Background Synchronous cancers have occasionally been detected at initial diagnosis among patients with breast and ovarian cancer. contralateral breast malignancy and coexistent breast and ovarian cancer have been reported at initial diagnosis [6, 7]. We report here the case of a woman with a germline BRCA2 mutation who presented with synchronous onset of breast malignancy and pancreatic cancer. Case Report The patient is usually a 41-year-old premenopausal woman who discovered a lump in the upper outer quadrant of the left breast. The workup was conducted in July 2015 within a week of symptom onset. Bilateral diagnostic mammography revealed pleomorphic calcifications Rabbit polyclonal to HOXA1 in the area of concern. An ultrasound revealed a 3.2-cm solid mass in the 2 2: 00 position 8 cm from the nipple, and 2 smaller masses in the 2 2: 30 position that were 4 cm from the nipple, which appeared to represent multifocal disease. An ultrasound-guided breast biopsy was performed. The 2 2: 00 o’clock lesion contained infiltrating duct carcinoma with intermediate- to high-grade features and duct carcinoma in situ (DCIS) with comedonecrosis. The 2 2: 30 Triapine manufacture lesion contained DCIS as well. The estrogen receptor (ER) stained 100%, and the progesterone receptor 12%. The HER2 FISH was 1.1. An MRI of the breast was performed which showed a suspicious lesion on the right side. A biopsy of the contralateral breast lesion was unfavorable. The left axillary lymph nodes (LNs) were sampled by ultrasound-guided fine needle aspiration Triapine manufacture and were negative. Because the breast malignancy was locally advanced by examination, a metastatic survey was undertaken. Metastatic disease was not discovered; however, a CT of the body (fig. ?(fig.1)1) revealed a 2.6-cm mass in the tail of the pancreas. The CA19-9 was 126 (normal 0C38). A positron emission tomography (PET) scan was positive in the pancreas with an SUV level of 3.6. A CT-guided biopsy of the lesion revealed adenocarcinoma. Immunostains for villin and CA19-9 were positive, and unfavorable for ER, establishing pancreatic origin and ruling out the diagnosis of a metastatic lesion (fig. ?(fig.22). Fig. 1 CT and FDG-PET/CT scans obtained at diagnosis. a A neoplastic lesion was identified in the tail of the pancreas. b Hypermetabolism is usually identified in the tail of pancreas lesion and axillary LNs. Primary breast lesion is not shown. Fig. 2 Histology and immunostains of breast and pancreas cancers diagnosed at presentation. Triapine manufacture Top panels: breast cancer, bottom panels: pancreas cancer. Left column: hematoxylin and eosin stains, middle column: villin stains, right column: ER stains. The patient was taken to the operating room in August 2015 and underwent a left altered radical mastectomy. Pathology revealed a 7.5-cm grade 2 (tubule 3, nuclear 3, mitoses 1 = 7/9) infiltrating duct carcinoma with lymphovascular invasion. A component of high-grade DCIS with solid and cribriform features occupying 50C60% of the tumor and made up of comedonecrosis was also identified. The deep margins for both the invasive and in situ components were clear by 0.6 cm and 8/23 LNs were found to contain metastatic cancer. She was considered to have a G2 pT3N2aM0, AJCC stage IIIA breast cancer. In September 2015, the patient underwent a laparoscopic, hand-assisted splenectomy, distal pancreatectomy, lymphadenectomy, and concomitant bilateral salpingo-oophorectomy. Pathology revealed a 3.2 2.3 2.0 cm moderately differentiated adenocarcinoma with invasion of the peripancreatic fat. Perineural invasion was present, but vascular invasion Triapine manufacture was not. The resection margins were 1.8 cm from proximal pancreatic margin; 1/13 regional LNs contained metastatic disease. She was considered to have G2, pT2N1M0, AJCC stage IIB pancreatic cancer. The fallopian tubes and ovaries were submitted entirely for microscopic examination and were histologically unremarkable. Germline genetic testing (Inherited Cancer Screen, Counsyl Inc., South San Francisco, Calif., USA) confirmed the presence of a deleterious BRCA2 mutation characterized as c.5681(dupA). Her father, who was diagnosed with Triapine manufacture prostate cancer at age 69, and her younger brother carry the same BRCA2 mutation..