Targeting the PI3K–Akt–mTOR Pathway in Cancers: Impact on Tumor Cells and Their Microenvironments

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (25 December 2023) | Viewed by 1845

Special Issue Editors


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Guest Editor
Translational Oncology Department, Edigene Biotechnology Inc., Cambridge, MA, USA
Interests: cancer; osteosarcoma; small round cell tumor; tumor microenvironment

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Guest Editor
Department of Biochemistry, School of Medicine, University of Crete, Heraklion, Greece
Interests: molecular and cellular mechanisms underlie tumor growth and metastasis; interplay between tumour cells and cells of the tumour microenvironment; PI3K-isoform specific signalling

Special Issue Information

Dear Colleagues, 

Increasing evidence has emerged suggesting that the PI3K–Akt–mTOR pathway is a critical driver of cancer progression. Tumors consist not only of cancer cells but also multiple residents or infiltrating normal host cells that comprise the tumor microenvironment (TME). The interactions of cancer cells with cells of the TME determine whether the primary tumor is regressing or progressing and metastasizing. Selective pharmacological inhibitors against molecular components of the PI3K–Akt–mTOR pathway have played critical roles in regulating TME cell fate and the differentiation of cancer cells. The clinical outcome of various hematologic and solid cancers has been improved by overcoming the resistance mechanisms generated through the blockade of one of these components. In addition, several preclinical studies using PI3K–Akt–mTOR inhibitors in combination have reported successful synergistic strategies.

This Special Issue aims to bridge the bibliographic history of the PI3K–Akt–mTOR pathway with new compelling therapeutic opportunities. We invite our colleagues to submit their original research articles and reviews considering new therapeutic approaches or novel targets of the mechanism of resistance to PI3K–Akt–mTOR to improve the effectiveness of existing cancer treatment in the clinic. We also encourage the submission of articles exploring the effects of new drugs that are under development in preclinical or translational evaluations for their impact on PI3K–Akt–mTOR and other crosstalk signaling pathways regulating cell proliferation, cell fate, metastasis, and other biological processes controlling tumor progression.

Dr. Salah-Eddine Lamhamedi-Cherradi
Dr. Evangelia A. Papakonstanti
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 submissions that pass pre-check are 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 semimonthly 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 2900 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.

Keywords

  • PI3K
  • PI3K isoforms
  • Akt
  • mTOR
  • cancer cells
  • tumor microenvironment
  • angiogenesis
  • cancer immunotherapy
  • solid tumors
  • hematologic malignancies

Published Papers (1 paper)

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Review

23 pages, 3664 KiB  
Review
An Observatory for the MET Oncogene: A Guide for Targeted Therapies
by Dogus M. Altintas and Paolo M. Comoglio
Cancers 2023, 15(18), 4672; https://doi.org/10.3390/cancers15184672 - 21 Sep 2023
Viewed by 1268
Abstract
The MET proto-oncogene encodes a pivotal tyrosine kinase receptor, binding the hepatocyte growth factor (HGF, also known as scatter factor, SF) and governing essential biological processes such as organogenesis, tissue repair, and angiogenesis. The pleiotropic physiological functions of MET explain its diverse role [...] Read more.
The MET proto-oncogene encodes a pivotal tyrosine kinase receptor, binding the hepatocyte growth factor (HGF, also known as scatter factor, SF) and governing essential biological processes such as organogenesis, tissue repair, and angiogenesis. The pleiotropic physiological functions of MET explain its diverse role in cancer progression in a broad range of tumors; genetic/epigenetic alterations of MET drive tumor cell dissemination, metastasis, and acquired resistance to conventional and targeted therapies. Therefore, targeting MET emerged as a promising strategy, and many efforts were devoted to identifying the optimal way of hampering MET signaling. Despite encouraging results, however, the complexity of MET’s functions in oncogenesis yields intriguing observations, fostering a humbler stance on our comprehension. This review explores recent discoveries concerning MET alterations in cancer, elucidating their biological repercussions, discussing therapeutic avenues, and outlining future directions. By contextualizing the research question and articulating the study’s purpose, this work navigates MET biology’s intricacies in cancer, offering a comprehensive perspective. Full article
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