1
|
Liu Y, Gu X, Xuan M, Lou N, Fu L, Li J, Xue C. Notch signaling in digestive system cancers: Roles and therapeutic prospects. Cell Signal 2024; 124:111476. [PMID: 39428027 DOI: 10.1016/j.cellsig.2024.111476] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/29/2024] [Revised: 09/20/2024] [Accepted: 10/17/2024] [Indexed: 10/22/2024]
Abstract
Digestive system cancers rank among the most prevalent malignant tumors, maintaining persistently high incidence and mortality rates. Notch signaling activity, often aberrant in esophageal, gastric, hepatic, pancreatic, and colorectal cancers, plays a pivotal role in the initiation, progression, and therapy resistance of these malignancies. As a highly conserved pathway, Notch signaling is integral to cell differentiation, survival, proliferation, stem cell renewal, development, and morphogenesis. Its dysregulation has been increasingly linked to various diseases, particularly digestive system cancers. In these malignancies, altered Notch signaling influences multiple biological processes, including cell proliferation, invasion, cell cycle progression, immune evasion, drug resistance, and stemness maintenance. Understanding the mechanisms of Notch signaling in digestive system cancers is essential for the development of novel targeted therapies. Numerous Notch pathway-targeting drugs are currently in preclinical studies, demonstrating promising efficacy both as monotherapies and in combination with conventional anti-cancer treatments. This review summarizes recent high-quality findings on the involvement of Notch signaling in digestive system cancers, focusing on the expression changes and pathological mechanisms of its dysregulated components. Special emphasis is placed on the potential of translating Notch-targeted approaches into therapeutic strategies, which hold promise for overcoming the limitations of existing treatments and improving the poor prognosis associated with these cancers.
Collapse
Affiliation(s)
- Yingru Liu
- Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China
| | - Xinyu Gu
- Department of Oncology, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471000, China
| | - Mengjuan Xuan
- Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China
| | - Na Lou
- Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China
| | - Leiya Fu
- Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China
| | - Juan Li
- Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.
| | - Chen Xue
- Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.
| |
Collapse
|
2
|
Pathoor NN, Ganesh PS, Gopal RK. Microbiome interactions: Acinetobacter baumannii biofilms as a co-factor in oral cancer progression. World J Microbiol Biotechnol 2024; 40:398. [PMID: 39612015 DOI: 10.1007/s11274-024-04208-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2024] [Accepted: 11/19/2024] [Indexed: 11/30/2024]
Abstract
Acinetobacter baumannii (A. baumannii) has long been recognized primarily as a hospital-acquired pathogen. However, recent studies have uncovered a potential link between this bacterium and oral cancer, necessitating a deeper exploration of this relationship. This review examines the relevance of A. baumannii biofilms in the context of oral cancer development. By synthesizing current knowledge, we seek to provide a comprehensive understanding of this emerging area of research and identify critical directions for future investigations. The review emphasizes the remarkable adaptability, environmental resilience, and antibiotic resistance of A. baumannii, delves into the molecular mechanisms of biofilm formation, and their potential connection to oral cancer progression. The review also evaluates how biofilm colonization on oral surfaces and medical devices, along with its role in chronic infections, inflammation, and increased antimicrobial resistance, could contribute to creating a microenvironment favourable for tumor development. This review underscores the broader healthcare implications of A. baumannii biofilms, evaluates current strategies for their prevention and eradication, and calls for interdisciplinary research in this emerging field. By shedding light on the complex interactions between A. baumannii biofilms and oral cancer, it aims to stimulate further research and guide the development of new diagnostic, preventive, and therapeutic strategies in both microbiology and oncology.
Collapse
Affiliation(s)
- Naji Naseef Pathoor
- Department of Microbiology, Centre for infectious Diseases, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University (Deemed to be University), Poonamallee, High Road Chennai, 600 077, Tamil Nadu, India
| | - Pitchaipillai Sankar Ganesh
- Department of Microbiology, Centre for infectious Diseases, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University (Deemed to be University), Poonamallee, High Road Chennai, 600 077, Tamil Nadu, India.
| | - Rajesh Kanna Gopal
- Department of Microbiology, Centre for infectious Diseases, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University (Deemed to be University), Poonamallee, High Road Chennai, 600 077, Tamil Nadu, India
| |
Collapse
|
3
|
Park J, Wu J, Szkop KJ, Jeong J, Jovanovic P, Husmann D, Flores NM, Francis JW, Chen YJC, Benitez AM, Zahn E, Song S, Ajani JA, Wang L, Singh K, Larsson O, Garcia BA, Topisirovic I, Gozani O, Mazur PK. SMYD5 methylation of rpL40 links ribosomal output to gastric cancer. Nature 2024; 632:656-663. [PMID: 39048817 PMCID: PMC11625416 DOI: 10.1038/s41586-024-07718-0] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/26/2023] [Accepted: 06/14/2024] [Indexed: 07/27/2024]
Abstract
Dysregulated transcription due to disruption in histone lysine methylation dynamics is an established contributor to tumorigenesis1,2. However, whether analogous pathologic epigenetic mechanisms act directly on the ribosome to advance oncogenesis is unclear. Here we find that trimethylation of the core ribosomal protein L40 (rpL40) at lysine 22 (rpL40K22me3) by the lysine methyltransferase SMYD5 regulates mRNA translation output to promote malignant progression of gastric adenocarcinoma (GAC) with lethal peritoneal ascites. A biochemical-proteomics strategy identifies the monoubiquitin fusion protein partner rpL40 (ref. 3) as the principal physiological substrate of SMYD5 across diverse samples. Inhibiting the SMYD5-rpL40K22me3 axis in GAC cell lines reprogrammes protein synthesis to attenuate oncogenic gene expression signatures. SMYD5 and rpL40K22me3 are upregulated in samples from patients with GAC and negatively correlate with clinical outcomes. SMYD5 ablation in vivo in familial and sporadic mouse models of malignant GAC blocks metastatic disease, including peritoneal carcinomatosis. Suppressing SMYD5 methylation of rpL40 inhibits human cancer cell and patient-derived GAC xenograft growth and renders them hypersensitive to inhibitors of PI3K and mTOR. Finally, combining SMYD5 depletion with PI3K-mTOR inhibition and chimeric antigen receptor T cell administration cures an otherwise lethal in vivo mouse model of aggressive GAC-derived peritoneal carcinomatosis. Together, our work uncovers a ribosome-based epigenetic mechanism that facilitates the evolution of malignant GAC and proposes SMYD5 targeting as part of a potential combination therapy to treat this cancer.
Collapse
Affiliation(s)
- Juhyung Park
- Department of Biology, Stanford University, Stanford, CA, USA
| | - Jibo Wu
- Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
| | - Krzysztof J Szkop
- Department of Oncology-Pathology, Science for Life Laboratories, Karolinska Institute, Stockholm, Sweden
| | - Jinho Jeong
- Department of Biology, Stanford University, Stanford, CA, USA
| | - Predrag Jovanovic
- Lady Davis Institute and Gerald Bronfman Department of Oncology, McGill University, Montreal, Quebec, Canada
| | - Dylan Husmann
- Department of Biology, Stanford University, Stanford, CA, USA
| | - Natasha M Flores
- Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
| | - Joel W Francis
- Department of Biology, Stanford University, Stanford, CA, USA
| | - Ying-Jiun C Chen
- Department of Biology, Stanford University, Stanford, CA, USA
- Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
| | - Ana Morales Benitez
- Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
| | - Emily Zahn
- Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St Louis, MO, USA
| | - Shumei Song
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
| | - Jaffer A Ajani
- Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
| | - Linghua Wang
- Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
| | - Kamini Singh
- Department of Molecular Pharmacology, Albert Einstein College of Medicine, Montefiore Einstein Cancer Center, Bronx, NY, USA
| | - Ola Larsson
- Department of Oncology-Pathology, Science for Life Laboratories, Karolinska Institute, Stockholm, Sweden
| | - Benjamin A Garcia
- Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St Louis, MO, USA
| | - Ivan Topisirovic
- Lady Davis Institute and Gerald Bronfman Department of Oncology, McGill University, Montreal, Quebec, Canada
| | - Or Gozani
- Department of Biology, Stanford University, Stanford, CA, USA.
| | - Pawel K Mazur
- Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
| |
Collapse
|
4
|
Singh H, Chopra H, Singh I, Mohanto S, Ahmed MG, Ghumra S, Seelan A, Survase M, Kumar A, Mishra A, Mishra AK, Kamal MA. Molecular targeted therapies for cutaneous squamous cell carcinoma: recent developments and clinical implications. EXCLI JOURNAL 2024; 23:300-334. [PMID: 38655092 PMCID: PMC11036065 DOI: 10.17179/excli2023-6489] [Citation(s) in RCA: 4] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Figures] [Subscribe] [Scholar Register] [Received: 08/18/2023] [Accepted: 02/14/2024] [Indexed: 04/26/2024]
Abstract
Cutaneous Squamous Cell Carcinoma (cSCC) is a common and potentially fatal type of skin cancer that poses a significant threat to public health and has a high prevalence rate. Exposure to ultraviolet radiation on the skin surface increases the risk of cSCC, especially in those with genetic syndromes like xerodermapigmentosum and epidermolysis bullosa. Therefore, understanding the molecular pathogenesis of cSCC is critical for developing personalized treatment approaches that are effective in cSCC. This article provides a comprehensive overview of current knowledge of cSCC pathogenesis, emphasizing dysregulated signaling pathways and the significance of molecular profiling. Several limitations and challenges associated with conventional therapies, however, are identified, stressing the need for novel therapeutic strategies. The article further discusses molecular targets and therapeutic approaches, i.e., epidermal growth factor receptor inhibitors, hedgehog pathway inhibitors, and PI3K/AKT/mTOR pathway inhibitors, as well as emerging molecular targets and therapeutic agents. The manuscript explores resistance mechanisms to molecularly targeted therapies and proposes methods to overcome them, including combination strategies, rational design, and optimization. The clinical implications and patient outcomes of molecular-targeted treatments are assessed, including response rates and survival outcomes. The management of adverse events and toxicities in molecular-targeted therapies is crucial and requires careful monitoring and control. The paper further discusses future directions for therapeutic advancement and research in this area, as well as the difficulties and constraints associated with conventional therapies.
Collapse
Affiliation(s)
- Harpreet Singh
- School of Pharmaceutical Sciences, IFTM University, Moradabad, U.P., India, 244102
| | - Hitesh Chopra
- Department of Biosciences, Saveetha School of Engineering, Saveetha Institute of Medical and Technical Sciences, Chennai - 602105, Tamil Nadu, India
| | - Inderbir Singh
- Chitkara College of Pharmacy, Chitkara University, Punjab, India
| | - Sourav Mohanto
- Department of Pharmaceutics, Yenepoya Pharmacy College & Research Center, Yenepoya (Deemed to be University), Mangalore, Karnataka, 575018, India
| | - Mohammed Gulzar Ahmed
- Department of Pharmaceutics, Yenepoya Pharmacy College & Research Center, Yenepoya (Deemed to be University), Mangalore, Karnataka, 575018, India
| | - Shruti Ghumra
- Department of Biological Sciences, Sunandan Divatia School of Science, NarseeMonjee Institute of Management Studies (NMIMS), Pherozeshah Mehta Rd, Mumbai, India, 400056
| | - Anmol Seelan
- Mahatma Gandhi Mission, Institute of Biosciences and Technology, Aurangabad, India
| | - Manisha Survase
- Mahatma Gandhi Mission, Institute of Biosciences and Technology, Aurangabad, India
| | - Arvind Kumar
- School of Pharmaceutical Sciences, IFTM University, Moradabad, U.P., India, 244102
| | - Amrita Mishra
- School of Pharmaceutical Sciences, Delhi Pharmaceutical Sciences and Research University, New Delhi, India, 110017
| | - Arun Kumar Mishra
- SOS School of Pharmacy, IFTM University, Moradabad, U.P., India, 244102
| | - Mohammad Amjad Kamal
- Institutes for Systems Genetics, Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, China
- King Fahd Medical Research Center, King Abdulaziz University, Saudi Arabia
- Department of Pharmacy, Faculty of Allied Health Sciences, Daffodil International University, Bangladesh
- Enzymoics, 7 Peterlee Place, Hebersham, NSW 2770; Novel Global Community Educational Foundation, Australia
| |
Collapse
|
5
|
Qiu Y, Lu G, Li N, Hu Y, Tan H, Jiang C. Exosome-mediated communication between gastric cancer cells and macrophages: implications for tumor microenvironment. Front Immunol 2024; 15:1327281. [PMID: 38455041 PMCID: PMC10917936 DOI: 10.3389/fimmu.2024.1327281] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/24/2023] [Accepted: 01/25/2024] [Indexed: 03/09/2024] Open
Abstract
Gastric cancer (GC) is a malignant neoplasm originating from the epithelial cells of the gastric mucosa. The pathogenesis of GC is intricately linked to the tumor microenvironment within which the cancer cells reside. Tumor-associated macrophages (TAMs) primarily differentiate from peripheral blood monocytes and can be broadly categorized into M1 and M2 subtypes. M2-type TAMs have been shown to promote tumor growth, tissue remodeling, and angiogenesis. Furthermore, they can actively suppress acquired immunity, leading to a poorer prognosis and reduced tolerance to chemotherapy. Exosomes, which contain a myriad of biologically active molecules including lipids, proteins, mRNA, and noncoding RNAs, have emerged as key mediators of communication between tumor cells and TAMs. The exchange of these molecules via exosomes can markedly influence the tumor microenvironment and consequently impact tumor progression. Recent studies have elucidated a correlation between TAMs and various clinicopathological parameters of GC, such as tumor size, differentiation, infiltration depth, lymph node metastasis, and TNM staging, highlighting the pivotal role of TAMs in GC development and metastasis. In this review, we aim to comprehensively examine the bidirectional communication between GC cells and TAMs, the implications of alterations in the tumor microenvironment on immune escape, invasion, and metastasis in GC, targeted therapeutic approaches for GC, and the efficacy of potential GC drug resistance strategies.
Collapse
Affiliation(s)
- Yue Qiu
- Medical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, China
| | - Guimei Lu
- Department of Laboratory, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, China
| | - Na Li
- Medical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, China
| | - Yanyan Hu
- Medical Oncology Department of Gastrointestinal Cancer, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, China
| | - Hao Tan
- Thoracic Esophageal Radiotherapy Department, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, China
| | - Chengyao Jiang
- Department of Gastric Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, Liaoning, China
| |
Collapse
|
6
|
Guarrera L, Kurosaki M, Garattini SK, Gianni' M, Fasola G, Rossit L, Prisciandaro M, Di Bartolomeo M, Bolis M, Rizzo P, Nastasi C, Foglia M, Zanetti A, Paroni G, Terao M, Garattini E. Anti-tumor activity of all-trans retinoic acid in gastric-cancer: gene-networks and molecular mechanisms. J Exp Clin Cancer Res 2023; 42:298. [PMID: 37951921 PMCID: PMC10638833 DOI: 10.1186/s13046-023-02869-w] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2023] [Accepted: 10/18/2023] [Indexed: 11/14/2023] Open
Abstract
BACKGROUND Gastric-cancer is a heterogeneous type of neoplastic disease and it lacks appropriate therapeutic options. There is an urgent need for the development of innovative pharmacological strategies, particularly in consideration of the potential stratified/personalized treatment of this tumor. All-Trans Retinoic-acid (ATRA) is one of the active metabolites of vitamin-A. This natural compound is the first example of clinically approved cyto-differentiating agent, being used in the treatment of acute promyelocytic leukemia. ATRA may have significant therapeutic potential also in the context of solid tumors, including gastric-cancer. The present study provides pre-clinical evidence supporting the use of ATRA in the treatment of gastric-cancer using high-throughput approaches. METHODS We evaluated the anti-proliferative action of ATRA in 27 gastric-cancer cell-lines and tissue-slice cultures from 13 gastric-cancer patients. We performed RNA-sequencing studies in 13 cell-lines exposed to ATRA. We used these and the gastric-cancer RNA-sequencing data of the TCGA/CCLE datasets to conduct multiple computational analyses. RESULTS Profiling of our large panel of gastric-cancer cell-lines for their quantitative response to the anti-proliferative effects of ATRA indicate that approximately half of the cell-lines are characterized by sensitivity to the retinoid. The constitutive transcriptomic profiles of these cell-lines permitted the construction of a model consisting of 42 genes, whose expression correlates with ATRA-sensitivity. The model predicts that 45% of the TCGA gastric-cancers are sensitive to ATRA. RNA-sequencing studies performed in retinoid-treated gastric-cancer cell-lines provide insights into the gene-networks underlying ATRA anti-tumor activity. In addition, our data demonstrate that ATRA exerts significant immune-modulatory effects, which seem to be largely controlled by IRF1 up-regulation. Finally, we provide evidence of a feed-back loop between IRF1 and DHRS3, another gene which is up-regulated by ATRA. CONCLUSIONS ATRA is endowed with significant therapeutic potential in the stratified/personalized treatment gastric-cancer. Our data represent the fundaments for the design of clinical trials focusing on the use of ATRA in the personalized treatment of this heterogeneous tumor. Our gene-expression model will permit the development of a predictive tool for the selection of ATRA-sensitive gastric-cancer patients. The immune-regulatory responses activated by ATRA suggest that the retinoid and immune-checkpoint inhibitors constitute rational combinations for the management of gastric-cancer.
Collapse
Affiliation(s)
- Luca Guarrera
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Mami Kurosaki
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Silvio-Ken Garattini
- Department of Oncology, Academic Hospital of Udine ASUFC, Piazzale Santa Maria della Misericordia 15, Udine, 33100, UD, Italy
| | - Maurizio Gianni'
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Gianpiero Fasola
- Department of Oncology, Academic Hospital of Udine ASUFC, Piazzale Santa Maria della Misericordia 15, Udine, 33100, UD, Italy
| | - Luca Rossit
- Department of General Surgery, Academic Hospital of Udine ASUFC, Piazzale Santa Maria della Misericordia 15, Udine, 33100, UD, Italy
| | - Michele Prisciandaro
- Department of Medical Oncology, Fondazione IRCCS Istituto Nazionale Dei Tumori, Via Venezian 1, Milan, 20133, Italy
| | - Maria Di Bartolomeo
- Department of Medical Oncology, Fondazione IRCCS Istituto Nazionale Dei Tumori, Via Venezian 1, Milan, 20133, Italy
| | - Marco Bolis
- Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
- Faculty of Biomedical Sciences, Institute of Oncology Research, USI, Bellinzona, 6500, TI, Switzerland
| | - Paola Rizzo
- Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, 24100, Italy
| | - Claudia Nastasi
- Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Marika Foglia
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Adriana Zanetti
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Gabriela Paroni
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Mineko Terao
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy
| | - Enrico Garattini
- Department of Biochemistry and Molecular Biology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, via Mario Negri 2, Milano, 20156, Italy.
| |
Collapse
|
7
|
Leowattana W, Leowattana P, Leowattana T. Immunotherapy for advanced gastric cancer. World J Methodol 2023; 13:79-97. [PMID: 37456977 PMCID: PMC10348086 DOI: 10.5662/wjm.v13.i3.79] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/01/2023] [Revised: 05/11/2023] [Accepted: 05/31/2023] [Indexed: 06/20/2023] Open
Abstract
Gastric cancer (GC) is believed to be the fifth most common cancer and the third most common cause of death worldwide. Treatment techniques include radiation, chemotherapy, gastrectomy, and targeted treatments are often employed. Some hopeful results from the development of GC immunotherapy have already changed treatment approaches. Along with previous combination medicines, new immunotherapies have been developed that target distinct molecules. Despite ongoing studies into the current therapeutic options and significant improvements in this field, the prognosis for the ailment is poor. Since there are few treatment options and a delay in detection, the illness actually advances, spreads, and metastasizes. The bulk of immunotherapies in use today rely on cytotoxic immune cells, monoclonal antibodies, and gene-transferred vaccines. Immune checkpoint inhibitors have become more popular. In this review, we sought to examine the viewpoint and development of several immunotherapy treatment modalities for advanced GC, as well as the clinical results thus far reported. Additionally, we outlined tumor immune escape and tumor immunosurveillance.
Collapse
Affiliation(s)
- Wattana Leowattana
- Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, Rachatawee 10400, Bangkok, Thailand
| | - Pathomthep Leowattana
- Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, Rachatawee 10400, Bangkok, Thailand
| | - Tawithep Leowattana
- Department of Medicine, Faculty of Medicine, Srinakharinwirot University, Wattana 10110, Bangkok, Thailand
| |
Collapse
|