Epigenetic and genetic alternation of PTEN in cervical neoplasm

Cheung, Tak‐Hong; Lo, KW; Yim, So Fan; Chan, Loucia Kit-Ying; Heung, Mei-Sze; Chan, C. K.; Cheung, Albert Y.; Chung, Tony K.H.; Wong, Yum-Shing

doi:10.1016/j.ygyno.2004.03.013

Cited by 83 publications

(70 citation statements)

References 21 publications

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“…Structural changes of PTEN in cervical carcinomas do not appear to be common. Previous reports have not identified mutations in the PTEN gene in this type of cancer 8,19 . However, Poetsch et al 27 demonstrated PTEN mutations in 23% of head and neck SCC tumor samples, and Kurose et al 28 found intragenic PTEN mutations in 15% (3/20) of cervical tumors.…”

Section: Discussionmentioning

confidence: 66%

“…Whether PTEN methylation contributes to the development of cervical cancer and affects the prognosis has not been elucidated. Cheung et al 8 found that PTEN methylation was significantly associated with reduced total and disease-free survival and suggested that tumors without normal PTEN functioning may be more aggressive.…”

Section: Referencesmentioning

confidence: 99%

“…Phosphatase and tensin homolog (PTEN) is a tumor suppressor gene localized on chromosome 10 (10q23.3) in a region that is often related to loss of heterozygosis and consequent predisposition to carcinogenesis in a number of malignancies [8][9][10] . Genetic, epigenetic and protein expression alterations in PTEN have been described in several types of tumors such as brain, prostate, breast, thyroid and endometrial tumors [11][12][13][14] .…”

Section: Introductionmentioning

confidence: 99%

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PTEN expression in patients with carcinoma of the cervix and its association with p53, Ki-67 and CD31

Loures¹,

Cândido²,

Vidigal³

et al. 2014

Rev. Bras. Ginecol. Obstet.

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PURPOSE: To investigate protein expression and mutations in phosphatase and tensin homolog (PTEN) in patients with stage IB cervical squamous cell carcinoma (CSCC) and the association with clinical-pathologic features, tumor p53 expression, cell proliferation and angiogenesis. METHODS: Women with stage IB CSCC (n=20 -Study Group) and uterine myoma (n=20 -Control Group), aged 49.1±1.7 years (mean±standard deviation, range 27-78 years), were prospectively evaluated. Patients with cervical cancer were submitted to Piver-Rutledge class III radical hysterectomy and pelvic lymphadenectomy and patients in the Control Group underwent vaginal hysterectomy. Tissue samples from the procedures were stained with hematoxylin and eosin for histological evaluation. Protein expression was detected by immunohistochemistry. Staining for PTEN, p53, Ki-67 and CD31 was evaluated. The intensity of PTEN immunostaining was estimated by computer-assisted image analysis, based on previously reported protocols. Data were analyzed using the Student's t-test to evaluate significant differences between the groups. Level of significance was set at p<0.05. RESULTS: The PTEN expression intensity was lower in the CSCC group than in the Control (benign cervix) samples (150.5±5.2 versus 204.2±2.6; p<0.001). Our study did not identify any mutations after sequencing all nine PTEN exons. PTEN expression was not associated with tumor expression of p53 (p=0.9), CD31 (p=0.8) or Ki-67 (p=0.3) or clinical-pathologic features in patients with invasive carcinoma of the cervix. CONCLUSIONS: Our findings demonstrate that the PTEN protein expression is significantly diminished in CSCC.

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Section: Discussionmentioning

confidence: 66%

Section: Referencesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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PTEN expression in patients with carcinoma of the cervix and its association with p53, Ki-67 and CD31

Loures¹,

Cândido²,

Vidigal³

et al. 2014

Rev. Bras. Ginecol. Obstet.

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“…Loss of PTEN can be due to mutations, deletions, gene promoter methylation, or microRNAs (miRs) [25][26][27][28]. Mutations and deletions of PTEN are rare events in cervical cancer [16,22,29]. In a study by Yang et al, PTEN methylation was observed in 20 (15.7%) of 127 cervical cancers, whereas Cheung et al [16] reported PTEN methylation in 36 (58%) of 62 of squamous cell cervical cancers.…”

Section: Discussionmentioning

confidence: 99%

“…pAKT and pERK immunostaining were considered positive if more than 10% of a tumor showed cytoplasmic and/or nuclear immunostaining [15]. Positive expression of PTEN was defined as more than 10% cytoplasmic immunostaining [16]. Positive pEGFR was defined as at least weak positive cytoplasmic immunostaining, as the activated EGFR is internalized [17].…”

Section: Evaluation Of Immunostainingmentioning

confidence: 99%

The epidermal growth factor receptor pathway in relation to pelvic lymph node metastasis and survival in early-stage cervical cancer

et al. 2010

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The epidermal growth factor receptor pathway in relation to pelvic lymph node metastasis and survival in early-stage cervical cancer Eijsink, J.J.; Noordhuis, M.G.; Ten Hoor, K.A.; Kok, M.; Hollema, Harry; de Bock, Gertruida H; Nijman, Hans; Schuuring, Eduardus; Wisman, G.B.A.; van der Zee, Ate Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. In multivariate analysis, only pelvic lymph node metastasis (hazard ratio, 6.11; 95% CI, 3.46-10.77, P b .001) and poor differentiation (hazard ratio, 1.91; 95% CI, 1.12-3.26, P = .018) were related to disease-specific survival. In early-stage cervical cancer, loss of PTEN expression is associated with pelvic lymph node metastasis, suggesting PTEN to be one of the tumor suppressor genes affecting pelvic lymph node metastasis. However, expression of EGFR pathway components does not appear to have prognostic impact in surgically treated early-stage cervical cancer.

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Human papillomavirus and molecular considerations for cancer risk

Whiteside

Siegel

Unger

2008

Cancer

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Human papillomaviruses (HPVs) are a major cause of cancer globally, including cervical cancer. The HPV 'early' proteins, E6 and E7, are the chief oncoproteins involved in cancer progression. These oncoproteins are more highly expressed in high-grade dysplasias and invasive cancer coincident with reduced viral DNA replication and reduced production of infective progeny virions. The E6 and E7 oncoproteins interact with several cellular proteins-classically TP53 and RB1, respectively-leading to the degradation of several of these proteins, although all interactions do not necessarily result in the degradation of a cellular protein.HPV infection is also associated with viral and host DNA methylation changes, many of which also occur in cancer types not associated with HPV infection. The E6 and E7 interactions with cellular proteins and DNA methylation changes are associated with changes in the integrity of key cellular pathways that regulate genomic integrity, cell adhesion, the immune response, apoptosis, and cell cycle control. The alterations in key cellular pathways may provide useful biomarkers to improve the sensitivity of current cancer screening methods, such as the Papanicolaou test. This review provides a detailed summary of the interactions of E6 and E7 with cellular proteins and alterations in cellular DNA methylation associated with HPV infection. The importance of molecular biomarkers to the clinical setting, underserved populations, and general public health is discussed.

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Epigenetic and genetic alternation of PTEN in cervical neoplasm

Cited by 83 publications

References 21 publications

PTEN expression in patients with carcinoma of the cervix and its association with p53, Ki-67 and CD31

PTEN expression in patients with carcinoma of the cervix and its association with p53, Ki-67 and CD31

The epidermal growth factor receptor pathway in relation to pelvic lymph node metastasis and survival in early-stage cervical cancer

Human papillomavirus and molecular considerations for cancer risk

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