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Review
. 2025 Feb 6;30(2):oyaf002.
doi: 10.1093/oncolo/oyaf002.

Management of vasomotor symptoms in cancer patients

Ling Zhu  1   2 , Tammy T Hshieh  3 , Tara K Iyer  4 , Alicia K Morgans  5 , Ole-Petter R Hamnvik  2
Affiliations
Review

Management of vasomotor symptoms in cancer patients

Ling Zhu et al. Oncologist. .

Abstract

Many cancer treatments can lead to reduced levels of sex hormones, which in turn may cause vasomotor symptoms (VMS) such as hot flashes. These symptoms are associated with impaired quality of life, as well as suboptimal tolerability of and adherence to cancer treatment. Hormone therapy, performed by increasing estradiol or testosterone levels, is the gold standard for treatment of VMS. However, this approach is generally contraindicated in patients with hormone-sensitive cancers. Nonhormone agents with low to moderate efficacy in controlling VMS are available, but their use may be limited by side effects and tolerability. In this narrative review, the approach to VMS in cancer patients will be discussed. The evidence for various treatment options, including novel agents such as fezolinetant that target the hypothalamic thermoregulatory pathway, will be evaluated. Finally, special considerations in different patient populations based on cancer types (eg, breast, prostate) and age groups (eg, older adults) will be explored.

Keywords: breast cancer; cancer survivors; hot flashes; menopause; prostate cancer.

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Conflict of interest statement

T.K.I. reports advisory roles at Astellas and Bayer. A.K.M. reports advisory roles at Astellas, AstraZeneca, Bayer, Exelixis, Lantheus, Curium, Merck, Myovant, Macrogenics, Pfizer, Novartis, SMPA, Sanofi, and Telix, and research funding from Astellas, AstraZeneca, Bayer, Lantheus, Curium, Myovant, Pfizer, Novartis, SMPA, and Telix. All other authors have no conflicts of interest.

Figures

Figure 1.
Figure 1.
Diagram illustrating the role of the KNDy neuron and its associated signaling pathway in generation of vasomotor symptoms. KNDy neuron is activated by NKB and inhibited by the endogenous opioid peptide dynorphin A. Following menopause, hypertrophy of KNDy neurons leads to increased kisspeptin release, and in turn GnRH secretion and LH pulses. In addition, NKB release is increased, which further stimulates kisspeptin release. NKB also acts on NK3R in the thermoregulatory center to trigger heat dissipation responses, leading to vasomotor symptoms. Abbreviations: FSH, follicle stimulating hormone; GnRH, gonadotropin-releasing hormone; KNDy, Kisspeptin/Neurokinin B/Dynorphin A; LH, luteinizing hormone; NK3R, neurokinin 3 receptor; NKB, neurokinin B.
Figure 2.
Figure 2.
Suggested approach to a cancer patient presenting with VMS. Abbreviations: ATE, arterial thromboembolism; CVD, cardiovascular disease; HT, hormone therapy; SNRI, serotonin norepinephrine reuptake inhibitors; SSRI, selective serotonin reuptake inhibitors; VMS, vasomotor symptoms; VTE, venous thromboembolism.
See this image and copyright information in PMC

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