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

Lyronis, Ioannis; Baritaki, Stavroula; Bizakis, Ioannis; Krambovitis, Elias; Spandidos, Demetrios Α.

doi:10.1007/s12253-008-9032-1

Cited by 34 publications

(33 citation statements)

References 30 publications

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“…Specific anatomic locations included oral mucosa (n=7), esophagus (n=2), larynx (n=2), adenoids/tonsils (n=2), and parotids (n=1) (Aggelopoulou et al, 1999; Blioumi et al, 2014; Bouda et al, 2000; Gorgoulis et al, 1999; Kouvousi, et al, 2013; Lambropoulos et al, 1997; Laskaris et al, 2014; Lyronis I., 2005; Lyronis, et al, 2008; Mammas, et al 2012; Mammas, et al, 2006; Tsimplaki et al, 2014; Vageli, et al, 2007). Only 5 studies included asymptomatic patients (Blioumi, et al, 2014; Bouda, et al, 2000; Lambropoulos, et al, 1997; Lyronis I., 2005; Lyronis, et al, 2008). The remaining studies focused on testing patients with dysplasia, hyperplasia or cancer.…”

Section: Resultsmentioning

confidence: 99%

Human papillomavirus infection by anatomical site among Greek men and women: a systematic review

Tsikis

Hoefer²,

Charnot-Katsikas³

et al. 2016

European Journal of Cancer Prevention

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Objectives We systematically reviewed the literature on anal, penile, cervical, and oropharyngeal HPV infection in Greece to provide a comprehensive overview of HPV prevalence and to explore the reporting of HPV in Greek men and women. Methods A total of 5 databases, including PubMed and Scopus, were searched up until January 1st, 2015 for studies looking at HPV prevalence, incidence, or risk factors by anatomical site. Results We identified 50 eligible studies for inclusion. The majority of them were cervical studies (n=26) followed by head and neck studies (n=13) with only two studies exclusively focusing on anal sites and two at penile sites. The remaining studies examined prevalence from multiple sites. Most studies looked at small, high-risk populations and HPV prevalence ranged from 2.5%–43.4% for cervical studies; 0%–91% for head and neck studies; 54.6%–78.4% for anal studies and 20.3%–66.7% for penile studies. Age, smoking, and number of sexual partners were commonly assessed risk factors. Conclusion There were significant gender and anatomic site disparities in the reporting of HPV prevalence. Given the relationship between HPV infection and the increasing incidence of anal cancer in men, more research is needed to reveal the prevalence of HPV at these sites in Greek men especially given reports of the declining health of the Greek population.

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Section: Resultsmentioning

confidence: 99%

Human papillomavirus infection by anatomical site among Greek men and women: a systematic review

Tsikis

Hoefer²,

Charnot-Katsikas³

et al. 2016

European Journal of Cancer Prevention

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“…It has been reported that RAS/RAF mutations are negatively associated with response to cetuximab. Ras gene and Raf gene mutations occur commonly in some tumors and lead to abnormal signaling, but the incidence of Ras and Raf mutation is very low in esophageal carcinoma [27][28][29]. In light of the relatively low frequency of Ras and Raf mutations and overexpression of EGFR, cetuximab would be appropriate as a combined monoclonal antibody for esophageal carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Pingyangmycin downregulates the expression of EGFR and enhances the effects of cetuximab on esophageal cancer cells and the xenograft in athymic mice

Gong

Liu

et al. 2012

Cancer Chemother Pharmacol

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“…The RAS family genes consist of three members, HRAS, KRAS and NRAS located on chromosomes 11, 12 and 1, respectively, encoding a 21 kDa membrane protein (p21), which possesses GTPase activity (5,6). HRAS has been shown to activate phosphatidylinositol 3 kinase (PI3K) more efficiently than KRAS and NRAS.…”

Section: Introductionmentioning

confidence: 99%

“…BRAF is one of the most commonly mutated oncogenes in human cancer. BRAF is a serine/threonine kinase of the RAF family, which consists of three genes, namely ARAF, BRAF and CRAF (5). More than 90% of the reported BRAF mutations occur in its kinase domain regarding a single nucleotide substitution V600E (also referred to as V599E according to the numbering system used) (13).…”

Section: Introductionmentioning

confidence: 99%

Novel mutations of the HRAS gene and absence of hotspot mutations of the BRAF genes in oral squamous cell carcinoma in a Greek population

et al. 2012

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Abstract. Oral squamous cell carcinoma (OSCC) is the sixth most common cancer in the world. The phosphatidylinositol 3 kinase (PI3K) signalling pathway has been reported to play an important role in OSCC. Since we have previously detected absence of hotspot PIK3CA gene mutations in the Greek population, we hypothesized that BRAF or HRAS may be activated as upstream effectors of the pathway. Furthermore, the status of the HRAS and BRAF mutations in OSCC has never been assessed before in the Greek population. Eighty-six primary paraffin-embedded tumors were screened for BRAF and HRAS hotspot mutations. In HRAS, two hotspot mutations in codon 12 (2.3%) and eight new genetic alterations were detected (8.6% overall). One new missense mutation, Alanine53Valine (Ala53Val), one silent mutation, two mutations in the 5'UTR region and four mutations in intron 1 were detected. No hotspot mutations in BRAF were found. A new silent mutation/polymorphism T1803C was detected at a percentage of 30%. This study is the first to report HRAS mutations in the Greek population. The results suggest that RAS is an important member of the PI3K signalling pathway and may play a role in the tumorigenesis of OSCC. IntroductionOral squamous cell carcinoma (OSCC) is a subset of head and neck squamous carcinoma (HNSCC) involving the oral tongue, upper gingival, lower gingival and alveolus, floor of the mouth, buccal mucosa, retromolar triangle, lip mucosa and hard palate. OSCC is considered to be the sixth most common cancer in the world (1). Smoking and alcohol consumption are major risks for HNSCC but only a fraction of people with these habits actually develop oral cancer, which implies that other genetic factors contribute to the pathogenesis of the disease (2,3). Infection by human papilloma virus has also emerged as a risk factor for HNSCC (4).The RAS family genes consist of three members, HRAS, KRAS and NRAS located on chromosomes 11, 12 and 1, respectively, encoding a 21 kDa membrane protein (p21), which possesses GTPase activity (5,6). HRAS has been shown to activate phosphatidylinositol 3 kinase (PI3K) more efficiently than KRAS and NRAS. Hotspots for RAS mutations are found in codons 12, 13 and 61, causing the mutant protein to lose its ability to exchange GTP with GDP thus remaining activated (7). RAS is also is an upstream regulator of PI3K. Thus an activated RAS could also activate the PI3K signalling pathway, which is shown to be activated in oral cancer (8,9). The incidence of RAS mutations varies greatly among different human tumors and different ethnicities. HRAS mutations are primarily found in cancers of the urinary tract and bladder.

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

Cited by 34 publications

References 30 publications

Human papillomavirus infection by anatomical site among Greek men and women: a systematic review

Human papillomavirus infection by anatomical site among Greek men and women: a systematic review

Pingyangmycin downregulates the expression of EGFR and enhances the effects of cetuximab on esophageal cancer cells and the xenograft in athymic mice

Novel mutations of the HRAS gene and absence of hotspot mutations of the BRAF genes in oral squamous cell carcinoma in a Greek population

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