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Cancers (Basel). 2018 Oct 10;10(10). pii: E376. doi: 10.3390/cancers10100376.

Molecular Markers of Anticancer Drug Resistance in Head and Neck Squamous Cell Carcinoma: A Literature Review.

Author information

1
Research Institute of Dentistry, Health Science Center, Universidad de Guadalajara, Guadalajara 4430, JAL, Mexico. patologiabucal@live.com.mx.
2
Department of Research, School of Dentistry, Universidad Juárez del Estado de Durango, Durango 34000, DGO, Mexico. lavallec@outlook.com.
3
Department of Research, School of Dentistry, Universidad Juárez del Estado de Durango, Durango 34000, DGO, Mexico. carreonburciaga55@hotmail.com.
4
Molecular Biology Department, School of Dentistry, Universidad Autónoma de Baja California, Mexicali 21040, Mexico. nserafin@uabc.edu.mx.
5
Department of Health Care, Xochimilco Unit, Universidad Autónoma Metropolitana (UAM) Xochimilco, Mexico City 04960, Mexico. nmolinaf@hotmail.com.
6
Department of Research, School of Dentistry, Universidad Juárez del Estado de Durango, Durango 34000, DGO, Mexico. rogegg@hotmail.com.
7
Department of Research, School of Dentistry, Universidad Juárez del Estado de Durango, Durango 34000, DGO, Mexico. ronellbologna@hotmail.com.
8
Molecular Pathology Area, School of Dentistry, Universidad de la República, Montevideo 11600, Uruguay. ronellbologna@hotmail.com.

Abstract

This manuscript provides an update to the literature on molecules with roles in tumor resistance therapy in head and neck squamous cell carcinoma (HNSCC). Although significant improvements have been made in the treatment for head and neck squamous cell carcinoma, physicians face yet another challenge-that of preserving oral functions, which involves the use of multidisciplinary therapies, such as multiple chemotherapies (CT) and radiotherapy (RT). Designing personalized therapeutic options requires the study of genes involved in drug resistance. This review provides an overview of the molecules that have been linked to resistance to chemotherapy in HNSCC, including the family of ATP-binding cassette transporters (ABCs), nucleotide excision repair/base excision repair (NER/BER) enzymatic complexes (which act on nonspecific DNA lesions generated by gamma and ultraviolet radiation by cross-linking and forming intra/interchain chemical adducts), cisplatin (a chemotherapeutic agent that causes DNA damage and induces apoptosis, which is a paradox because its effectiveness is based on the integrity of the genes involved in apoptotic signaling pathways), and cetuximab, including a discussion of the genes involved in the cell cycle and the proliferation of possible markers that confer resistance to cetuximab.

KEYWORDS:

drug resistance; epigenetics; oral squamous cell carcinoma

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