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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, among 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 (drugs@fda) and the NCCN (National Comprehensive Cancer Network). Table 71–1 provides the details and focuses on the complexities of treatment of two cancers.



ADT: androgen deprivation therapy

AI: aromatase inhibitor

ALL: acute lymphoblastic leukemia

AR: androgen receptor

AUC: area under the curve

BAT: bipolar androgen deprivation therapy

BCRP: breast cancer resistance protein

CDK: cyclin-dependent kinase

CLL: chronic lymphocytic leukemia

CRPC: castration-resistant prostate cancer

CYP: cytochrome P450

ER: estrogen receptor

ERE: estrogen-response element

FSH: follicle-stimulating hormone

GnRH: gonadotropin-releasing hormone

GR: glucocorticoid receptor

HER: human epidermal growth factor

HL: Hodgkin lymphoma

HR: hormone receptor

LH(RH): luteinizing hormone (–releasing hormone)

MM: multiple myeloma

mTOR: mechanistic (or mammalian) target of rapamycin

NHL: non-Hodgkin lymphoma

OATP: organic anion transporting polypeptide

Pgp: P-glycoprotein

PR: progesterone receptor

PROTAC: proteolysis targeting chimeras

SERD: selective estrogen receptor downregulator

SERM: selective estrogen receptor modulator

UGT: UDP-glucuronosyltransferase


The growth of a number of cancers is hormone-dependent or regulated by hormones. Therapies that employ estrogen and androgen receptor antagonists, steroid hormone synthesis inhibitors, and gonadotropin-releasing hormone (GnRH) analogues or antagonists extend survival and delay or prevent tumor recurrence of both breast and prostate cancer. These molecules interrupt the normal feedback controls regulating steroid hormone synthesis, inhibit androgen and estrogen production, or inhibit binding of these hormones to their cognate receptors, which are ligand-activated transcription factors. By inhibiting the activation and actions of androgen and estrogen receptors, these drugs block or reduce expression of genes and gene networks that ultimately promote tumor growth and survival. Glucocorticoids are used for their antiproliferative and lympholytic properties in hematologic malignancies and, in other oncological settings, to mitigate untoward responses to other treatments as well as some cancer-related symptoms.

The pharmacology of the estrogens and androgens is described in detail in Chapters 48 and 49. Decreasing the actions of these steroid hormones is the therapeutic goal in certain cancers, most notably those of the prostate and breast, because these organs are dependent on steroid hormones for their growth, function, and morphological integrity.


The presence of the estrogen receptor (ER) and/or progesterone receptor (PR) (ER+/PR+) in female breast cancer tissue identifies the subset of hormone receptor–positive cancers with a greater than 60% likelihood of responding to endocrine therapy. The response rate to ...

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