EGFR mutations and human papillomavirus in lung cancer

Kato, Takuya; Koriyama, Chihaya; Khan, Noureen; Samukawa, Takuya; Yanagi, Masakazu; Hamada, Tsutomu; Yokomakura, Naoya; Otsuka, Takeshi; Inoue, Hiromasa; Sato, Masami; Natsugoe, Shoji; Akiba, Suminori

doi:10.1016/j.lungcan.2012.08.011

Cited by 32 publications

(21 citation statements)

References 25 publications

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“…5 Sequencing the EGFR gene revealed that lung cancer patients who responded to EGFR TKIs have dramatic mutations within the EGFR kinase domain. 6 Thus, evaluation of the EGFR mutational status before and after the treatment is important in determining optimal therapy of lung cancers.…”

mentioning

confidence: 99%

99mTc-HYNIC-MPG: A novel SPECT probe for targeting mutated EGFR

Yan¹,

Xiao²,

Song³

et al. 2015

Bioorganic & Medicinal Chemistry Letters

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mentioning

confidence: 99%

99mTc-HYNIC-MPG: A novel SPECT probe for targeting mutated EGFR

Yan¹,

Xiao²,

Song³

et al. 2015

Bioorganic & Medicinal Chemistry Letters

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“…Baba et al (2010) observed lower viral load in lung tumors, geometric average of 0.02 copies per cell, than in cervical cancers 333 copies per cell. Similarly, Kato et al (2012) observed much lower HPV load in lung tumors, about 0.003 per cell, than in cervical cancer, 333 copies per cell.…”

Section: Viral Load Hpv In Lung Tumorsmentioning

confidence: 75%

“…The −2.325/2.260 region of the p21 promoter recruits p53. In turn, p53 recruits DDX3, and this interaction increases the affinity of Sp1 in the p21 promoter and increases the activation of the p21 transcription low exposure to tobacco (Kato et al 2012). HPV 16/18 E6 may lead to EGFR mutation in lung cancer and an elevation of 8-OH-dG formation through increased ROS levels.…”

Section: E6 and Egfr Mutationsmentioning

confidence: 99%

“…According to Kato et al (2012), this may be due to an HPV infection in cancer stem cells or also by chromosomal instability induced by E6 and high-risk HPV E7 leading to an advantageous selective growth of malignant cells. It may be that such malignant cells containing unstable chromosomes tend to suffer loss of chromosome that contains integrated HPV or loss of part of the integrated HPV replication after numerous cycles (Baba et al 2010).…”

Section: Viral Load Hpv In Lung Tumorsmentioning

confidence: 99%

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Human papillomavirus and lung cancinogenesis: an overview

Freitas

Gurgel

Lima

et al. 2016

J Cancer Res Clin Oncol

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Lung cancer is the most common cause of cancer deaths worldwide. Although tobacco smoking is considered to be the main risk factor and the most well-established risk factor for lung cancer, a number of patients who do not smoke have developed this disease. This number varies between 15 % to over one-half of lung cancer cases, and the deaths from lung cancer in non-smokers are increasing every year. There are many other agents that are thought to be etiological, including diesel exhaust exposure, metals, radiation, radon, hormonal factors, cooking oil, air pollution and infectious diseases, such as human papillomavirus (HPV). Studies in various parts of the world have detected HPV DNA at different rates in lung tumors. However, the role of HPV in lung cancer is still unclear. Thus, in this review, we investigated some molecular mechanisms of HPV protein activity in host cells, the entry of HPV into lung tissue and the possible route used by the virus to reach the lung cells.

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“…The presence of HPV DNA was significantly related to epidermal growth factor receptor (EGFR) mutations, and EGFR TK domain mutations that can lead to lung cancer pathogenesis were much more frequent in never smokers (Ohtsuka et al, 2006;Kato et al, 2012). cIAP-2 up-regulated by E6 was not only through NF-κB pathway but also through EGFR/PI3K/AKT pathway (Wu et al, 2010).…”

Section: E6 Oncoprotein and Cellular Inhibitor Of Apoptotic Proteinmentioning

confidence: 99%

Human Papillomavirus Type 16/18 Oncoproteins: Potential Therapeutic Targets in Non-smoking Associated Lung Cancer

Zhang¹,

Tang²

2012

Asian Pacific Journal of Cancer Prevention

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High-risk human papillomavirus (HPV) especially HPV-16 and HPV-18 types are speculated to be important risk factors in non-smoking associated lung cancer in Asia. Increasing evidence has demonstrated that HPV oncoproteins may contribute to lung tumorigenesis and cell transformation. Importantly, HPV 16/18 E6 and E7 oncoproteins can mediate expression of multiple target genes and proteins, such as p53/pRb, VEGF, HIF-1α, cIAP-2, and hTERT, and contribute to cell proliferation, angiogenesis and cell immortalization through different signaling pathways in lung cancer. This article provides an overview of experiment data on HPV-associated lung cancer, describes the main targets on which HPV E6/E7 oncoproteins act, and further discusses the potential signaling pathways in which HPV E6/E7 oncoproteins are involved. In addition, we also raise questions regarding existing problems with the study of HPV-associated lung cancer.

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EGFR mutations and human papillomavirus in lung cancer

Cited by 32 publications

References 25 publications

99mTc-HYNIC-MPG: A novel SPECT probe for targeting mutated EGFR

99mTc-HYNIC-MPG: A novel SPECT probe for targeting mutated EGFR

Human papillomavirus and lung cancinogenesis: an overview

Human Papillomavirus Type 16/18 Oncoproteins: Potential Therapeutic Targets in Non-smoking Associated Lung Cancer

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