P53 Gene Mutation in a T-Acute Lymphoblastic Leukemia Cell Line (Loucy) with t(16:20) and 5q-Chromosomal Aberrations

Miron Prokocimer; Shoshana Peller; Hannah Ben-Bassat; Naomi Goldfinger; Varda Rotter

doi:10.3109/10428199809050920

P53 Gene Mutation in a T-Acute Lymphoblastic Leukemia Cell Line (Loucy) with t(16:20) and 5q-Chromosomal Aberrations

Miron Prokocimer, Shoshana Peller, Hannah Ben-Bassat, Naomi Goldfinger, Varda Rotter

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

A human T-acute lymphoblastic leukemia (ALL) cell line (Loucy), derived from cells from a patient with resistant ALL with a t(16:20) and 5q-chromosomal aberrations was evaluated for p53 gene alterations and expression. Western blot analysis of p53 showed elevated levels of the protein. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and direct sequencing identified a point mutation at codon 272 (GTG → ATG) of the p53 gene. Possible molecular mechanisms underlying these alterations and their role in the establishment of this cell line and in leukemogenesis in general are discussed.

Original language	English
Pages (from-to)	607-611
Number of pages	5
Journal	Leukemia and Lymphoma
Volume	29
Issue number	42130
DOIs	https://doi.org/10.3109/10428199809050920
State	Published - 1 Jan 1998
Externally published	Yes

Keywords

ALL
Tumor suppressor
codon 272
mutation
p53

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.3109/10428199809050920

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title = "P53 Gene Mutation in a T-Acute Lymphoblastic Leukemia Cell Line (Loucy) with t(16:20) and 5q-Chromosomal Aberrations",

abstract = "A human T-acute lymphoblastic leukemia (ALL) cell line (Loucy), derived from cells from a patient with resistant ALL with a t(16:20) and 5q-chromosomal aberrations was evaluated for p53 gene alterations and expression. Western blot analysis of p53 showed elevated levels of the protein. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and direct sequencing identified a point mutation at codon 272 (GTG → ATG) of the p53 gene. Possible molecular mechanisms underlying these alterations and their role in the establishment of this cell line and in leukemogenesis in general are discussed.",

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author = "Miron Prokocimer and Shoshana Peller and Hannah Ben-Bassat and Naomi Goldfinger and Varda Rotter",

note = "Funding Information: This work was supported in part by grmts from the Leo and Julia Forchheimer Center for Molecular Genetics, and the Israel Cancer Association (S. P. and V. R.). V. R. is the incumbent of the Norman and Helen Asher Professorial Chair in Cancer Research at the Weizmann Institute.",

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AU - Peller, Shoshana

AU - Ben-Bassat, Hannah

AU - Goldfinger, Naomi

AU - Rotter, Varda

N1 - Funding Information: This work was supported in part by grmts from the Leo and Julia Forchheimer Center for Molecular Genetics, and the Israel Cancer Association (S. P. and V. R.). V. R. is the incumbent of the Norman and Helen Asher Professorial Chair in Cancer Research at the Weizmann Institute.

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N2 - A human T-acute lymphoblastic leukemia (ALL) cell line (Loucy), derived from cells from a patient with resistant ALL with a t(16:20) and 5q-chromosomal aberrations was evaluated for p53 gene alterations and expression. Western blot analysis of p53 showed elevated levels of the protein. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and direct sequencing identified a point mutation at codon 272 (GTG → ATG) of the p53 gene. Possible molecular mechanisms underlying these alterations and their role in the establishment of this cell line and in leukemogenesis in general are discussed.

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KW - codon 272

KW - mutation

KW - p53

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P53 Gene Mutation in a T-Acute Lymphoblastic Leukemia Cell Line (Loucy) with t(16:20) and 5q-Chromosomal Aberrations

Abstract

Keywords

UN SDGs

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