Menopause following cancer treatment-induced menopause: unique considerations and current recommendations.

This research did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sector.

Tibolone is a selective tissue regulator with oestrogenic, progestogenic, and androgenic activity and has demonstrated efficacy comparable to conventional HRT. Due to its weak oestrogenic activity, it is less effective at managing severe symptoms in POI. However, it does effectively improve BMD and reduce fracture risk (HR: 0.73; 95% CI: 0.59–0.92) ( Barrionuevo et al. 2019 ). It may also offer a lower venous thromboembolism risk (RR: 0.92; 95% CI: 0.77–1.10 relative to non-use) compared with oral oestradiol (RR: 1.54; 95% CI: 1.44–1.65) ( Renoux et al. 2010 ) and therefore provide an alternative option for poor transdermal absorbers. Although tibolone appears to have a less stimulatory effect on breast tissue and does not increase mammographic density, its oncological safety continues to be uncertain. The LIBERATE trial was terminated early due to increased risk of breast cancer recurrence in those with oestrogen receptor-positive tumours (HR: 1.56, 95% CI: 1.22–2.01, P = 0.0005) ( Kenemans et al. 2009 ). Consequently, tibolone cannot be assumed to be a safer alternative and should not be prescribed where standard HRT is contraindicated. Transdermal testosterone therapy at physiological doses for premenopausal women improves sexual function in hypoactive sexual desire disorder (HSDD) when other causes have been excluded and baseline serum levels are low. Current evidence does not support its use for cognition, mood, or musculoskeletal outcomes (e.g. BMD and muscle strength). However, trials such as the ESTEEM study are anticipated to address some of these evidence gaps ( ISRCTN Registry 2025 ). Epidemiological studies have demonstrated that increased endogenous testosterone may be associated with increased breast cancer risk (HR: 1.18; 95% CI: 1.14–1.23) ( Tin Tin et al. 2021 ). In contrast, a randomised, double-blind, placebo-controlled trial involving 250 women, with no history of breast cancer, reported that exogenous testosterone therapy did not significantly increase mammographic breast density, and short-term use was not associated with increased breast cancer incidence ( Davis et al. 2009 ). However, the follow-up was only 52 weeks, which limits the ability of this study to establish the long-term breast safety of testosterone. A single-arm small pilot study of 29 breast cancer survivors undergoing ovarian suppression and aromatase inhibitor therapy evaluated a 3-month course of low-dose testosterone and demonstrated maintenance of baseline oestradiol levels alongside significant improvements in sexual function scores ( Taranto et al. 2024 ). Long-term safety was not a reported outcome, and larger, longitudinal randomised controlled trials are required to assess this. As there is limited information on the oncological safety of testosterone, particularly after hormone-positive cancers, such as breast cancer, and concerns over the peripheral conversion of testosterone to oestradiol, testosterone is not recommended. Tamoxifen and aromatase inhibitors are associated with menopausal symptoms. Symptoms typically become apparent within 3–6 months of treatment, after which they often stabilise or improve ( Marsden 2016 ). Switching endocrine therapies may help alleviate specific adverse effects (such as arthralgia and hair loss) but should only be considered in consultation with the oncology team. The use of HRT with selective oestrogen receptor modulators (SERMs) is not routinely recommended. In selected cases if HRT is considered, switching from an aromatase inhibitor to tamoxifen may provide theoretical reassurance, as tamoxifen antagonises oestrogen receptors in breast tissue. Although bazedoxifene combinations show some favourable breast safety in the general population, they remain contraindicated after breast cancer. Non-hormonal therapies play a key role in managing cancer treatment-induced menopause, especially in those for whom HRT is contraindicated or declined. However, their value extends beyond this subgroup of patients. As previously outlined, symptoms in cancer survivors often coalesce, due to the combined effects of endocrine changes, disease factors, and treatment-related toxicities. Therefore, HRT alone may not be sufficient to address the full range of symptoms or to improve quality of life. Also, confidence in counselling women on non-hormonal therapies facilitates patient choice. Non-hormonal approaches can be used to target individual symptoms. These include pharmacological agents, behavioural and psychological interventions, and lifestyle-based strategies, each with variable efficacy. A tailored approach should prioritise the most burdensome symptoms, whilst accounting for comorbidities, concurrent cancer treatments, and patient preferences. Pharmacological therapies ( Table 2 ) can be less effective than HRT if used individually. Their use for managing menopause is off-label, except for clonidine and neurokinin receptor antagonists. Most prescribable agents target vasomotor symptoms, with individual selective benefits for mood (antidepressants), pain or arthralgia (gabapentinoids), and urinary symptoms (oxybutynin). As such, by providing targeted symptom control, they can achieve improvements in quality of life without complete menopause symptom resolution. However, for many women, the side effect profile of these agents outweighs the benefits of these agents, and longer-term complications, such as sexual dysfunction with the SSRIs and addiction potential (SSRIs/gabapentinoids), should be discussed before initiating treatment. Drug interactions must also be considered, particularly cytochrome P4502D6 inhibition in tamoxifen users. Non-hormonal therapies for vasomotor symptoms: efficacy, safety, and considerations in oncology populations. SSRIs, selective serotonin reuptake inhibitors; SNRIs, serotonin–norepinephrine reuptake inhibitors. Other pharmacological agents may offer selective symptom benefit. For example, mirtazapine can improve sleep and mood, although its use is limited by side effects, including weight gain, sedation, and cognitive effects. Daridorexant, approved for chronic insomnia where non-pharmacological measures have been insufficient, reduces nocturnal awakenings without significant daytime sedation. It should only be used as a short-term intervention with appropriate monitoring and coordination with primary care.

In addition to menopausal symptoms, patients also experience cancer-related symptoms, treatment toxicities, and psychosocial stressors. These factors often intertwine with each other and can exacerbate menopausal symptom severity and negatively impact quality of life. Table 1 summarises the prevalence, severity, and clinical considerations of symptoms, highlighting the unique challenges faced by women experiencing cancer treatment-induced menopause. These symptoms rarely occur in isolation; cancer survivors frequently experience a convergence of symptoms that are driven by both menopausal hormonal changes and cancer treatment-related toxicities. Additionally, fatigue can act as a central amplifier of symptom burden, increasing the severity of hot flashes, mood disturbance, sexual dysfunction, and weight gain ( Glaus et al. 2006 ). Understanding how these symptoms occur together and interact is important for individualised menopause management. Clinical manifestations of cancer treatment-induced menopause: mechanisms and contributing factors. Summary of key symptom domains, showing the relative contributions of early menopause-related hormonal changes and cancer- or treatment-specific factors. DEXA, dual-energy X-ray absorptiometry; HR, hazard ratio; HRT, hormone replacement therapy; OR, odds ratio; PARPis, poly (ADP-ribose) polymerase inhibitors; AIs, aromatase inhibitors; POI, premature ovarian insufficiency. Aside from symptom burden, a major concern is accelerated biological ageing and the associated long-term morbidity. Increasing evidence suggests that early loss of ovarian function contributes to biological age acceleration due to epigenetic changes, telomere shortening, and markers of cellular senescence ( Zhou et al. 2025 ). In parallel, cancer survivors demonstrate treatment-related biological ageing, with similar alterations linked to increased cardiovascular and metabolic risk ( Mandelblatt et al. 2021 ). Therefore, cancer treatment-induced menopause may be conceptualised as a ‘double-hit’ model. Both disruption of the endocrine system and cancer therapies increase biological ageing and long-term morbidity in this population. A graded relationship is also observed for all-cause mortality across the menopause spectrum. A meta-analysis of seven studies showed that POI is associated with a 40% increased risk of all-cause mortality (RR: 1.40; 95 CI: 1.10–1.77), whilst EM confers a more modest risk (RR: 1.09; 95% CI: 1.00–1.18) ( Tao et al. 2016 ). Similarly, there is a 55% higher cardiovascular risk in women with POI, compared with a 30% in those aged 40–44 years relative to the average age of menopause. This gradient is observed in a number of cardiovascular outcomes and persists even after adjustment for other risk factors ( Zhu et al. 2019 ). These findings depict a dose–response relationship such that earlier loss of ovarian function is associated with progressively greater adverse health outcomes. Bone health is also influenced by age at menopause, with earlier ovarian insufficiency associated with a greater risk of low bone density. Data from the Women’s Health Initiative Observational Study ( n = 21,711) reported that menopause before 40 years was associated with a significantly higher fracture risk and lower bone mineral density (BMD) compared with menopause at age 50 years or older (HR: 1.21; 95% CI: 1.02–1.44) ( Sullivan et al. 2015 ). Interventional data demonstrate that this risk is reversible, with hormone replacement therapy (HRT) restoring BMD in women with POI to levels comparable with age-matched controls over 12 months ( Popat et al. 2014 ). In the context of cancer treatment-induced menopause, BMD loss is further increased. Population-based data indicate that there is a 10–30% excess fracture risk among cancer survivors compared with the general population ( Ye et al. 2024 ). Given this cumulative risk, early prevention strategies are essential. International guidelines recommend baseline BMD assessment at the time of POI diagnosis ( Panay et al. 2024 ). If normal and appropriate hormone replacement therapy (HRT) is initiated, a repeat evaluation within 5 years is not required. However, if osteopenia or osteoporosis is reported, then repeat assessment is advised. Routine advice should include adequate dietary calcium, vitamin D supplementation, and weight-bearing exercise. Where HRT is not recommended, non-hormonal alternatives, such as bisphosphonates, provide comparable benefits in preserving BMD but are associated with different side effect profiles. Zoledronic acid not only improves BMD but also reduces the risk of breast cancer recurrence in postmenopausal women ( Early Breast Cancer Trialist’s Collaborative Group 2015 ). Additionally, cardiovascular risk should be reviewed at diagnosis and monitored yearly, with optimisation of modifiable risk factors including smoking cessation, weight management, physical activity, blood pressure, and metabolic health (lipids and insulin resistance). Early initiation of HRT in POI, if not contraindicated, can mitigate cardiovascular and bone risk and is advised by international guidelines ( Panay et al. 2024 , National Institute for Health & Care Excellence 2025 ), although long-term data are limited. Beyond the average age of menopause, decisions regarding continuation of HRT should be individualised, using the lowest effective dose with regular review. Infertility following a diagnosis of POI is one of the most distressing outcomes for women, particularly those who have not completed their family. Furthermore, the loss of reproductive choice along with the disruption of anticipated life trajectories contributes to the psychological burden. In a cross-sectional survey of 136 women with POI, including women with menopause as a result of cancer treatment, fertility was the most frequently reported specific concern (75%) ( Singer et al. 2011 ). The impact of cancer treatment-induced menopause also extends to broader aspects of identity and self-perception. In the same cohort, 78% of women reported that POI negatively affected their self-image and confidence. Menopause occurring earlier than expected may create a perceived mismatch between chronological age and bodily ageing, contributing to feelings of social isolation from peers who have not yet experienced menopause ( Parton et al. 2017 ). Qualitative studies suggest that reproductive capacity remains closely linked to perceptions of femininity, thus contributing to the psychological impact of infertility and menopause ( Parton et al. 2017 ). Sexual dysfunction is also highly prevalent and multifactorial. It can include the loss of libido, vaginal dryness, dyspareunia, and diminished sexual confidence. These symptoms can negatively affect intimate relationships and are often compounded by fatigue, mood disturbance, and body image concerns associated with cancer treatment. Despite the significant symptom burden associated with cancer treatment-induced menopause, substantial gaps remain in counselling, access to specialist care, and symptom management among cancer survivors. Many women report receiving limited information beyond cancer risk reduction, with issues such as sexual health, cardiovascular risk, and body image often under-discussed. Consequently, survivors enter menopause with insufficient knowledge or support, amplifying distress and impairing quality of life. This is reflected in patient-reported survivorship data, in which menopause symptoms and associated health changes were reported to significantly impact quality of life in 86%, whilst 95% reported not receiving adequate support from their healthcare team during or after cancer treatment ( Talaulikar et al. 2025 ). Access to specialised menopause care is limited, with care commonly fragmented across specialities, primary care, and self-management ( Peate et al. 2021 ). Effective therapies are often underutilised due to lack of resources, clinician uncertainty, concerns regarding oncological safety, and inconsistent guidance ( Yongue et al. 2023 ). In the VIVROVAIRE study of ovarian cancer survivors, only 5 of 59 women (8.5%) received HRT despite 76% having no clear contraindication ( Gernier et al. 2021 ). Additionally, patient-reported barriers, such as concerns about treatment efficacy, treatment cost, stigma, and inadequate clinician knowledge about treatment options ( Hirschberg et al. 2025 ), further restrict timely intervention. A key structural contributor to these gaps is the limited recognition of cancer treatment-induced menopause as a distinct clinical entity within existing healthcare frameworks. Menopause following cancer treatment is often subsumed within general menopause guidance, without adequately addressing the specific risks and survivorship needs of this population. This lack of tailored guidance has implications for service provision and care pathways. However, it is also important to recognise that whilst some patients require specialist multidisciplinary input, a substantial proportion can be effectively supported within current services, provided that clinicians are equipped with appropriate knowledge and resources.

Menopause induced by cancer treatment presents a unique and complex clinical challenge that extends beyond the natural physiological process of menopause. Its abrupt onset, combined with the effects of oncological therapies, results in a multidimensional burden encompassing physical, psychological, and social domains. Although there is a growing awareness of cancer treatment-induced menopause as a significant survivorship issue, gaps remain in access to care, clinician education, and integration of menopause management within care pathways. Therefore, multidisciplinary and scalable models of care are required to address this unmet need. Such models would utilise specialist menopause services, integrate oncology pathways, and employ digital health interventions. Through a coordinated, patient-centred approach, survivorship and menopause care would balance both oncological safety and quality-of-life priorities. Future research should focus on the safety and efficacy of therapeutic interventions in cancer populations, including hormone replacement therapy, novel non-hormonal agents, and integrative approaches. Additionally, greater emphasis is required on translating existing evidence into routine clinical practice. Ultimately, improving outcomes for women with menopause induced by cancer treatment requires a shift away from the reactive management of symptoms and towards a more proactive integrative model that recognises menopause as an important component of cancer survivorship rather than a secondary consequence of treatment.

Management of menopause following cancer treatment requires an individualised, risk-stratified approach that balances oncological safety with quality-of-life priorities and prevention of future morbidity. As symptoms are driven by both menopause and oncological processes, HRT alone often does not adequately address the full spectrum of symptom burden, and a multimodal management approach is required. Figure 1 provides a practical framework to guide clinical decision-making, integrating key considerations including oncological risk, symptom burden, and long-term health outcomes. Algorithm outlining a stepwise, individualised approach to the management of menopause following cancer treatment-induced menopause. *Neurokinin-3 receptor antagonists are not currently approved by NICE for use in breast cancer populations, with guidance pending results from ongoing trials (including the HIGHLIGHT study). However, fezolinetant is now available on NHS prescription for non-oncological populations. SSRIs, selective serotonin reuptake inhibitors; SNRIs, serotonin–norepinephrine reuptake inhibitors; CBT, cognitive behavioural therapy; DEXA, dual-energy X-ray absorptiometry; CV, cardiovascular. HRT remains the most effective treatment for menopausal symptoms and for the prevention of long-term sequelae of oestrogen deficiency in those with premature/early menopause. However, its use in cancer survivors requires careful consideration according to recurrence risk, tumour biology (see Fig. 2 ), and individual patient factors and preferences. In women at low oncological risk, HRT can be prescribed and should be actively considered, particularly in those with POI. In this group, treatment is indicated not only to improve symptoms but also to mitigate the risks of long-term morbidity. HRT is recommended up until the average age of natural menopause (51 years) at which point its risks and benefits should be re-evaluated. In women at intermediate risk, HRT may be considered following an individualised risk–benefit assessment. Non-hormonal treatments should be explored in the first instance; however, if they are not effective or there is patient preference, then HRT can be considered. In women at high risk, systemic HRT is generally not recommended. In these patients, management should prioritise non-hormonal strategies and targeted local therapies where appropriate. For some women, an individualised multidisciplinary approach to HRT may be required if symptoms are severe and non-hormonal options are not acceptable or effective. When prescribing HRT for women with cancer treatment-induced menopause, it is important to recognise that this population often carries a higher baseline risk profile. Oral oestradiol is an effective option and may be used in appropriately selected women. However, transdermal oestrogen is recommended in those receiving active cancer treatment or with comorbidities, such as an increased risk of venous thromboembolism ( Vinogradova et al. 2019 ). Additionally, oral oestradiol should be used with caution in women at risk of drug interactions, such as those receiving systemic anticancer therapies, or in those with gastrointestinal malabsorption (e.g. radiation enteritis), as absorption may be unreliable. Women with an intact uterus, including those who have undergone pelvic radiotherapy, should be prescribed an adequate dose of progesterone/progestogen for endometrial protection. This should also be considered in hysterectomised women with a history of endometrial cancer, or endometriosis where there is a theoretical risk of stimulating residual disease. The choice of progestogen may also be clinically relevant. Limited evidence suggests that micronized progesterone and dydrogesterone may have a more favourable breast safety profile in low-risk women ( Fournier et al. 2007 ). Therefore, they may also be preferred in those with a history or increased risk of breast cancer, including BRCA mutation carriers. Off-label use of vaginal progesterone should be avoided in women who have undergone vaginal radiotherapy due to the risk of poor absorption.

Menopause marks the end of ovarian endocrine function and is associated with physiological and psychosocial changes. Menopause resulting from cancer treatment, surgery and systemic therapies, is often abrupt in onset and associated with increased severity of symptoms, with increased long-term health impacts in those experiencing an early menopause. Menopause symptoms can also overlap with ongoing cancer treatment side effects, introducing additional management complexity, particularly around the use of menopause hormone replacement therapy, which may impact cancer recurrence risk. This review synthesises current evidence in this area, examines contemporary management strategies, and highlights areas of controversy and ongoing need. By consolidating current perspectives and recommendations, we aim to support clinicians in providing individualised, evidence-based menopause care following cancer treatment.

SN declares receiving consulting fees from GSK, AbbVie, Bayer, and Pharma&; payment for lectures/presentations from GKS, AbbVie, and Pharma&; and travel expenses for attending meetings from MSD, GSK, and AbbVie; is on advisory boards at GSK, Biotech, Tubulis, Regeneron, Immunocore, AbbVie, Bayer, Pharma&; and has stock ownership in GSK, AstraZeneca, and Roche Family.

Cancer treatment-induced menopause is associated with the loss of ovarian function before the expected age of natural menopause. It is classified as premature ovarian insufficiency (POI) if occurring before age 40 and as early menopause (EM) between ages 40 and 44. Globally, the estimated prevalence of POI and EM is 3.7 and 12.2%, respectively ( Golezar et al. 2019 ). Although ovarian function may recover in some cases, many experience abrupt and complete ovarian failure leading to more severe symptoms ( Marino et al. 2014 ). Natural menopause usually results in a more gradual endocrine decline, with the postmenopausal ovary continuing to produce androgens, particularly testosterone, that contribute to a small amount of peripheral oestrogen synthesis. Conversely, surgical menopause results in more acute and marked reductions in circulating oestradiol, testosterone, and dehydroepiandrosterone (DHEA) ( Wu et al. 2025 ). Chemotherapy-induced ovarian insufficiency results from damage to the primordial follicle pool, although partial preservation of primordial follicles may allow recovery, particularly in younger women ( Meirow et al. 2010 ). The most gonadotoxic drugs are alkylating agents, particularly cyclophosphamide, causing damage to oocytes and granulosa cells in a dose-dependent fashion ( Wallace et al. 2005 ). Other drugs, such as platinum agents and doxorubicin, pose a moderate risk of gonadal dysfunction. Radiotherapy causes ovarian injury through dose-dependent destruction of follicles and vascular compromise. Pelvic irradiation directly exposes the ovaries to ionising radiation and causes menopause within the first six months ( Viswanathan et al. 2014 ). Total body irradiation results in ovarian failure in 90% of patients during long-term follow-up ( Viswanathan et al. 2014 ). Endocrine therapies further contribute to hypoestrogenism. Gonadotropin-releasing hormone agonists (GnRHas) induce a reversible hypogonadal state by pituitary desensitisation and suppression of gonadotrophin secretion. This suppresses ovarian steroidogenesis, with full effect achieved within 7–14 days ( Conn & Crowley Jr 1991 ). Aromatase inhibitors suppress oestradiol (E2) and oestrone (E1) production by inhibiting the peripheral conversion of androgens. Letrozole, the most potent agent in this class, reduces circulating oestradiol from a typical postmenopausal range of 10–60 pmol/L to below 1–3 pmol/L ( Faltinová et al. 2023 ). They are widely used as adjuvant therapy in oestrogen receptor-positive breast cancer and in selected gynaecological malignancies, including low-grade serous ovarian carcinoma. This profound suppression of oestrogen exacerbates menopausal symptoms and can significantly impact quality of life ( Faltinová et al. 2023 ). Tamoxifen is a selective oestrogen receptor modulator with anti-oestrogenic effects on the hypothalamic–pituitary axis. It can cause amenorrhoea and menopause symptoms but without permanently affecting ovarian function. A cohort study demonstrated that, in the absence of chemotherapy, tamoxifen use is not associated with earlier onset of menopause ( Chien et al. 2015 ). However, assessment of menopausal status can be challenging, as tamoxifen alters follicle-stimulating hormone (FSH) levels, and therefore, serial hormone measurements may be required ( Gradishar et al. 2026 ). Additionally, tamoxifen increases the risk of endometrial hyperplasia and adenocarcinoma, stroke, pulmonary embolism, and embryo-fetal toxicity ( National Library of Medicine (NLM), 2021 ). The increasing use of cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors in the management of hormone receptor-positive breast cancer has raised questions regarding their potential impact on ovarian function ( Scavone et al. 2023 ). Preclinical data suggest a biological basis for ovarian toxicity, as the cyclin D–CDK4/6 complex plays a key role in granulosa cell proliferation, primordial follicle activation, and oocyte meiosis. However, clinical data remain insufficient and are confounded by the routine co-administration of ovarian suppression in premenopausal women.

Cognitive behavioural therapy (CBT) is an evidence-based intervention grounded in a biopsychosocial model of menopause. Randomised controlled trials, including MENOS-2 ( Ayers et al. 2012 ), have demonstrated significant and sustained reductions in vasomotor symptoms (50%) and improvements in sleep and quality of life with the use of either group or self-help CBT. Lifestyle interventions provide modest but clinically meaningful benefits in both menopause symptoms and longer-term health. Practical measures, such as smoking cessation, reducing alcohol and caffeine intake, avoiding triggers and cooling strategies, alleviate vasomotor symptoms. Mind–body interventions (e.g. yoga, Pilates, and Tai Chi) may improve musculoskeletal symptoms, emotional well-being, and energy levels. Emerging evidence links diet and microbiome, with reduced intake of saturated fats and ultra-processed foods linked to improvements in cognition and mood ( Cuozzo et al. 2026 ). Additionally, optimisation of modifiable risk factors can be beneficial for symptom management. For example, improving metabolic health can support cognitive function, whilst weight loss may improve both arthralgia and vasomotor symptoms ( Anekwe et al. 2025 ). A wide range of over-the-counter supplements ( Table 3 ) are commonly used by women to manage menopausal symptoms despite variable and often limited evidence of activity. Some may have oestrogenic effects or interact with cancer therapies and therefore careful counselling regarding safety and efficacy is required. Over-the-counter supplements for menopausal symptoms: efficacy and safety considerations ( Mullin & Manley 2025 ). QOL, quality of life; VMS, vasomotor symptoms; RCT, randomised controlled trial. Low-dose topical vaginal oestrogen is the most effective therapy for GSM with minimal systemic absorption. As such, it is recommended by the National Institute for Health and Care Excellence as the first-line management of GSM ( National Institute for Health & Care Excellence 2025 ). The main exception to this guidance is for those with breast cancer using an aromatase inhibitor (see also Fig. 2 ). For this subgroup, non-hormonal moisturisers and lubricants should be offered as a first-line treatment with escalation to vaginal oestrogen on an individualised basis. Furthermore, switching to tamoxifen may permit safer use but must be balanced against oncological efficacy ( Baumgart et al. 2013 ). Where vaginal oestrogen is considered, the preparation choice may be relevant. Oestriol is a weaker oestrogen with a preferential affinity for urogenital rather than breast oestrogen receptors ( Katzenellenbogen 1984 ) and does not convert to the more potent oestradiol in vivo . In women with persistent symptoms, consider irritant reactions or alternative diagnoses, such as vulval dermatoses, radiotherapy changes, or graft-versus-host disease, after allogenic stem cell transplants. Risk stratification for hormone replacement therapy in cancer survivors. Risk categories are derived from available evidence, including British Gynaecological Cancer Society recommendations for gynaecological cancers ( Taylor et al. 2024 ) and expert guidance ( Hickey et al. 2024 , Yongue et al. 2026 ). *Endometrial cancers are stratified using ESGO prognostic risk groups. **Inconsistent results in studies, some showing increased risk whilst others do not. DCIS, ductal carcinoma in situ ; LCIS, lobular carcinoma in situ ; AI, aromatase inhibitor; HG, high grade; LG, low grade; ESS, endometrial stromal sarcoma. Alternative treatments for GSM include ospemifene and vaginal DHEA. Ospemifene is an oral SERM that improves vaginal dryness and dyspareunia by up to 80% at 12 months ( Di Donato et al. 2019 ). It can be useful when vaginal treatment is impractical. However, there are no safety data for its use in hormone-sensitive cancers. Similarly, prasterone, a vaginal dehydroepiandrosterone (DHEA) insert, is approved for moderate-to-severe dyspareunia in menopause. In a randomised controlled trial of 464 women with prior breast or gynaecological cancer, it improved symptoms and sexual function without increasing serum oestradiol levels ( Barton et al. 2018 ). The management of menopause after cancer requires a multidisciplinary approach due to the complex and evolving needs of cancer survivors, which are shaped by disease characteristics, treatment exposures, comorbidities, and individual preferences. Despite this, access to specialist menopause services remains limited, and many clinicians report uncertainty on how to apply existing evidence to clinical practice ( Yongue et al. 2023 ). Multidisciplinary menopause and survivorship services offer a strategy to address these challenges, by offering expertise from oncology, gynaecology, endocrinology, primary care, and allied health. An example of this type of approach is the Menopausal Service after Cancer (MSAC) in Australia. This service is reported to have resulted in significant improvements in patient-reported outcomes, including vasomotor symptoms, fatigue, sleep disturbance, and sexual well-being ( Hollingworth et al. 2022 ). However, such resource-intensive models may not be feasible in all healthcare settings. A more practical approach is through the integration of menopause care within routine oncology pathways. Given the frequency of oncology follow-up, embedding menopause assessment and management into cancer care, supported by multidisciplinary discussions, supports the provision of individualised, evidence-based care whilst continuing access to specialist input ( Brierley et al. 2026 ). Mind–body interventions, lifestyle modification, and non-pharmacological therapies can help improve overall well-being whilst complementing conventional treatments. Digital health initiatives have also been shown to improve symptoms, increase education, and empower patients with early menopause ( Yeganeh et al. 2022 ). A priority for future service development is the establishment of consensus across societies that recognise cancer treatment-induced menopause as a distinct clinical entity. There also needs to be clear guidance that delineates suitable care pathways. Existing models currently do not distinguish between patients who can be managed effectively in primary care and those requiring specialist or tertiary input. A stratified approach may help guide referral pathways and optimise resource utilisation to ensure that specialist services are targeted to those with the greatest need. Despite increasing recognition of cancer treatment-induced menopause as a significant survivorship issue, there are significant evidence gaps. The international Menopause Priority Setting Partnership (MAPS) ( Nash et al. 2024 ) and the National Institute for Health and Care Excellence ( National Institute for Health & Care Excellence 2025 ) have both identified key areas requiring further investigation. These include the identification of safe and effective non-hormonal therapies, particularly for women in whom HRT is contraindicated; optimisation of management strategies in breast cancer populations, where uncertainty regarding oncological safety persists; and clarification of the long-term safety, duration, and optimal regimens of hormone replacement therapy in higher-risk groups. In addition, high-quality longitudinal studies evaluating the safety of low-dose vaginal oestrogen in women using aromatase inhibitors and testosterone after breast cancer would also be of benefit.

GY drafted the manuscript. ZN, KM, MD, and SN contributed with significant edits to the final version.