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A Note on Treatment Regimens

Cancer treatment regimens change to reflect continuous advances in basic and clinical science: new drugs, both small molecules and biologicals; improved methods of targeting and timing of drug delivery; agents with altered pharmacokinetic properties and selectivities; the use of rational multidrug combinations; and greater knowledge of the basic cell biology of tumorigenesis, metastasis, and immune function, amongst other advances. As a consequence, this chapter presents relatively few detailed treatment regimens; rather, we refer the reader to the web-based resources of the U.S. FDA and the NCCN. Table 67–1 provides the details and demonstrates the complexities of treatment of two cancers.


The growth of a number of cancers is hormone dependent or regulated by hormones. Glucocorticoids are used for their antiproliferative and lympholytic properties and to ameliorate untoward responses to other treatments. Estrogen and androgen antagonists, steroid synthesis inhibitors, and GnRH analogues and antagonists are all effective in extending survival and delaying or preventing tumor recurrence of both breast and prostate cancer. These molecules interrupt the stimulatory axis created by systemic pools of androgens and estrogens, inhibit hormone production or hormone binding to receptors, and ultimately block expression of genes that promote tumor growth and survival.





ADME: absorption, distribution, metabolism, excretion

ADT: androgen deprivation therapy

AI: aromatase inhibitor

ALL: acute lymphoblastic leukemia

AR: androgen receptor

CDK: cyclin-dependent kinase

CLL: chronic lymphocytic leukemia

CRPC: castration-resistant prostate cancer

CYP: cytochrome P450

DHEA: dehydroepiandrosterone

ER: estrogen receptor

ERE: estrogen-response element

FDA: Food and Drug Administration

FSH: follicle-stimulating hormone

HL: Hodgkin lymphoma

HR: hormone receptor

GI: gastrointestinal

GnRH: gonadotropin-releasing hormone

GR: glucocorticoid receptor

HR: hormone receptor (i.e., ER+/PR+)

LH: luteinizing hormone

MM: multiple myeloma

mTOR: mechanistic target of rapamycin

NCCN: National Comprehensive Cancer Network

NHL: non-Hodgkin lymphoma

PR: progesterone receptor

PSA: prostate-specific antigen

SERD: selective estrogen receptor downregulator

SERM: selective estrogen receptor modulator




The pharmacology, major therapeutic uses, and toxic effects of the glucocorticoids are discussed in Chapter 46. Only the applications of these drugs in the treatment of neoplastic disease are considered here.


Glucocorticoids act by binding to a specific GR that is a member of the nuclear receptor family of transcription factors. The GR translocates to the nucleus and induces complex gene expression changes (Chapter 46) that lead to antiproliferative and apoptotic responses in sensitive cells. Because of their lympholytic effects and their ability to suppress mitosis in lymphocytes, glucocorticoids are used as cytotoxic agents in the treatment of acute leukemia in children and malignant lymphoma in children and adults. In acute lymphoblastic or undifferentiated leukemia of childhood, glucocorticoids may produce prompt clinical improvement and objective hematological remissions in 30% of children. However, the duration of remission is brief. Remissions occur more rapidly with glucocorticoids than with antimetabolites, and there is no evidence of cross-resistance ...

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