Search

Your search keyword '"Manjunath, Yariswamy"' showing total 38 results
Start Over Author "Manjunath, Yariswamy"
38 results on '"Manjunath, Yariswamy"'

10. NSCLC patient-derived xenografts perpetuating tumor-associated, tumor-reactive T cells that respond to immunotherapy but do not cause GVHD in host mice

Author

Radhakrishnan, Vijay, primary, Venkateshaiah, Sathisha Upparahalli, additional, Mahadevappa, Chandrashekara Puthanapura, additional, Okpasuo, Onyekachi Juliet, additional, Cheatham, Christa, additional, Nagaraj, Suvilesh Kanve, additional, Manjunath, Yariswamy, additional, Li, Guangfu, additional, Kaifi, Jussuf T, additional, Schrum, Adam G, additional, Gil, Diana, additional, and Avella, Diego M, additional

Published
2023
Full Text
View/download PDF

11. Abstract 205: Patient-derived organoids from surgically treated, localized non-small cell lung cancer as high-throughput drug testing platforms for conventional and repurposed drugs

Author

Manjunath, Yariswamy, primary, Nagaraj, Suvilesh Kanve, additional, Nussbaum, Yulia I., additional, Gadelkarim, Mohamed, additional, Staveley-O’Carroll, Kevin F., additional, Kimchi, Eric T., additional, Li, Guangfu, additional, Warren, Wesley, additional, Shyu, Chi-Ren, additional, Ciorba, Matthew, additional, Mitchem, Jonathan B., additional, and Kaifi, Jussuf T., additional

Published
2023
Full Text
View/download PDF

13. 87. Somatic mutation variant analysis in rural, resectable non-small cell lung carcinoma patients

Author

Kaifi, Jussuf, primary, Mitchem, Jonathan, additional, Miller, Amanda, additional, Manjunath, Yariswamy, additional, Barbirou, Mouadh, additional, Murugesan, Raju, additional, Shen, Yuanyuan, additional, Li, Guangfu, additional, Avella, Diego, additional, Chaudhuri, Aadel, additional, Shyu, Chi-Ren, additional, Warren, Wesley, additional, and Tonellato, Peter, additional

Published
2022
Full Text
View/download PDF

15. Epigenetic Regulation of Cancer Immune Cells

Author

Avella Patino, Diego M., primary, Radhakrishnan, Vijay, additional, Suvilesh, Kanve N., additional, Manjunath, Yariswamy, additional, Li, Guangfu, additional, Kimchi, Eric T., additional, Staveley-O’Carroll, Kevin F., additional, Warren, Wesley C., additional, Kaifi, Jussuf T., additional, and Mitchem, Jonathan B., additional

Published
2022
Full Text
View/download PDF

16. Abstract 267: Xenograft models of non-metastatic non-small cell lung cancer reveals micrometastasis-associated single cell composition

Author

Suvilesh, Kanve Nagaraj, primary, Nussbaum, Yulia I., additional, Radhakrishnan, Vijay, additional, Manjunath, Yariswamy, additional, Avella, Diego M., additional, Staveley-O’Carroll, Kevin F., additional, Kimchi, Eric T., additional, Chaudhuri, Aadel A., additional, Shyu, Chi-Ren, additional, Li, Guangfu, additional, Pantel, Klaus, additional, Warren, Wesley C., additional, Mitchem, Jonathan B., additional, and Kaifi, Jussuf T., additional

Published
2022
Full Text
View/download PDF

18. Additional file 4 of Tumorigenic circulating tumor cells from xenograft mouse models of non-metastatic NSCLC patients reveal distinct single cell heterogeneity and drug responses

Author

Suvilesh, Kanve N., Nussbaum, Yulia I., Radhakrishnan, Vijay, Manjunath, Yariswamy, Avella, Diego M., Staveley-O���Carroll, Kevin F., Kimchi, Eric T., Chaudhuri, Aadel A., Shyu, Chi-Ren, Li, Guangfu, Pantel, Klaus, Warren, Wesley C., Mitchem, Jonathan B., and Kaifi, Jussuf T.

Abstract

Additional file 4. Supplementary methods.

Published
2022
Full Text
View/download PDF

19. Single Circulating-Tumor-Cell-Targeted Sequencing to Identify Somatic Variants in Liquid Biopsies in Non-Small-Cell Lung Cancer Patients

Author

Barbirou, Mouadh, primary, Miller, Amanda, additional, Manjunath, Yariswamy, additional, Ramirez, Arturo B., additional, Ericson, Nolan G., additional, Staveley-O’Carroll, Kevin F., additional, Mitchem, Jonathan B., additional, Warren, Wesley C., additional, Chaudhuri, Aadel A., additional, Huang, Yi, additional, Li, Guangfu, additional, Tonellato, Peter J., additional, and Kaifi, Jussuf T., additional

Published
2022
Full Text
View/download PDF

23. Sunitinib and Sorafenib Modulating Antitumor Immunity in Hepatocellular Cancer

Author

Liu, Dai, Qi, Xiaoqiang, Manjunath, Yariswamy, Kimchi, Eric T., Ma, Lixin, Kaifi, Jussuf T., Staveley-O’Carroll, Kevin F., and Li, Guangfu

Subjects
Regulatory T cells (Tregs), Myeloid-derived suppressive cells (MDSCs), Hepatocellular cancer (HCC), Sunitinib, Chemoimmunotherapy, Sorafenib, urologic and male genital diseases, neoplasms, digestive system diseases, female genital diseases and pregnancy complications, Article
Abstract

Sorafenib and sunitinib are multiple tyrosine kinase inhibitors. Both of them have been approved by the US FDA in the treatment of patients with malignancies. In order to develop an effective and clinically useful chemoimmunotherapy modality against hepatocellular cancer (HCC), we investigate their tumoricidal and immune modulatory effect in the setting of HCC. In vitro experiments suggested that sunitinib and sorafenib both induced HCC cell apoptosis at an equivalent level, but stronger suppressive function to cell proliferation was detected in sorafenib. Correspondingly, treatment of tumor-bearing mice with sorafenib led to the suppression of tumor growth to a larger extent than sunitinib. Flow cytometry showed that treatment with sunitinib, not sorafenib, significantly reduced the frequency of regulatory T cells (Tregs) and myeloid-derived suppressive cells (MDSCs) in tumor-bearing mice; and allowed splenic lymphocytes to produce equivalent levels of IFN-γ and TNF-α in response to vaccination as that in wild type mice. This activation was not detected in control and sorafenib-treated tumor mice. In addition, treatment of tumor-bearing mice with sunitinib followed by adoptive transfer of tumor antigen-specific CD8+ T cells and immunization resulted in the additional suppression to tumor growth compared to sunitinib monotherapy. These results imply treatment with sunitinib, not sorafenib, is able to prevent tumor-induced immunotolerance and activate antitumorimmunity. Our data suggest that sunitinib may be a preferable chemotherapeutic agent to use in combination with immunotherapy for the treatment of HCC.

Published
2018

25. Abstract 5375: Large, polymorphonuclear circulating cancer-associated cell with dual epithelial and macrophage/myeloid phenotype is prognostic in non-small cell lung cancer and has an impact on anti-tumor immune responses

Author

Manjunath, Yariswamy, primary, Suvilesh, Kanve N., additional, Avella, Diego M., additional, Kimchi, Eric T., additional, Staveley-O'Carroll, Kevin F., additional, Deroche, Chelsea B., additional, Li, Guangfu, additional, and Kaifi, Jussuf T., additional

Published
2020
Full Text
View/download PDF

28. 18F-FDG PET/CT total lesion glycolysis is associated with circulating tumor cell counts in patients with stage I to IIIA non-small cell lung cancer

Author

Avella, Diego M., primary, Manjunath, Yariswamy, additional, Singh, Amolak, additional, Deroche, Chelsea B., additional, Kimchi, Eric T., additional, Staveley-O’Carroll, Kevin F., additional, Mitchem, Jonathan B., additional, Kwon, Eric, additional, Li, Guangfu, additional, and Kaifi, Jussuf T., additional

Published
2020
Full Text
View/download PDF

32. Abstract 917: Circulating tumor cells accurately detect and characterize lung cancers in high-risk subjects undergoing low-dose CT screening

Author

MANJUNATH, YARISWAMY, primary, Venkateshaiah, Sathisha Upparahalli, additional, Kimchi, Eric T., additional, Staveley-O'Carroll, Kevin F., additional, Coberly, Jared, additional, Avella, Diego M., additional, Hoffman, Timothy J., additional, Deroche, Chelsea, additional, Pantel, Klaus, additional, Li, Guangfu, additional, and Kaifi, Jussuf T., additional

Published
2019
Full Text
View/download PDF

33. PD-L1 Expression with Epithelial Mesenchymal Transition of Circulating Tumor Cells Is Associated with Poor Survival in Curatively Resected Non-Small Cell Lung Cancer

Author

Manjunath, Yariswamy, primary, Upparahalli, Sathisha V., additional, Avella, Diego M., additional, Deroche, Chelsea B., additional, Kimchi, Eric T., additional, Staveley-O’Carroll, Kevin F., additional, Smith, Charles J., additional, Li, Guangfu, additional, and Kaifi, Jussuf T., additional

Published
2019
Full Text
View/download PDF

36. Targeting AKR1B10 by Drug Repurposing with Epalrestat Overcomes Chemoresistance in Non-Small Cell Lung Cancer Patient-Derived Tumor Organoids.

Author

Suvilesh KN, Manjunath Y, Nussbaum YI, Gadelkarim M, Raju M, Srivastava A, Li G, Warren WC, Shyu CR, Gao F, Ciorba MA, Mitchem JB, Rachagani S, and Kaifi JT

Subjects
Humans, Animals, Mice, Female, Cell Line, Tumor, Male, Cell Proliferation drug effects, Rhodanine analogs & derivatives, Thiazolidines, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung pathology, Carcinoma, Non-Small-Cell Lung genetics, Carcinoma, Non-Small-Cell Lung metabolism, Drug Repositioning methods, Drug Resistance, Neoplasm drug effects, Organoids drug effects, Lung Neoplasms drug therapy, Lung Neoplasms pathology, Lung Neoplasms genetics, Lung Neoplasms metabolism, Aldo-Keto Reductases genetics, Aldo-Keto Reductases metabolism, Xenograft Model Antitumor Assays
Abstract

Purpose: Systemic treatments given to patients with non-small cell lung cancer (NSCLC) are often ineffective due to drug resistance. In the present study, we investigated patient-derived tumor organoids (PDTO) and matched tumor tissues from surgically treated patients with NSCLC to identify drug repurposing targets to overcome resistance toward standard-of-care platinum-based doublet chemotherapy., Experimental Design: PDTOs were established from 10 prospectively enrolled patients with non-metastatic NSCLC from resected tumors. PDTOs were compared with matched tumor tissues by histopathology/immunohistochemistry, whole exome sequencing, and transcriptome sequencing. PDTO growths and drug responses were determined by measuring 3D tumoroid volumes, cell viability, and proliferation/apoptosis. Differential gene expression analysis identified drug-repurposing targets. Validations were performed with internal/external data sets of patients with NSCLC. NSCLC cell lines were used for aldo-keto reductase 1B10 (AKR1B10) knockdown studies and xenograft models to determine the intratumoral bioavailability of epalrestat., Results: PDTOs retained histomorphology and pathological biomarker expression, mutational/transcriptomic signatures, and cellular heterogeneity of the matched tumor tissues. Five (50%) PDTOs were chemoresistant toward carboplatin/paclitaxel. Chemoresistant PDTOs and matched tumor tissues demonstrated overexpression of AKR1B10. Epalrestat, an orally available AKR1B10 inhibitor in clinical use for diabetic polyneuropathy, was repurposed to overcome chemoresistance of PDTOs. In vivo efficacy of epalrestat to overcome drug resistance corresponded to intratumoral epalrestat levels., Conclusions: PDTOs are efficient preclinical models recapitulating the tumor characteristics and are suitable for drug testing. AKR1B10 can be targeted by repurposing epalrestat to overcome chemoresistance in NSCLC. Epalrestat has the potential to advance to clinical trials in patients with drug-resistant NSCLC due to favorable toxicity, pharmacological profile, and bioavailability., (©2024 The Authors; Published by the American Association for Cancer Research.)

Published
2024
Full Text
View/download PDF

37. Induction of Ferroptosis by an Amalgam of Extracellular Vesicles and Iron Oxide Nanoparticles Overcomes Cisplatin Resistance in Lung Cancer.

Author

Paramanantham A, Asfiya R, Manjunath Y, Xu L, McCully G, Das S, Yang H, Kaifi JT, and Srivastava A

Abstract

Extracellular vesicles (EVs) hold potential as effective carriers for drug delivery, providing a promising approach to resolving challenges in lung cancer treatment. Traditional treatments, such as with the chemotherapy drug cisplatin, encounter resistance in standard cell death pathways like apoptosis, prompting the need to explore alternative approaches. This study investigates the potential of iron oxide nanoparticles (IONP) and EVs to induce ferroptosis-a regulated cell death mechanism-in lung cancer cells. We formulated a novel EV and IONP-based system, namely 'ExoFeR', and observed that ExoFeR demonstrated efficient ferroptosis induction, evidenced by downregulation of ferroptosis markers (xCT/SLC7A11 and GPX4), increased intracellular and mitochondrial ferrous iron levels, and morphological changes in mitochondria. To enhance efficacy, tumor-targeting transferrin (TF)-conjugated ExoFeR (ExoFeR TF ) was developed. ExoFeR TF outperformed ExoFeR, exhibiting higher uptake and cell death in lung cancer cells. Mechanistically, nuclear factor erythroid 2-related factor 2 (Nrf2)-a key regulator of genes involved in glutathione biosynthesis, antioxidant responses, lipid metabolism, and iron metabolism-was found downregulated in the ferroptotic cells. Inhibition of Nrf2 intracellular translocation in ExoFeR TF -treated cells was also observed, emphasizing the role of Nrf2 in modulating ferroptosis-dependent cell death. Furthermore, ExoFeR and ExoFeR TF demonstrated the ability to sensitize chemo-resistant cancer cells, including cisplatin-resistant lung cancer patient-derived tumoroid organoids. In summary, ExoFeR TF presents a promising and multifaceted therapeutic approach for combating lung cancer by intrinsically inducing ferroptosis and sensitizing chemo-resistant cells.

Published
2024
Full Text
View/download PDF

38. 18 F-FDG PET/CT total lesion glycolysis is associated with circulating tumor cell counts in patients with stage I to IIIA non-small cell lung cancer.

Author

Avella DM, Manjunath Y, Singh A, Deroche CB, Kimchi ET, Staveley-O'Carroll KF, Mitchem JB, Kwon E, Li G, and Kaifi JT

Abstract

Background: In non-small cell lung cancer (NSCLC), 18 F-fluoro-2-deoxy-D-glucose ( 18 F-FDG) uptake determined by PET and presence of circulating tumor cells (CTCs) in the peripheral blood independently predict outcomes. For 18 F-FDG PET/CT staging interpretation, standardized uptake values (SUV max/avg ) are routinely used in clinical reporting. The goal was to investigate whether 18 F-FDG uptake measured by SUV max/avg , but also measures of metabolic tumor volume (MTV) and total lesion glycolysis (TLG) (MTV × SUV avg ), are associated with CTCs., Methods: Prospectively, 7.5 mL blood was drawn from NSCLC patients at the time of staging 18F-FDG PET/CT and from healthy control subjects. CTCs were identified by immunofluorescent staining (CK8/18/19 pos /EpCAM pos /CD45 neg /DAPI pos nucleus). 18 F-FDG PET/CTs were analyzed for SUV max , SUV avg , MTV, and TLG., Results: In 16 NSCLC patients with stage I-IIIA, MTV and TLG, in contrast to SUV max and SUV avg , were positively associated with CTCs (linear regression analysis). No CTCs were detectable in 20 healthy control subjects., Conclusions: This pilot study demonstrates that 18 F-FDG PET/CT TLG correlates with CTCs in NSCLC patients without distant metastases. TLG might be a more appropriate marker for hematogenous micrometastatic potential than SUVs., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/tlcr.2020.04.10). The authors have no conflicts of interest to declare., (2020 Translational Lung Cancer Research. All rights reserved.)

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results