K‐<i>ras</i> codon 12 mutations in Barrett’s oesophagus and adenocarcinomas of the oesophagus and oesophagogastric junction

Lord, Reginald V.; O'grady, Roslynn; Sheehan, Catherine; Field, Andrew; Ward, Robyn L.

doi:10.1046/j.1440-1746.2000.02163.x

Cited by 58 publications

(41 citation statements)

References 34 publications

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“…Reports at point mutations in K-Ras in Barrett's esophagus and in esophageal adenocarcinomas showed them to be rare [50][51][52]. Another report described K-Ras mutations in 0% of Barrett's metaplasias, 0% of low grade dysplasias, 30% of high grade dysplasias, and 40% of adenocarcinomas [53]. Activation of the Ras proto-oncogenes seems to be of little importance in Barrett's adenocarcinomas.…”

Section: Growth Factors and Their Receptorsmentioning

confidence: 99%

The molecular biology of esophageal adenocarcinoma

Koppert

Wijnhoven

Dekken

et al. 2005

Journal of Surgical Oncology

123

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Within the multistep process of esophageal adenocarcinogenesis, to date no single molecular marker came forward able to predict who will and who will not develop cancer in the setting of Barrett's esophagus. Instead, panels of markers need to be developed in the future allowing to indicate disease progression. Identification of crucial molecular pathways involved in esophageal adenocarcinogenesis would ultimately improve therapy and facilitate development of new treatment strategies.

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Section: Growth Factors and Their Receptorsmentioning

confidence: 99%

The molecular biology of esophageal adenocarcinoma

Koppert

Wijnhoven

Dekken

et al. 2005

Journal of Surgical Oncology

123

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“…Recent data have shown that B-raf is mutated in about 7% of cancers, identifying it as another important oncogene on this pathway [11]. The highest incidence of B-raf mutations is in malignant melanoma (27%-70%), papillary thyroid cancer [15] (36%-53%), colorectal cancer [18] (5%-22%), and ovarian cancer (30%), but they also occur at a low frequency (1%-3%) in a wide variety of other cancers, including stomach cancer [14], squamous cell carcinomas of the head and neck, and lung cancer [7].…”

Section: Introductionmentioning

confidence: 99%

K-ras Mutation, HPV Infection and Smoking or Alcohol Abuse Positively Correlate with Esophageal Squamous Carcinoma

Lyronis

Baritaki

Bizakis

et al. 2008

Pathol. Oncol. Res.

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The Ras/Raf/MEK/ERK (MAPK) signal transduction cascade is an important mediator of a number of cellular fates including growth, survival and apoptosis. The aim of this study was to determine the incidence of B-raf, Kirsten-ras (K-ras) and Neuroblastoma-ras (N-ras) gene mutations in esophageal squamous cell carcinoma (ESCC) in the Greek population. DNA was extracted from 30 ESCC and 32 normal esophageal specimens and screened for V600E B-raf, and K-ras/N-ras codon 12 mutations, by PCR-RFLP based analysis. Among the genes tested, only the heterozygous K-ras mutation was detected in 5 out of the 30 ESCC specimens (16%), whereas no mutation was found in the normal esophageal tissue (P < 0.022). The normal samples were screened negative for N-ras and V600E B-raf mutations. The increased risk of esophageal cancer was correlated with tobacco use (OR = 3.5, P < 0.023) and alcohol abuse (OR = 7.22, P < 0.001), accompanied with the high incidence of the k-ras codon 12 mutation (22%, OR = 1.77 and 21%, OR = 1.52), respectively. A similar positive association was seen in human papilloma virus (HPV)-infected patients (OR = 5.66, P < 0.003). Our overall findings demonstrate that the mutational activation of the K-ras gene, HPV infection and tobacco or alcohol abuse, can be considered independently or in combination as high risk factors for ESCC development.

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“…58 Recently, studies have demonstrated K-ras mutations in 11% to 40% of esophageal adenocarcinomas, but few data are available on the frequency of Ras mutations in gastric cardia adenocarcinomas. 57,59 Moreover, available data do not support an important role for oncogenic B-raf in adenocarcinomas of the upper gastrointestinal tract. 57,60,61 Given the pivotal role of Ras proteins in the regulation of cell growth, it is not surprising that inhibitors of Ras are in development as anticancer therapies.…”

Section: Independence From Exogenous Stimulationmentioning

confidence: 99%

Concepts in the Prevention of Adenocarcinoma of the Distal Esophagus and Proximal Stomach

Souza

Spechler

2005

CA: A Cancer Journal for Clinicians

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For decades, the incidence rates for squamous cell carcinoma of the esophagus and adenocarcinoma of the distal stomach have been declining while the rates for adenocarcinomas of the esophagus and gastric cardia have increased profoundly. Recent studies have shown that the gastroesophageal junction (GEJ) is regularly exposed to concentrated gastric acid and to a variety of nitrosating species, noxious agents that may contribute to carcinogenesis in this region. For adenocarcinomas that straddle the GEJ, it can be difficult to determine whether the tumor originated in the esophagus or in the gastric cardia. This classification problem hampers studies on the epidemiology and pathogenesis of GEJ tumors. Current concepts in the prevention of cancers of the distal esophagus and proximal stomach have emerged from advances in our understanding of the specific molecular events that occur during the evolution of these tumors. This report reviews those events and focuses on current concepts in the prevention of adenocarcinomas at the GEJ. The similarities and differences in risk factors, molecular pathogenesis, and in preventive strategies for adenocarcinomas of the esophagus and gastric cardia are highlighted. (CA Cancer J Clin 2005;55:334-351.)

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K‐ras codon 12 mutations in Barrett’s oesophagus and adenocarcinomas of the oesophagus and oesophagogastric junction

Cited by 58 publications

References 34 publications

The molecular biology of esophageal adenocarcinoma

The molecular biology of esophageal adenocarcinoma

K-ras Mutation, HPV Infection and Smoking or Alcohol Abuse Positively Correlate with Esophageal Squamous Carcinoma

Concepts in the Prevention of Adenocarcinoma of the Distal Esophagus and Proximal Stomach

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