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4 results on '"Khiabanian H"'

1. Recurrent Rhoa Mutations In Peripheral T-Cell Lymphoma

Author

Palomero, T., Couronne, L., Khiabanian, H., Kim, M., Ambesi, A., Carpenter, Z., Abate, Francesco, Allegretta, M., Lossos, I. S., Nicolas, C., Balbin, M., Bastard, C., Bhagat, G., M. A. A., Campo, E., Bernard, O. A., and Rabadan, R.

Published
2013

2. PHF6 mutations in T-cell lymphoblastic leukemia

Author

Vlierberghe, P, Palomero, T, Khiabanian, H, van der Meulen, J, Castillo, M, van Roy, N, de Moerloose, B, Philippe, J, Conzalez-Garcia, S, Toribio, ML, Taghon, T, Zuurbier, Linda, Cauwelier, B, Harrison, CJ, Schwab, C, Pisecker, M, Strehl, S, Langerak, Ton, Gecz, J, Sonneveld, E, Pieters, Rob, Paietta, E, Rowe, J, Wiernik, PH, Benoit, Y, Soulier, J, Poppe, B, Yao, X, Cordon-Cardo, C, Meijerink, Jules, Rabadan, R, Speleman, F, Ferrando, AA, Pediatrics, and Immunology

Published
2010

3. A Case of T-cell Acute Lymphoblastic Leukemia Relapsed As Myeloid Acute Leukemia

Author

Paganin, Maddalena, Buldini, Barbara, Germano, Giuseppe, Seganfreddo, Elena, Meglio, Annamaria di, Magrin, Elisa, Grillo, Francesca, Pigazzi, Martina, Rizzari, Carmelo, Cazzaniga, Giovanni, Khiabanian, Hossein, Palomero, Teresa, Rabadan, Raul, Ferrando, Adolfo A., Basso, Giuseppe, Paganin, M, Buldini, B, Germano, G, Seganfreddo, E, Meglio, A, Magrin, E, Grillo, F, Pigazzi, M, Rizzari, C, Cazzaniga, G, Khiabanian, H, Palomero, T, Rabadan, R, Ferrando, A, and Basso, G

Subjects
Male, MED/03 - GENETICA MEDICA, Hematology, Gene Rearrangement, T-Lymphocyte, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Leukemia, Myeloid, Acute, Oncology, Recurrence, Child, Preschool, switch lineage, Pediatrics, Perinatology and Child Health, Mutation, Humans, whole-exome sequencing, T-ALL, Gene Deletion, Human
Abstract

A 4-year-old male with the diagnosis of T-cell acute lymphoblastic leukemia (T-ALL) relapsed after 19 months with an acute myeloid leukemia (AML). Immunoglobulin and T-cell receptor gene rearrangements analyses reveal that both leukemias were rearranged with a clonal relationship between them. Comparative genomic hybridization (Array-CGH) and whole-exome sequencing analyses of both samples suggest that this leukemia may have originated from a common T/myeloid progenitor. The presence of homozygous deletion of p16/INK4A, p14/ARF, p15/INK4B, and heterozygous deletion of WT1 locus remained stable in the leukemia throughout phenotypic switch, revealing that this AML can be genetically associated to T-ALL.

Published
2016

4. Activating mutations and translocations in the guanine exchange factor VAV1 in peripheral T-cell lymphomas

Author

Govind Bhagat, Mi-Yeon Kim, S. Aidan Quinn, Xosé R. Bustelo, Teresa Palomero, Olivier Bernard, Elias Campo, Raul Rabadan, Stefano Pileri, Izidore S. Lossos, Maria Antonella Laginestra, Javier Robles-Valero, Adolfo A. Ferrando, Giorgio Inghirami, Lucile Couronné, Francesco Abate, Miguel A. Piris, Ana C. da Silva-Almeida, Hossein Khiabanian, Danilo Fiore, Christine Y. Kim, Sakellarios Zairis, Universitat de Barcelona, Abate, F., Da Silva-Almeida, A. C., Zairis, S., Robles-Valero, J., Couronne, L., Khiabanian, H., Quinn, S. A., Kim, M. -Y., Laginestra, M. A., Kim, C., Fiore, D., Bhagat, G., Piris, M. A., Campo, E., Lossos, I. S., Bernard, O. A., Inghirami, G., Pileri, S., Bustelo, X. R., Rabadan, R., Ferrando, A. A., and Palomero, T.

Subjects
0301 basic medicine, MAPK/ERK pathway, VAV1, Guanine, T cell, T cells, Jurkat Cell, Biology, Translocation, Genetic, 03 medical and health sciences, Jurkat Cells, Cell Line, Tumor, medicine, Guanine Nucleotide Exchange Factors, Humans, Amino Acid Sequence, Proto-Oncogene Proteins c-vav, Gene, Sequence Deletion, Multidisciplinary, Base Sequence, Effector, Alternative splicing, Mutació (Biologia), Peripheral T-cell lymphoma, Lymphoma, T-Cell, Peripheral, NFAT, Biological Sciences, Mutation (Biology), Guanine Nucleotide Exchange Factor, Molecular biology, Alternative Splicing, 030104 developmental biology, medicine.anatomical_structure, Cèl·lules T, Genes, Mutation, Cancer research, Guanine nucleotide exchange factor, Gene fusion, Human, Gens
Abstract

Peripheral T-cell lymphomas (PTCLs) are a heterogeneous group of non-Hodgkin lymphomas frequently associated with poor prognosis and for which genetic mechanisms of transformation remain incompletely understood. Using RNA sequencing and targeted sequencing, here we identify a recurrent in-frame deletion (VAV1 Δ778-786) generated by a focal deletion-driven alternative splicing mechanism as well as novel VAV1 gene fusions (VAV1-THAP4, VAV1-MYO1F, and VAV1-S100A7) in PTCL. Mechanistically these genetic lesions result in increased activation of VAV1 catalytic-dependent (MAPK, JNK) and non-catalytic-dependent (nuclear factor of activated T cells, NFAT) VAV1 effector pathways. These results support a driver oncogenic role for VAV1 signaling in the pathogenesis of PTCL.

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