Madi Y. Cissé

ORCID: 0000-0001-6760-3381
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About
Contact & Profiles
Research Areas
  • Cancer-related Molecular Pathways
  • Epigenetics and DNA Methylation
  • Cancer, Hypoxia, and Metabolism
  • Histone Deacetylase Inhibitors Research
  • Acute Myeloid Leukemia Research
  • Sarcoma Diagnosis and Treatment
  • Calpain Protease Function and Regulation
  • Mesenchymal stem cell research
  • Mitochondrial Function and Pathology
  • Microbial Metabolic Engineering and Bioproduction
  • Mast cells and histamine
  • Cancer, Lipids, and Metabolism
  • Autophagy in Disease and Therapy
  • PI3K/AKT/mTOR signaling in cancer
  • Tuberous Sclerosis Complex Research
  • Pancreatic function and diabetes
  • Cancer-related gene regulation
  • Endoplasmic Reticulum Stress and Disease
  • Viral-associated cancers and disorders

Université de Montpellier
2016-2024

Institut de Recherche en Cancérologie de Montpellier
2016-2024

Inserm
2016-2024

Harvard University
2021

La Ligue Contre le Cancer
2018-2020

Institut Regional du Cancer de Montpellier
2016

Mutations in IDH induce epigenetic and transcriptional reprogramming, differentiation bias, susceptibility to mitochondrial inhibitors cancer cells. Here, we first show that cell lines, PDXs, patients with acute myeloid leukemia (AML) harboring an mutation displayed enhanced oxidative metabolism. Along increase TCA cycle intermediates, this AML-specific metabolic behavior mechanistically occurred through the electron transport chain complex I activity, respiration, methylation-driven...

10.1084/jem.20200924 article EN cc-by-nc-sa The Journal of Experimental Medicine 2021-03-24

Sarcomas are still unsolved therapeutic challenges. Cancer stem cells believed to contribute sarcoma development, but lack of specific markers prevents their characterization and targeting. Here, we show that calpain-6 expression is associated with cancer cell features. In mouse models bone sarcoma, calpain-6-expressing have unique tumor-initiating metastatic capacities. Calpain-6 levels especially high in tumors been successfully propagated establish patient-derived xenografts. We found...

10.1172/jci.insight.121225 article EN JCI Insight 2018-09-05

Dedifferentiated and Well-differentiated liposarcoma are characterized by a systematic amplification of the Murine Double Minute 2 (MDM2) oncogene. We demonstrate that p53-independent metabolic functions chromatin-bound MDM2 exacerbated in mediate an addiction to serine metabolism sustain tumor growth. However, origin exogenous remains unclear. Here, we show elevated levels mice harboring liposarcoma-patient derived xenograft, released distant muscle is essential for cell survival....

10.1038/s41467-024-51827-3 article EN cc-by-nc-nd Nature Communications 2024-09-12

Studies of the topology, functioning, and regulation metabolic systems are based on two main types information that can be measured by mass spectrometry: (absolute or relative) concentration metabolites their isotope incorporation in 13C-labeling experiments. These data currently obtained from independent experiments because 13C-labeled internal standard (IS) used to determine a given metabolite overlaps 13C-mass fractions which its 13C-isotopologue distribution (CID) is quantified. Here, we...

10.1021/acs.analchem.9b05709 article EN Analytical Chemistry 2020-03-26

Mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) integrates diverse intracellular and extracellular growth signals to regulate cell tissue growth. How the molecular mechanisms regulating mTORC1 signaling established through biochemical biological studies function under physiological states in specific mammalian tissues are unknown. Here, we characterize a genetic mouse model lacking 5 phosphorylation sites on tuberous sclerosis 2 (TSC2) protein which factor-stimulated kinase AKT can...

10.1101/2024.09.23.614519 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-09-23

Isocitrate dehydrogenases (IDH) are involved in redox control and central metabolism. We hypothesized that key metabolic fluxes selectively reprogrammed to maintain biosynthetic homeostasis lower drug responses IDH mutant acute myeloid leukemia cells. Here we show reprogramming initiated by IDH1 mutation leads marked increases glucose, glutamine fatty acid catabolism along with enhancement of wild-type enzyme activity contribute provision α-KG required for 2-HG synthesis replenish Krebs...

10.2139/ssrn.3255557 article EN SSRN Electronic Journal 2018-01-01
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