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Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 26949

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Prof. Dr. Simona Gurzu

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Department of Pathology, George Emil Palade University of Medicine, Pharmacy, Sciences and Technology, 38 Gheorghe Marinescu Street, 540139 Targu Mures, Romania
Interests: oncopathology; gastric cancer; colorectal cancer; hepatocellular carcinoma; epithelial–mesenchymal transition; targeted therapy of cancer; histopathology; molecular pathology
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Special Issue Information

Dear Colleague,

The scope of this special issue is to collect papers referring to the molecular profile of gastrointestinal cancer cells. It can be focused on tissue samples or circulating cells, but experimental studies are also welcomed. Histochemical, immunohistochemical, or other molecular techniques used to create a cancer cell profile can also be included. This Special Issue which is guest edited by a professor of pathology might be extended to those clinical studies in which the prognostic or predictive value of biomarkers is checked. Of course, extensive literature reviews and meta-analyses can complete the circle of the molecular profile of cancer cells, which is far from being understood. The submitted papers can be about tumors of the gastrointestinal tract as well as liver, pancreas, and metastatic tumors.

Prof. Dr. Simona Gurzu
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

Molecular pathology
Histology
Oncology
Biomarkers
Gene profile
Immunohistochemistry
Prognosis
Targeted therapy
Colorectal cancer
Gastric cancer
Esophagus
Small intestine
Liver
Pancreas
Bile ducts

Published Papers (12 papers)

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Editorial

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3 pages, 185 KiB

Open AccessEditorial

Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms

by Simona Gurzu

Int. J. Mol. Sci. 2023, 24(13), 11136; https://doi.org/10.3390/ijms241311136 - 06 Jul 2023

Viewed by 922

Abstract

This Special Issue aims to highlight the advances made regarding the molecular profile of digestive system tumors in experimental and clinical studies [...] Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

Research

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23 pages, 2264 KiB

Open AccessArticle

A Phase II Exploratory Study to Identify Biomarkers Predictive of Clinical Response to Regorafenib in Patients with Metastatic Colorectal Cancer Who Have Failed First-Line Therapy

by Karen Gambaro, Maud Marques, Suzan McNamara, Mathilde Couetoux du Tertre, Cyrla Hoffert, Archana Srivastava, Anna Schab, Thierry Alcindor, Adrian Langleben, Lucas Sideris, Mahmoud Abdelsalam, Mustapha Tehfe, Felix Couture, Gerald Batist and Petr Kavan

Int. J. Mol. Sci. 2024, 25(1), 43; https://doi.org/10.3390/ijms25010043 - 19 Dec 2023

Viewed by 1059

Abstract

Single-agent regorafenib is approved in Canada for metastatic colorectal cancer (mCRC) patients who have failed previous lines of therapy. Identifying prognostic biomarkers is key to optimizing therapeutic strategies for these patients. In this clinical study (NCT01949194), we evaluated the safety and efficacy of single-agent regorafenib as a second-line therapy for mCRC patients who received it after failing first-line therapy with an oxaliplatin or irinotecan regimen with or without bevacizumab. Using various omics approaches, we also investigated putative biomarkers of response and resistance to regorafenib in metastatic lesions and blood samples in the same cohort. Overall, the safety profile of regorafenib seemed similar to the CORRECT trial, where regorafenib was administered as ≥ 2 lines of therapy. While the mutational landscape showed typical mutation rates for the top five driver genes (APC, KRAS, BRAF, PIK3CA, and TP53), KRAS mutations were enriched in intrinsically resistant lesions. Additional exploration of genomic-phenotype associations revealed several biomarker candidates linked to unfavorable prognoses in patients with mCRC using various approaches, including pathway analysis, cfDNA profiling, and copy number analysis. However, further research endeavors are necessary to validate the potential utility of these promising genes in understanding patients’ responses to regorafenib treatment. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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14 pages, 4667 KiB

Open AccessArticle

The Correlation of Ten Immune Checkpoint Gene Expressions and Their Association with Gastric Cancer Development

by Danzan Mansorunov, Natalya Apanovich, Fatimat Kipkeeva, Maxim Nikulin, Olga Malikhova, Ivan Stilidi and Alexander Karpukhin

Int. J. Mol. Sci. 2022, 23(22), 13846; https://doi.org/10.3390/ijms232213846 - 10 Nov 2022

Cited by 3 | Viewed by 1559

Abstract

In the immunotherapy based on immune checkpoint inhibition (IC), additional ICs are being studied to increase its effectiveness. An almost unstudied feature is the possible co-expression of ICs, which can determine the therapeutic efficacy of their inhibition. For the selection of promising ICs, information on the association of their expression with cancer development may be essential. We have obtained data on the expression correlation of ADAM17, PVR, TDO2, CD274, CD276, CEACAM1, IDO1, LGALS3, LGALS9, and HHLA2 genes in gastric cancer (GC). All but one, TDO2, have other IC genes with co-expression at some stage. At the metastatic stage, the expression of the IDO1 does not correlate with any other gene. The correlations are positive, but the expressions of the CD276 and CEACAM1 genes are negatively correlated. The expression of TDO2 and LGALS3 is associated with GC metastasis. The expression of TDO2 four-fold higher in metastatic tumors than in non-metastatic tumors, but LGALS3 was two-fold lower. The differentiation is associated with IDO1. The revealed features of TDO2, with a significant increase in expression at the metastatic stage and the absence of other IC genes with correlated expression indicates that the prospect of inhibiting TDO2 in metastatic GC. IDO1 may be considered for inhibition in low-differentiated tumors. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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17 pages, 2395 KiB

Open AccessArticle

PD-L1 Expression in High-Risk Early-Stage Colorectal Cancer—Its Clinical and Biological Significance in Immune Microenvironment

by Bing-Syuan Chung, I-Chuang Liao, Peng-Chan Lin, Shang-Yin Wu, Jui-Wen Kang, Bo-Wen Lin, Po-Chuan Chen, Ren-Hao Chan, Chung-Ta Lee, Meng-Ru Shen, Shang-Hung Chen and Yu-Min Yeh

Int. J. Mol. Sci. 2022, 23(21), 13277; https://doi.org/10.3390/ijms232113277 - 31 Oct 2022

Cited by 4 | Viewed by 2601

Abstract

Programmed death-ligand 1 (PD-L1) is an immune checkpoint molecule that can regulate immune responses in the tumor microenvironment (TME); however, the clinical applications of PD-L1 in early-stage colorectal cancer (CRC) remain unclear. In this study, we aimed to investigate the relationship between PD-L1 expression and survival outcome and explore its relevant immune responses in CRC. PD-L1 expression was evaluated by immunohistochemical staining to determine the tumor proportion score and combined positive score (CPS) in a Taiwanese CRC cohort. The oncomine immune response research assay was conducted for immune gene expression analyses. CRC datasets from the TCGA database were reappraised for PD-L1-associated gene enrichment analyses using GSEA. The high expression of PD-L1 (CPS ≥ 5) was associated with longer recurrence-free survival (p = 0.031) and was an independent prognostic factor as revealed by multivariate analysis. High PD-L1 expression was related to six immune-related gene signatures, and CXCL9 is the most significant overexpressed gene in differential analyses. High CXCL9 expression correlated with increased infiltration levels of immune cells in the TME, including CD8+ T lymphocytes and M1 macrophages. These findings suggest that high PD-L1 expression is a prognostic factor of early-stage CRC, and CXCL9 may play a key role in regulating PD-L1 expression. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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17 pages, 3500 KiB

Open AccessArticle

Molecular Pathogenesis of Colorectal Cancer: Impact of Oncogenic Targets Regulated by Tumor Suppressive miR-139-3p

by Ryutaro Yasudome, Naohiko Seki, Shunichi Asai, Yusuke Goto, Yoshiaki Kita, Yuto Hozaka, Masumi Wada, Kan Tanabe, Tetsuya Idichi, Shinichiro Mori and Takao Ohtsuka

Int. J. Mol. Sci. 2022, 23(19), 11616; https://doi.org/10.3390/ijms231911616 - 01 Oct 2022

Cited by 8 | Viewed by 1536

Abstract

We recently determined the RNA sequencing-based microRNA (miRNA) expression signature of colorectal cancer (CRC). Analysis of the signature showed that the expression of both strands of pre-miR-139 (miR-139-5p, the guide strand, and miR-139-3p, the passenger strand) was significantly reduced in CRC tissues. Transient transfection assays revealed that expression of miR-139-3p blocked cancer cell malignant transformation (e.g., cell proliferation, migration, and invasion). Notably, expression of miR-139-3p markedly blocked RAC-alpha serine/threonine-protein kinase (AKT) phosphorylation in CRC cells. A combination of in silico database and gene expression analyses of miR-139-3p-transfected cells revealed 29 putative targets regulated by miR-139-3p in CRC cells. RNA immunoprecipitation analysis using an Argonaute2 (AGO2) antibody revealed that KRT80 was efficiently incorporated into the RNA-induced silencing complex. Aberrant expression of Keratin 80 (KRT80) was detected in CRC clinical specimens by immunostaining. A knockdown assay using small interfering RNA (siRNA) targeting KRT80 showed that reducing KRT80 expression suppressed the malignant transformation (cancer cell migration and invasion) of CRC cells. Importantly, inhibiting KRT80 expression reduced AKT phosphorylation in CRC cells. Moreover, hexokinase-2 (HK2) expression was reduced in cells transfected with the KRT80 siRNAs or miR-139-3p. The involvement of miRNA passenger strands (e.g., miR-139-3p) in CRC cells is a new concept in miRNA studies. Our tumor-suppressive miRNA-based approach helps elucidate the molecular pathogenesis of CRC. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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14 pages, 2680 KiB

Open AccessArticle

Chrysin-Induced G Protein-Coupled Estrogen Receptor Activation Suppresses Pancreatic Cancer

by Hyun Kyung Lim, Hee Jung Kwon, Ga Seul Lee, Jeong Hee Moon and Joohee Jung

Int. J. Mol. Sci. 2022, 23(17), 9673; https://doi.org/10.3390/ijms23179673 - 26 Aug 2022

Cited by 4 | Viewed by 1807

Abstract

Pancreatic cancer (PC) has a high mortality rate due to its poor prognosis and the possibility of surgical resection in patients with the disease. Importantly, adjuvant chemotherapy is necessary to improve PC prognosis. Chrysin, a natural product with anti-inflammatory, antioxidant, and anticancer properties, has been studied for several years. Our previous study demonstrated that chrysin induced G protein-coupled estrogen receptor (GPER) expression and regulated its activity in breast cancer. Herein, we investigated whether chrysin-induced GPER activation suppresses PC progression in MIA PaCa-2 cells and a xenograft model. To determine its mechanism of action, cytotoxicity and clonogenic assays, a FACS analysis, and Western blotting were performed. Furthermore, the delay in tumor growth was evaluated in the MIA PaCa-2-derived xenograft model. Tumor tissues were investigated by Western blotting, immunohistochemistry, and a proteomic analysis. Chrysin caused cell cycle arrest and significantly decreased cell viability. Following co-treatment with chrysin and 17β-estradiol, the inhibitory effect of chrysin on cell proliferation was enhanced. In the xenograft model, chrysin and G1 (a GPER agonist) significantly delayed tumor growth and reduced both Ki-67 (a proliferation marker) and c-Myc expressions in tumor tissues. The proteomic analysis of tumor tissues identified that rho-associated coiled-coil containing protein kinase 1 (ROCK1), transgelin 2 (TAGLN2), and FCH and Mu domain containing endocytic adaptor 2 (FCHO2) levels were significantly reduced in chrysin-treated tumor tissues. High ROCK1, TAGLN2, and FCHO2 expressions were indicative of low overall PC survival as found using the Kaplan–Meier plotter. In conclusion, our results suggest that chrysin suppresses PC progression through the activation of GPER and reductions in ROCK1, TAGLN2, and FCHO2 expressions. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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17 pages, 1864 KiB

Open AccessArticle

SPDL1 Is an Independent Predictor of Patient Outcome in Colorectal Cancer

by Anna Klimaszewska-Wiśniewska, Karolina Buchholz, Justyna Durślewicz, Emilly Schlee Villodre, Maciej Gagat and Dariusz Grzanka

Int. J. Mol. Sci. 2022, 23(3), 1819; https://doi.org/10.3390/ijms23031819 - 05 Feb 2022

Cited by 2 | Viewed by 2007

Abstract

Spindle Apparatus Coiled-Coil Protein 1 (SPDL1) is a relatively recently identified coiled-coil domain containing protein and an important determinant of DNA fidelity by ensuring faithful mitosis. Hence, SPDL1 is suspected to underlie genomic (in-)stability in human cancers, yet its exact roles in these diseases remain largely underexplored. Given that genomic instability (GIN) is a crucial feature in colorectal cancer (CRC), we primarily asked whether the expression of this protein may account for differences in clinicopathological features and survival rates of CRC patients. Protein expression was evaluated by immunohistochemistry in the institutional tissue microarray (TMA), and gene expression by the analysis of publicly available datasets. To place the prognostic relevance in a predicted biological context, gene co-expression set around SPDL1 identified by public data mining was annotated and assessed for enrichment in gene ontology (GO) categories, BRITE hierarchies, and Reactome pathways. The comparison with adjacent normal tissue revealed a high expression of SPDL1 protein in a subset of tumor cases (48.84%), and these had better prognosis than the SPDL1-low expression counterpart even after adjustment for multiple confounders. SPDL1-high expression within tumors was associated with a median 56-month survival advantage, but not with any clinicopathological characteristics of our cohort. In the TCGA cohort, SPDL1 was overexpressed in tumor tissue and positively associated with improved survival, chromosome instability phenotype, and various GIN markers. In addition to the genes critically involved in the cell cycle and mitosis, a gene set co-expressed with SPDL1 contained checkpoint members of both chromosome segregation and DNA replication, as well as those associated with defective DNA repair, and retrograde vesicle-mediated transport. In conclusion, SPDL1 is an independent predictor of CRC patient survival in a possible connection with chromosomal instability. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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14 pages, 3511 KiB

Open AccessArticle

MiR-29a Curbs Hepatocellular Carcinoma Incidence via Targeting of HIF-1α and ANGPT2

by Ying-Hsien Huang, Wei-Shiung Lian, Feng-Sheng Wang, Pei-Wen Wang, Hung-Yu Lin, Ming-Chao Tsai and Ya-Ling Yang

Int. J. Mol. Sci. 2022, 23(3), 1636; https://doi.org/10.3390/ijms23031636 - 31 Jan 2022

Cited by 16 | Viewed by 2763

Abstract

A high-fat diet is responsible for hepatic fat accumulation that sustains chronic liver damage and increases the risks of steatosis and hepatocellular carcinoma (HCC). MicroRNA-29a (miR-29a), a key regulator of cellular behaviors, is present in anti-fibrosis and modulator tumorigenesis. However, the increased transparency of the correlation between miR-29a and the progression of human HCC is still further investigated. In this study, we predicted HIF-1α and ANGPT2 as regulators of HCC by the OncoMir cancer database and showed a strong positive correlation with HIF-1α and ANGPT2 gene expression in HCC patients. Mice fed the western diet (WD) while administered CCl4 for 25 weeks induced chronic liver damage and higher HCC incidence than without fed WD mice. HCC section staining revealed signaling upregulation in ki67, severe fibrosis, and steatosis in WD and CCl4 mice and detected Col3a1 gene expressions. HCC tissues significantly attenuated miR-29a but increased in HIF-1α, ANGPT2, Lox, Loxl2, and VEGFA expression. Luciferase activity analysis confirms that miR-29a specific binding 3′UTR of HIF-1α and ANGPT2 to repress expression. In summary, miR-29a control HIF-1α and ANGPT2 signaling in HCC formation. This study insight into a novel molecular pathway by which miR-29a targeting HIF-1α and ANGPT2 counteracts the incidence of HCC development. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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16 pages, 20182 KiB

Open AccessArticle

MVP Expression Facilitates Tumor Cell Proliferation and Migration Supporting the Metastasis of Colorectal Cancer Cells

by Paulina Pietras, Marta Leśniczak-Staszak, Aldona Kasprzak, Małgorzata Andrzejewska, Karol Jopek, Mateusz Sowiński, Marcin Rucinski, Shawn M. Lyons, Pavel Ivanov and Witold Szaflarski

Int. J. Mol. Sci. 2021, 22(22), 12121; https://doi.org/10.3390/ijms222212121 - 09 Nov 2021

Cited by 4 | Viewed by 1863

Abstract

Cancer cells show significant dysregulation of genes expression, which may favor their survival in the tumor environment. In this study, the cellular vault’s components MVP (major vault protein), TEP1 (telomerase-associated protein 1) and vPARP (vault poly(ADP-ribose) polymerase) were transiently or completely inhibited in U2OS cells (human bone osteosarcoma epithelial cells) to evaluate their impact on the cell proliferative and migratory capacity as well as on the development of their resistance to the drug vinorelbine. Comparative analysis of MVP protein expression level in normal colon tissue, primary colorectal tumor, and metastasis showed that the expression of this protein does not increase significantly in the primary tumor, but its expression increases in metastatic cells. Further comparative molecular analysis using the whole transcriptome microarrays for MVP-positive and MVP-negative cells showed that MVP is involved in regulating proliferation and migration of cancer cells. MVP may facilitate metastasis of colon cancer due to its impact on cell migration. Moreover, two vault proteins, MVP and TEP1, contribute the resistance to vinorelbine, while vPARP does not. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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Review

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20 pages, 1715 KiB

Open AccessReview

Immune Microenvironment and Immunotherapeutic Management in Virus-Associated Digestive System Tumors

by Panagiotis Sarantis, Eleni-Myrto Trifylli, Evangelos Koustas, Kostas A. Papavassiliou, Michalis V. Karamouzis and Athanasios G. Papavassiliou

Int. J. Mol. Sci. 2022, 23(21), 13612; https://doi.org/10.3390/ijms232113612 - 06 Nov 2022

Cited by 4 | Viewed by 2073

Abstract

The development of cancer is a multifactorial phenomenon, while it constitutes a major global health problem. Viruses are an important factor that is involved in tumorigenesis and is associated with 12.1% of all cancer cases. Major examples of oncogenic viruses which are closely associated with the digestive system are HBV, HCV, EBV, HPV, JCV, and CMV. EBV, HPV, JCV, and CMV directly cause oncogenesis by expressing oncogenic proteins that are encoded in their genome. In contrast, HBV and HCV are correlated indirectly with carcinogenesis by causing chronic inflammation in the infected organs. In addition, the tumor microenvironment contains various immune cells, endothelial cells, and fibroblasts, as well as several growth factors, cytokines, and other tumor-secreted molecules that play a key role in tumor growth, progression, and migration, while they are closely interrelated with the virus. The presence of T-regulatory and B-regulatory cells in the tumor microenvironment plays an important role in the anti-tumor immune reaction. The tumor immune microenvironments differ in each type of cancer and depend on viral infection. The alterations in the immune microenvironment caused by viruses are also reflected in the effectiveness of immunotherapy. The present review aims at shedding light on the association between viruses and digestive system malignancies, the characteristics of the tumor immune microenvironment that develop, and the possible treatments that can be administered. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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14 pages, 1617 KiB

Open AccessReview

From Dukes-MAC Staging System to Molecular Classification: Evolving Concepts in Colorectal Cancer

by Laura Banias, Ioan Jung, Rebeca Chiciudean and Simona Gurzu

Int. J. Mol. Sci. 2022, 23(16), 9455; https://doi.org/10.3390/ijms23169455 - 21 Aug 2022

Cited by 7 | Viewed by 4377

Abstract

This historical review aimed to summarize the main changes that colorectal carcinoma (CRC) staging systems suffered over time, starting from the creation of the classical Duke’s classification, modified Astler–Coller staging, internationally used TNM (T—primary tumor, N—regional lymph nodes’ status, M—distant metastases) staging system, and ending with molecular classifications and epithelial–mesenchymal transition (EMT) concept. Besides currently used staging parameters, this paper briefly presents the author’s contribution in creating an immunohistochemical (IHC)-based molecular classification of CRC. It refers to the identification of three molecular groups of CRCs (epithelial, mesenchymal and hybrid) based on the IHC markers E-cadherin, β-catenin, maspin, and vimentin. Maspin is a novel IHC antibody helpful for tumor budding assessment, which role depends on its subcellular localization (cytoplasm vs. nuclei). The long road of updating the staging criteria for CRC has not come to an end. The newest prognostic biomarkers, aimed to be included in the molecular classifications, exert predictive roles, and become more and more important for targeted therapy decisions. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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26 pages, 1040 KiB

Open AccessReview

Immunotherapy as a Therapeutic Strategy for Gastrointestinal Cancer—Current Treatment Options and Future Perspectives

by Evangelos Koustas, Eleni-Myrto Trifylli, Panagiotis Sarantis, Nikolaos Papadopoulos, Eleni Karapedi, Georgios Aloizos, Christos Damaskos, Nikolaos Garmpis, Anna Garmpi, Kostas A. Papavassiliou, Michalis V. Karamouzis and Athanasios G. Papavassiliou

Int. J. Mol. Sci. 2022, 23(12), 6664; https://doi.org/10.3390/ijms23126664 - 15 Jun 2022

Cited by 13 | Viewed by 2780

Abstract

Gastrointestinal (GI) cancer constitutes a highly lethal entity among malignancies in the last decades and is still a major challenge for cancer therapeutic options. Despite the current combinational treatment strategies, including chemotherapy, surgery, radiotherapy, and targeted therapies, the survival rates remain notably low for patients with advanced disease. A better knowledge of the molecular mechanisms that influence tumor progression and the development of optimal therapeutic strategies for GI malignancies are urgently needed. Currently, the development and the assessment of the efficacy of immunotherapeutic agents in GI cancer are in the spotlight of several clinical trials. Thus, several new modalities and combinational treatments with other anti-neoplastic agents have been identified and evaluated for their efficiency in cancer management, including immune checkpoint inhibitors, adoptive cell transfer, chimeric antigen receptor (CAR)-T cell therapy, cancer vaccines, and/or combinations thereof. Understanding the interrelation among the tumor microenvironment, cancer progression, and immune resistance is pivotal for the optimal therapeutic management of all gastrointestinal solid tumors. This review will shed light on the recent advances and future directions of immunotherapy for malignant tumors of the GI system. Full article

(This article belongs to the Special Issue Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms)

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