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Academic literature on the topic 'Inhibiteurs CDK4/6'
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Journal articles on the topic "Inhibiteurs CDK4/6"
Gonçalves, Anthony. "Inhibiteurs de CDK4/6 : biomarqueurs, mécanismes de résistance et étude de l’ADN tumoral circulant potentielle." Bulletin du Cancer 105, no. 6 (June 2018): 545–46. http://dx.doi.org/10.1016/j.bulcan.2018.04.003.
Full textMassard, V., A. Harlé, L. Uwer, and J. L. Merlin. "Mutations du gène ESR1 : du fondamental à la clinique." Oncologie 21, no. 1-4 (January 2019): 29–32. http://dx.doi.org/10.3166/onco-2019-0027.
Full textBaldé, S. "C95: Place de l’Evérolimus dans le cancer du sein avancé M+ RH+/Her2- : Stratégies thérapeutiques." African Journal of Oncology 2, no. 1 Supplement (March 1, 2022): S40—S41. http://dx.doi.org/10.54266/ajo.2.1s.c95.hcih5777.
Full text"Inhibiteurs de CDK4/6 et cancers du sein, du métastatique à l’adjuvant : données cliniques." Innovations & Thérapeutiques en Oncologie 8, no. 3 (May 1, 2022): 157–65. http://dx.doi.org/10.1684/ito.2022.0317.
Full textDissertations / Theses on the topic "Inhibiteurs CDK4/6"
Richard, Mathilde. "Les vésicules extracellulaires plasmatiques, de potentiels biomarqueurs de suivi thérapeutique dans le cancer du sein métastatique." Electronic Thesis or Diss., Nantes Université, 2024. http://www.theses.fr/2024NANU1012.
Full textExtracellular vesicles (EVs), nanoparticle entities derived from cellular membranes, transport biological materials and circulate through body fluids. They are currently positioned as potential biomarkers for cancer progression and therapeutic response. Despite numerous innovative therapeutic strategies improving management and survival rates, breast cancer (BC) remains the leading cause of cancer-related death in women. Thus, the identification of specific biomarkers represents a significant hope for monitoring disease progression and predicting treatment efficacy. The primary objective of this research project was to characterize plasma EVs as potential biomarkers of response to CDK4/6 inhibitors treatment in metastatic breast cancer (MBC) patients with hormone receptor-positive (HR+) status. To facilitate translational research on the use of EVs as circulating biomarkers, we established a three-step procedure clinically applicable: 1- EVs were isolated from plasma using semi-automated size-exclusion chromatography (SEC); 2- plasma EV concentration (i.e., vesiclemia) was determined using the VideoDrop, a microscope utilizing interferometry; and 3- the sphingo-lipidic signature was analyzed by mass spectrometry. We initially measured vesiclemia in a healthy population to establish a reference value, accounting for sex and age. Subsequently, we monitored the physiological vesiclemia evolution over 24 months and compared it with that of MBC HR+ patients at different treatment stages. Our results reveal that an increase in vesiclemia two months after treatment initiation is significantly associated with early disease progression. Furthermore, we analyzed the lipid composition of EVs to reinforce their potential as biomarkers of disease progression. A specific signature of 16 EV-associated sphingolipids enabled us to establish a score identifying CDK4/6 inhibitor-resistant patients with82% accuracy. Finally, this characterization of plasma EVs as biomarkers led us to explore their potential in MBC patients with triple-negative and HER2+ status
Fourmentraux, Emmanuelle. "Modulation de l'activité lymphocytaire T CD4⁺ par le récepteur inhibiteur KIR2DL1." Paris 7, 2009. http://www.theses.fr/2009PA077022.
Full textThe functional activity of immune cells is controlled by a balance between activators and inhibitors signals. The Inhibitory killer Ig-like receptors (KIR) expressed on NK cells and memory effectors T-cell recognize the CMH-I molecules and inhibit cellular activation by SHP-1 recruitment. To better understand the fonction of KIR receptors on CD4⁺ T-cells, KIR2DL1 transfectants were obtained from human T-cell line and from primary CD4⁺ T-cells. Following TCR stimulation, IL-2 production is increased in CD4+ T cells transfected by KIR2DL1 independently of its engagement. When KIR2DL1 is engaged by its cognate ligand the TCR activation is inhibited. Co-stimulation of the TCR signaling by KIR2DL1 requires intact ITIM and their phosphorylation. It induces a subséquent SHP-2 recruitment and an increased of PKCθ and ERK phosphorylation. Synapses leading to activation are characterized by an increase in the recruitment of p-Tyr, SHP-2, and p-PKCθ. Interaction of KIR2DL1 with its ligand leads to a strong synaptic KIR2DL1 accumulation and SHP-1/SHP-2 recruitment resulting in the inhibition of TCR-induced IL-2 production. These data reveal that KIR2DL1 may induce two opposite signaling outputs in CD4⁺ T cells, depending on whether the KIR receptor is bound to its ligand. The unexpected results observed on the regulation of CD4⁺ T cells by KIR2DL1 receptors, through the functional duality of ITIM, is fundamental to determine the immune System capacity to develop an adapted answer, i. E. To maintain the balance between tolerance and immunity