Special Issue "PTEN: A Multifaceted Tumor Suppressor"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 15 June 2019

Special Issue Editors

Guest Editor
Dr. Ludovica Ciuffreda

IRCCS, Regina Elena National Cancer Institute, Oncologia Medica 1, Via Elio Chianesi 53, 00144 Rome, Italy
Interests: PTEN; biomarkers; targeted therapy; molecular biology
Guest Editor
Dr. Emilio Bria

Medical Oncology, Fondazione Policlinico, Universitario A. Gemelli, IRCCS, Università Cattolica del Sacro Cuore, Rome, Italy
Website | E-Mail
Interests: methodology of clinical trials; biomarker clinical validation; meta-analyses
Guest Editor
Dr. Robert Pilarski

Department of Internal Medicine, The Ohio State University, Columbus, USA
Website | E-Mail
Interests: PTEN; Cowden syndrome; hereditary cancer

Special Issue Information

Dear Colleagues,

PTEN is the main negative regulator of PI3K pathway. PTEN levels and/or function can be regulated through multiple mechanisms (e.g., epigenetic silencing, post-translational modifications, etc.), and its protein and lipid phosphatase activity is involved in different cell functions, such as survival, growth, DNA repair, and protein synthesis. Its function is determined, at least in part, by its subcellular localization and a longer PTEN variant, named PTEN long, which may be implicated in paracrine cell-cell communication.

Germline loss of PTEN expression/function results in hereditary cancer predisposition syndromes, clinically referred to as PTEN hamartoma syndromes (PHTS) or PTENopaties, which carry a high lifetime risk of developing either benign or malignant growth in different target organs. Moreover, somatic PTEN aberrations are frequently observed in a wide spectrum of sporadic cancers, such as glioblastoma multiforme, malignant melanoma, endometrial, prostate, breast, colorectal, and lung cancers. Indeed, PTEN is a haploinsufficient tumor suppressor, and even subtle reductions in its active levels dictate cancer susceptibility in a dose-dependent manner.

In this Special Issue, we will focus on the mechanisms regulating PTEN expression and function, as well as on its functional role in PTENopaties and cancer, highlighting its prognostic/predictive potential and examining possible strategies to target PTEN-deficient tumors.

Dr. Ludovica Ciuffreda
Dr. Emilio Bria
Dr. Robert Pilarski
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • PTEN
  • hereditary syndrome
  • hereditary cancer
  • biomarker clinical validation

Published Papers (1 paper)

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Open AccessFeature PaperReview PTEN as a Prognostic/Predictive Biomarker in Cancer: An Unfulfilled Promise?
Cancers 2019, 11(4), 435; https://doi.org/10.3390/cancers11040435
Received: 28 February 2019 / Revised: 22 March 2019 / Accepted: 25 March 2019 / Published: 28 March 2019
PDF Full-text (13350 KB) | HTML Full-text | XML Full-text
Identifying putative biomarkers of clinical outcomes in cancer is crucial for successful enrichment, and for the selection of patients who are the most likely to benefit from a specific therapeutic approach. Indeed, current research in personalized cancer therapy focuses on the possibility of [...] Read more.
Identifying putative biomarkers of clinical outcomes in cancer is crucial for successful enrichment, and for the selection of patients who are the most likely to benefit from a specific therapeutic approach. Indeed, current research in personalized cancer therapy focuses on the possibility of identifying biomarkers that predict prognosis, sensitivity or resistance to therapies. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a tumor suppressor gene that regulates several crucial cell functions such as proliferation, survival, genomic stability and cell motility through both enzymatic and non-enzymatic activities and phosphatidylinositol 3-kinase (PI3K)-dependent and -independent mechanisms. Despite its undisputed role as a tumor suppressor, assessment of PTEN status in sporadic human tumors has yet to provide clinically robust prognostic, predictive or therapeutic information. This is possibly due to the exceptionally complex regulation of PTEN function, which involves genetic, transcriptional, post-transcriptional and post-translational events. This review shows a brief summary of the regulation and function of PTEN and discusses its controversial aspects as a prognostic/predictive biomarker. Full article
(This article belongs to the Special Issue PTEN: A Multifaceted Tumor Suppressor)

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