Japanese Journal of Clinical Oncology 30:188-190 (2000)
© 2000 Foundation for Promotion of Cancer Research
Bilateral Male Breast Cancer and Prostate Cancer: A Case Report
Gülhane Military Academy, 1Department of Medical Oncology and BMT Center and 2Department of Pathology, Ankara, Turkey
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONCASE REPORTDISCUSSIONREFERENCES |
|---|
Male breast cancer, consisting only 1% of all breast cancers, is occasionally associated with other primary malignancies, especially in patients with familial breast cancer history. Sporadic male breast cancers with another primary tumor are extremely rare. We report a 67-year-old male with asynchronous bilateral breast cancer and prostate cancer without familial breast cancer history.
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONCASE REPORTDISCUSSIONREFERENCES |
|---|
Breast carcinoma is rarely seen in males. Infiltrating ductal carcinoma is the predominant histologic type. Because most men with breast carcinoma have estrogen and progesterone receptor positive tumors, male breast cancer is likely to respond to hormonal manipulation (1–3). The incidence of contralateral breast cancer was reported as 2.7% in male breast cancer patients, similar to that in women (4). Prostate cancer is one of the leading causes of cancer death in men aged 65 or older. Little is yet known about the etiopathogenesis of the prostate cancer. There is some evidence regarding genetic predispositions and familial associations for this cancer (5–8). Despite male breast and prostate cancers being very similar in etiopathogenetic properties, their combination is unusual. We report here a male patient with asynchronous bilateral breast cancer and prostate cancer, which is a rarely reported situation.
|
CASE REPORT |
|---|
|
TOPABSTRACTINTRODUCTIONCASE REPORTDISCUSSIONREFERENCES |
|---|
A 67-year-old male was hospitalized with a 3 cm mass in his left breast. He had no history of familial breast cancer, any solid organ tumors or gynecomastia. Tumor markers and hormonal profile were normal [carcinoembryonic antigen (CEA) 0.01 µg/ml, CA 15-3 29 kU/l, follicle stimulating hormone 10.3 IU/l, luteinizing hormone 8.0 IU/l, total testosterone 14.35 nmol/l, progesterone 2.1 nmol/l, estradiol 102 pmol/l, aldosterone 80 pmol/l]. Examination of modified radical mastectomy and axillary dissection specimens revealed an estrogen receptor positive (90%), progesterone receptor positive (20%) and HER-2/neu amplification positive, poorly differentiated infiltrative carcinoma mostly growing as solid areas and virtually devoid of gland formation (Fig. 1). No axillary lymph node involvement was found. He was treated with external radiotherapy to the chest wall, axilla and supraclavicular fossa with doses of 50 Gy (2 Gy dose daily, five weekly fractions). Adjuvant chemo- or hormone therapy was not carried out owing to our concept at that time.
|
Multiple metastatic lesions in both lobes of the liver were determined by abdominal CT, 3 years after radiotherapy. Histopathological examination of the lesions revealed breast ductal carcinoma metastasis. Oral tamoxifen 20 mg daily was started for up to 5 years and the patient was treated with hepatic arterial chemoembolization, which was done by percutaneous catheterization of the femoral artery using the Seldinger technique (50 mg adriamycin and 10 ml lipiodol were mixed as an emulsion and injected slowly under fluoroscopic guidance). Chemoembolization was done every 6 weeks. At the end of the fifth chemoembolization session there was no heterogeneity and no mass lesion was visible in the liver. Two months later, the patient was admitted to the hospital with frequent urination, hesitancy and narrowing of urine stream. Prostate irregularity was observed on digital rectal examination and trans-rectal ultrasonography showed a 15.1 mm lesion in the left peripheral zone of the prostate and the capsule was intact. Prostate-specific antigen (PSA) level was fivefold higher than the reference value (20.8 µg/l). Examination of the needle biopsy material revealed a progesterone receptor positive (70%), estrogen receptor negative (0%), HER-2/neu negative, moderately differentiated adenocarcinoma (Gleason score = 6) (Fig. 2). The tumor was composed of single, separate, variable glands infiltrating among larger benign glands and smoothly circumscribed cribriform nodules. One month later, metastasis to the sternum and sacrum was detected by bone scintigraphy. The PSA, CA 15-3 and CEA values were 26.3 µg/l, 115.2 kU/l and 2.4 µg/l, respectively. After external radiotherapy to the pelvic region in doses of 40 Gy (2 Gy dose daily, five weekly fractions) and to the prostate with boost doses of 20 Gy in 2 weeks, he was treated with oral medroxyprogesterone acetate, 320 mg daily for eight months. The PSA and CA 15-3 levels decreased to the normal ranges quickly (0.38 µg/l and 22.3 kU/l, respectively) and the patient became symptom free within 19 months.
|
About 7 years after the diagnosis of the left breast cancer, two nodules were detected in the contralateral breast; one in the subareolar region and the other in the inferomedial area of the breast, both 0.5 cm in diameter. The CA 15-3 level was high (59.9 kU/l) and the PSA level was normal (1.2 µg/l) at that time. The histopathological diagnosis of both lesions was moderately differentiated infiltrative carcinoma (Fig. 3). The tumor showed well-developed glandular differentiation, well-defined nests and some individual cell infiltrations. External radiotherapy was given to right chest wall in dose of 36 Gy in 12 fractions and six cycles of paclitaxel, 175 mg/m2, were administered. Despite achieving partial remission initially, the patient died from progressive breast cancer 102 months after the first diagnosis. The terminal findings were local recurrence on the chest wall, pulmonary parenchymal metastases, mediastinal lymph node metastases, extensive bone metastases and liver metastasis. A graph documenting the clinical course of this case chronologically is shown in Fig. 4.
|
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONCASE REPORTDISCUSSIONREFERENCES |
|---|
The overall incidence of multiple primary cancers among cancer patients is 0.83%. The interval between the onsets of two cancers varies from 1 month to 30 years. The majority of the patients are male. The most commonly diagnosed multiple primary cancers are larynx and lung cancers, followed by lip and larynx cancers. Such malignancies, which occur together, probably have similar etiopathogenetic mechanisms (9).
The incidence of synchronous or metachronous contralateral breast cancer was reported as 2.7% in male breast cancer patients, similar to that of women (4). However, the incidence of synchronous or metachronous cancer was reported as 10.6% for male breast cancer patients, higher than that of women, and the most frequent sites were the prostate (21%), lung (14%), colon and rectum (14%) and esophagus (9%) (4). Combination of bilateral male breast cancer and prostate cancer is a rare condition, which has been reported in only 19 patients in the literature (4,10). As with our patient, just a few cases of this combination without a family history of breast cancer have been reported (7,11–13).
Prostate and male breast cancers have some similarities in terms of etiology, epidemiology and treatment approaches (4,8). Hormonal, genetic and environmental factors appear to be important in the development of male breast and prostate cancers (6–14). In our case, we could not find any morphological similarity between the two tumors. The first appearing tumor in the left breast was a poorly differentiated invasive carcinoma showing high nuclear grade. The tumor in the prostate had the typical morphology of prostatic adenocarcinoma such as growth pattern, glandular differentiation and cytological features. The tumor in the right breast that finally appeared was a moderately differentiated carcinoma revealing glandular differentiation. The lesion in the inferomedial area of the right breast had the same morphology as the last one. Neither of the tumors of the left and right breast had an intraductal component. We found it difficult to interpret tumors of the prostate and right breast as metastatic because of the striking morphological differences. The prostatic tumor revealed the typical histology of prostate adenocarcinoma and the tumor in the right breast was much more differentiated than the first one.
Several other etiopathogenetic mechanisms have been described in the literature for these tumors, including: (a) androgen receptor mutations (15,16), (b) the loss of heterozygosity at specific genetic loci (17), (c) BRCA2 mutation (18,19) and (d) Bcl-2 expression (20); however, their effects on the relationship between these tumors need to be clarified. Unfortunately, we could not evaluate our patient in terms of these etiopathogenetic mechanisms because of the lack of some technical facilities. Despite the absence of familial breast cancer history, we cannot be sure that our patient was a sporadic case because of the possibility of a new germline mutation of BRCA2. HER-2/neu gene amplification and protein overexpression have been established as a prognostic factor in breast and prostate cancers (21), but we did not find any relation between the two tumors in terms of HER-2/neu gene.
This case is a rare combination of multiple primary tumors. The absence of familial breast cancer history and the discordance of the HER-2/neu and hormone receptors status between the two tumors in our patient do not confirm the common opinion that breast and prostate cancers may develop due to similar factors. In our opinion, it is too early to conclude that the presence of breast cancer in a male can increase the risk of prostate cancer or vice versa. However, because such a combination is rarely diagnosed, it may be recommended that when either a breast or prostate cancer is diagnosed in a male patient, clinicians should be alert for the other.
|
FOOTNOTES |
|---|
+ For reprints and all correspondence: Ahmet Özet, Gülhane Military Academy, Department of Medical Oncology and BMT Center, Etlik 06018, Ankara, Turkey. E-mail: aozet@gata.edu.tr
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONCASE REPORTDISCUSSIONREFERENCES |
|---|
1 Rizk SN, Assimacopoulos CA, Ryan JJ. Male breast cancer: three case reports and review of the literature. S D J Med 1994;47:343–6.[Medline]
2 Bounds WE, Burton GV, Schwalke MA. Male breast cancer. J La State Med Soc 1993;145:353–6.[Medline]
3 Hecht JR, Winchester DJ. Male breast cancer. Am J Clin Pathol 1994;102:25–30.
4 Cutuli BF, Lacroze M, Dilhuydy JM, Florentz P, Velten M, Allavena C, et al. Breast cancer in men: incidence and types of associated previous synchronous and metachronous cancers. Bull Cancer 1992;79:689–96.[ISI][Medline]
5 DeAntoni EP, Crawford ED. Pretreatment of metastatic disease. Prostate cancer in the older male. Cancer 1994;74:2182–7.[ISI][Medline]
6 Wilding G. Endocrine control of prostate cancer. Cancer Surv 1995;23:43–62.[ISI][Medline]
7 Carter BS, Bova GS, Beaty TH, Steinberg GD, Childs B, Isaacs WB, et al. Hereditary prostate cancer: epidemiologic and clinical features. J Urol 1993;146:1305.
8 Pienta KJ, Goodson JA, Esper PS. Epidemiology of prostate cancer: molecular and environmental clues. Urology 1996;48:676–83.[ISI][Medline]
9 Engin K. Cancers in multiple primary sites. Int Surg 1994;79:33–7.[ISI][Medline]
10 Tajika M, Tuchiya T, Yasuda M, Ito Y, Nakamura T, Yamauchi K, et al. A male case of synchronous double cancers of the breast and prostate. Intern Med 1994;33:31–5.[ISI][Medline]
11 Akashi-Tanaka S, Fukutomi T, Fukami A, Fujiki T. Male breast cancer in patients with a familial history of breast cancer. Surg Today 1996;26:975–9.[ISI][Medline]
12 Tulinius H, Olafsdottir GH, Sigvaldason H, Tryggvadottir L, Bjarnadottir K. Neoplastic diseases in families of breast cancer patients. J Med Genet 1994;31:618–21.[Abstract]
13 Anderson DE, Badzioch MD. Familial effects of prostate and other cancers on lifetime breast cancer risk. Breast Cancer Res Treat 1993;28:107–13.[ISI][Medline]
14 Stephens RL, Schimke RN. Case report: breast cancer in males – a genetic consideration. Am J Med Sci 1992;304:91–2.[ISI][Medline]
15 MacLean HE, Warne GL, Zajac JD. Defects of androgen receptor function: from sex reversal to motor neurone disease. Mol Cell Endocrinol 1995;112:133–41.[ISI][Medline]
16 Namer M, Cutuli BF, Pujol H, Sultan C. Androgen receptor gene mutation in male breast cancer. Hum Mol Genet 1993;2:1799–802.
17 Chuaqui RF, Sanz Ortega J, Vocke C, Linehan WM, Sanz Esponera J, Zhuang Z, et al. Loss of heterozygosity on the short arm of chromosome 8 in male breast carcinomas. Cancer Res 1995;55:4995–8.
18 Thorlacius S, Olafsdottir G, Tryggvadottir L, Neuhausen S, Jonasson JG, Tavtigian SV, et al. A single BRCA2 mutation in male and female breast cancer families from Iceland with varied cancer phenotypes. Nature Genet 1996,13:117–9.[ISI][Medline]
19 Tonin P, Ghadirian P, Phelan C, Lenoir GM, Lynch HT, Letendre F, et al. A large multisite cancer family is linked to BRCA2. J Med Genet 1995;32:982–4.[Abstract]
20 Bhargava V, Kell DL, Van de Rijn M, Warnke RA. Bcl-2 immunoreactivity in breast carcinoma correlates with hormone receptor positivity. Am J Pathol 1994;145:535–40.[Abstract]
21 Ross JS, Sheehan CE, Hayner-Buchan AM, Ambros RA, Kallakury BV, Kaufman RP Jr, et al. Prognostic significance of HER-2/neu gene amplification status by fluorescence in situ hybridization of prostate carcinoma. Cancer 1997;79:2162–70.[ISI][Medline]
Received December 7, 1999; accepted February 4, 2000.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||