Kavitha Gowrishankar
YOU?
Author Swipe
View article: Current developments in T-cell receptor therapy for acute myeloid leukemia
Current developments in T-cell receptor therapy for acute myeloid leukemia Open
T-cell receptor (TCR) therapies are a promising modality for the treatment of cancers, with significant efforts being directed toward acute myeloid leukemia (AML), a particularly challenging disease. Chimeric antigen receptor (CAR) T cells…
View article: CAR+ and CAR− T cells share a differentiation trajectory into an NK-like subset after CD19 CAR T cell infusion in patients with B cell malignancies
CAR+ and CAR− T cells share a differentiation trajectory into an NK-like subset after CD19 CAR T cell infusion in patients with B cell malignancies Open
View article: CAR+ and CAR− T cells differentiate into an NK-like subset that is associated with increased inflammatory cytokines following infusion
CAR+ and CAR− T cells differentiate into an NK-like subset that is associated with increased inflammatory cytokines following infusion Open
Chimeric antigen receptor (CAR) T cells have demonstrable efficacy in treating B-cell malignancies. Factors such as product composition, lymphodepletion and immune reconstitution are known to influence CAR+ T cell survival and persistence,…
View article: Supplementary Figure Legend from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure Legend from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 81K
View article: Supplementary Figure 3 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 3 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 1073K, BRAF inhibition does not reduce the proliferation of wild-type BRAF melanoma cells.
View article: Supplementary Figure 4 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 4 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 5091K, CT scans illustrating growth of subcutaneous lesion while on MAPK inhibitor treatment.
View article: Supplementary Figure 1 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 1 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 2188K, Melanoma sub-lines with acquired resistance to MAPK inhibition, survive in the presence of MAPK inhibitor.
View article: Supplementary Figure 2 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 2 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 1142K, Resistant melanoma sub-lines display a diminished proliferative transcriptome signatured when exposed to MAPK inhibitors.
View article: Data from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Data from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
Inhibitors of the mitogen-activated protein kinases (MAPK), BRAF, and MAP–ERK kinase (MEK) induce tumor regression in the majority of patients with BRAF-mutant metastatic melanoma. The clinical benefit of MAPK inhibitors is restricted by t…
View article: Supplementary Figure 6 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 6 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 452K, Identification of BRAFV600E splice variant lacking exons 2-10 in dabrafenib resistant WMD009 tumour and derived cell line.
View article: Supplementary Figure 3 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 3 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 1073K, BRAF inhibition does not reduce the proliferation of wild-type BRAF melanoma cells.
View article: Supplementary Figure 6 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 6 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 452K, Identification of BRAFV600E splice variant lacking exons 2-10 in dabrafenib resistant WMD009 tumour and derived cell line.
View article: Supplementary Figure Legend from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure Legend from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 81K
View article: Supplementary Figure 2 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 2 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 1142K, Resistant melanoma sub-lines display a diminished proliferative transcriptome signatured when exposed to MAPK inhibitors.
View article: Supplementary Figure 4 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 4 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 5091K, CT scans illustrating growth of subcutaneous lesion while on MAPK inhibitor treatment.
View article: Data from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Data from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
Inhibitors of the mitogen-activated protein kinases (MAPK), BRAF, and MAP–ERK kinase (MEK) induce tumor regression in the majority of patients with BRAF-mutant metastatic melanoma. The clinical benefit of MAPK inhibitors is restricted by t…
View article: Supplementary Figure 5 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 5 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 918K, MAPK inhibitor treatment does not induce apoptosis in MAPK inhibitor resistant patient derived cell lines.
View article: Supplementary Figure 1 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 1 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 2188K, Melanoma sub-lines with acquired resistance to MAPK inhibition, survive in the presence of MAPK inhibitor.
View article: Supplementary Figure 5 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma
Supplementary Figure 5 from Antiproliferative Effects of Continued Mitogen-Activated Protein Kinase Pathway Inhibition following Acquired Resistance to BRAF and/or MEK Inhibition in Melanoma Open
PDF file - 918K, MAPK inhibitor treatment does not induce apoptosis in MAPK inhibitor resistant patient derived cell lines.
View article: Evolving Strategies to Eliminate the CD4 T Cells HIV Viral Reservoir via CAR T Cell Immunotherapy
Evolving Strategies to Eliminate the CD4 T Cells HIV Viral Reservoir via CAR T Cell Immunotherapy Open
Although the advent of ART has significantly reduced the morbidity and mortality associated with HIV infection, the stable pool of HIV in latently infected cells requires lifelong treatment adherence, with the cessation of ART resulting in…
View article: CAR+ and CAR- T cells differentiate into an NK-like subset that is associated with increased inflammatory cytokines following infusion
CAR+ and CAR- T cells differentiate into an NK-like subset that is associated with increased inflammatory cytokines following infusion Open
Chimeric antigen receptor (CAR) T cells have demonstrable efficacy in treating B-cell malignancies. Factors such as product composition, lymphodepletion and immune reconstitution are known to influence functional persistence of CAR+ T cell…
View article: CAR<sup>+</sup> and CAR<sup>-</sup> T cells differentiate into an NK-like subset that is associated with increased inflammatory cytokines following infusion
CAR<sup>+</sup> and CAR<sup>-</sup> T cells differentiate into an NK-like subset that is associated with increased inflammatory cytokines following infusion Open
Chimeric antigen receptor (CAR) T cells have demonstrable efficacy in treating B-cell malignancies. Factors such as product composition, lymphodepletion and immune reconstitution are known to influence functional persistence of CAR + T cel…
View article: Characterizing piggyBat—a transposase for genetic modification of T cells
Characterizing piggyBat—a transposase for genetic modification of T cells Open
View article: Investigation of product-derived lymphoma following infusion of <i>piggyBac</i>-modified CD19 chimeric antigen receptor T cells
Investigation of product-derived lymphoma following infusion of <i>piggyBac</i>-modified CD19 chimeric antigen receptor T cells Open
We performed a phase 1 clinical trial to evaluate outcomes in patients receiving donor-derived CD19-specific chimeric antigen receptor (CAR) T cells for B-cell malignancy that relapsed or persisted after matched related allogeneic hemopoie…
View article: CAR T Cell Generation by piggyBac Transposition from Linear Doggybone DNA Vectors Requires Transposon DNA-Flanking Regions
CAR T Cell Generation by piggyBac Transposition from Linear Doggybone DNA Vectors Requires Transposon DNA-Flanking Regions Open
CD19-specific chimeric antigen receptor (CAR19) T cells, generated using viral vectors, are an efficacious but costly treatment for B cell malignancies. The nonviral piggyBac transposon system provides a simple and inexpensive alter…
View article: <i>Ex vivo</i> enrichment of PRAME antigen‐specific T cells for adoptive immunotherapy using CD137 activation marker selection
<i>Ex vivo</i> enrichment of PRAME antigen‐specific T cells for adoptive immunotherapy using CD137 activation marker selection Open
Objective Adoptive immunotherapy with ex vivo expanded tumor‐specific T cells has potential as anticancer therapy. Preferentially expressed antigen in melanoma (PRAME) is an attractive target overexpressed in several cancers including mela…
View article: CD13 and CD33 CAR-T cells for the treatment of myeloid malignancies
CD13 and CD33 CAR-T cells for the treatment of myeloid malignancies Open
Background: Chimeric antigen receptor (CAR) T-cells can eliminate acute myeloid leukaemia (AML) blasts, but also cause haematological toxicity due to presence of leukaemia associated antigens on normal haemopoietic progenitor cells. Target…
View article: PD-L1 expression in melanoma cells.
PD-L1 expression in melanoma cells. Open
A. KMJR138 cells were treated with indicated doses of IFN-γ for 48 hours and the cell surface expression of PD-L1 was determined by flow cytometry. The corresponding mean fluorescence intensity (MFI) with values is shown in the hist…
View article: Targeting activating mutations of EZH2 leads to potent cell growth inhibition in human melanoma by derepression of tumor suppressor genes
Targeting activating mutations of EZH2 leads to potent cell growth inhibition in human melanoma by derepression of tumor suppressor genes Open
The epigenetic modifier EZH2 is part of the polycomb repressive complex that suppresses gene expression via histone methylation. Activating mutations in EZH2 are found in a subset of melanoma that contributes to disease progression by inac…
View article: Combining BET and HDAC inhibitors synergistically induces apoptosis of melanoma and suppresses AKT and YAP signaling
Combining BET and HDAC inhibitors synergistically induces apoptosis of melanoma and suppresses AKT and YAP signaling Open
Histone acetylation marks have an important role in controlling gene expression and are removed by histone deacetylases (HDACs). These marks are read by bromodomain and extra-terminal (BET) proteins and novel inhibitiors of these proteins …