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Health Protocols

Chemotherapy

How Does Chemotherapy Work?

Traditional chemotherapy destroys rapidly dividing cells by disrupting processes vital for cell division and survival. The aim of chemotherapy drugs is to kill cancer cells, or at least stop their growth and multiplication (Mihlon 2010; Baszkowsky 2012). Chemotherapy is most successful at treating rapidly proliferating tumors, such as certain leukemias, lymphomas, and testicular tumors, as well as smaller tumors that are growing rapidly (Baszkowsky 2012; Mitchison 2012).

The field of cancer therapy has expanded considerably in recent decades, and specialized classes of medicines are now incorporated into treatment regimens alongside classical cell-killing (cytotoxic) chemotherapy. These include molecularly targeted therapies, immunotherapies, cancer vaccines, hormonal therapies, and others. Although these more specific types of cancer medicine have helped improve outcomes in some types of cancer, traditional systemic chemotherapy—along with its side effects—is still a mainstay of cancer treatment today, and will likely remain so for some time (Galmarini 2012; Slater 2001; Joo 2013; NCI 2014c).

This protocol will review cytotoxic drugs and their side effects. Specialized cancer therapies are discussed in other Life Extension Disease Prevention and Treatment protocols.

Types of Chemotherapy Drugs

There are many different types of chemotherapy drugs. They are grouped into classes based on their mechanism of action, chemical structure, and relationship to other drugs. Some chemotherapy drugs fit into more than one class. Generally, cancer patients receive chemotherapy drugs from more than one class at the same time (Mihlon 2010; Baszkowsky 2012; Doroshow 2017). This strategy, called combination chemotherapy, aims to maximize the number of cancer cells killed and minimize development of chemoresistance. Combination chemotherapy has historically increased treatment efficacy in many types of cancer (Galmarini 2012; Yardley 2013; Pritchard 2012).

Table 1: Examples of Chemotherapy Drug Classes and Their Mechanisms of Action

Chemotherapy Class

Mechanism of Action

Types of Cancer Treated

Alkylating Agents : eg, bendamustine, carboplatin, chlorambucil, cisplatin, cyclophosphamide, procarbazine, streptozotocin

Bind to DNA, causing cell death by inhibiting protein and DNA synthesis

Leukemias, lymphomas, myelomas, and sarcomas; lung, reproductive system (breast, prostate, cervical, testicular, endometrial, ovarian), gastric, and head and neck cancers; and many other types of cancer

Antimetabolites : eg, fludarabine phosphate, methotrexate, mercaptopurine, 5-fluorouracil (5-FU), hydroxyurea

Interfere with metabolic pathways, including DNA and RNA synthesis

Leukemias and lymphomas; reproductive system, gastrointestinal, lung, bladder, and head and neck cancers; and many other types of cancer

Antitumor Antibiotics : eg, daunorubicin, doxorubicin, epidoxorubicin, idarubicin, actinomycin-D, bleomycin, mitomycin-C, mitoxantrone

Interfere with DNA and RNA synthesis; inhibit topoisomerase enzymes, which are involved in DNA synthesis

Leukemias, lymphomas, multiple myeloma, sarcomas, and many solid cancers

Topoisomerase Inhibitors : eg, topotecan, irinotecan, etoposide, teniposide

Inhibit topoisomerase enzymes

Certain leukemias, as well as lung, ovarian, gastrointestinal, and other cancers

Mitotic Inhibitors : eg, paclitaxel, ixabepilone, vinblastine, vincristine, vinorelbine, estramustine

Interfere with cell division

Myelomas, lymphomas, leukemias, and breast, lung, and other cancers

Others (chemotherapy drugs that do not fit into typical classes) : eg, L-asparaginase, bortezomib

L-asparaginase breaks down the amino acid asparagine, which cannot be synthesized by some cancers

Acute lymphoblastic leukemia

Bortezomib is a proteasome inhibitor that interferes with cells’ ability to break down damaged proteins

Secondary treatment of multiple myeloma and certain lymphomas

(Doroshow 2017; ACS 2017a; Healthwise 2013; Millenium Pharmaceuticals 2014; Piatkowska-Jakubas 2008; ACS 2013a)