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Article ; Online: Spatial and temporal pattern of rice yield growth in Asian countries from 1961 to 2016

Mukhopadhyay Debabrata

Ekonomika Poljoprivrede (1979), Vol 68, Iss 1, Pp 23-

An exploratory econometric analysis

2021 Volume 35

Abstract: The present paper attempts to find out the spatial and temporal movement of rice yield in twelve countries in Asia which is its lifeline over the period 1961 to 2016 by following Bai-Perron multiple structural break tests. The results based on endogenous ...

Abstract	The present paper attempts to find out the spatial and temporal movement of rice yield in twelve countries in Asia which is its lifeline over the period 1961 to 2016 by following Bai-Perron multiple structural break tests. The results based on endogenous multiple structural break analysis show that many of these countries passed through several phases of acceleration and deceleration in rice yield over this period The results also demonstrate that except Japan, all the twelve countries considered in our study experienced at least one structural break in rice yield at level during the period 1961 to 2016. The acceleration phases of rice yield growth observed mostly during 1970's and 1980's are resulted from improved technological innovations in agriculture whereas deceleration phases observed in the last two decades are mainly caused by environmental challenges on rice production. Cross country yield gaps have been showing declining trend since early 80's.
Keywords	rice production ; yield ; structural break ; technology innovations ; environmental challenges ; Agriculture ; S
Subject code	339
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Naučno društvo agrarnih ekonomista Balkana, Beograd; Institut za ekonomiku poljoprivrede, Beograd i Akademija ekonomskih nauka, Bukurešt
Document type	Article ; Online
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Article ; Online: Machine learning-based approach for automated classification of cell and extracellular matrix using nanomechanical properties.

Kulkarni, Tanmay / Robinson, Olivia-Marie / Dutta, Ayan / Mukhopadhyay, Debabrata / Bhattacharya, Santanu

Materials today. Bio

2024 Volume 25, Page(s) 100970

Abstract: Fibrosis characterized by excess accumulation of extracellular matrix (ECM) due to complex cell-ECM interactions plays a pivotal role in pathogenesis. Herein, we employ the pancreatic ductal adenocarcinoma (PDAC) model to investigate dynamic alterations ... ...

Abstract	Fibrosis characterized by excess accumulation of extracellular matrix (ECM) due to complex cell-ECM interactions plays a pivotal role in pathogenesis. Herein, we employ the pancreatic ductal adenocarcinoma (PDAC) model to investigate dynamic alterations in nanomechanical attributes arising from the cell-ECM interactions to study the fibrosis paradigm. Several segregated studies performed on cellular and ECM components fail to recapitulate their complex collaboration. We utilized collagen and fibronectin, the two most abundant PDAC ECM components, and studied their nanomechanical attributes. We demonstrate alteration in morphology and nanomechanical attributes of collagen with varying thicknesses of collagen gel. Furthermore, by mixing collagen and fibronectin in various stoichiometry, their nanomechanical attributes were observed to vary. To demonstrate the dynamicity and complexity of cell-ECM, we utilized Panc-1 and AsPC-1 cells with or without collagen. We observed that Panc-1 and AsPC-1 cells interact differently with collagen and vice versa, evident from their alteration in nanomechanical properties. Further, using nanomechanics data, we demonstrate that ML-based techniques were able to classify between ECM as well as cell, and cell subtypes in the presence/absence of collagen with higher accuracy. This work demonstrates a promising avenue to explore other ECM components facilitating deeper insights into tumor microenvironment and fibrosis paradigm.
Language	English
Publishing date	2024-01-20
Publishing country	England
Document type	Journal Article
ISSN	2590-0064
ISSN (online)	2590-0064
DOI	10.1016/j.mtbio.2024.100970
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Article ; Online: Dynamic alteration of poroelastic attributes as determinant membrane nanorheology for endocytosis of organ specific targeted gold nanoparticles.

Kulkarni, Tanmay / Mukhopadhyay, Debabrata / Bhattacharya, Santanu

Journal of nanobiotechnology

2022 Volume 20, Issue 1, Page(s) 74

Abstract: Background: Efficacy of targeted drug delivery using nanoparticles relies on several factors including the uptake mechanisms such as phagocytosis, macropinocytosis, micropinocytosis and receptor mediated endocytosis. These mechanisms have been studied ... ...

Abstract	Background: Efficacy of targeted drug delivery using nanoparticles relies on several factors including the uptake mechanisms such as phagocytosis, macropinocytosis, micropinocytosis and receptor mediated endocytosis. These mechanisms have been studied with respect to the alteration in signaling mechanisms, cellular morphology, and linear nanomechanical properties (NMPs). Commonly employed classical contact mechanics models to address cellular NMPs fail to address mesh like structure consisting of bilayer lipids and proteins of cell membrane. To overcome this technical challenge, we employed poroelastic model which accounts for the biphasic nature of cells including their porous behavior exhibiting both solid like (fluid storage) and liquid like (fluid dissipate) behavior. Results: In this study, we employed atomic force microscopy to monitor the influence of surface engineering of gold nanoparticles (GNPs) to the alteration of nonlinear NMPs such as drained Poisson's ratio, effective shear stress, diffusion constant and pore dimensions of cell membranes during their uptake. Herein, we used pancreatic cancer (PDAC) cell lines including Panc1, AsPC-1 and endothelial cell (HUVECs) to understand the receptor-dependent and -independent endocytosis of two different GNPs derived using plectin-1 targeting peptide (PTP-GNP) and corresponding scrambled peptide (sPEP-GNP). Compared to untreated cells, in case of receptor dependent endocytosis of PTP-GNPs diffusion coefficient altered ~ 1264-fold and ~ 1530-fold and pore size altered ~ 320-fold and ~ 260-fold in Panc1 and AsPC-1 cells, respectively. Whereas for receptor independent mechanisms, we observed modest alteration in diffusion coefficient and pore size, in these cells compared to untreated cells. Effective shear stress corresponding to 7.38 ± 0.15 kPa and 20.49 ± 0.39 kPa in PTP-GNP treatment in Panc1 and AsPC-1, respectively was significantly more than that for sPEP-GNP. These results demonstrate that with temporal recruitment of plectin-1 during receptor mediated endocytosis affects the poroelastic attributes of the membrane. Conclusion: This study confirms that nonlinear NMPs of cell membrane are directly associated with the uptake mechanism of nanoparticles and can provide promising insights of the nature of endocytosis mechanism involved for organ specific drug delivery using nanoparticles. Hence, nanomechanical analysis of cell membrane using this noninvasive, label-free and live-cell analytical tool can therefore be instrumental to evaluate therapeutic benefit of nanoformulations.
MeSH term(s)	Cell Membrane/metabolism ; Endocytosis ; Gold/chemistry ; Humans ; Metal Nanoparticles/chemistry ; Pancreatic Neoplasms/metabolism
Chemical Substances	Gold (7440-57-5)
Language	English
Publishing date	2022-02-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2100022-0
ISSN	1477-3155 ; 1477-3155
ISSN (online)	1477-3155
ISSN	1477-3155
DOI	10.1186/s12951-022-01276-1
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Article ; Online: Divergent roles of Plexin D1 in cancer.

Vivekanadhan, Sneha / Mukhopadhyay, Debabrata

Biochimica et biophysica acta. Reviews on cancer

2019 Volume 1872, Issue 1, Page(s) 103–110

Abstract: Plexin D1 belongs to a family of transmembrane proteins called plexins. It was characterized as a receptor for semaphorins and is known to be essential for axonal guidance and vascular patterning. Mutations in Plexin D1 have been implicated in pathologic ...

Abstract	Plexin D1 belongs to a family of transmembrane proteins called plexins. It was characterized as a receptor for semaphorins and is known to be essential for axonal guidance and vascular patterning. Mutations in Plexin D1 have been implicated in pathologic conditions such as truncus arteriosus and Möbius syndrome. Emerging data show that expression of Plexin D1 is deregulated in several cancers; it can support tumor development by aiding in tumor metastasis and EMT; and conversely, it can act as a dependence receptor and stimulate cell death in the absence of its canonical ligand, semaphorin 3E. The role of Plexin D1 in tumor development and progression is thereby garnering research interest for its potential as a biomarker and as a therapeutic target. In this review, we describe its discovery, structure, mutations, role(s) in cancer, and therapeutic potential.
MeSH term(s)	Biomarkers, Tumor/genetics ; Cell Adhesion Molecules, Neuronal/genetics ; Humans ; Mobius Syndrome/complications ; Mobius Syndrome/genetics ; Mobius Syndrome/therapy ; Molecular Targeted Therapy ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/pathology ; Neoplasms/complications ; Neoplasms/genetics ; Neoplasms/therapy ; Signal Transduction/genetics ; Truncus Arteriosus/pathology
Chemical Substances	Biomarkers, Tumor ; Cell Adhesion Molecules, Neuronal ; PLXND1 protein, human
Language	English
Publishing date	2019-05-30
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2918802-7
ISSN	1879-2561 ; 0304-419X
ISSN (online)	1879-2561
ISSN	0304-419X
DOI	10.1016/j.bbcan.2019.05.004
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Article ; Online: Conditional, Tissue-Specific CRISPR/Cas9 Vector System in Zebrafish Reveals the Role of Nrp1b in Heart Regeneration.

Singh Angom, Ramcharan / Wang, Ying / Wang, Enfeng / Dutta, Shamit Kumar / Mukhopadhyay, Debabrata

Arteriosclerosis, thrombosis, and vascular biology

2023 Volume 43, Issue 10, Page(s) 1921–1934

Abstract: Background: CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/clustered regularly interspaced short palindromic repeat-associated 9) technology-mediated genome editing has significantly improved the targeted inactivation of genes in ...

Abstract	Background: CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/clustered regularly interspaced short palindromic repeat-associated 9) technology-mediated genome editing has significantly improved the targeted inactivation of genes in vitro and in vivo in many organisms. Neuropilins play crucial roles in zebrafish heart regeneration, heart failure in mice, and electrical remodeling after myocardial infarction in rats. But the cell-specific functions of nrp1 have not been described before. In this study, we have investigated the role of Methods: In this study, we have reported a novel CRISPR-based vector system for conditional tissue-specific gene ablation in zebrafish. Specifically, the cardiac-specific Results: We observed that both the isoforms ( Conclusions: To our knowledge, this study is novel where we have reported a heat-shock-mediated conditional knockdown of
MeSH term(s)	Animals ; CRISPR-Cas Systems ; Gene Editing ; Myocytes, Cardiac/physiology ; Neuropilin-1/genetics ; Regeneration ; Ventricular Remodeling ; Zebrafish/genetics ; Zebrafish Proteins/physiology
Chemical Substances	Neuropilin-1 (144713-63-3) ; Zebrafish Proteins
Language	English
Publishing date	2023-08-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.123.319189
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Article ; Online: Genetic status of KRAS influences Transforming Growth Factor-beta (TGF-β) signaling: An insight into Neuropilin-1 (NRP1) mediated tumorigenesis.

Vivekanandhan, Sneha / Mukhopadhyay, Debabrata

Seminars in cancer biology

2018 Volume 54, Page(s) 72–79

Abstract: Oncogenic RAS and deregulated transforming growth factor-beta (TGF)-β signaling have been implicated in several cancers. So far, attempts to target either one of them therapeutically have been futile as both of them are involved in multiple fundamental ... ...

Abstract	Oncogenic RAS and deregulated transforming growth factor-beta (TGF)-β signaling have been implicated in several cancers. So far, attempts to target either one of them therapeutically have been futile as both of them are involved in multiple fundamental cellular processes and the normal forms are expressed by almost all cells. Hence, their inhibition would disrupt several physiological processes. Besides, their downregulation stimulates the tumor cells to develop adaptive mechanisms and would most likely be ineffective as therapeutic targets. Furthermore, growing literature suggests that both of these signaling pathways converge to enhance tumor development. Therefore, a lot of interest has been generated to explore the areas where these pathways interface that might identify new molecules that could potentially serve as novel therapeutic targets. In this review, we focus on such convergent signaling and cross-interaction that is mediated by neuropilin-1 (NRP1), a receptor that can interact with multiple growth factors including TGF-β for promoting tumorigenesis process.
MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cytokines/metabolism ; Gene Expression Regulation, Neoplastic ; Genetic Variation ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neuropilin-1/genetics ; Neuropilin-1/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Signal Transduction ; Transforming Growth Factor beta/metabolism
Chemical Substances	Cytokines ; Intercellular Signaling Peptides and Proteins ; Transforming Growth Factor beta ; Neuropilin-1 (144713-63-3) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2018-02-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2018.01.014
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Zs.A 2922: Show issues

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Article: Foreign investment inflows and the role of governance

Mukhopadhyay, Debabrata

The Asian economic review : journal of the Indian Institute of Economics Vol. 57, No. 1 , p. 107-118

an Indian perspective

2015 Volume 57, Issue 1, Page(s) 107–118

Author's details	Debabrata Mukhopadhyay
Keywords	foreign institutional investment ; Kapitalimport ; Investitionsklima ; Investitionspolitik ; Politische Instabilität ; Indien
Language	English
Size	graph. Darst.
Publisher	Indian Institute of Economics
Publishing place	Hyderabad
Document type	Article
ZDB-ID	410142x
ISSN	0004-4555
Database	ECONomics Information System

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Article ; Online: Nanomechanical Insight of Pancreatic Cancer Cell Membrane during Receptor Mediated Endocytosis of Targeted Gold Nanoparticles.

Kulkarni, Tanmay / Mukhopadhyay, Debabrata / Bhattacharya, Santanu

ACS applied bio materials

2020 Volume 4, Issue 1, Page(s) 984–994

Abstract: Nanoscale alterations in the cellular membrane transpire during cellular interactions with the extracellular environment through the endocytosis processes. Although the biological innuendos as well as alterations in cellular morphology during endocytosis ...

Abstract	Nanoscale alterations in the cellular membrane transpire during cellular interactions with the extracellular environment through the endocytosis processes. Although the biological innuendos as well as alterations in cellular morphology during endocytosis are well-known, nanomechanical amendments in the cellular membrane are poorly understood. In this manuscript, atomic force microscope is employed to demonstrate the nanomechanical alterations in membrane dynamics during receptor mediated endocytosis of gold nanoparticles conjugated with either plectin-1 targeted peptide (PTP-GNP) or scrambled peptide (sPEP-GNP). Plectin-1 is aberrantly overexpressed at cell membrane of pancreatic cancer cells and is known to provide and maintain cellular mechanical integrity. During receptor mediated endocytosis of nanoparticles, we demonstrate temporal nanomechanical changes of cell membrane in both immortal pancreatic cancer Panc1 cells and patient derived primary pancreatic cancer cell, 4911. We further confirm the alterations of plectin-1 expression in Panc1 cell membrane during the receptor mediated endocytosis using classical streptavidin-biotin reaction and establish its association with nanomechanical alteration in membrane dynamics. Withdrawal of PTP-GNPs from the cell culture restores the plectin-1 expression at the membrane and reverses the mechanical properties of Panc1. We also show a distinctly opposite trend in nanomechanical behavior in cancer and endothelial cells when treated with sPEP-GNP and PTP-GNP, respectively, signifying receptor independent endocytosis process. This study illustrates the nanomechanical perspective of cell membrane in receptor mediated endocytosis of nanoparticles designed for organ specific drug delivery.
MeSH term(s)	Cell Line, Tumor ; Cell Membrane/metabolism ; Endocytosis/physiology ; Gold/chemistry ; Human Umbilical Vein Endothelial Cells ; Humans ; Metal Nanoparticles/chemistry ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Plectin/chemistry ; Plectin/genetics ; Plectin/metabolism
Chemical Substances	PLEC protein, human ; Plectin ; Gold (7440-57-5)
Language	English
Publishing date	2020-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2576-6422
ISSN (online)	2576-6422
DOI	10.1021/acsabm.0c01443
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Article ; Online: Aurora kinase a inhibitor MLN8237 suppresses pancreatic cancer growth.

Zhang, Yuebo / Ma, Yong / Wang, Ying / Mukhopadhyay, Debabrata / Bi, Yan / Ji, Baoan

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.

2022 Volume 22, Issue 5, Page(s) 619–625

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is notorious for high mortality due to limited options of appropriate chemotherapy drugs. Here we report that Aurora kinase-A expression is elevated in both human and mouse PDAC samples. MLN8237, an inhibitor of ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is notorious for high mortality due to limited options of appropriate chemotherapy drugs. Here we report that Aurora kinase-A expression is elevated in both human and mouse PDAC samples. MLN8237, an inhibitor of Aurora kinase-A, efficiently reduced the proliferation and motility of PDAC cells in vitro as well as tumor growth in orthotropic xenograft model and genetic pancreatic cancer animal models (p53/LSL/Pdx-Cre mice) in vivo. MLN8237 exhibited tumor inhibitory effect through inhibiting proliferation and migration, and inducing apoptosis and senescence. These results provide the molecular basis for a novel chemotherapy strategy for PDAC patients.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Aurora Kinase A/antagonists & inhibitors ; Aurora Kinase A/genetics ; Aurora Kinase A/metabolism ; Azepines/pharmacology ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/enzymology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Humans ; Mice ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/enzymology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/pathology ; Protein Kinase Inhibitors/pharmacology ; Pyrimidines/pharmacology ; Pancreatic Neoplasms
Chemical Substances	Azepines ; MLN 8237 ; Protein Kinase Inhibitors ; Pyrimidines ; Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2022-04-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2056680-3
ISSN	1424-3911 ; 1424-3903
ISSN (online)	1424-3911
ISSN	1424-3903
DOI	10.1016/j.pan.2022.03.019
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Zs.A 5553: Show issues

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Article: Targeting mTOR and Survivin Concurrently Potentiates Radiation Therapy in Renal Cell Carcinoma by Suppressing DNA Damage Repair and Amplifying Mitotic Catastrophe.

Rachamala, Hari K / Madamsetty, Vijay S / Angom, Ramcharan S / Nakka, Naga M / Kumar Dutta, Shamit / Wang, Enfeng / Mukhopadhyay, Debabrata / Pal, Krishnendu

Research square

2023

Abstract: Background: Renal cell carcinoma (RCC) was historically considered to be less responsive to radiation therapy (RT) compared to other cancer indications. However, advancements in precision high-dose radiation delivery through single-fraction and multi- ... ...

Abstract	Background: Renal cell carcinoma (RCC) was historically considered to be less responsive to radiation therapy (RT) compared to other cancer indications. However, advancements in precision high-dose radiation delivery through single-fraction and multi-fraction stereotactic ablative radiotherapy (SABR) have led to better outcomes and reduced treatment-related toxicities, sparking renewed interest in using RT to treat RCC. Moreover, numerous studies have revealed that certain therapeutic agents including chemotherapies can increase the sensitivity of tumors to RT, leading to a growing interest in combining these treatments. Here, we developed a rational combination of two radiosensitizers in a tumor-targeted liposomal formulation for augmenting RT in RCC. The objective of this study is to assess the efficacy of a tumor-targeted liposomal formulation combining the mTOR inhibitor everolimus (E) with the survivin inhibitor YM155 (Y) in enhancing the sensitivity of RCC tumors to radiation. Experimental design: We slightly modified our previously published tumor-targeted liposomal formulation to develop a rational combination of E and Y in a single liposomal formulation (EY-L) and assessed its efficacy in RCC cell lines in vitro and in RCC tumors in vivo. We further investigated how well EY-L sensitizes RCC cell lines and tumors toward radiation and explored the underlying mechanism of radiosensitization. Results: EY-L outperformed the corresponding single drug-loaded formulations E-L and Y-L in terms of containing primary tumor growth and improving survival in an immunocompetent syngeneic mouse model of RCC. EY-L also exhibited significantly higher sensitization of RCC cells towards radiation in vitro than E-L and Y-L. Additionally, EY-L sensitized RCC tumors towards radiation therapy in xenograft and murine RCC models. EY-L mediated induction of mitotic catastrophe via downregulation of multiple cell cycle checkpoints and DNA damage repair pathways could be responsible for the augmentation of radiation therapy. Conclusion: Taken together, our study demonstrated the efficacy of a strategic combination therapy in sensitizing RCC to radiation therapy via inhibition of DNA damage repair and a substantial increase in mitotic catastrophe. This combination therapy may find its use in the augmentation of radiation therapy during the treatment of RCC patients.
Language	English
Publishing date	2023-12-23
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3770403/v1
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