Diseases of the Male Breast: Gynecomastia and Breast Cancer

Background: Gynecomastia (GM) is the most common abnormality of the male breast; it is benign and usually bilateral. GM is a manifestation of disease and not a diagnosis in itself. An important differential diagnosis of unilateral GM is breast cancer.

Methods: This narrative review is based on pertinent publications from 2010 onward that were retrieved by a PubMed search, with special attention to the guidelines of the AWMF and the European Academy of Andrology (EAA) and the recommendations of the German Society for Gynecology and Obstetrics.

Results: GM can occur physiologically in newborns, during puberty, and in men over age 65. The basic diagnostic evaluation of GM consists of a thorough history and physical examination (especially of the breast area and genitals), breast and testicular sonography, and laboratory testing for total testosterone (tT), estradiol (E2), luteinizing hormone (LH), human chorionic gonadotropin (hCG), and prolactin (PRL) levels. Further tests to be carried out as indicated according to the clinical findings include the determination of follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), fT4, alpha-1-fetoprotein (AFP), dehydroepiandrosterone (DHEA), and free testosterone (fT) levels, liver and kidney function tests, chromosomal analysis, and supplementary imaging procedures. The treatment depends on the underlying disease and the severity of symptoms, ranging from further observation alone to pharmacotherapy and surgery. Approximately 700 men receive a diagnosis of breast cancer each year in Germany. Because breast cancer in men is rare, there are no pertinent studies, and its treatment is analogous to the treatment of breast cancer in women as recommended in the guidelines.

Conclusion: Men should be included in clinical trials of treatment for breast cancer whenever this is feasible, so that the evidence base can be enlarged and men can be given access to innovative treatment methods.

Cite this as: Faridi A, Gerber B, Hartmann S: Diseases of the male breast: Gynecomastia and breast cancer. Dtsch Arztebl Int 2025; 122: 406–11. DOI: 10.3238/arztebl.m2025.0071

Gynecomastia vera (GM) is the most common benign abnormality of the male breast, with a prevalence of 32–65% (1). GM is not an independent entity but a manifestation of disease that leads to an imbalance of estrogen and androgen in the organism (1, 2, 3). It is defined as hypertrophy of the glandular body of the male breast, and it needs to be distinguished from lipomastia—an increase in fatty tissue without involvement of the glandular tissue (1, 4). GM can occur physiologically in different life phases. In neonates and infants, 65–90 of all neonates develop GM which spontaneously regresses several weeks after the birth. The prevalence of GM in adolescents varies between 22% and 69%, spontaneous regression is to be expected within 6–24 months. The prevalence of GM in adult men is reported in the literature as 36–57% (1, 3, 5, 6, 7). Gynecothelia is the term used to describe the isolated enlargement of the nipple-areola. We undertook a literature search in PubMed, covering the time period after 2010. In particular, we considered guidelines and recommendations regarding gynecomastia and breast cancer.

Physiology and pathophysiology

Neonatal GM is caused among others by the high fetal blood concentrations of estradiol and progesterone, which the mother produces, as well as by the increased conversion of steroid hormone precursors in sexual steroids and the increased aromatization of androgens as a result of the neonatal rise in luteinizing hormone (LH) (3). GM in puberty can be due to either reduced androgen production or increased aromatization of circulating androgens, with the estrogen to androgen ratio increased (2, 3, 8). Physiological GM in men older than 65 is often the result of relative hypogonadism with raised sexual hormone binding globulin (SHBG), lowered total testosterone (tT), and lowered free testosterone (fT) (9). Furthermore, the peripheral aromatization of androgens may be increased by a higher body mass index (9, 10). In obese men of all ages, lipomastia may develop in isolation or concomitantly with GM (11). Causes (Box 1) of pathological GM are medications, drug misuse, anabolic steroids, different diseases, obesity, paraneoplastic hormone production in testicular or other neoplasms, disorders of sexual differentiation, androgen ablation of advanced prostate cancer, and hypogonadism, which, among others, lead to:

Box 1

Causes of gynecomastia

• An (excessively) raised estrogen concentration or lowered androgen concentration
• Reduced androgen activity
• Androgen insensitivity
• Raised prolactin concentration, and
• Raised HCG values (2, 3, 12, 13).

In 45–50% of adult men with GM, no cause is found (13). Yang et al. determined that medication-induced GM is most often caused by antipsychotic medications, especially risperidone (Box 2). What is crucial, however, is the discovery that medication-induced GM accounts for only 0.17% of all reports of adverse events, which underlines its rarity in the clinical setting.

Box 2

Medications, drugs, and other substances that can cause gynecomastia

Pathology

In women, progesterone induces lobular development and proliferation and thus the formation of the terminal ductal-lobular unit (TDLU), which consists of the terminal duct and the lobules branching from it and represents the secretory and functional compartment of the breast (15). Although ductal and stromal proliferation can be very pronounced in men with gynecomastia vera, the lack of progesterone means that substantial lobular proliferation is rare, and for this reason, lobular changes—such as fibroadenomas, phyllodes tumors, most fibrocystic changes, lobular carcinoma in situ, and invasive lobular cancer—are rare in men (16). By contrast, lipomastia is due to a diffuse increase in fatty tissue without ductal or stromal proliferation (17). Under the influence of maternal estrogens in pregnancy, neonates may develop physiological transient GM, which is occasionally accompanied by milk secretion (18). In puberty, girls experience under the influence of estrogen and progesterone rapid growth of the breast with glandular proliferation, whereas in boys, this effect is counteracted by androgens. As a result, the normal male breast consists mainly of subcutaneous fatty tissue, rudimentary milk ducts, and some stroma elements. Cooper ligaments, fibrous ligaments that connect skin and breast tissue, are lacking (15, 17).

Clinical symptoms and diagnostic evaluation

The main symptom of GM is a palpable, mostly painless unilateral or bilateral retroareolar increase in the size of the glandular body (sonography/sonographic ≥2 cm) (5, 6, 19). In 50 men with GM in adolescence, Acharya et al. (20) found in 68% a bilateral and in 32% a unilateral occurrence. Especially in adolescence, GM may be associated with a substantial level of suffering and psychological strain, body dysphoria, and social isolation (18). Kinsela et al. (21) diagnosed in 24 young men adjustment (79.2%) and anxiety (16.7%) disorders, dysthymia (16.7%), and social phobias (4.2%). In lipomatous GM, an increase in fatty tissue without enlargement of the glandular body is the main symptom. In addition to a detailed medical history (among others, medications/drug misuse, sexual development, other disorders) and a thorough physical examination (breast and genitals), basic diagnostics include breast ultrasound to distinguish lipomatosis from GM, testicular ultrasound (to rule out testicular tumors), evaluation of total testosterone (tT), estradiol (E2), luteinizing hormone (LH), human chorionic gonadotropin (hCG), and prolactin, as well as in the extended diagnostic evaluation, adapted to the clinical findings, testing for liver enzymes, kidney function, follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), fT4, alpha-1-fetoprotein (AFP), dehydroepiandrosterone (DHEA), free testosterone (fT), chromosomal analysis, and complementary imaging procedures (Box 3) (1, 2, 3, 7, 9, 18, 22). The symptom triad of GM, loss of libido, and testicular tumor is characteristic for Leydig cell tumor (2, 18). The differential diagnostic evaluation of GM is of particular importance to rule out breast cancer. If on the basis of the clinical examination including breast ultrasound, breast cancer is suspected, mammography is recommended (suspect microcalcifications, multifocal/multicentric carcinoma?) before the necessary confirmation on histology by punch biopsy (Box 3) (1, 3, 16, 18, 22).

Box 3

Diagnostic evaluation in gynecomastia

Therapy

The treatment of GM is based on the underlying cause, its duration, its conspicuousness, and the degree of suffering. The spectrum ranges from watchful waiting, especially in GM in puberty (up to 24 months), via treating the underlying disease, lifestyle modifications (for example, weight loss, discontinuing medications, avoiding other substances that may be a contributing cause), medication therapy to surgical measures, which are indicated if the GM is persistent after the underlying cause has been eliminated and if the waiting period has been adequate, if spontaneous remission has not occurred, or if, after an attempt at medication (off label), the finding remains pronounced and/or the level of suffering is substantial. The latter particularly applies for GM in puberty; in this setting, a decision regarding surgery should be made once the patient has completed his puberty development. To correct estrogen-androgen imbalances, androgens, anti-estrogens, and aromatase inhibitors can be used (1, 2, 4, e1). Medication treatment for GM should be initiated before the tissue starts to fibrose (<6 months, where a high level of suffering in GM in puberty is experienced, this should be weighed up against spontaneous remission). Anti-estrogen active substances—for example, tamoxifen—are used especially in incident GM because of the good response rate (regression of 50% in 41–77.5% of patients) and a short treatment period of up to 6 months; according to the literature the recurrence rate is up to 14% (22). Nieschlag (18) comments that assessing the existing studies is difficult because the case and control groups (if the latter were included at all) are small and the results are difficult to interpret because of the frequent spontaneous remissions. The authors from the European Academy of Andrology (EAA) are opposed to the general use of selective estrogen receptor modulators (SERMs), aromatase inhibitors (AIs), or non-aromatizable androgens in the treatment of GM. They reason that scientific proof for these substances is currently lacking and they are not licensed for this indication (1, 8). In spite of this, tamoxifen is most often used in a curative attempt (off label) at a dosage of 10–20 mg/day and should be discontinued after three month depending on the extent of the GM, the expected spontaneous course, and the patient’s level of suffering if no significant improvement has occurred (2, 18).

Currently in the US, more than 24 000 lipomastia operations are undertaken every year , which corresponds to a notable increase in the number of surgeries by 36% since 2013 (5, 6, 23). The German Society of Plastic, Reconstructive and Aesthetic Surgeons (DGPRÄC) (24) also reported a notable nationwide increase in GM/lipomastia operations from 5.3% (2015) to 12.3% (2024). The motives for having an operation are lacking self-confidence and emotional stress (80%); pain or other physical symptoms are rarer (25).

In GM, the combination of different techniques of liposuction and surgical resection of the glandular body of the breast is a safe method that is low in complications (26). Knoedler et al. (23) reported a complication rate of 4.4% (among others, infections and impaired wound healing 1.8%, reoperations 2/4%). In pseudo-GM/lipomastia, liposuction can be carried out without any surgical measures. Satisfaction after GM/lipomastia surgery is high—regarding the postoperative course as well as the cosmetic result; overall satisfaction rates range from 62.5% to more than 80% (25, e2-e6).

Other benign diseases

Further less common benign changes of the male breast are cysts, abscesses that can develop (peri-)ductally in persons who smoke or who have diabetes mellitus as a sequela of mastitis, and hemangiomas—benign vascular neoplasms that arise from proliferation of vascular canals lined with endothelium. Furthermore, myofibroblastomas, spindle cell tumors (syn. stromal tumor) typically in the sixth and seventh decade of life, and intraductal papillomas, a ductal hyperplasia as a consequence of long-term GM (16). Pseudoangiomatous stromal hyperplasia (PASH)—first described in 1986—is a benign disease of the breast that has been observed in pre- and perimenopausal women; only individual cases have been described in men (27).

Breast cancer

Epidemiology

About 1% of breast cancers affect men (28), which means this cancer is rare in men. In 2020 in Germany, 740 of all 71,290 cases of breast cancer were in men; 166 men died as a result in the same year. On average, men develop breast cancer at an older age than women (71 years versus 65 years). In women, by contrast, breast cancer is the most common malignancy by some margin, with a lifetime risk of 13.2% (1 in 8 women) (e7). Because breast cancer is so rare in men, most studies focus on breast cancer in women, and the principles regarding diagnosis and treatment are in principle based on those of breast cancer treatment in women.

Risk factors

The demographic risk factors are increasing age (29) and familial breast cancer burden (30). Absolutely or relatively raised serum estrogen concentrations as in liver disease, testicular disorders, obesity, Klinefelter syndrome, and exposure to radiation in childhood or adolescence are also associated with an increased risk (31). Gynecomastia is also associated with a greater risk for breast cancer (OR=9.78; 95% confidence interval: [7.52; 12.7]) (e8). The cause of breast cancer in men may be a pathogenic mutation in breast cancer risk genes.

The prevalence of such mutations in the high-risk gene BRCA1/2 in the general population is 0.2–0.2% (e9), whereas in a German study population they were confirmed in 27.6% of all men with breast cancer, and pathogenic mutations in rarer risk genes, such as CHEK2, PALB2, and ATM occurred in clusters. Even without the existence of other family members with breast or ovarian cancer the probability for a pathogenic mutation in BRCA1/2 was 11% (32), consequently, if breast cancer is found in a man the recommendation is for genetic counseling and if needed genetic testing (e10). Men with a faulty BRCA1/2 gene do not only have an increased risk for developing breast cancer (lifetime risk for BRCA1 mutation 1–5%, for BRCA2 mutation it is 5–10%) (33) but also for prostate cancer (BRCA1 mutation 29%, BRCA2 mutation 60% lifetime risk) (34). Although no special cancer screening program is recommended for men with a confirmed mutation, those affected should be educated regarding the risk of developing disease and family members should be informed, since the inheritance is autosomal-dominant.

Clinical symptoms and diagnostic evaluation

A typical symptom is a poorly defined, rough, painless palpation-detected lesion in 97% of cases, which in 67% is located behind the nipple-areola (35). Because men have smaller breasts, their nipples are more commonly involved than those in women, in the form of retraction (9%), ulceration (6%), or pathological secretion (6%) (36). No screening measures are recommended in men. In addition to the lacking awareness of the disease, this is a reason for why the tumor is comparatively more often diagnosed at locally advanced or distant metastatic stages. In more than 40% of affected men, regional lymph node metastases are confirmed at the initial diagnosis (37), which can manifest clinically as rough, possibly fixed, axillary, infraclavicular or supraclavicular lymph node swellings.

The clinical examination of breast and lymph drainage pathways should be followed by imaging diagnostics in the form of breast ultrasound (including ultrasound of the axillary lymph nodes) and mammography (e11). On mammography, most invasive cancers present as hyperdense, irregularly shaped focal lesions with spiculated or lobulated edges (Figure). Microcalcifications are detectable in only 13–30% of tumors. On sonography, low-echo, irregularly shaped, spiculated or lobulated subareolar focal lesions may appear (38) . Once a suspect imaging finding is confirmed, a minimally invasive biopsy under local anesthesia is recommended for the purposes of further clarification. Staging for distant metastases is recommended—in analogy to the recommendation for women (e11)—only if the risk for distant metastases is high and/or symptoms exist and/or an indication exists for (neo-)adjuvant chemo-/antibody therapy, and then preferably in the form of computed tomography of thorax and abdomen and skeletal scintigraphy (e12).

Figure

Highly suspect focal lesion on mammography in two planes in a case of cancer in the left craniomedial breast in a 75 year old patient

Therapy

Because evidence from clinical studies for male breast cancer patients is lacking, the treatment is recommended according to the guidelines for female patients (e11). This is also the case for locoregional therapy in the form of surgical treatment and radiotherapy. In principle, breast-conserving therapy with subsequent radiotherapy is possible, but 88% of affected men have a mastectomy (e13). If tumor extirpation is possible with free margins, breast-conserving treatment in men probably does not lead to poorer survival rates (e14, e15). The reasons for the high mastectomy rate include the often unfavorable correlation of breast-tumor-volume and the retroareolar tumor position (e11, e17). If the tumor is clinically node negative, the less radical axillary sentinel lymph node biopsy (SLNB) is recommended (e11, e17). In men too, this is associated with lower postoperative morbidity than axillary lymphadenectomy with oncological safety (e18) remaining the same.

The recommendations for systemic therapy (at the early stage as well as at the distant-metastatic stage) are also articulated in analogy to those for female patients (e11, e17) (Table). The recommendation for carrying out chemotherapy and in HER2 positive cancer for anti-HER2 therapy in early breast cancer is made depending on tumor stage and tumor biology. There are no data from prospectively randomized trials in which only men were treated.

Table

Systemic therapeutic options for male patients with breast cancer

In hormone receptor positive tumors, endocrine therapy is indicated. In men, the selective estrogen receptor modulator tamoxifen is the active ingredient of choice (e17). The most commonly reported side effects are a loss of libido (9.7%), hot flushes (7.3%), fatigue (5.7%), anxiety disorders (4.2%), erectile dysfunction and sleep disorders (each 4%) (39). To avoid early discontinuation of treatment in confirmed benefit with significantly better survival and reduction in the rate of recurrence when carrying out endocrine therapy (e24), the adverse effects in affected patients should receive interdisciplinary care at breast centers with integrated psycho-oncology, independent gynecologists, general practitioners, urologists, and andrologists (Box 4) (e11). If, alternatively, aromatase inhibitors are used, the man should also be given a gonadotropin-releasing hormone (GnRH) agonist (e17) since 80% of estrogens in men are formed from testosterone by aromatase and 20% directly in the testicular Leydig cells (e25).

Box 4

Management of male breast cancer

Follow-up

Follow-up in male breast cancer patients is provided mainly in the treating hospitals (60%), but also by independent oncologists (24%) and gynecologists (23%) as well as general practitioners (17%). In addition to detecting and treating adverse effects of the therapy , follow-up care aims to detect locoregional, curatively treatable recurrences and contralateral breast cancers at an early stage. Annual breast imaging (mammography and breast ultrasound) should be carried out. Further imaging investigations are indicated only if a clinical suspicion exists of distant metastases (e26).

Conflict of interest statement
The authors declare that no conflict of interest exists.

Manuscript received on 6 December 2024, revised version accepted on 10 April 2025.

Translated from the original German by Birte Twisselmann, PhD.

Corresponding author
Prof. Dr. med. Andree Faridi

References

1. Kanakis GA, Nordkap L, Bang AK, et al.: EAA clinical practice guidelines-gynecomastia evaluation and management. Andrology 2019; 7: 778–93

2. Schanz S, Schreiber G, Zitzmann M, et al.: S1-Leitlinie: GM im Erwachsenenalter. AWMF Registernummer 013–039. J Dtsch Dermatol Ges 2017; 15: 465–72

3. Swerdloff RS, Ng JCM. Gynecomastia: Etiology, diagnosis, and treatment. In: Feingold KR, Anawalt B, Blackman MR et al. (eds): Endotext [Internet]. South Dartmouth (MA): MDText.com 2023.

4. Braunstein GD: Clinical practice. Gynecomastia. N Engl J Med 2007; 357: 1229–37

5. Braunstein GD: What accounts for the increased incidnce of gynecomastia diagnosis in Denmark from 1998–2017? J Clin Endocrinol Metab 2020; 105: e3810–1

6. Braunstein GD, Anawalt BD: Epidemiology, pathophysiology, and causes of gynecomastia. In: Post TW (eds). UpToDate. Waltham, MA: UpToDate; 2020.

7. AWMF GM: S1 Leitlinie der Deutschen Gesellschaft für Kinderheilkunde und Jugendmedizin. Register Nr. 027/028 (in Überarbeitung unter der Register Nr. 174/023) register.awmf.org/assets/guidelines/174–004m_S1_Kleinwuchs_2023–07.pdf (ast accessed on 25 April 2025)

8. Metwalley KA, Farghaly HS: Gynecomastia in adolescent males: Current understanding of its etiology, pathophysiology, diagnosis, and treatment. Ann Pediatr Endocrinol Metab 2024; 29: 75–81

9. Hohl A , Ronsoni MF, van de Sande Lee S, Gynecomastia. In: Hohl A, (eds.) Testosterone: From basic to clinical aspect. Springer 2024; 159–76

10. Braunstein GD: Aromatase and gynecomastia. Endocr Relat Cancer 1999; 6: 315–2

11. Rosen H, Webb ML, DiVasta AD, et al.: Adolescent gynecomastia: Not only an obesity issue. Ann Plast Surg 2010; 64: 688–90

12. Köhn FM, Schuppe HC: [Check list Gynecomastia]. MMW Fortschr Med 2022; 164: 65–9

13. Mieritz MG, Christiansen P, Jensen MB, et al.: Gynaecomastia in 786 adult men: Clinical and biochemical findings. Eur J Endocrinol 2017; 176: 555–66

14. Yang X, Zheng X, Zhang M, Huang J, Huang P, Wang J: Drug-induced gynecomastia: Data mining and analysis of the FDA Adverse Event Reporting System Database. Clin Epidemiol 2024; 16: 617–30

15. Boecker W, Weigel S, Heindel W, Stute P: The normal breast. In: Boecker W (ed.): Preneoplasia of the Breast. München: Saunders 2006; 2–27.

16. Mannix J, Duke H, Almajnooni A, Ongkeko M: Imaging the male breast: Gynecomastia, male breast cancer, and beyond. Radiographics 2024; 44: e230181

17. Yang S, Leng Y, Chau CM, et al.: The ins and outs of male breast and anterior chest wall lesions from childhood to adulthood. Clin Radiol 2022; 77: 503–13

18. Nieschlag E: Gynecomastia. In: Nieschlag E, Behre HM, Kliesch S, Nieschlag S (eds.): Andrology. Male Reproductive Health and Dysfunction. 4. Edition. Cham: Springer 2023; 479–90

19. Klang E, Kanana N, Grossman A, et al.: Quantitative CT assessment of gynecomastia in the general population and in dialysis, cirrhotic, and obese patients. Acad Radiol 2018; 25: 626–35

20. Acharya SV: Clinical features, presentation and hormonal parameters in patients with pubertal gynecomastia. J Family Med Prim Care 2021; 10: 648–51

21. Kinsella Jr. C, Landfair A, Rottgers SA, et al.: The psychological burden of idiopathic adolescent gynecomastia. Plast Reconstr Surg 2012; 129: 1–7

22. Berger O, Landau Z, Talisman R: Gynecomastia: A systematic review of pharmacological treatments. Front Pediatr 2022; 10: 1–8

23. Knoedler L, Knoedler S, Alfertshofer M, et al.: Gynecomastia surgery in 4996 male patients over 14 years: A retrospective analysis of surgical trends, predictive risk factors, and short-term outcomes. Aesthetic Plast Surg 2024; 48: 4642–50

24. DGÄPC: Zahlen, Fakten und Trends der Ästhetisch-Plastischen Chirurgie. Statistik 2015 und 2023–2024. www.dgaepc.de/aktuelles/dgaepc-statistik/ (last accessed on 25 April 2025).

25. Ridha H, Colville RJ, Vesely MJ: How happy are patients with their gynaecomastia reduction surgery? J Plast Reconstr Aesthet Surg 2009; 62: 1473–8

26. Fagerlund A, Lewin R, Rufolo G, et al. Gynecomastia: A systematic review. J Plast Surg Hand Surg 2015; 9: 311–8

27. Owji SC, Shroff N, Robinson AS, Posleman Monetto FE: Pseudoangiomatous stromal hyperplasia in a healthy young adult male. Radiol Case Rep 2022; 17: 2919–22

28. Gucalp A, Traina TA, Eisner JR, et al.: Male breast cancer: A disease distinct from female breast cancer. Breast Cancer Res Treat 2019; 173: 37–48

29. Giordano SH, Cohen DS, Buzdar AU, et al.: Breast carcinoma in men: A population-based study. Cancer 2004; 101: 51–7

30. Brinton LA, Richesson DA, Gierach GL, et al.: Prospective evaluation of risk factors for male breast cancer. J Natl Cancer Inst 2008; 100: 1477–81

31. Giordano SH: Breast cancer in men. N Engl J Med 2018; 378: 2311–20

32. Rolfes M, Borde J, Möllenhoff K, et al.: Prevalence of cancer predisposition germline variants in male breast cancer patients: Results of the German consortium for hereditary breast and ovarian cancer. Cancers 2022; 14: 3292

33. Ottini L: Male breast cancer: A rare disease that might uncover underlying pathways of breast cancer. Nat Rev Cancer 2014; 14: 643–4

34. Nyberg T, Frost D, Barrowdale D, et al.: Prostate cancer risks for male BRCA1 and BRCA2 mutation carriers: A prospective cohort study. Eur Urol 2020; 77: 24–35

35. Liu T, Tong Z, He L, Zhang L: Clinicopathological characteristics and survival analysis of 87 male breast cancer cases. Breast Care (Basel) 2011; 6: 446–51

36. Nofal MN, Yousef AJ: The diagnosis of male breast cancer. Neth J Med 2019; 77: 356–9.

37. Greif JM, Pezzi CM, Klimberg VZ, Bailey L, Zuraek M: Gender differences in breast cancer: Analysis of 13,000 breast cancers in men from the National Cancer Data Base. Ann Surg Oncol 2012; 19: 3199–204

38. Kim SH, Kim YS: Ultrasonographic and mammographic findings of male breast disease. J Ultrasound Med 2019; 38: 243–52

39. Wibowo E, Pollock PA, Hollis N, Wassersug RJ: Tamoxifen in men: A review of adverse events. Andrology 2016; 4: 776–88

40. Halbach SM, Midding E, Ernstmann N, et al.: Male breast cancer patients‘ perspectives on their health care situation: A mixed-methods study. Breast Care (Basel) 2020; 15: 22–9

e1. Billa E, Kanakis GA, Goulis DG: Imaging in gynecomastia. Andrology 2021; 9 :1444–56

e2. Frigerio G, Serre A, Engels PE, Kalbermatten DF, André-Lévigne D: Available techniques to minimize scars in surgical management of gynecomastia—a comprehensive review. JPRAS Open 2024; 42: 256–67

e3. Kasielska-Trojan A, Antoszewski B: Gynecomastia Surgery—impact on life quality: A prospective case-control study. Ann Plast Surg 2017; 78: 264–8

e4. Holzmer SW, Lewis PG, Landau MJ, et al.: Surgical management of gynecomastia: A comprehensive review of the literature. Plast Reconstr Surg Glob Open 2020; 8: e3161

e5. Wiesman IM, Lehman JA, Parker MG, et al.: Gynecomastia: An outcome analysis. Ann Plast Surg 2024; 53: 97–101

e6. Zhenzhen L, Yichun D, Xiaojing L: Study on the clinical effects of liposuction and small incision gland resection for the treatment of gynecomastia. Altern Ther Health Med 2023; 29: 222–7.

e7. Zentrum für Krebsregisterdaten und Gesellschaft der epidemiologischen Krebsregister in Deutschland e.V.: Krebs in Deutschland für 2019/2020. 14. Ausgabe. www.krebsdaten.de/Krebs/DE/Content/Publikationen/Krebs_in_Deutschland/krebs_in_deutschland_2023.pdf (last accessed on 18 September 2024).

e8. Brinton LA, Cook MB, McCormack V, et al.: Anthropometric and hormonal risk factors for male breast cancer: Male breast cancer pooling project results. J Natl Cancer 2014; 106: djt465

e9. BRCA Gene Changes: Cancer risk and genetic testing fact sheet–NCI (last accessed on 6 February 2025).

e10. Arbeitsgemeinschaft gynäkologische Onkologie e.V. Empfehlungen gynäkologische Onkologie Kommission Mamma. www.ago2025.de/fileadmin/2025/Slides_DE/AGO_2025D_02_Genetik.pdf (last accessed on 3 April 2025).

e11. Leitlinienprogramm Onkologie: S3-Leitlinie Mammakarzinom, Version 4.4, Juni 2021.

e12. Arbeitsgemeinschaft gynäkologische Onkologie e.V. Empfehlungen gynäkologische Onkologie Kommission Mamma. www.ago2025.de/fileadmin/2025/Slides_DE/AGO_2025D_03_Frueherkennung_und_Diagnostik.pdf (last accessed on 3 April 2025).

e13. Schulte-Vorwick FRM: Versorgungsrealität des Mammakarzinoms beim Mann: 10 Jahres-Analyse an zwei Brustzentren. www.edoc.ub.uni-muenchen.de/31945/6/Schulte-Vorwick_Felicitas.pdf (last accessed on 27 October 2023)

e14. Cloyd JM, Hernandez-Boussard T, Wapnir IL: Outcomes of partial mastectomy in male breast cancer patients: Analysis of SEER, 1983–2009. Ann Surg Oncol 2013; 20: 1545–50

e15. Bateni SB, Perry LM, Zhao X, et al.: The role of radiation therapy in addition to lumpectomy and hormone therapy in men 70 years of age and older with early breast cancer: A NCDB analysis. Ann Surg Oncol 2021; 28: 2463–71

e16. Arzanova E, Mayrovitz HN: Male breast cancer: Treatment trends, reported outcomes, and suggested recommendations. Cureus 2021; 13: e18337

e17. Arbeitsgemeinschaft gynäkologische Onkologie e.V. Empfehlungen gynäkologische Onkologie Kommission Mamma. www.ago2025.de/fileadmin/2025/Slides_DE/AGO_2025D_15_Brustkrebs_Spezielle_Situationen.pdf (last accessed on 3 April 2025).

e18. Maráz R, Boross G, Pap-Szekeres J, et al.: The role of sentinel node biopsy in male breast cancer. Breast Cancer 2016; 23: 85–91

e19. Arbeitsgemeinschaft gynäkologische Onkologie e.V. Empfehlungen gynäkologische Onkologie Kommission Mamma. www.ago2025.de/download-empfehlungen/download-empfehlungen-2022-3-1-1-1 (last accessed on 3 April 2025).

e20. Johnston SRD, Harbeck N, Hegg R, et al.: Abemaciclib combined with endocrine therapy for the adjuvant treatment of HR+, HER2−, node-positive, high-risk, early breast cancer (monarchE). J Clin Oncol 2020; 38: 3987–98

e21. Slamon D, Lipatov O, Nowecki Z, et al.: Ribociclib plus endocrine therapy in early breast cancer. N Engl J Med 2024; 390: 1080–91

e22. Schmid P, Cortes J, Pusztai L, et al.: Pembrolizumab for early triple-negative breast cancer. N Engl J Med 2020; 382: 810–21

e23. Tutt ANJ, Garber JE, Kaufman B, et al.: Adjuvant olaparib for patients with BRCA1- or BRCA2-mutated breast cancer. N Engl J Med 2021; 384: 2394–2405

e24. Giordano SH, Perkins GH, Broglio K, et al.: Adjuvant systemic therapy for male breast carcinoma. Cancer 2005; 104: 2359–64

e25. Hesse A, Hester A, König A, et al.: Management des Mammakarzinoms beim Mann. InFo Hämatol Onkol 2020; 23: 35–42

e26. Arbeitsgemeinschaft gynäkologische Onkologie e.V. Empfehlungen gynäkologische Onkologie Kommission Mamma. www.ago2025.de/fileadmin/2025/Slides_DE/AGO_2025D_16_Nachsorge.pdf (last accessed on 3 April 2025).