cancers-logo

Journal Browser

Journal Browser

Tumorigenesis Mechanism of Colorectal Cancer

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

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 1836

Special Issue Editor

Department of Anatomy and Cell Biology, McGill University, Montreal, QC H3A 0G4, Canada
Interests: colorectal cancer

Special Issue Information

Dear Colleagues, 

Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second deadliest cancer worldwide. CRC accounts for approximately 10% of cancer-related deaths in men and women. Although screening techniques and treatment have progressed substantially in recent years, the prevalence of CRC is still on the rise. Therefore, further studies are necessary to determine the molecular mechanisms that underline CRC initiation and progression.

In this Special Issue, we are pleased to invite authors to submit articles addressing recent advances regarding the mechanistic pathways involved in CRC tumorigenesis.

This Special Issue was established to prompt researchers to perform studies on the following subjects in CRC:

  • Mechanistic pathways involved in the evolution of primary, metastatic, and recurrent lesions;
  • Metabolism dysregulation;
  • The molecular mechanisms of resistance to anti-cancer agents;
  • The role of extracellular vesicles in tumorigenesis.

Basic studies or translational studies are welcome. Reviews are also appreciated.

Dr. Miran Rada
Guest Editor

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 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

  • colorectal cancer
  • molecular mechanisms
  • mechanistic pathways
  • cancer initiation
  • cancer progression

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

15 pages, 3153 KiB  
Article
Impaired Expression of the Salvador Homolog-1 Gene Is Associated with the Development and Progression of Colorectal Cancer
by Anna Ewa Kowalczyk, Bartlomiej Emil Krazinski, Aleksandra Piotrowska, Jedrzej Grzegrzolka, Janusz Godlewski, Piotr Dziegiel and Zbigniew Kmiec
Cancers 2023, 15(24), 5771; https://doi.org/10.3390/cancers15245771 - 8 Dec 2023
Viewed by 1386
Abstract
Salvador homolog-1 (SAV1) is a component of the Hippo pathway that regulates tissue growth and homeostasis by affecting diverse cell processes, including apoptosis, cell division, and differentiation. The aberrant expression of Hippo pathway components has been observed in various human cancers. This study [...] Read more.
Salvador homolog-1 (SAV1) is a component of the Hippo pathway that regulates tissue growth and homeostasis by affecting diverse cell processes, including apoptosis, cell division, and differentiation. The aberrant expression of Hippo pathway components has been observed in various human cancers. This study aimed to examine the expression level of the SAV1 gene in colorectal cancer (CRC) and its prognostic value and associations with tumor progression. We obtained matched pairs of tumor tissue and non-cancerous mucosa of the large intestine from 94 CRC patients as well as 40 colon biopsies of healthy subjects collected during screening colonoscopy. The tissue samples and CRC cell lines were quantified for SAV1 mRNA levels using the quantitative polymerase chain reaction method, while SAV1 protein expression was estimated in the paired tissues of CRC patients using immunohistochemistry. The average level of SAV1 mRNA was decreased in 93.6% of the tumor tissues compared to the corresponding non-cancerous tissues and biopsies of healthy colon mucosa. A downregulated expression of SAV1 mRNA was also noted in the CRC cell lines. Although the average SAV1 immunoreactivity was increased in the CRC samples compared to the non-cancerous tissues, a decreased immunoreactivity of the SAV1 protein in the tumor specimens was associated with lymph node involvement and higher TNM disease stage and histological grade. The results of our study suggest that the impaired expression of SAV1 is involved in CRC progression. Full article
(This article belongs to the Special Issue Tumorigenesis Mechanism of Colorectal Cancer)
Show Figures

Figure 1

Back to TopTop