RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status

Mohd Feroz Mohd Omar; Kosei Ito; Min En Nga; Ross Soo; Bee Keow Peh; Tuty Muliana Ismail; Bhavin Thakkar; Richie Soong; Yoshiaki Ito; Manuel Salto-Tellez

doi:10.1007/s12253-011-9485-5

RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status

Mohd Feroz Mohd Omar, Kosei Ito, Min En Nga, Ross Soo, Bee Keow Peh, Tuty Muliana Ismail, Bhavin Thakkar, Richie Soong, Yoshiaki Ito, Manuel Salto-Tellez

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

13 Citations (Scopus)

Abstract

RUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMA was also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications.

Original language	English
Pages (from-to)	783-92
Number of pages	10
Journal	GBER, Global Built Environment Review (issn: 1474-6824)
Volume	18
Issue number	4
DOIs	https://doi.org/10.1007/s12253-011-9485-5
Publication status	Published - Oct 2012

Keywords

ras Proteins
Tumor Suppressor Protein p53
Receptor, Epidermal Growth Factor
DNA Mutational Analysis
Humans
Cell Line, Tumor
Proto-Oncogene Proteins
Tissue Array Analysis
DNA Methylation
Down-Regulation
Lung Neoplasms
Core Binding Factor Alpha 3 Subunit
Adenocarcinoma
Carcinoma, Squamous Cell
Immunohistochemistry
Mutation

ASJC Scopus subject areas

Cancer Research
Oncology
Pathology and Forensic Medicine

UN SDGs

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

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10.1007/s12253-011-9485-5

Cite this

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title = "RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status",

abstract = "RUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMA was also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications.",

keywords = "ras Proteins, Tumor Suppressor Protein p53, Receptor, Epidermal Growth Factor, DNA Mutational Analysis, Humans, Cell Line, Tumor, Proto-Oncogene Proteins, Tissue Array Analysis, DNA Methylation, Down-Regulation, Lung Neoplasms, Core Binding Factor Alpha 3 Subunit, Adenocarcinoma, Carcinoma, Squamous Cell, Immunohistochemistry, Mutation",

author = "Omar, {Mohd Feroz Mohd} and Kosei Ito and Nga, {Min En} and Ross Soo and Peh, {Bee Keow} and Ismail, {Tuty Muliana} and Bhavin Thakkar and Richie Soong and Yoshiaki Ito and Manuel Salto-Tellez",

year = "2012",

month = oct,

doi = "10.1007/s12253-011-9485-5",

language = "English",

volume = "18",

pages = "783--92",

journal = "GBER, Global Built Environment Review (issn: 1474-6824)",

issn = "1436-3291",

publisher = "Springer Japan",

number = "4",

}

RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status. / Omar, Mohd Feroz Mohd; Ito, Kosei; Nga, Min En; Soo, Ross; Peh, Bee Keow; Ismail, Tuty Muliana; Thakkar, Bhavin; Soong, Richie; Ito, Yoshiaki; Salto-Tellez, Manuel.

In: GBER, Global Built Environment Review (issn: 1474-6824), Vol. 18, No. 4, 10.2012, p. 783-92.

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

TY - JOUR

T1 - RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status

AU - Omar, Mohd Feroz Mohd

AU - Ito, Kosei

AU - Nga, Min En

AU - Soo, Ross

AU - Peh, Bee Keow

AU - Ismail, Tuty Muliana

AU - Thakkar, Bhavin

AU - Soong, Richie

AU - Ito, Yoshiaki

AU - Salto-Tellez, Manuel

PY - 2012/10

Y1 - 2012/10

N2 - RUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMA was also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications.

AB - RUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMA was also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications.

KW - ras Proteins

KW - Tumor Suppressor Protein p53

KW - Receptor, Epidermal Growth Factor

KW - DNA Mutational Analysis

KW - Humans

KW - Cell Line, Tumor

KW - Proto-Oncogene Proteins

KW - Tissue Array Analysis

KW - DNA Methylation

KW - Down-Regulation

KW - Lung Neoplasms

KW - Core Binding Factor Alpha 3 Subunit

KW - Adenocarcinoma

KW - Carcinoma, Squamous Cell

KW - Immunohistochemistry

KW - Mutation

U2 - 10.1007/s12253-011-9485-5

DO - 10.1007/s12253-011-9485-5

M3 - Article

C2 - 22729835

VL - 18

SP - 783

EP - 792

JO - GBER, Global Built Environment Review (issn: 1474-6824)

JF - GBER, Global Built Environment Review (issn: 1474-6824)

SN - 1436-3291

IS - 4

ER -

RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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