Pavlina Chuntova
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View article: EXTH-123. Novel Dyrk1a inhibitors impair glioblastoma proliferation and enhance the effectiveness of other cell-cycle-directed therapies
EXTH-123. Novel Dyrk1a inhibitors impair glioblastoma proliferation and enhance the effectiveness of other cell-cycle-directed therapies Open
INTRODUCTION Dysregulated cell proliferation is a hallmark of glioblastoma, and DYRK1A kinase, a key cell cycle regulator, may provide a novel therapeutic target. METHODS The effects of two DYRK1A inhibitors (Leucettinib-21 and #423) were …
View article: P08.07.A COMPREHENSIVE EVALUATION OF CAR-ENGINEERED IMMUNE CELL SUBSETS REVEALS THERAPEUTIC SYNERGY IN AN IMMUNE-COMPETENT GLIOBLASTOMA MODEL
P08.07.A COMPREHENSIVE EVALUATION OF CAR-ENGINEERED IMMUNE CELL SUBSETS REVEALS THERAPEUTIC SYNERGY IN AN IMMUNE-COMPETENT GLIOBLASTOMA MODEL Open
BACKGROUND Chimeric antigen receptor (CAR)-based therapies have yet to achieve meaningful success in solid tumors such as glioblastoma (GBM). Recent efforts have focused on leveraging alternative immune cell types for CAR engineering, but …
View article: Comparative evaluation of CAR-expressing T-, NK-, NKT-cells, and macrophages in an immunocompetent mouse glioma model
Comparative evaluation of CAR-expressing T-, NK-, NKT-cells, and macrophages in an immunocompetent mouse glioma model Open
Background While chimeric antigen receptor (CAR) T-cells are promising, there is a rapidly growing interest in developing other CAR-expressing immune cells. However, to date, no reported studies evaluated these cells side-by-side in immune…
View article: IMMU-28. LOW-INTENSITY PULSED ULTRASOUND COMBINED WITH POLY-ICLC AND INTERLEUKIN-2 UNLOCKS THE IMMUNE PRIVILEGE OF THE BRAIN BY PROMOTING EPITOPE SPREADING AND ACTIVATION OF CNS-SPECIFIC NAÏVE T CELLS
IMMU-28. LOW-INTENSITY PULSED ULTRASOUND COMBINED WITH POLY-ICLC AND INTERLEUKIN-2 UNLOCKS THE IMMUNE PRIVILEGE OF THE BRAIN BY PROMOTING EPITOPE SPREADING AND ACTIVATION OF CNS-SPECIFIC NAÏVE T CELLS Open
Immunotherapies targeting glioma, such as chimeric antigen receptor (CAR) T cell therapies, offer new therapeutic avenues; however, their application has yielded limited success in clinical trials so far. Due to the antigenic heterogeneity…
View article: DDEL-10. MICROBUBBLE-ENHANCED FOCUSED ULTRASOUND REGULATES THE ENRICHMENT OF INFLAMMATORY PATHWAYS IN THE BLOOD-BRAIN BARRIER AND IMPROVES CAR T CELL ACCUMULATION IN GLIOMAS
DDEL-10. MICROBUBBLE-ENHANCED FOCUSED ULTRASOUND REGULATES THE ENRICHMENT OF INFLAMMATORY PATHWAYS IN THE BLOOD-BRAIN BARRIER AND IMPROVES CAR T CELL ACCUMULATION IN GLIOMAS Open
A major challenge to brain cancer immunotherapy is posed by the rate-limiting obstacles to the systemic delivery of cytotoxic T cells, such as chimeric antigen receptor (CAR) T cells, in brain tumors posed by the blood brain barrier (BBB).…
View article: Non-lytic replicating viral delivery of an IL15 superagonist enhances antitumor immunity and extends survival in glioblastoma
Non-lytic replicating viral delivery of an IL15 superagonist enhances antitumor immunity and extends survival in glioblastoma Open
Glioblastoma (GBM) is the most lethal primary brain neoplasm due to its highly immunosuppressive microenvironment and resistance to conventional therapies. To overcome this challenge, we engineered a replicating retrovirus (RRV) to deliver…
View article: KS05.6.A T-CELL THERAPY COMBINED WITH LOW-INTENSITY PULSED FOCUSED ULTRASOUND, MICROBUBBLES AND POLY-ICLC PROMOTES THE PRESENTATION OF BRAIN-DERIVED ANTIGENS, BREAKING CNS TOLERANCE AND INDUCING ACTIVE T-CELL RESPONSES
KS05.6.A T-CELL THERAPY COMBINED WITH LOW-INTENSITY PULSED FOCUSED ULTRASOUND, MICROBUBBLES AND POLY-ICLC PROMOTES THE PRESENTATION OF BRAIN-DERIVED ANTIGENS, BREAKING CNS TOLERANCE AND INDUCING ACTIVE T-CELL RESPONSES Open
BACKGROUND Immunotherapies targeting glioma, such as chimeric antigen receptor (CAR) T cell therapies, offer new therapeutic opportunities; however, their application has yielded limited success. Due to the antigenic heterogeneity of gliom…
View article: P02.16.A IRF8-DRIVEN REPROGRAMMING OF THE IMMUNE MICROENVIRONMENT ENHANCES ANTI-TUMOR ADAPTIVE IMMUNITY AND REDUCES IMMUNOSUPPRESSION IN MURINE GLIOBLASTOMA
P02.16.A IRF8-DRIVEN REPROGRAMMING OF THE IMMUNE MICROENVIRONMENT ENHANCES ANTI-TUMOR ADAPTIVE IMMUNITY AND REDUCES IMMUNOSUPPRESSION IN MURINE GLIOBLASTOMA Open
BACKGROUND Glioblastoma (GBM) has a highly immunosuppressive tumor immune microenvironment (TIME), largely mediated by myeloid-derived suppressor cells (MDSCs). Here, we utilized a retroviral replicating vector (RRV) to deliver Interferon …
View article: Interferon regulatory factor 8-driven reprogramming of the immune microenvironment enhances antitumor adaptive immunity and reduces immunosuppression in murine glioblastoma
Interferon regulatory factor 8-driven reprogramming of the immune microenvironment enhances antitumor adaptive immunity and reduces immunosuppression in murine glioblastoma Open
Background Glioblastoma (GBM) has a highly immunosuppressive tumor immune microenvironment (TIME), largely mediated by myeloid-derived suppressor cells (MDSCs). Here, we utilized a retroviral replicating vector (RRV) to deliver Interferon …
View article: IRF8-driven reprogramming of the immune microenvironment enhances anti-tumor adaptive immunity and reduces immunosuppression in murine glioblastoma
IRF8-driven reprogramming of the immune microenvironment enhances anti-tumor adaptive immunity and reduces immunosuppression in murine glioblastoma Open
Background Glioblastoma (GBM) has a highly immunosuppressive tumor immune microenvironment (TIME), largely mediated by myeloid-derived suppressor cells (MDSCs). Here, we utilized a retroviral replicating vector (RRV) to deliver Interferon …
View article: Enhancing CAR-T cell metabolism to overcome hypoxic conditions in the brain tumor microenvironment
Enhancing CAR-T cell metabolism to overcome hypoxic conditions in the brain tumor microenvironment Open
The efficacy of chimeric antigen receptor T cell (CAR-T) therapy has been limited against brain tumors to date. CAR-T cells infiltrating syngeneic intracerebral SB28 EGFRvIII gliomas revealed impaired mitochondrial ATP production and a mar…
View article: Enhancing CAR-T Cell Metabolism to Overcome Hypoxic Conditions in the Brain Tumor Microenvironment
Enhancing CAR-T Cell Metabolism to Overcome Hypoxic Conditions in the Brain Tumor Microenvironment Open
The efficacy of chimeric antigen receptor (CAR)-T therapy has been limited against brain tumors to date. CAR-T cells infiltrating syngeneic intracerebral SB28-EGFRvIII glioma revealed impaired mitochondrial ATP production and a markedly hy…
View article: IMMU-52. LOW-INTENSITY PULSED ULTRASOUND CONDUCTS ANTIGEN-INDEPENDENT T CELL HOMING INTO THE BRAIN PARENCHYMA WITH THE INTACT BLOOD-BRAIN BARRIER
IMMU-52. LOW-INTENSITY PULSED ULTRASOUND CONDUCTS ANTIGEN-INDEPENDENT T CELL HOMING INTO THE BRAIN PARENCHYMA WITH THE INTACT BLOOD-BRAIN BARRIER Open
The blood-brain barrier (BBB) protects the brain parenchyma from excessive inflammation but also leads to poor immune cell homing, hampering the success of immunotherapies, such as ones for low-grade glioma, where the BBB is intact. Low-in…
View article: IMMU-21. LOW-INTENSITY PULSED ULTRASOUND PROMOTES THE PRESENTATION OF BRAIN-DERIVED ANTIGENS THROUGH ENHANCED TRAFFICKING OF ANTIGEN-PRESENTING CELLS FROM THE BRAIN INTO THE PERIPHERY
IMMU-21. LOW-INTENSITY PULSED ULTRASOUND PROMOTES THE PRESENTATION OF BRAIN-DERIVED ANTIGENS THROUGH ENHANCED TRAFFICKING OF ANTIGEN-PRESENTING CELLS FROM THE BRAIN INTO THE PERIPHERY Open
The central nervous system, immunologically unique due to specialized lymphatics and anatomical barriers, often conceals brain neoplasm from the peripheral immune system. Low-intensity pulsed ultrasound with microbubbles (LIPU/MB) enables …
View article: EXTH-34. LOCAL DELIVERY OF AN IL-15 SUPERAGONIST USING A REPLICATING RETROVIRUS SYNGERIZES WITH TEMOZOLOMIDE TO INCREASE LYMPHOCYTE INFILTRATION AND SURVIVAL IN TWO POORLY IMMUNOGENIC GLIOBLASTOMA MOUSE MODELS
EXTH-34. LOCAL DELIVERY OF AN IL-15 SUPERAGONIST USING A REPLICATING RETROVIRUS SYNGERIZES WITH TEMOZOLOMIDE TO INCREASE LYMPHOCYTE INFILTRATION AND SURVIVAL IN TWO POORLY IMMUNOGENIC GLIOBLASTOMA MOUSE MODELS Open
Glioblastoma (GBM) leads to systemic and local immunosuppression and immunotherapies have had limited clinical success. We evaluated the treatment efficacy of RLI (receptor-linker-IL-15), a superagonist of T-cell activator IL-15, delivered…
View article: EXTH-18. DEVELOPMENT OF A TRANSGENIC MOUSE MODEL ENABLING COMPARATIVE ANALYSIS OF CHIMERIC ANTIGEN RECEPTOR (CAR)-EXPRESSING IMMUNE CELL POPULATIONS FOR CANCER IMMUNOTHERAPY
EXTH-18. DEVELOPMENT OF A TRANSGENIC MOUSE MODEL ENABLING COMPARATIVE ANALYSIS OF CHIMERIC ANTIGEN RECEPTOR (CAR)-EXPRESSING IMMUNE CELL POPULATIONS FOR CANCER IMMUNOTHERAPY Open
We reported the creation of C57BL/6J-background transgenic (Tg) mice carrying the anti-epidermal growth factor receptor (EGFR)vIII-CAR with CD3z-CD28-4-1BB downstream of a Lox-Stop-Lox cassette in the Rosa26 locus. Breeding these mice with…
View article: IMMU-09. DISSECTING THE INTERPLAY BETWEEN THE ENDOGENOUS IMMUNE RESPONSE AND ONCOLYTIC VIRUS THERAPY IN PEDIATRIC BRAIN TUMORS
IMMU-09. DISSECTING THE INTERPLAY BETWEEN THE ENDOGENOUS IMMUNE RESPONSE AND ONCOLYTIC VIRUS THERAPY IN PEDIATRIC BRAIN TUMORS Open
Oncolytic virus (OV) elicits an antitumor immune response in addition to tumor-cell killing. However, it is unknown if a pre-existing antitumor immune response aids or hinders OV therapy. To study the interplay between the endogenous immun…
View article: Supplementary Figure 4 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 4 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 116K, Supplemental Figure 4. Activation of FGFR (1) leads to increased gene expression and secretion of IL-6 family members (2). These bind to the gp130 receptor (3) which activates STAT3 (4). Phosphorylated STAT3 regulates HAS2…
View article: Supplementary Figure 2 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 2 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 78K, Effect on proliferation and apoptosis of Stattic treated Hs578T cells.
View article: Supplementary Figure 1 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 1 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 66K, IHC control images.
View article: Supplementary Table 1 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Table 1 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 38K, Proportional odds logistic regression results evaluating the association between pSTAT3 and pFRS2.
View article: Supplementary Figure 3 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 3 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 45K, Supplemental Figure 3. HC-11 or HC-11/R1 cells were injected into the mammary fat pads of Balb/c mice. Mice were palpated to determine the % tumor free.
View article: Supplementary Figure 1 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 1 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 66K, IHC control images.
View article: Supplementary Figure 3 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 3 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 45K, Supplemental Figure 3. HC-11 or HC-11/R1 cells were injected into the mammary fat pads of Balb/c mice. Mice were palpated to determine the % tumor free.
View article: Data from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Data from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
Aberrant activation of fibroblast growth factor receptors (FGFR) contributes to breast cancer growth, progression, and therapeutic resistance. Because of the complex nature of the FGF/FGFR axis, and the numerous effects of FGFR activation …
View article: Supplementary Figure 2 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 2 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 78K, Effect on proliferation and apoptosis of Stattic treated Hs578T cells.
View article: Data from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Data from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
Aberrant activation of fibroblast growth factor receptors (FGFR) contributes to breast cancer growth, progression, and therapeutic resistance. Because of the complex nature of the FGF/FGFR axis, and the numerous effects of FGFR activation …
View article: Supplementary Figure Legend from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure Legend from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 45K
View article: Supplementary Figure 4 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation
Supplementary Figure 4 from Activation of the FGFR–STAT3 Pathway in Breast Cancer Cells Induces a Hyaluronan-Rich Microenvironment That Licenses Tumor Formation Open
PDF file - 116K, Supplemental Figure 4. Activation of FGFR (1) leads to increased gene expression and secretion of IL-6 family members (2). These bind to the gp130 receptor (3) which activates STAT3 (4). Phosphorylated STAT3 regulates HAS2…