Falguni Mishra

ORCID: 0000-0003-0092-5559
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Research Areas
  • Cancer Cells and Metastasis
  • Cancer, Hypoxia, and Metabolism
  • Cancer Research and Treatments
  • Cell Adhesion Molecules Research
  • Electrospun Nanofibers in Biomedical Applications
  • Pancreatic and Hepatic Oncology Research
  • Medical Imaging and Pathology Studies
  • Chronic Lymphocytic Leukemia Research
  • Cancer Diagnosis and Treatment
  • Immune cells in cancer
  • Virus-based gene therapy research
  • Cancer Immunotherapy and Biomarkers
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Hedgehog Signaling Pathway Studies
  • Liver Disease and Transplantation
  • Fibroblast Growth Factor Research
  • Cardiac Fibrosis and Remodeling
  • Liver Disease Diagnosis and Treatment
  • Immunotherapy and Immune Responses
  • Animal Virus Infections Studies
  • Colorectal Cancer Treatments and Studies
  • Liver physiology and pathology
  • Glycosylation and Glycoproteins Research
  • Virology and Viral Diseases
  • Immunodeficiency and Autoimmune Disorders

Georgia State University
2018-2024

Tata Memorial Hospital
2017

Fibrotic tumor stroma plays an important role in facilitating triple-negative breast cancer (TNBC) progression and chemotherapeutic resistance. We previously reported a rationally designed protein (ProAgio) that targets integrin αvβ3 at novel site. ProAgio induces apoptosis via the integrin. Cancer-associated fibroblasts (CAFs) angiogenic endothelial cells (aECs) TNBC express high levels of αvβ3. effectively CAFs aECs. The depletion by reduces intratumoral collagen decreases growth factors...

10.1084/jem.20200712 article EN cc-by-nc-sa The Journal of Experimental Medicine 2021-02-09

Rationale: Fibrosis is a pathologic condition of abnormal accumulation collagen fibrils. Collagen major extracellular matrix (ECM) protein synthesized and secreted by myofibroblasts, composing mainly (Gly-X-Y)n triplet repeats with >30% Gly residue. During fibrosis progression, myofibroblasts must upregulate glycine metabolism to meet the high demands amino acids for synthesis. Method: Expression PKM2 in was analyzed cultured fibroblasts disease tissues. Functional roles activator...

10.7150/thno.60385 article EN cc-by Theranostics 2021-01-01

Background & AimsPancreatic ductal adenocarcinoma (PDAC) is resistant to most therapeutics owing dense fibrotic stroma orchestrated by cancer-associated pancreatic stellate cells (CAPaSC). CAPaSC also support cancer cell growth, metastasis, and resistance apoptosis. Currently, there no effective therapy for PDAC that specifically targets CAPaSC. We previously reported a rationally designed protein, ProAgio, integrin αvβ3 at novel site induces apoptosis in αvβ3-expressing cells. Because both...

10.1016/j.jcmgh.2020.08.004 article EN cc-by-nc-nd Cellular and Molecular Gastroenterology and Hepatology 2020-08-15

Nonalcoholic steatohepatitis (NASH) and alcoholic hepatitis (AH) affect a large part of the general population worldwide. Dysregulation lipid metabolism alcohol toxicity drive disease progression by activation hepatic stellate cells capillarization liver sinusoidal endothelial cells. Collagen deposition, along with remodeling, alters sinusoid structure, resulting in inflammation, portal hypertension, failure, other complications. Efforts were made to develop treatments for NASH AH. However,...

10.3390/ijms25137447 article EN International Journal of Molecular Sciences 2024-07-06

Fibrotic stroma and angiogenic tumor vessels play an important role in modulating immunity. We previously reported a rationally designed protein (ProAgio) that targets integrin αvβ3 at novel site. ProAgio induces the apoptosis of cells express high levels integrin. Both activated cancer-associated fibroblasts (CAFs) endothelial (aECs) tumors αvβ3. simultaneously specifically CAFs aECs tumors. provide evidence here depletion elimination leaky by alter reduces CD4+ Treg Myeloid-derived...

10.3390/cancers16132483 article EN Cancers 2024-07-08

Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed inserting a transgene express Smac/DIABLO during (VSV-S). Endogenous Smac in HeLa cells diminished wtVSV infection, whereas the level enhanced VSV-S infection. Apoptosis readily induced VSV-S, but not wtVSV, More importantly, tumor volume reduced larger extent when xenografts 4T1 BALB/c mice and...

10.1016/j.omto.2019.05.006 article EN cc-by-nc-nd Molecular Therapy — Oncolytics 2019-06-04

Cytogenetic aberrations as well presence of IGVH mutations are the underlying reason for clinical heterogeneity in Chronic Lymphocytic Leukemia (CLL). The predominant gene usage shows geographical variations. However, there is no study from India addressing immunogenetics CLL. In a first Indian we document CLL large tertiary hospital.We analyzed mutation status, VH usage, cytogenetic abnormalities using FISH, immunophenotyping data and correlated them with standard variables 84 patients...

10.4103/0377-4929.200051 article EN cc-by-nc-sa Indian Journal of Pathology and Microbiology 2017-01-01

Abstract Background/Objective: One of the common mechanisms resistance solid tumors, including colon cancers, is activation integrins on endothelial cells (ECs) and cancer-associated fibroblasts (CAFs). ProAgio a small molecule developed to target integrin alpha V beta 3 (αvβ3), located surface abnormal ECs CAFs. enhances apoptosis inhibits angiogenesis via targeting αvβ3. The aim current study evaluate combination with FOLFIRI immune profile tumor growth cancer. Material Methods: Female...

10.1158/1538-7445.am2024-4571 article EN Cancer Research 2024-03-22

Substantial loss of cardiomyocytes during heart attacks and onset other cardiovascular diseases is a major cause mortality. Preservation cardiac injury would be the most effective strategy to manage these in clinic. However, there no treatment that able prevent cardiomyocyte loss. We demonstrate here systemic administration recombinant PKM2 mutant (G415R) preserves reduces fibrosis myocardial infarction. G415R by protecting from dying promoting proliferation. extracellular (EcPKM2) because...

10.3390/ijms252413246 article EN International Journal of Molecular Sciences 2024-12-10

Abstract Background: TNBC metastasis is responsible for a majority of the mortalities associated with breast cancer across globe. Cancers metastasize to various distant organs such as lungs, liver, and bones, which accounts low 5-year survival rate. Lung offers most favorable environment is, therefore, common metastatic site in patients. Currently, there are no effective targeted therapies hence dire clinical need establish treatment this disease. It noteworthy that tumor growth supported by...

10.1158/1538-7445.am2018-2124 article EN cc-by-nc Cancer Research 2018-07-01

Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer with five-year survival rate of just 9% after diagnosis. Despite large efforts in developing treatments, the outcome therapies for patient only improves marginally. Dense fibrotic stroma and ECM orchestrated by cancer-associated pancreatic stellate cells (CAPaSC) considered to be one major contributors resistance anti-tumor this disease. The presence dense collagen fibrils forms physical block drug delivery...

10.1158/1538-7445.am2019-110 article EN cc-by-nc Cancer Research 2019-07-01

Abstract Background: Pancreatic ductal adenocarcinoma (PDA) is the most lethal form of cancer owing to its insensitivity many chemotherapeutic drugs. Gemcitabine remains a cornerstone PDA treatment despite suboptimal efficacy in clinics. One major mechanism by which becomes resistant gemcitabine conversion inactive derivative, dFdU upregulation enzyme, cytidine deaminase (Cda) cells. Activated pancreatic stellate cells (PSC) are source IGF1 tumor microenvironment, may be responsible for an...

10.1158/1538-7445.am2019-117 article EN cc-by-nc Cancer Research 2019-07-01

Background: Pancreatic ductal adenocarcinoma (PDA) is the most lethal form of cancer owing to its insensitivity many chemotherapeutic drugs. Gemcitabine remains a cornerstone PDA treatment despite suboptimal efficacy in clinics. One major mechanism by which becomes resistant gemcitabine conversion inactive derivative, dFdU upregulation enzyme, cytidine deaminase (Cda) cells. Activated pancreatic stellate cells (PSC) are source IGF1 tumor microenvironment, may be responsible for an increase...

10.1158/1538-7445.sabcs18-117 article EN cc-by-nc Tumor Biology 2019-07-01

Background: Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer with five-year survival rate of just 9% after diagnosis. Despite large efforts in developing treatments, the outcome therapies for patient only improves marginally. Dense fibrotic stroma and ECM orchestrated by cancer-associated pancreatic stellate cells (CAPaSC) considered to be one major contributors resistance anti-tumor this disease. The presence dense collagen fibrils forms physical block drug delivery completely...

10.1158/1538-7445.sabcs18-110 article EN cc-by-nc Tumor Biology 2019-07-01
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