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      Head and neck cancer management and cancer stem cells implication

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          Abstract

          Head and neck squamous cell carcinomas (HNSCCs) arise in the mucosal linings of the upper aerodigestive tract and are heterogeneous in nature. Risk factors for HNSCCs are smoking, excessive alcohol consumption, and the human papilloma virus. Conventional treatments are surgery, radiotherapy, chemotherapy, or a combined modality; however, no international standard mode of therapy exists. In contrast to the conventional model of clonal evolution in tumor development, there is a newly proposed theory based on the activity of cancer stem cells (CSCs) as the model for carcinogenesis. This “CSC hypothesis” may explain the high mortality rate, low response to treatments, and tendency to develop multiple tumors for HNSCC patients. We review current knowledge on HNSCC etiology and treatment, with a focus on CSCs, including their origins, identifications, and effects on therapeutic options.

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          Identification of pancreatic cancer stem cells.

          Chenwei Li, David G Heidt, Piero Dalerba … (2007)
          Emerging evidence has suggested that the capability of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. Although data have been provided to support this theory in human blood, brain, and breast cancers, the identity of pancreatic cancer stem cells has not been determined. Using a xenograft model in which primary human pancreatic adenocarcinomas were grown in immunocompromised mice, we identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA). Pancreatic cancer cells with the CD44(+)CD24(+)ESA(+) phenotype (0.2-0.8% of pancreatic cancer cells) had a 100-fold increased tumorigenic potential compared with nontumorigenic cancer cells, with 50% of animals injected with as few as 100 CD44(+)CD24(+)ESA(+) cells forming tumors that were histologically indistinguishable from the human tumors from which they originated. The enhanced ability of CD44(+)CD24(+)ESA(+) pancreatic cancer cells to form tumors was confirmed in an orthotopic pancreatic tail injection model. The CD44(+)CD24(+)ESA(+) pancreatic cancer cells showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog. Identification of pancreatic cancer stem cells and further elucidation of the signaling pathways that regulate their growth and survival may provide novel therapeutic approaches to treat pancreatic cancer, which is notoriously resistant to standard chemotherapy and radiation.
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            The clonal evolution of tumor cell populations.

            P C Nowell (1976)
            It is proposed that most neoplasms arise from a single cell of origin, and tumor progression results from acquired genetic variability within the original clone allowing sequential selection of more aggressive sublines. Tumor cell populations are apparently more genetically unstable than normal cells, perhaps from activation of specific gene loci in the neoplasm, continued presence of carcinogen, or even nutritional deficiencies within the tumor. The acquired genetic insta0ility and associated selection process, most readily recognized cytogenetically, results in advanced human malignancies being highly individual karyotypically and biologically. Hence, each patient's cancer may require individual specific therapy, and even this may be thwarted by emergence of a genetically variant subline resistant to the treatment. More research should be directed toward understanding and controlling the evolutionary process in tumors before it reaches the late stage usually seen in clinical cancer.
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              Head and neck cancer.

              Athanassios Argiris, Michalis V. Karamouzis, David Raben … (2008)
              Most head and neck cancers are squamous cell carcinomas that develop in the upper aerodigestive epithelium after exposure to carcinogens such as tobacco and alcohol. Human papillomavirus has also been strongly implicated as a causative agent in a subset of these cancers. The complex anatomy and vital physiological role of the tumour-involved structures dictate that the goals of treatment are not only to improve survival outcomes but also to preserve organ function. Major improvements have been accomplished in surgical techniques and radiotherapy delivery. Moreover, systemic therapy including chemotherapy and molecularly targeted agents--namely, the epidermal growth factor receptor inhibitors--has been successfully integrated into potentially curative treatment of locally advanced squamous-cell carcinoma of the head and neck. In deciding which treatment strategy would be suitable for an individual patient, important considerations include expected functional outcomes, ability to tolerate treatment, and comorbid illnesses. The collaboration of many specialties is the key for optimum assessment and decision making. We review the epidemiology, molecular pathogenesis, diagnosis and staging, and the latest multimodal management of squamous cell carcinoma of the head and neck.
              Article 0 comments Cited 531 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Simon D. Tran
                Journal
                Journal ID (nlm-ta): Saudi Dent J
                Journal ID (iso-abbrev): Saudi Dent J
                Title: The Saudi Dental Journal
                Publisher: Elsevier
                ISSN (Print): 1013-9052
                ISSN (Electronic): 1658-3558
                Publication date PMC-release: 10 June 2019
                Publication date (Print): October 2019
                Publication date (Electronic): 10 June 2019
                Volume: 31
                Issue: 4
                Pages: 395-416
                Affiliations
                [a ]McGill Craniofacial Tissue Engineering and Stem Cells Laboratory, Faculty of Dentistry, McGill University, Montreal, QC, Canada
                [b ]Oral Pathology Department, Faculty of Dentistry, Mansoura University, Mansoura, Egypt
                Author notes
                [* ]Corresponding author at: McGill University, Faculty of Dentistry, McGill Craniofacial Tissue Engineering and Stem Cells Laboratory, 3640 University Street, Montreal, Quebec H3A 0C7, Canada. simon.tran@ 123456mcgill.ca
                Article
                Publisher ID: S1013-9052(19)30562-0
                DOI: 10.1016/j.sdentj.2019.05.010
                PMC ID: 6823822
                PubMed ID: 31700218
                SO-VID: c01be177-1141-4795-9d82-8d58f0edfaa0
                Copyright © © 2019 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 20 May 2019
                Date accepted : 27 May 2019
                Categories
                Subject: Review Article

                Keywords: abc, atp-binding cassette transporters,atc, amplifying transitory cell,bmi-1, b cell-specific moloney murine leukemia virus integration site 1,egfr, epidermal growth factor receptor,hifs, hypoxia-inducible factors,mdr1, multidrug resistance protein 1,nf-κb, nuclear factor kappa-light-chain-enhancer of activated b cells,pi3k, phosphatidylinositol-4,5-bisphosphate 3-kinase,tkis, tyrosine kinase inhibitors,head and neck cancer,carcinoma,squamous cell,cancer stem cells,cancer treatment,antineoplastic agents
                Data availability:
                Keywords: abc, atp-binding cassette transporters, atc, amplifying transitory cell, bmi-1, b cell-specific moloney murine leukemia virus integration site 1, egfr, epidermal growth factor receptor, hifs, hypoxia-inducible factors, mdr1, multidrug resistance protein 1, nf-κb, nuclear factor kappa-light-chain-enhancer of activated b cells, pi3k, phosphatidylinositol-4,5-bisphosphate 3-kinase, tkis, tyrosine kinase inhibitors, head and neck cancer, carcinoma, squamous cell, cancer stem cells, cancer treatment, antineoplastic agents

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