Sara Basbous
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View article: Wild-type and mutated ß-catenin differently repress <i>RND3/RHOE</i> expression in hepatocellular carcinoma
Wild-type and mutated ß-catenin differently repress <i>RND3/RHOE</i> expression in hepatocellular carcinoma Open
Background & Aims Tumor development and progression are mainly driven by oncogenic mutations but are also regulated by physical factors, such as applied forces or microenvironment stiffness. Through its structural and transcriptional funct…
View article: Specific features of ß-catenin-mutated hepatocellular carcinomas
Specific features of ß-catenin-mutated hepatocellular carcinomas Open
CTNNB1 , encoding the ß-catenin protein, is a key oncogene contributing to liver carcinogenesis. Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer in adult, representing the third leading cause of cancer-relate…
View article: Loss of RND3/RHOE controls entosis through LAMP1 expression in hepatocellular carcinoma
Loss of RND3/RHOE controls entosis through LAMP1 expression in hepatocellular carcinoma Open
Entosis is a process that leads to the formation of cell-in-cell structures commonly found in cancers. Here, we identified entosis in hepatocellular carcinoma and the loss of Rnd3 (also known as RhoE) as an efficient inducer of this mechan…
View article: Loss of<i>RND3/RHOE</i>controls entosis through<i>LAMP1</i>expression in hepatocellular carcinoma
Loss of<i>RND3/RHOE</i>controls entosis through<i>LAMP1</i>expression in hepatocellular carcinoma Open
Entosis is a process that leads to the formation of cell-in-cell structures commonly found in cancers. Here, we identified entosis in hepatocellular carcinoma and the loss of Rnd3 as an efficient inducer of this mechanism. We characterized…
View article: Supplementary Figure 1 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 1 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 200KB, The kinase activity of BCR-ABL induces upregulation of ST2 in UT7 cells.
View article: Supplementary Figure 1 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 1 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 200KB, The kinase activity of BCR-ABL induces upregulation of ST2 in UT7 cells.
View article: Supplementary Figure 2 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 2 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 192KB, CML-CP CD34(+) cells proliferate in response to IL-33.
View article: Supplementary Figure Legends from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure Legends from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 89KB
View article: Supplementary Figure 3 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 3 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 118KB, IL-33 does not modulate apoptosis of CD34(+) cells from CML-CP patients.
View article: Data from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Data from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
Although it is generally acknowledged that cytokines regulate normal hematopoiesis in an autocrine/paracrine fashion, their possible role in chronic myelogenous leukemia (CML) and resistance to imatinib mesylate treatment remain poorly inv…
View article: Supplementary Figure 5 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 5 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 154KB, CML-CP CD34(+) cells proliferate in response to IL-33 independently from GM-CSF.
View article: Supplementary Figure 3 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 3 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 118KB, IL-33 does not modulate apoptosis of CD34(+) cells from CML-CP patients.
View article: Supplementary Figure 4 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 4 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 145KB, IL-33 is as efficient as SCF in inducing proliferation of CML-CP CD34(+) cells.
View article: Supplementary Figure 7 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 7 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 208KB, Xenotransplant experiments in immunodeficient NOG mice (A); Mouse model of CML-like induced syndrome (B-C).
View article: Supplementary Figure 6 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 6 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 105KB, CML is associated with high circulating levels of soluble ST2: reversion after IM therapy.
View article: Supplementary Figure 6 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 6 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 105KB, CML is associated with high circulating levels of soluble ST2: reversion after IM therapy.
View article: Supplementary Figure 4 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 4 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 145KB, IL-33 is as efficient as SCF in inducing proliferation of CML-CP CD34(+) cells.
View article: Supplementary Figure Legends from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure Legends from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 89KB
View article: Supplementary Figure 2 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 2 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 192KB, CML-CP CD34(+) cells proliferate in response to IL-33.
View article: Supplementary Figure 5 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 5 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 154KB, CML-CP CD34(+) cells proliferate in response to IL-33 independently from GM-CSF.
View article: Data from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Data from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
Although it is generally acknowledged that cytokines regulate normal hematopoiesis in an autocrine/paracrine fashion, their possible role in chronic myelogenous leukemia (CML) and resistance to imatinib mesylate treatment remain poorly inv…
View article: Supplementary Figure 7 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients
Supplementary Figure 7 from BCR-ABL–Induced Deregulation of the IL-33/ST2 Pathway in CD34(+) Progenitors from Chronic Myeloid Leukemia Patients Open
PDF file - 208KB, Xenotransplant experiments in immunodeficient NOG mice (A); Mouse model of CML-like induced syndrome (B-C).
View article: Pathophysiological functions of Rnd proteins
Pathophysiological functions of Rnd proteins Open
Rnd proteins constitute a subfamily of Rho GTPases represented in mammals by Rnd1, Rnd2 and Rnd3. Despite their GTPase structure, their specific feature is the inability to hydrolyse GTP-bound nucleotide. This aspect makes them atypical am…
View article: Phenotype of NK-Like CD8(+) T Cells with Innate Features in Humans and Their Relevance in Cancer Diseases
Phenotype of NK-Like CD8(+) T Cells with Innate Features in Humans and Their Relevance in Cancer Diseases Open
Unconventional T cells are defined by their capacity to respond to signals other than the well-known complex of peptides and major histocompatibility complex proteins. Among the burgeoning family of unconventional T cells, innate-like CD8(…
View article: The Hypothesis of the Human iNKT/Innate CD8(+) T-Cell Axis Applied to Cancer: Evidence for a Deficiency in Chronic Myeloid Leukemia
The Hypothesis of the Human iNKT/Innate CD8(+) T-Cell Axis Applied to Cancer: Evidence for a Deficiency in Chronic Myeloid Leukemia Open
We recently identified a new human subset of NK-like [KIR/NKG2A(+)] CD8(+) T cells with a marked/memory phenotype, high Eomesodermin expression, potent antigen-independent cytotoxic activity, and the capacity to generate IFN-γ rapidly afte…
View article: La voie Rho/ROCK, un nouveau mécanisme d'échappement des cellules leucémiques au contrôle de l'immunité T innée
La voie Rho/ROCK, un nouveau mécanisme d'échappement des cellules leucémiques au contrôle de l'immunité T innée Open
Les cellules iNKT et T CDS innees sont presumees contribuer a l'irnmunosurveillance (IS) des cancers et sont fonctionnellement deficientes dans la leucemie myeloide chronique (LMC). Notre hypothese etait que ces defauts resultent de l'inca…
View article: Evidence for eomesodermin‐expressing innate‐like CD8<sup>+</sup> KIR/NKG2A<sup>+</sup> T cells in human adults and cord blood samples
Evidence for eomesodermin‐expressing innate‐like CD8<sup>+</sup> KIR/NKG2A<sup>+</sup> T cells in human adults and cord blood samples Open
Polyclonal CD8 + T cells, with a marked innate/memory phenotype, high eomesodermin (Eomes) expression, and the capacity to generate IFN‐γ rapidly without prior exposure to antigen, have been described in mice. However, even though a pool o…