PRIMA-1Met/APR-246 induces apoptosis and tumor growth delay in small cell lung cancer expressing mutant p53

Roza Zandi; Galina Selivanova; Camilla Laulund Christensen; Thomas Alexander Gerds; Berthe Marie Willumsen; Hans Skovgaard Poulsen

doi:10.1158/1078-0432.CCR-10-3168

PRIMA-1Met/APR-246 induces apoptosis and tumor growth delay in small cell lung cancer expressing mutant p53

Roza Zandi, Galina Selivanova, Camilla Laulund Christensen, Thomas Alexander Gerds, Berthe Marie Willumsen, Hans Skovgaard Poulsen

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

119 Citationer (Scopus)

Abstract

Small cell lung cancer (SCLC) is a highly malignant disease with poor prognosis, necessitating the need to develop new and efficient treatment modalities. PRIMA-1(Met) (p53-dependent reactivation of massive apoptosis), also known as APR-246, is a small molecule, which restores tumor suppressor function to mutant p53 and induces cancer cell death in various cancer types. Since p53 is mutated in more than 90% of SCLC, we investigated the ability of PRIMA-1(Met) to induce apoptosis and inhibit tumor growth in SCLC with different p53 mutations.

Originalsprog	Engelsk
Tidsskrift	Clinical Cancer Research
Vol/bind	17
Udgave nummer	9
Sider (fra-til)	2830-2841
Antal sider	12
ISSN	1078-0432
DOI	https://doi.org/10.1158/1078-0432.CCR-10-3168
Status	Udgivet - 1 maj 2011

Adgang til dokumentet

10.1158/1078-0432.CCR-10-3168

Citationsformater

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title = "PRIMA-1Met/APR-246 induces apoptosis and tumor growth delay in small cell lung cancer expressing mutant p53",

abstract = "Small cell lung cancer (SCLC) is a highly malignant disease with poor prognosis, necessitating the need to develop new and efficient treatment modalities. PRIMA-1(Met) (p53-dependent reactivation of massive apoptosis), also known as APR-246, is a small molecule, which restores tumor suppressor function to mutant p53 and induces cancer cell death in various cancer types. Since p53 is mutated in more than 90% of SCLC, we investigated the ability of PRIMA-1(Met) to induce apoptosis and inhibit tumor growth in SCLC with different p53 mutations.",

author = "Roza Zandi and Galina Selivanova and Christensen, {Camilla Laulund} and Gerds, {Thomas Alexander} and Willumsen, {Berthe Marie} and Poulsen, {Hans Skovgaard}",

note = "{\textcopyright}2011 AACR.",

year = "2011",

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doi = "10.1158/1078-0432.CCR-10-3168",

language = "English",

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TY - JOUR

T1 - PRIMA-1Met/APR-246 induces apoptosis and tumor growth delay in small cell lung cancer expressing mutant p53

AU - Zandi, Roza

AU - Selivanova, Galina

AU - Christensen, Camilla Laulund

AU - Gerds, Thomas Alexander

AU - Willumsen, Berthe Marie

AU - Poulsen, Hans Skovgaard

PY - 2011/5/1

Y1 - 2011/5/1

N2 - Small cell lung cancer (SCLC) is a highly malignant disease with poor prognosis, necessitating the need to develop new and efficient treatment modalities. PRIMA-1(Met) (p53-dependent reactivation of massive apoptosis), also known as APR-246, is a small molecule, which restores tumor suppressor function to mutant p53 and induces cancer cell death in various cancer types. Since p53 is mutated in more than 90% of SCLC, we investigated the ability of PRIMA-1(Met) to induce apoptosis and inhibit tumor growth in SCLC with different p53 mutations.

AB - Small cell lung cancer (SCLC) is a highly malignant disease with poor prognosis, necessitating the need to develop new and efficient treatment modalities. PRIMA-1(Met) (p53-dependent reactivation of massive apoptosis), also known as APR-246, is a small molecule, which restores tumor suppressor function to mutant p53 and induces cancer cell death in various cancer types. Since p53 is mutated in more than 90% of SCLC, we investigated the ability of PRIMA-1(Met) to induce apoptosis and inhibit tumor growth in SCLC with different p53 mutations.

U2 - 10.1158/1078-0432.CCR-10-3168

DO - 10.1158/1078-0432.CCR-10-3168

M3 - Journal article

C2 - 21415220

SN - 1078-0432

VL - 17

SP - 2830

EP - 2841

JO - Clinical Cancer Research

JF - Clinical Cancer Research

IS - 9

ER -