TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy

Sabina Chiaretti; Fulvia Brugnoletti; Simona Tavolaro; Silvia Bonina; Francesca Paoloni; Marilisa Marinelli; Nancy Patten; Massimiliano Bonifacio; Maria Grazia Kropp; Simona Sica; Anna Guarini; Robin Foà

doi:10.3324/haematol.2012.076786

TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy

Sabina Chiaretti, Fulvia Brugnoletti, Simona Tavolaro, Silvia Bonina, Francesca Paoloni, Marilisa Marinelli, Nancy Patten, Massimiliano Bonifacio, Maria Grazia Kropp, Simona Sica, Anna Guarini, Robin Foà

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Abstract

Acute lymphoblastic leukemia (ALL) is a disease of either B-cell (80–85%) or T-cell (20–25%) derivation. Several molecular aberrations (i.e. BCR-ABL1, MLL/AFF1, SIL/TAL1 and E2A/PBX1) confer an overall poor outcome.1,2 However, a proportion of patients do not carry known genetic abnormalities and have a heterogeneous clinical course. P53 plays a crucial role in cell cycle regulation and apoptosis after DNA damage, and its role in tumorigenesis is well-recognized in solid and hematologic malignancies, particularly acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), in which its deregulation represents an important predictor of poor outcome.3–10

Lingua originale	English
pagine (da-a)	e59-e59-61
Rivista	Haematologica
Volume	98
DOI	https://doi.org/10.3324/haematol.2012.076786
Stato di pubblicazione	Pubblicato - 2013

Keywords

Adult
Humans
Mutation
Oncogene Proteins, Fusion
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Remission Induction
TP53 mutations
Treatment Outcome
Tumor Suppressor Protein p53
adult acute lymphoblastic leukemia
response to induction chemotherapy

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Chiaretti, S., Brugnoletti, F., Tavolaro, S., Bonina, S., Paoloni, F., Marinelli, M., Patten, N., Bonifacio, M., Kropp, M. G., Sica, S., Guarini, A., & Foà, R. (2013). TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy. Haematologica, 98, e59-e59-61. https://doi.org/10.3324/haematol.2012.076786

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title = "TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy",

abstract = "Acute lymphoblastic leukemia (ALL) is a disease of either B-cell (80–85%) or T-cell (20–25%) derivation. Several molecular aberrations (i.e. BCR-ABL1, MLL/AFF1, SIL/TAL1 and E2A/PBX1) confer an overall poor outcome.1,2 However, a proportion of patients do not carry known genetic abnormalities and have a heterogeneous clinical course. P53 plays a crucial role in cell cycle regulation and apoptosis after DNA damage, and its role in tumorigenesis is well-recognized in solid and hematologic malignancies, particularly acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), in which its deregulation represents an important predictor of poor outcome.3–10",

keywords = "Adult, Humans, Mutation, Oncogene Proteins, Fusion, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Remission Induction, TP53 mutations, Treatment Outcome, Tumor Suppressor Protein p53, adult acute lymphoblastic leukemia, response to induction chemotherapy, Adult, Humans, Mutation, Oncogene Proteins, Fusion, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Remission Induction, TP53 mutations, Treatment Outcome, Tumor Suppressor Protein p53, adult acute lymphoblastic leukemia, response to induction chemotherapy",

author = "Sabina Chiaretti and Fulvia Brugnoletti and Simona Tavolaro and Silvia Bonina and Francesca Paoloni and Marilisa Marinelli and Nancy Patten and Massimiliano Bonifacio and Kropp, {Maria Grazia} and Simona Sica and Anna Guarini and Robin Fo{\`a}",

year = "2013",

doi = "10.3324/haematol.2012.076786",

language = "English",

volume = "98",

pages = "e59--e59--61",

journal = "Haematologica",

issn = "0390-6078",

publisher = "Pavia : Fondazione Ferrata Storti",

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Chiaretti, S, Brugnoletti, F, Tavolaro, S, Bonina, S, Paoloni, F, Marinelli, M, Patten, N, Bonifacio, M, Kropp, MG, Sica, S, Guarini, A & Foà, R 2013, 'TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy', Haematologica, vol. 98, pagg. e59-e59-61. https://doi.org/10.3324/haematol.2012.076786

TY - JOUR

T1 - TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy

AU - Chiaretti, Sabina

AU - Brugnoletti, Fulvia

AU - Tavolaro, Simona

AU - Bonina, Silvia

AU - Paoloni, Francesca

AU - Marinelli, Marilisa

AU - Patten, Nancy

AU - Bonifacio, Massimiliano

AU - Kropp, Maria Grazia

AU - Sica, Simona

AU - Guarini, Anna

AU - Foà, Robin

PY - 2013

Y1 - 2013

N2 - Acute lymphoblastic leukemia (ALL) is a disease of either B-cell (80–85%) or T-cell (20–25%) derivation. Several molecular aberrations (i.e. BCR-ABL1, MLL/AFF1, SIL/TAL1 and E2A/PBX1) confer an overall poor outcome.1,2 However, a proportion of patients do not carry known genetic abnormalities and have a heterogeneous clinical course. P53 plays a crucial role in cell cycle regulation and apoptosis after DNA damage, and its role in tumorigenesis is well-recognized in solid and hematologic malignancies, particularly acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), in which its deregulation represents an important predictor of poor outcome.3–10

AB - Acute lymphoblastic leukemia (ALL) is a disease of either B-cell (80–85%) or T-cell (20–25%) derivation. Several molecular aberrations (i.e. BCR-ABL1, MLL/AFF1, SIL/TAL1 and E2A/PBX1) confer an overall poor outcome.1,2 However, a proportion of patients do not carry known genetic abnormalities and have a heterogeneous clinical course. P53 plays a crucial role in cell cycle regulation and apoptosis after DNA damage, and its role in tumorigenesis is well-recognized in solid and hematologic malignancies, particularly acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), in which its deregulation represents an important predictor of poor outcome.3–10

KW - Adult

KW - Humans

KW - Mutation

KW - Oncogene Proteins, Fusion

KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma

KW - Remission Induction

KW - TP53 mutations

KW - Treatment Outcome

KW - Tumor Suppressor Protein p53

KW - adult acute lymphoblastic leukemia

KW - response to induction chemotherapy

KW - Adult

KW - Humans

KW - Mutation

KW - Oncogene Proteins, Fusion

KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma

KW - Remission Induction

KW - TP53 mutations

KW - Treatment Outcome

KW - Tumor Suppressor Protein p53

KW - adult acute lymphoblastic leukemia

KW - response to induction chemotherapy

UR - http://hdl.handle.net/10807/50970

U2 - 10.3324/haematol.2012.076786

DO - 10.3324/haematol.2012.076786

M3 - Article

SN - 0390-6078

VL - 98

SP - e59-e59-61

JO - Haematologica

JF - Haematologica

ER -

TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy

Abstract

Keywords

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