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Cancers
Special Issues
Metastatic Gastrointestinal (GI) Cancers
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Metastatic Gastrointestinal (GI) Cancers

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

Deadline for manuscript submissions: closed (10 August 2021) | Viewed by 8888

Special Issue Editor

Prof. Dr. Subhash C. Chauhan

E-Mail Website
Guest Editor
Department of Immunology and Microbiology, South Texas Center of Excellence in Cancer Research, School of Medicine, University of Texas Rio Grande Valley, Biomedical Research Building, 5300 North L Street, Room 1.200, McAllen, TX 78504, USA
Interests: cancer; cancer metastasis; tumor microenvironment; tumor progression; cancer treatment; cancer diagnosis; tumor imaging; targeted therapies; antibody therapies; immune checkpoint immunotherapies; tumor microbiome; oncogenic cell signaling; nanomedicine

Special Issue Information

Dear Colleagues,

The management of gastrointestinal (GI) cancer patients’ diagnosis and treatment remains challenging, particularly in solid tumors, due to the variable histo-architecture, the tumor microenvironment, and the metastatic potential. Moreover, the prognosis of GI cancer patients with metastatic disease is extremely grim. We still have very limited options for the management of metastatic GI cancer patients. Among all GI cancers, the diagnosis and treatment of pancreatic cancer has been the most difficult due to excessive desmoplasia, poor infusion of drugs into tumors, and the very high metastatic potential of tumors. This Special Issue aims to shed light on the cellular and molecular mechanisms of different metastatic GI cancers and provide new insights into these oncogenic signaling pathways. This Special Issue also aims to cover the involvement of nanomedicine in the management of cancer patients and potential upcoming nanotechnology platforms that may be useful in the future for cancer treatment, cancer diagnosis, and tumor imaging.

Prof. Dr. Subhash C. Chauhan
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 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

  • gastrointestinal (GI) cancer
  • cancer metastasis
  • tumor microenvironment
  • tumor progression
  • cancer treatment
  • cancer diagnosis
  • tumor imaging
  • targeted therapies
  • antibody therapies
  • immune checkpoint immunotherapies
  • tumor microbiome
  • oncogenic cell signaling
  • nanomedicine

Published Papers (3 papers)

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Research

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14 pages, 4247 KiB  
Article
Identification of Gene Co-Expression Networks Associated with Consensus Molecular Subtype-1 of Colorectal Cancer
by Sha’Kayla K. Nunez, Corey D. Young, Ti’ara L. Griffen, Adaugo Q. Ohandjo, Lawrence P. McKinney, Scott Kopetz and James W. Lillard, Jr.
Cancers 2021, 13(22), 5824; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13225824 - 20 Nov 2021
Cited by 3 | Viewed by 2762
Abstract
Colorectal cancer (CRC) is driven in part by dysregulated Wnt, Ras-Raf-MAPK, TGF-β, and PI3K-Akt signaling. The progression of CRC is also promoted by molecular alterations and heterogeneous—yet interconnected—gene mutations, chromosomal instability, transcriptomic subtypes, and immune signatures. Genomic alterations of CRC progression lead to [...] Read more.
Colorectal cancer (CRC) is driven in part by dysregulated Wnt, Ras-Raf-MAPK, TGF-β, and PI3K-Akt signaling. The progression of CRC is also promoted by molecular alterations and heterogeneous—yet interconnected—gene mutations, chromosomal instability, transcriptomic subtypes, and immune signatures. Genomic alterations of CRC progression lead to changes in RNA expression, which support CRC metastasis. An RNA-based classification system used for CRC, known as consensus molecular subtyping (CMS), has four classes. CMS1 has the lowest survival after relapse of the four CRC CMS phenotypes. Here, we identify gene signatures and associated coding mRNAs that are co-expressed during CMS1 CRC progression. Using RNA-seq data from CRC primary tumor samples, acquired from The Cancer Genome Atlas (TCGA), we identified co-expression gene networks significantly correlated with CMS1 CRC progression. CXCL13, CXCR5, IL10, PIK3R5, PIK3AP1, CCL19, and other co-expressed genes were identified to be positively correlated with CMS1. The co-expressed eigengene networks for CMS1 were significantly and positively correlated with the TNF, WNT, and ERK1 and ERK2 signaling pathways, which together promote cell proliferation and survival. This network was also aligned with biological characteristics of CMS1 CRC, being positively correlated to right-sided tumors, microsatellite instability, chemokine-mediated signaling pathways, and immune responses. CMS1 also differentially expressed genes involved in PI3K-Akt signaling. Our findings reveal CRC gene networks related to oncogenic signaling cascades, cell activation, and positive regulation of immune responses distinguishing CMS1 from other CRC subtypes. Full article
(This article belongs to the Special Issue Metastatic Gastrointestinal (GI) Cancers)
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20 pages, 7368 KiB  
Article
Pimavanserin: A Novel Autophagy Modulator for Pancreatic Cancer Treatment
by Sharavan Ramachandran, Itishree S. Kaushik and Sanjay K. Srivastava
Cancers 2021, 13(22), 5661; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13225661 - 12 Nov 2021
Cited by 7 | Viewed by 2166
Abstract
Pancreatic tumors exhibit high basal autophagy compared to that of other cancers. Several studies including those from our laboratory reported that enhanced autophagy leads to apoptosis in cancer cells. In this study, we evaluated the autophagy and apoptosis inducing effects of Pimavanserin tartrate [...] Read more.
Pancreatic tumors exhibit high basal autophagy compared to that of other cancers. Several studies including those from our laboratory reported that enhanced autophagy leads to apoptosis in cancer cells. In this study, we evaluated the autophagy and apoptosis inducing effects of Pimavanserin tartrate (PVT). Autophagic effects of PVT were determined by Acridine Orange assay and Transmission Electron Microscopy analysis. Clinical significance of ULK1 in normal and pancreatic cancer patients was evaluated by R2 and GEPIA cancer genomic databases. Modulation of proteins in autophagy signaling was assessed by Western blotting and Immunofluorescence. Apoptotic effects of PVT was evaluated by Annexin-V/APC assay. Subcutaneous xenograft pancreatic tumor model was used to evaluate the autophagy-mediated apoptotic effects of PVT in vivo. Autophagy was induced upon PVT treatment in pancreatic ducal adenocarcinoma (PDAC) cells. Pancreatic cancer patients exhibit reduced levels of autophagy initiator gene, ULK1, which correlated with reduced patient survival. Interestingly, PVT induced the expression of autophagy markers ULK1, FIP200, Atg101, Beclin-1, Atg5, LC3A/B, and cleavage of caspase-3, an indicator of apoptosis in several PDAC cells. ULK1 agonist LYN-1604 enhanced the autophagic and apoptotic effects of PVT. On the other hand, autophagy inhibitors chloroquine and bafilomycin blocked the autophagic and apoptotic effects of PVT in PDAC cells. Notably, chloroquine abrogated the growth suppressive effects of PVT by 25% in BxPC3 tumor xenografts in nude mice. Collectively, our results indicate that PVT mediated pancreatic tumor growth suppression was associated with induction of autophagy mediated apoptosis. Full article
(This article belongs to the Special Issue Metastatic Gastrointestinal (GI) Cancers)
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Review

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20 pages, 1404 KiB  
Review
TGFβ Signaling in the Pancreatic Tumor Microenvironment
by Daniel R. Principe, Kaytlin E. Timbers, Luke G. Atia, Regina M. Koch and Ajay Rana
Cancers 2021, 13(20), 5086; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13205086 - 11 Oct 2021
Cited by 21 | Viewed by 3077
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is associated with poor clinical outcomes, largely attributed to incomplete responses to standard therapeutic approaches. Recently, selective inhibitors of the Transforming Growth Factor β (TGFβ) signaling pathway have shown early promise in the treatment of PDAC, particularly as a [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is associated with poor clinical outcomes, largely attributed to incomplete responses to standard therapeutic approaches. Recently, selective inhibitors of the Transforming Growth Factor β (TGFβ) signaling pathway have shown early promise in the treatment of PDAC, particularly as a means of augmenting responses to chemo- and immunotherapies. However, TGFβ is a potent and pleiotropic cytokine with several seemingly paradoxical roles within the pancreatic tumor microenvironment (TME). Although TGFβ signaling can have potent tumor-suppressive effects in epithelial cells, TGFβ signaling also accelerates pancreatic tumorigenesis by enhancing epithelial-to-mesenchymal transition (EMT), fibrosis, and the evasion of the cytotoxic immune surveillance program. Here, we discuss the known roles of TGFβ signaling in pancreatic carcinogenesis, the biologic consequences of the genetic inactivation of select components of the TGFβ pathway, as well as past and present attempts to advance TGFβ inhibitors in the treatment of PDAC patients. Full article
(This article belongs to the Special Issue Metastatic Gastrointestinal (GI) Cancers)
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