Sherven Sharma
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View article: Financial burden of cancer in Nepal: Factors associated with annual cost and catastrophic health expenditure
Financial burden of cancer in Nepal: Factors associated with annual cost and catastrophic health expenditure Open
Background There is a dearth of comprehensive research on the financial burden of cancer in low-resource settings. This study aims to identify factors associated with annual cost of cancer care and catastrophic health expenditure as well a…
View article: Supplementary Table 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Supplementary Table 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
PDF file - 47K, Patient characteristics.
View article: Supplementary Figure 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Supplementary Figure 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
PDF file - 37K, Stable knockdown of c-myc expression by shRNA in NSCLC cells.
View article: Supplementary Figure Legends from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Supplementary Figure Legends from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
PDF file - 38K
View article: Data from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Data from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
Aberrant expression of microRNAs (miRNA) with oncogenic capacities (oncomiRs) has been described for several different malignancies. The first identified oncomiR, miR-17-92, is frequently overexpressed in a variety of cancers and its targe…
View article: Supplementary Table 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Supplementary Table 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
PDF file - 47K, Patient characteristics.
View article: Data from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Data from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
Aberrant expression of microRNAs (miRNA) with oncogenic capacities (oncomiRs) has been described for several different malignancies. The first identified oncomiR, miR-17-92, is frequently overexpressed in a variety of cancers and its targe…
View article: Supplementary Figure Legends from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Supplementary Figure Legends from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
PDF file - 38K
View article: Supplementary Figure 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC
Supplementary Figure 1 from PGE2-Driven Expression of c-Myc and OncomiR-17-92 Contributes to Apoptosis Resistance in NSCLC Open
PDF file - 37K, Stable knockdown of c-myc expression by shRNA in NSCLC cells.
View article: Supplementary Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma
Supplementary Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma Open
Supplementary Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma
View article: Figures S5-S6 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figures S5-S6 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figures S5-S6 provide additional evidence that Snail malignantly transforms epithelial cells in vitro. Information on the mutational background and stem phenotype of the cells transformed by Snail is provided.
View article: Figure S8 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figure S8 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figure S8 provides evidence that ESRP1 loss alone (without Snail expression) is not sufficient to transform epithelial cells in vitro.
View article: Figure S1 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figure S1 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figure S1 provides additional evidence that Snail is expressed during pulmonary premalignancy.
View article: Data from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Data from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Epithelial-to-mesenchymal transition (EMT) is organized in cancer cells by a set of key transcription factors, but the significance of this process is still debated, including in non–small cell lung cancer (NSCLC). Here, we report increase…
View article: Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma
Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma Open
Purpose: As a transcriptional repressor of E-cadherin, Snail has predominantly been associated with epithelial-mesenchymal transition, invasion, and metastasis. However, other important Snail-dependent malignant phenotypes have not been fu…
View article: Figure S7 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figure S7 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figure S7 provides additional evidence that Snail malignantly transforms epithelial cells in vivo. Information on the stem cell phenotype of the cells transformed by Snail is provided.
View article: Figure S7 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figure S7 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figure S7 provides additional evidence that Snail malignantly transforms epithelial cells in vivo. Information on the stem cell phenotype of the cells transformed by Snail is provided.
View article: Supplemental Methods-References-Tables from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Supplemental Methods-References-Tables from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Detailed supplemental methods and key references are provided. Tables S1-S2-S3-S4 provide antibody information, mouse study design information, PCR primer information, and an abbreviations list, respectively.
View article: Supplementary Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma
Supplementary Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma Open
Supplementary Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma
View article: Figures S5-S6 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figures S5-S6 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figures S5-S6 provide additional evidence that Snail malignantly transforms epithelial cells in vitro. Information on the mutational background and stem phenotype of the cells transformed by Snail is provided.
View article: Figures S2-S3-S4 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figures S2-S3-S4 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figures S2-S3-S4 provide additional evidence that Snail is a potent driver of EMT, carcinogenic signaling programs, and stem cell expansion in vitro.
View article: Figure S8 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figure S8 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figure S8 provides evidence that ESRP1 loss alone (without Snail expression) is not sufficient to transform epithelial cells in vitro.
View article: Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma
Data from Snail Promotes CXCR2 LigandDependent Tumor Progression in NonSmall Cell Lung Carcinoma Open
Purpose: As a transcriptional repressor of E-cadherin, Snail has predominantly been associated with epithelial-mesenchymal transition, invasion, and metastasis. However, other important Snail-dependent malignant phenotypes have not been fu…
View article: Figures S2-S3-S4 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figures S2-S3-S4 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figures S2-S3-S4 provide additional evidence that Snail is a potent driver of EMT, carcinogenic signaling programs, and stem cell expansion in vitro.
View article: Data from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Data from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Epithelial-to-mesenchymal transition (EMT) is organized in cancer cells by a set of key transcription factors, but the significance of this process is still debated, including in non–small cell lung cancer (NSCLC). Here, we report increase…
View article: Supplemental Methods-References-Tables from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Supplemental Methods-References-Tables from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Detailed supplemental methods and key references are provided. Tables S1-S2-S3-S4 provide antibody information, mouse study design information, PCR primer information, and an abbreviations list, respectively.
View article: Figure S1 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells
Figure S1 from Silencing the Snail-Dependent RNA Splice Regulator ESRP1 Drives Malignant Transformation of Human Pulmonary Epithelial Cells Open
Figure S1 provides additional evidence that Snail is expressed during pulmonary premalignancy.
View article: CCL21-DC tumor antigen vaccine augments anti-PD-1 therapy in lung cancer
CCL21-DC tumor antigen vaccine augments anti-PD-1 therapy in lung cancer Open
Targeting inhibitory immune checkpoint molecules has highlighted the need to find approaches enabling the induction and activation of an immune response against cancer. Therapeutic vaccination, which can induce a specific immune response …
View article: Targeting BMI-1-mediated epithelial–mesenchymal transition to inhibit colorectal cancer liver metastasis
Targeting BMI-1-mediated epithelial–mesenchymal transition to inhibit colorectal cancer liver metastasis Open
Liver is the most common metastatic site for colorectal cancer (CRC), there is no satisfied approach to treat CRC liver metastasis (CRCLM). Here, we investigated the role of a polycomb protein BMI-1 in CRCLM. Immunohistochemical analysis s…