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Molecular mechanisms associated with chemoresistance in esophageal cancer.

Abstract
Esophageal cancer (EC) is one of the most incident and lethal tumors worldwide. Although surgical resection is an important approach in EC treatment, late diagnosis, metastasis and recurrence after surgery have led to the management of adjuvant and neoadjuvant therapies over the past few decades. In this scenario, 5-fluorouracil (5-FU) and cisplatin (CISP), and more recently paclitaxel (PTX) and carboplatin (CBP), have been traditionally used in EC treatment. However, chemoresistance to these agents along EC therapeutic management represents the main obstacle to successfully treat this malignancy. In this sense, despite the fact that most of chemotherapy drugs were discovered several decades ago, in many cases, including EC, they still represent the most affordable and widely employed treatment approach for these tumors. Therefore, this review summarizes the main mechanisms through which the response to the most widely chemotherapeutic agents used in EC treatment is impaired, such as drug metabolism, apoptosis resistance, cancer stem cells (CSCs), cell cycle, autophagy, energetic metabolism deregulation, tumor microenvironment and epigenetic modifications.
AuthorsMatheus Lohan-Codeço, Maria Luísa Barambo-Wagner, Luiz Eurico Nasciutti, Luis Felipe Ribeiro Pinto, Nathalia Meireles Da Costa, Antonio Palumbo Jr
JournalCellular and molecular life sciences : CMLS (Cell Mol Life Sci) Vol. 79 Issue 2 Pg. 116 (Feb 03 2022) ISSN: 1420-9071 [Electronic] Switzerland
PMID35113247 (Publication Type: Journal Article, Review)
Copyright© 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.
Chemical References
  • Antineoplastic Agents
  • Biomarkers, Tumor
  • Carboplatin
  • Paclitaxel
  • Cisplatin
  • Fluorouracil
Topics
  • Antineoplastic Agents (therapeutic use)
  • Biomarkers, Tumor (antagonists & inhibitors, genetics, metabolism)
  • Carboplatin (therapeutic use)
  • Cisplatin (therapeutic use)
  • Drug Resistance, Neoplasm (drug effects, genetics)
  • Esophageal Neoplasms (drug therapy, genetics, metabolism)
  • Fluorouracil (therapeutic use)
  • Humans
  • Molecular Targeted Therapy (methods)
  • Mutation
  • Paclitaxel (therapeutic use)
  • Tumor Microenvironment (drug effects, genetics)

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