Nasopharyngeal Cancer Medication

Updated: Nov 17, 2016
  • Author: Arnold C Paulino, MD; Chief Editor: Cameron K Tebbi, MD  more...
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Medication

Medication Summary

Medical therapy consists of radiation therapy and chemotherapy. Concurrent treatment with cisplatin, 5-fluorouracil, and radiotherapy has been shown to improve survival rates. Other studies have used neoadjuvant chemotherapy followed by radiation therapy with improvement in local control or progression-free survival rates.

In November 2016, nivolumab was approved for SCCHN that has advanced on or after platinum-based therapy. Nivolumab significantly improved overall survival when compared with the comparator (investigator's choice of methotrexate, docetaxel, or cetuximab) in the phase 3 CheckMate-141 trial. [22]

Anesthetic lozenges and sprays may be helpful during the course of radiotherapy to minimize oral or throat pain, and pilocarpine with or without artificial salivary products (ie, oral sprays, gels, gums) may improve radiation-associated xerostomia.

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Antineoplastic agents

Class Summary

Chemotherapy is used to decrease the bulk of disease and to limit the risk of recurrence. Cancer chemotherapy is based on an understanding of tumor cell growth and how drugs affect this growth. After cells divide, they enter a period of growth (ie, phase G1), followed by DNA synthesis (ie, phase S). The next phase is a premitotic phase (ie, G2); then, finally a mitotic cell division (ie, phase M) occurs.

Cell division rate varies for different tumors. Most common cancers increase very slowly in size compared to normal tissues, and the rate may decrease further in large tumors. This difference allows normal cells to recover more quickly than malignant ones from chemotherapy and is the rationale behind current cyclic dosage schedules. Dosage cycles are determined by cancer stage and tolerance of adverse effects.

Antineoplastic agents interfere with cell reproduction. Some agents are cell cycle specific, whereas others (eg, alkylating agents, anthracyclines, cisplatin) are not. Cellular apoptosis (ie, programmed cell death) is also a potential mechanism of many antineoplastic agents.

Cisplatin (Platinol)

Inhibits DNA synthesis and, thus, cell proliferation by causing DNA crosslinks and denaturation of double helix.

5-Fluorouracil (5-FU, Adrucil)

Fluorinated pyrimidine antimetabolite that inhibits thymidylate synthase and also interferes with RNA synthesis and function. Has some effect on DNA. Useful in symptom palliation for patients with progressive disease.

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PD-1/PD-L1 Inhibitors

Class Summary

PD-1 and related target PD-ligand 1 (PD-L1) are expressed on the surface of activated T cells under normal conditions. PD-L1/PD-1 interaction inhibits immune activation and reduces T-cell cytotoxic activity when bound. This negative feedback loop is essential for maintaining normal immune responses and limits T-cell activity to protect normal cells during chronic inflammation. Tumor cells may circumvent T-cell–mediated cytotoxicity by expressing PD-L1 on the tumor itself or on tumor-infiltrating immune cells, resulting in the inhibition of immune-mediated killing of tumor cells.

Nivolumab (Opdivo)

Nivolumab is a monoclonal antibody to programmed cell death-1 protein (PD-1); blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2. It is indicated for recurrent or metastatic squamous cell carcinoma of the head and neck (SCCHN) with disease progression on or after a platinum-based therapy.

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Antiemetic agents

Class Summary

Prevention and treatment of chemotherapy-induced nausea and vomiting. Prevention is essential for highly emetogenic drugs (eg, cisplatin-based chemotherapy).

Antineoplastic-induced vomiting is stimulated through the chemoreceptor trigger zone (CTZ), which then stimulates the vomiting center (VC) in the brain. Increased activity of central neurotransmitters, dopamine in CTZ, or acetylcholine in VC appears to be a major mediator for inducing vomiting. Following administration of antineoplastic agents, serotonin (5-HT) is released from enterochromaffin cells in the GI tract. With serotonin release and subsequent binding to 5-HT3-receptors, vagal neurons are stimulated and transmit signals to the VC, resulting in nausea and vomiting.

Antineoplastic agents may cause nausea and vomiting so intolerable that patients may refuse further treatment. Some antineoplastic agents are more emetogenic than others. Prophylaxis with antiemetic agents prior to and following cancer treatment is often essential to ensure administration of the entire chemotherapy regimen.

Ondansetron (Zofran)

Selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally. Prevents nausea and vomiting associated with emetogenic cancer chemotherapy (eg, high-dose cisplatin) and complete body radiotherapy.

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Colony-stimulating factors

Class Summary

These agents act as a hematopoietic growth factor that stimulates the development of granulocytes. They are used to treat or prevent neutropenia in patients receiving myelosuppressive cancer chemotherapy and to reduce the period of neutropenia associated with bone marrow transplantation. They are also used to mobilize autologous peripheral blood progenitor cells for bone marrow transplantation and in the management of chronic neutropenia.

Filgrastim (G-CSF, Neupogen)

Granulocyte colony-stimulating factor that activates and stimulates production, maturation, migration, and cytotoxicity of neutrophils. Is most often administered to prevent neutropenia, starting 1 d after completion of highly myelosuppressive chemotherapy. Can also be used to treat neutropenia in the setting of significant infection.

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