Helga Simon‐Molas
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View article: Mitigating T-cell mitochondrial dysfunction in CLL to augment CAR T-cell therapy: evaluation in an immunocompetent model
Mitigating T-cell mitochondrial dysfunction in CLL to augment CAR T-cell therapy: evaluation in an immunocompetent model Open
An unmet clinical need in chronic lymphocytic leukemia (CLL) is emerging due to the rapidly expanding group of patients with double refractory (Bruton's tyrosine kinase- and B-cell lymphoma 2-inhibitor) disease. So far, autologous T-cell–b…
View article: Reprogramming CLL T-Cell Mitochondrial Fitness Using PI3K Inhibition for Enhancing CAR T-Cell Therapy
Reprogramming CLL T-Cell Mitochondrial Fitness Using PI3K Inhibition for Enhancing CAR T-Cell Therapy Open
Chronic lymphocytic leukemia (CLL) presents a significant clinical shortfall, as the number of patients developing resistance to both BTK inhibitors and Bcl2-targeted therapies is rapidly increasing. To date, chimeric antigen receptor (CAR…
View article: Metabolic signature and response to glutamine deprivation are independent of p53 status in B cell malignancies
Metabolic signature and response to glutamine deprivation are independent of p53 status in B cell malignancies Open
The tumor suppressor p53 has been described to control various aspects of metabolic reprogramming in solid tumors, but in B cell malignancies that role is as yet unknown. We generated pairs of p53 functional and knockout (KO) clones from d…
View article: Metabolic reprogramming in the CLL TME; potential for new therapeutic targets
Metabolic reprogramming in the CLL TME; potential for new therapeutic targets Open
Chronic lymphocytic leukemia (CLL) cells circulate between peripheral (PB) blood and lymph node (LN) compartments, and strictly depend on microenvironmental factors for proliferation, survival and drug resistance. All cancer cells display …
View article: Glucose metabolism in B cell malignancies: a focus on glycolysis branching pathways
Glucose metabolism in B cell malignancies: a focus on glycolysis branching pathways Open
Glucose catabolism, one of the essential pathways sustaining cellular bioenergetics, has been widely studied in the context of tumors. Nevertheless, the function of various branches of glucose metabolism that stem from ‘classical’ glycolys…
View article: T-cell dysfunction by pseudohypoxia and autocrine purinergic signaling in chronic lymphocytic leukemia
T-cell dysfunction by pseudohypoxia and autocrine purinergic signaling in chronic lymphocytic leukemia Open
Acquired T-cell dysfunction is common in chronic B-cell malignancies. Given the strong connection between T-cell metabolism and function, we investigated metabolic alterations as the basis of T-cell dysfunction induced by malignant cells. …
View article: P595: DEFECTIVE MITOCHONDRIAL METABOLISM IS AT THE BASIS OF T-CELL DYSFUNCTION IN CHRONIC LYMPHOCYTIC LEUKEMIA PATIENTS
P595: DEFECTIVE MITOCHONDRIAL METABOLISM IS AT THE BASIS OF T-CELL DYSFUNCTION IN CHRONIC LYMPHOCYTIC LEUKEMIA PATIENTS Open
Background: Chronic lymphocytic leukemia (CLL) remains incurable despite availability of targeted therapies. Successful autologous cell-based anti-cancer therapies require functionality and longevity of effector cells, features that highly…
View article: P593: T-CELL DYSFUNCTION BY PSEUDOHYPOXIA AND AUTOCRINE PURINERGIC SIGNALING IN CHRONIC LYMPHOCYTIC LEUKEMIA
P593: T-CELL DYSFUNCTION BY PSEUDOHYPOXIA AND AUTOCRINE PURINERGIC SIGNALING IN CHRONIC LYMPHOCYTIC LEUKEMIA Open
Background: Acquired T-cell dysfunction is a prominent feature in chronic B-cell malignancies, such as chronic lymphocytic leukemia (CLL). This is widely assumed to hinder the efficacy of T-cell based immunotherapy. T cells rely on metabol…
View article: Electron transport chain and mTOR inhibition synergistically decrease CD40 signaling and counteract venetoclax resistance in chronic lymphocytic leukemia
Electron transport chain and mTOR inhibition synergistically decrease CD40 signaling and counteract venetoclax resistance in chronic lymphocytic leukemia Open
CD40 signaling upregulates BCL-XL and MCL-1 expression in the chronic lymphocytic leukemia (CLL) lymph node microenvironment (TME), affording resistance to the BCL-2 inhibitor venetoclax (VEN). VEN resistance in the therapeutic setting and…
View article: P612: CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)-DERIVED T-CELLS HAVE DISTURBED FATTY ACID METABOLISM, POSSIBLY CONTRIBUTING TO T-CELL DYSFUNCTION
P612: CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)-DERIVED T-CELLS HAVE DISTURBED FATTY ACID METABOLISM, POSSIBLY CONTRIBUTING TO T-CELL DYSFUNCTION Open
Background: T-cells from CLL patients are dysfunctional and display reduced activation, proliferation and cytotoxicity upon in-vitro activation. Whilst the role of glucose metabolism in activated T cells is extensively studied, the contrib…
View article: Characterization of metabolic alterations of chronic lymphocytic leukemia in the lymph node microenvironment
Characterization of metabolic alterations of chronic lymphocytic leukemia in the lymph node microenvironment Open
Altered metabolism is a hallmark of both cell division and cancer. Chronic lymphocytic leukemia (CLL) cells circulate between peripheral blood (PB) and lymph nodes (LNs), where they receive proliferative and prosurvival signals from surrou…
View article: The Expression of TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Can Be Controlled by the Antioxidant Orchestrator NRF2 in Human Carcinoma Cells
The Expression of TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Can Be Controlled by the Antioxidant Orchestrator NRF2 in Human Carcinoma Cells Open
Hyperactivation of the KEAP1-NRF2 axis is a common molecular trait in carcinomas from different origin. The transcriptional program induced by NRF2 involves antioxidant and metabolic genes that render cancer cells more capable of dealing w…
View article: TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Is Upregulated in Lymphocytes Stimulated with Concanavalin A
TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Is Upregulated in Lymphocytes Stimulated with Concanavalin A Open
The glycolytic modulator TP53-Inducible Glycolysis and Apoptosis Regulator (TIGAR) is overexpressed in several types of cancer and has a role in metabolic rewiring during tumor development. However, little is known about the role of this e…
View article: Fructose 2,6-Bisphosphate in Cancer Cell Metabolism
Fructose 2,6-Bisphosphate in Cancer Cell Metabolism Open
For a long time, pioneers in the field of cancer cell metabolism, such as Otto Warburg, have focused on the idea that tumor cells maintain high glycolytic rates even with adequate oxygen supply, in what is known as aerobic glycolysis or th…
View article: <scp>TGF</scp>‐β1 targets Smad, p38 <scp>MAPK</scp>, and <scp>PI</scp>3K/Akt signaling pathways to induce <scp>PFKFB</scp>3 gene expression and glycolysis in glioblastoma cells
<span>TGF</span>‐β1 targets Smad, p38 <span>MAPK</span>, and <span>PI</span>3K/Akt signaling pathways to induce <span>PFKFB</span>3 gene expression and glycolysis in glioblastoma cells Open
In human cancers, transforming growth factor‐β1 ( TGF ‐β1) plays a dual role by acting as both a tumor suppressor and a promoter of tumor metastasis. Although TGF ‐β1 contributes to the metabolic reprogramming of cancer cells and tumor‐ass…
View article: Akt mediates <scp>TIGAR</scp> induction in HeLa cells following <scp>PFKFB</scp>3 inhibition
Akt mediates <span>TIGAR</span> induction in HeLa cells following <span>PFKFB</span>3 inhibition Open
Neoplastic cells metabolize higher amounts of glucose relative to normal cells in order to cover increased energetic and anabolic needs. Inhibition of the glycolytic enzyme 6‐phosphofructo‐2‐kinase/fructose‐2,6‐bisphosphatase 3 ( PFKFB 3) …