic reprogramming to JAK-STAT signaling in triple-negative breast cancer brain metastasis

  Cancer Research · 2026-04-03

  article1st authorCorresponding

  Abstract Introduction: Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype disproportionately affects younger patients and associated with high recurrence rates and rapid disease progression. TNBC cells that colonize the brain undergo extensive metabolic reprogramming to survive in this specialized microenvironment. Understanding the mechanisms by which TNBC cells adapt their metabolism and signaling networks to thrive in the brain niche is critical to uncovering novel vulnerabilities for therapeutic intervention. Materials and Methods: To address this knowledge gap, we conducted integrated metabolomic and transcriptomic analyses utilizing a TNBC brain metastasis (BM) xenograft mouse model, with validation in human patient-derived tissues. Metabolite profiling was performed using liquid chromatography-mass spectrometry equipped with an ACQUITY UPLC BEH C18 column. Matched samples from primary tumors, brain metastases, and serum were analyzed. Metabolite deconvolution employed AMDIS software, and compound identification was cross-referenced with NIST and HMDB spectral databases. Unique metabolites enriched in brain metastases and serum were identified and subjected to pathway enrichment analysis using MetaboAnalyst. To integrate metabolic findings with gene expression, pathway-associated genes were cross-referenced against transcriptomic datasets (GEO GSE76714), enabling network analysis of metabolite-gene interactions. Results: Our integrative analyses revealed that RNF125, an E3 ubiquitin ligase involved in immune regulation and oncogenesis, functions as a central regulatory node connecting metabolic pathways to the JAK-STAT signaling axis. RNF125 upregulation was inversely correlated with JAK3 activity, suggesting a role in modulating cytokine signaling to promote TNBC cell adaptation within the brain microenvironment. Conclusion: This study identifies RNF125 as a novel biomarker and potential therapeutic target in TNBC brain metastasis. Citation Format: Jayshree Mishra, Narendra Kumar. Linking metabolic reprogramming to JAK-STAT signaling in triple-negative breast cancer brain metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 6132.

  PublisherDOI

• A Study on the Russia-Ukraine War and Asian Stock Markets

  2025-08-21

  book-chapter

  This study examines how the conflict between Russia and Ukraine has affected Asian stock markets. We examined the performance of the major indices from the top Asian stock markets based on their market capitalization like Shanghai Stock Exchange (SSE), Japan Exchange Group (JPX), Hong Kong Stock Exchange (SEHK), National Stock Exchange of India (NSE), and Bombay Stock Exchange of India (BSE) after the war broke out on February 24, 2022, using time series analysis. Historical data is taken to calculate the returns of three months before and three months during the war. After comparing both the graphs for each exchange we found that there are no significant differences between the before the war and during the war metrics of the stock exchanges.

  PublisherDOI

• Mucosal implications of oral Jak3-targeted drugs in COVID patients

  Molecular Medicine · 2025-05-23 · 2 citations

  reviewOpen accessSenior author

  The JAK family, particularly JAK3, plays a crucial role in immune signaling and inflammatory responses. Dysregulated JAK3 activation in SARS-CoV-2 infections has been associated with severe inflammation and respiratory complications, making JAK inhibitors a viable therapeutic option. However, their use raises concerns regarding immunosuppression, which could increase susceptibility to secondary infections. While long-term adverse effects are less of a concern in acute COVID-19 treatment, patient selection and monitoring remain critical. Furthermore, adverse effects associated with oral JAK3 inhibitors necessitate the exploration of alternative strategies to optimize therapeutic efficacy while minimizing risks. This review highlights the role of JAK3 in immune and epithelial cells, examines the adverse effects of oral JAK3 inhibitors in COVID-19 and other treatments, and discusses alternative therapeutic strategies for improving patient outcomes.

  PublisherOA PDFDOI

• Correction: Mucosal implications of oral Jak3-targeted drugs in COVID patients

  Molecular Medicine · 2025-09-06 · 1 citations

  erratumOpen accessSenior author
  PublisherOA PDFDOI

• Abstract 616: TYK2: A novel therapeutic target in triple-negative breast cancer brain metastasis

  Cancer Research · 2025-04-21

  article1st authorCorresponding

  Breast cancer (BC) is one of the deadliest cancers that affect 300,000 women annually where 15-25% are Triple negative in nature and spreads quickly to the brain causing brain metastasis (TNBC-BM). Triple-negative breast cancer (TNBC) is a heterogeneous disease characterized by lack of hormone receptor expression and is known for high rates of recurrence, distant metastases, and poor clinical outcomes. The 5-year survival rate for TNBC-BM is only 9%. Current standard of care to treat TNBC-BM include whole brain radiation therapy, surgery and chemotherapy which leads to sever side effects, high level of neurotoxicity, neurological complication that leads to low survival rate and low quality of life. Because of such a low survival rate, there is an unmet clinical need to treat these patients differently to decrease neurotoxicity, and TNBC-BM cell death. In our study, we identified and characterized novel therapeutic targets and targeted pharmacologic inhibitors of natural compound origin for the treatment of TNBC-BM. Our preliminary data suggest (1) overexpression of Tyk2 ( JAK Family meber) gene in TNBC-BM compared to TNBC and TNBC lung metastasis using a PDX database. Overall Survival analysis of TNBC patients databases suggest that higher expression of Tyk2 gene and it’s downstream signaling partner gene STAT5A. Tyk2 is overexpressed in the TNBC-BM metastatic brain sample and TNBC -BM specific cell line ( BrM-831). Based on the published literature and our strong preliminary data, we hypothesize that over expression of Tyk2 promotes brain metastasis in TNBC cells through the activation of Tyk2-STA5A signaling pathway stimulating epithelial-to-mesenchymal transition, cell migration and invasion of TNBC cells, leading to tumorigenesis and metastasis in TNBC; Together, this study will demonstrate Tyk2 as a new target and Tyk2 targeted therapeutic agent will be capable of inhibiting TNBC-metastasis through blocking the activation of the Tyk2-/STAT5 molecular targets. In future, we plan to develop Tyk2 targeted drug compounds originated from natural products to treat TNBC-BM. Citation Format: Jayshree Mishra, Priyam Kumar, Narendra Kumar. TYK2: A novel therapeutic target in triple-negative breast cancer brain metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 616.

  PublisherDOI

• Abstract 1996 Development of a AI-driven highly selective JAK3 inhibitor for the treatment of Metastatic Triple negative breast cancer

  Journal of Biological Chemistry · 2024-03-01

  articleOpen access1st authorCorresponding

  Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, having a poor prognosis and rapid metastases to the brain. TNBC is characterized by the absence of estrogen, progesterone, and human epidermal growth receptor-2 (HER2) expressions and has a 7% five-year survival rate. Compared to other breast cancer subtypes, TNBC patients only respond to conventional chemotherapies, and even then, with limited success. Therefore, there is a critical need to develop novel targeted therapeutic strategies to re-store the anti-cancer actions to treat metastasis of Triple negative breast cancer to reduce disease morbidity and mortality.

  PublisherOA PDFDOI

• Brain-Gut and Microbiota-Gut-Brain Communication in Type-2 Diabetes Linked Alzheimer’s Disease

  Nutrients · 2024-08-03 · 15 citations

  reviewOpen access

  The gastrointestinal (GI) tract, home to the largest microbial population in the human body, plays a crucial role in overall health through various mechanisms. Recent advancements in research have revealed the potential implications of gut-brain and vice-versa communication mediated by gut-microbiota and their microbial products in various diseases including type-2 diabetes and Alzheimer's disease (AD). AD is the most common type of dementia where most of cases are sporadic with no clearly identified cause. However, multiple factors are implicated in the progression of sporadic AD which can be classified as non-modifiable (e.g., genetic) and modifiable (e.g. Type-2 diabetes, diet etc.). Present review focusses on key players particularly the modifiable factors such as Type-2 diabetes (T2D) and diet and their implications in microbiota-gut-brain (MGB) and brain-gut (BG) communication and cognitive functions of healthy brain and their dysfunction in Alzheimer's Disease. Special emphasis has been given on elucidation of the mechanistic aspects of the impact of diet on gut-microbiota and the implications of some of the gut-microbial products in T2D and AD pathology. For example, mechanistically, HFD induces gut dysbiosis with driven metabolites that in turn cause loss of integrity of intestinal barrier with concomitant colonic and systemic chronic low-grade inflammation, associated with obesity and T2D. HFD-induced obesity and T2D parallel neuroinflammation, deposition of Amyloid β (Aβ), and ultimately cognitive impairment. The review also provides a new perspective of the impact of diet on brain-gut and microbiota-gut-brain communication in terms of transcription factors as a commonly spoken language that may facilitates the interaction between gut and brain of obese diabetic patients who are at a higher risk of developing cognitive impairment and AD. Other commonality such as tyrosine kinase expression and functions maintaining intestinal integrity on one hand and the phagocytic clarence by migratory microglial functions in brain are also discussed. Lastly, the characterization of the key players future research that might shed lights on novel potential pharmacological target to impede AD progression are also discussed.

  PublisherOA PDFDOI

• Abstract 1620 Kinases in Gut-Liver-brain communication and neuroinflammation

  Journal of Biological Chemistry · 2024-03-01

  articleOpen access

  Background and Aims: Alzheimer's disease (AD) is the commonest form of dementia where its incidence is rising and expected to quadruple worldwide by 2050. Type-2 diabetes (T2D) is a risk factor for AD, where AD is now being considered as Type-3 diabetes (T3D). Though we all say, “you are what you eat, and everyone has a gut-feeling”, the role of gut in AD pathology is still not completely clear. Previously we reported reduced expression of intestinal Janus kinase-3 (Jak3), a non-receptor tyrosine kinase in humans with type-2 diabetes (T2D). In this study we model total body and tissue-specific Jak3-deficiency in mice and demonstrate its role in T2D and AD through interorgan communication mediated by gut-liver-brain axis. Our data show that high fat diet (HFD) suppresses Jak3 expression both in intestinal mucosa and in brain of wild-type mice and genetic manipulation-led Jak3-deficiency causes gut-dysbiosis, T2D, and AD-like symptoms. Methodology: Global (Jak3-KO) and intestinal epithelial cell-specific conditional (IEC-Jak3-KO) mice were used to measure fasting blood glucose, glucose tolerance, serum insulin, cognitive functions, western analysis, flow-cytometry, immunofluorescence microscopy, and 16s rRNA sequencing of fecal pellets. Results: We reveal that Jak3 deficiency leads to gut-dysbiosis, intestinal and liver inflammation and these together compromises TREM-2 functions-mediated activation of microglial cells. Moreover, these increase TLR-4 expression and HIF1-a-mediated neuroinflammation in the brain. Altogether, these led to compromised microglial functions-mediated increased level of b-amyloid (Aβ) and hyperphosphorylated Tau (pTau) and cognitive impairments. Collectively, these data illustrate how the drivers of T2D promote cognitive impairment and demonstrate the underlying mechanism where diet-mediated impact on intestinal-Jak3 gut-liver-brain miscommunication, reduced microglial-TREM2 expression, microglial-activation, and compromised clearance of Aβ and pTau as the mechanism during T2D linked neuroinflammation and cognitive impairments. Conclusion: Thus, we not only demonstrate the tissue-specific role of Jak3 but also show the evidence of Gut-Liver-brain communication and cognitive impairments during Jak3 deficiency through mucosal tolerance, gut-dysbiosis, hepatitis, and neuroinflammation. Global Institute of Hispanic Health (GIHH), Discovery Foundation, Texas A&M University.

  PublisherOA PDFDOI

• Abstract 1947 Exploring the Interplay of Social- Economic, and Racial Disparities Stress and Their Impact on Breast Cancer, with a Focus on Triple Negative Breast Cancer and Hormonal Imbalance-Induced Early Immune Cell Aging

  Journal of Biological Chemistry · 2024-03-01

  articleOpen access1st authorCorresponding

  Breast cancer remains a complex and multifaceted health challenge, with emerging evidence suggesting a profound interconnection between social, economic, and racial disparities, chronic stress, and the development of breast cancer (BC) notably in Triple negative breast cancer (TNBC). TNBC is prevalent in African American, Hispanic. This study investigates the intricate pathways through which socio-economic status, and the stress from the racial inequities contribute to the onset and progression of BC , with a specific focus on the hormonal imbalances induced premature aging of immune cells. Socioeconomic factors, including income disparities and limited access to healthcare resources, are explored as potential stressors that trigger chronic psychological and physiological stress. These stressors, in turn, are linked to disruptions in hormonal balance, particularly the dysregulation of cortisol and sex hormones. Racial and ethnic disparities are analyzed as crucial components of this complex interplay, with a focus on understanding how systemic inequalities contribute to chronic stress experienced by marginalized populations. For Black women and the Hispanic women have constant exposure to race-related stresses that causes hormonal imbalances leading to pre-mature immune aging. This study further develops into the specific impact of chronic stress-induced hormonal imbalances on the immune system leading to premature immune aging, revealing a potential mechanism by which stress-induced hormonal imbalances accelerates the aging of immune cells thereby delayed immune response leading poor breast cancer outcome. We will test a novel hypothesis that declining of the immune fitness in the Black and Hispanic Women leads to transcriptional heterogeneity in the immune cells leading to increase in low-grade inflammation, changes in the composition of microbiome and the mediators of this systemic inflammation such as pro-inflammatory cytokines such as interleukin-6 and tumor necrosis factor (TNF-alpha) and changes in the female sex hormone estrogen and progesterone. For this our study will analyze the check the race -specific immune signatures through multi parametric immunoprofiling due to the racial disparities in a small cohort of sample and will corelate the data with the change in the level of female sex hormone. Finally, all data were correlated with patient outcome. The results obtained from this study will identify therapeutic strategies for improving anti-tumor immunity and can be used as a part of clinical risk assessment. Discovery Foundation Advancing the Discovery to Market.

  PublisherOA PDFDOI

• 314P Perioperative outcomes in advanced epithelial ovarian cancer treated with neoadjuvant bevacizumab and chemotherapy: Real-world experience from an Indian cancer centre

  Annals of Oncology · 2023-11-01

  articleOpen access
  PublisherOA PDFDOI

Frequent coauthors

• Narendra Kumar

  Sankalchand Patel University

  50 shared

• Satya Sridhar Karanki

  Texas A&M University – Kingsville

  9 shared

• Longxiang Kuang

  Texas A&M University – Kingsville

  9 shared

• Priyam Kumar

  7 shared

• Sohel H. Quazi

  Texas College

  7 shared

• Jugal Kishore Das

  Utkal University

  6 shared

• Premranjan Kumar

  Baylor College of Medicine

  6 shared

• Gianfranco Alpini

  Richard L. Roudebush VA Medical Center

  5 shared

Labs

• Pharmaceutical SciencesPI

Education

• PhD, Biotechnology

  Indian Institute of Technology Kharagpur

  2005

Awards & honors

• Presidential Impact Fellow