Neuroendocrine Breast Cancer Research Articles

PO-1089 Long-term follow-up of a single-center neuroendocrine breast cancer cohort

PO-1089 Long-term follow-up of a single-center neuroendocrine breast cancer cohort

Breast cancer with neuroendocrine differentiation: an update based on the latest WHO classification.

Breast cancers with neuroendocrine (NE) differentiation are very heterogeneous, comprising broadly cancers that are morphologically similar to NE tumors (NET) of other anatomic sites, infiltrating breast carcinomas, no special type (IBC-NST) and other special subtypes with NE morphology and/or NE markers expression. Depending on the classification schemes, they are variably included into "NE breast cancers". The latest WHO classification harmonized NE breast cancers with NE neoplasms (NEN) of other organ systems, defined NEN into well-differentiated NET (low Nottingham grade) and poorly-differentiated NE carcinoma (NEC) (high Nottingham grade). Other IBC with NE differentiation are diagnosed based on solely the non-NEN component. Due to the changes in diagnostic criteria, variable results were obtained in the previous studies on NE breast cancers. Hence, the clinical value of NE differentiation in breast cancers is not well investigated and understood. In this review, the current understanding in the pathogenesis, clinical, prognostic, immunhistochemical, and molecular features of "NE breast cancers" is summarized. Controversial issues in their diagnosis and classification are also discussed.

Rare presentation of metastasized primary neuroendocrine breast carcinoma to the right colon and literature review of primary neuroendocrine breast carcinoma metastasized to other organs of the body: case report

Primary neuroendocrine breast tumors account for less than 0.1% of all breast cancers, hence, unique in nature. This paper aims to report a 56 years old female, known case of primary neuroendocrine breast cancer with a metastatic right colonic neuro-endocrine tumor. The article also aims to review and acclaim the literature regarding primary breast neuroendocrine tumors metastasized to other parts of the body. The patient presented complaining of a breast mass, ulceration, and discharge, which was rapidly progressing. Examination revealed a right breast mass with skin erythema and impending ulceration and right axillary lymph nodes fixed with palpable supra-clavicular lymph nodes. Ultrasound-guided biopsy of right breast mass and axilla disclosed a large cell neuroendocrine carcinoma. CT abdomen and chest revealed metastases to the ascending colon. The patient was treated with palliative radiotherapy along with multiple cycles of chemotherapy for the primary breast cancer. She also underwent a laparoscopic-assisted right hemicolectomy with complete mesocolic excision and primary anastomosis for the metastatic colon cancer. The paper compares the reported case to other similar cases using the framework of an analysis based on age of the patient, primary breast cancer location, method of detection, presence of neuroendocrine markers, primary cancer presentation, metastases symptoms, and location and treatment approach. In conclusion, metastasized primary neuroendocrine breast cancer is a very rare presentation. Incidence and prevalence maybe influenced by age, primary breast cancer location, and presence of neuroendocrine markers. Prognosis may also be a product of metastatic location, associated symptoms and treatment approaches.

Neuroendocrine Cancer of the Breast: A Rare Entity.

Neuroendocrine breast cancer (NEBC) is a rare histotype of breast carcinoma that presents, in most cases, positive hormone receptors and negative HER2. Indeed, the analysis of gene expression profiles revealed that NEBC belongs mainly to the luminal subtype. Cases of HER2-positive and triple-negative NEBC are rare. The cardinal treatment of early NEBC is surgery, similar to the treatment of invasive non-special histological type carcinoma. The use of radiotherapy follows the criteria applied in infiltrating breast cancer of non-special histotype. In the post-operative phase, therefore after the surgical treatment of mammary quadrantectomy, or mastectomy associated with homolateral sentinel lymph node removal ± axillary dissection, based on the histopathological characteristics of the tumor, the use of chemotherapy (anthracycline + taxane) and/or hormone therapy, whether or not associated with anti-HER2 therapy (trastuzumab) is the rule. Literature data report the use of cisplatin and etoposide, as in small cell lung cancers. Most of the information currently available derive from single case reports or a series of clinical cases; it follows the difficulty of formulating definite recommendations on the correct management of this histological type of breast cancer. This review describes available knowledge on this rare entity to improve the diagnostic and therapeutic strategies and offer insights to stimulate exploration of the many aspects still unknown.

(Radio)Theranostic Patient Management in Oncology Exemplified by Neuroendocrine Neoplasms, Prostate Cancer, and Breast Cancer.

The role of nuclear medicine in the management of oncological patients has expanded during last two decades. The number of radiopharmaceuticals contributing to the realization of theranostics/radiotheranostics in the context of personalized medicine is increasing. This review is focused on the examples of targeted (radio)pharmaceuticals for the imaging and therapy of neuroendocrine neoplasms (NENs), prostate cancer, and breast cancer. These examples strongly demonstrate the tendency of nuclear medicine development towards personalized medicine.

90Y-microsphere radioembolization: The method, clinical evidence and perspective.

The current review unfolds the procedural steps and the clinical evidence for yttrium-90 (90Y)-microspheres radioembolization. Radioembolization is part of the loco-regional therapeutic spectrum for liver malignancy and involves the invasive, intra-arterial delivery of microspheres carrying β-emitter isotopes in order to destroy cancerous tissue via ionizing radiation. The main steps of the therapeutic process are selection of eligible patients, angiographic workup, simulation scintigraphy, pre-treatment dosimetry, actual treatment and post-treatment imaging/dosimetry. Radioembolization is routinely applied in advanced stage hepatocellular carcinoma (HCC), yet its role is being investigated even in earlier stages. Prospective, randomized controlled trials did not verify increased overall survival of radioembolization over systemic treatment with sorafenib in HCC; however, it showed survival benefit in certain sub-groups and a favorable toxicity profile with fewer adverse events. Radioembolization is also applied in metastatic colon cancer showing tumoral liver responses, which however did not translate into an overall survival benefit. Data regarding applications of this method in other neoplasms, such as neuroendocrine tumors, breast cancer and melanoma are also presented. There are ongoing clinical trials to define the role of radioembolization within recent treatments algorithms, to determine optimal combinations of this treatment with systemic and targeted therapies and to decide the patients' sub-groups, who will benefit the most.

Abstract 1123: Bcl-xL promotes metastasis via a novel nuclear function

Abstract Cancer cells often evade apoptosis through upregulation of anti-apoptotic proteins and/or downregulation of pro-apoptotic proteins. Bcl-xL, a negative regulator of mitochondria-mediated apoptosis, is frequently overexpressed in cancer cells. Bcl-xL has long been known for its function in regulating apoptosis during embryonic development and in pathological conditions. Any role that Bcl-xL might play in tumor metastasis has been ascribed to its anti-apoptotic function; i.e. Bcl-xL may increase metastasis by lending survival advantage to the tumor cells during the course of metastasis. However, we have demonstrated that Bcl-xL’s metastatic function is independent of its canonical anti-apoptotic activity and instead requires a novel nuclear function in cancer. We found that Bcl-xL promotes migration, even when cells are defective in mitochondria-mediated apoptosis. Consistently, Bcl-xL mutants lacking anti-apoptotic activity can still promote migration, induce epithelial-mesenchymal transition (EMT), upregulate TGFβ, and increase migration and invasion of pancreatic neuroendocrine tumor cells and breast cancer cells. Importantly, our data demonstrated that forcible localization of Bcl-xL outside the nucleus impairs its metastatic function. As a mitochondrial membrane protein in healthy cells, Bcl-xL’s transmembrane domain prevents its nuclear import. This suggests that Bcl-xL enters the nucleus by an active nuclear transport. We hypothesized that unique transporters likely exist so as to transport this normally mitochondria membrane-bound Bcl-xL protein to the nucleus. By using immunoprecipitation in combination with mass spectrometry, we identified a novel interacting partner of Bcl-xL. We are investigating whether this protein transports Bcl-xL into the nucleus to promote metastasis. Citation Format: Tiantian Zhang, Sha Li, Joseph Na, Soyoung Chi, George Zhang, Yi-Chieh Nancy Du. Bcl-xL promotes metastasis via a novel nuclear function [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1123.

Retrospective study of neuroendocrine breast cancer cases from a single institution in Québec.

e12588 Background: Within numerous breast cancer types, the neuroendocrine subtype distinguishes itself from the others by its rarity. Most of the actual data comes from European and Asian retrospective studies, whom were mostly published before the 2012 WHO classification. Methods: The aim of our study was to describe a North American cohort of neuroendocrine breast cancer tumors homogenized for the latest WHO classification of 2012. We describe the clinical presentation, diagnostic, therapeutic management and prognosis of our population recensed between 2006 and 2016 at the CHUS in Sherbrooke, Québec. A pathological review of the cases was done to unify the cohort by the latest WHO classification. Results: 59 cases were identified from the 5238 cases of breast cancer evaluated between 2006 and 2016. After review from the pathologist, 9 cases were discarded since they did not meet the diagnostic criterias. 47 patients had invasive breast carcinoma with neuroendocrine differentiation, 4 patients had poorly differentiated/small cell carcinoma and none had well differentiated neuroendocrine tumor. 44 patients were not metastatic whereas 7 patients were metastatic at disease onset with a mean age at diagnosis of 70 and 67 years respectively. 10% (4/44) developed a metastatic disease with a median time of 30 months. The mean size of the tumor was 26,1 mm and had a mean Ki67% of 28,3%. All of our patients were ER+, 98% PR+ and 4% Her2+. None had a triple negative disease. 6 patients were SBR grade 1, 31 were grade 2 and 12 were grade 3. The median follow-up for the non-metastatic patients was 42 months and 23 months for the metastatic patients. The median overall survival of our metastatic cohort was 30 months. The histologic subtype did not statistically influence the overall survival and the progression-free survival. Conclusions: Our study is the largest North American cohort of neuroendocrine breast cancer tumors classified with the latest WHO classification of 2012. More details about each subgroup analysis will be presented at the meeting. Even with this classification, the histologic diagnosis remains challenging. Further studies are needed to better characterize these patients and define their optimal management.

ALK7 Signaling Manifests a Homeostatic Tissue Barrier That Is Abrogated during Tumorigenesis and Metastasis

Herein, we report that the TGFß superfamily receptor ALK7 is a suppressor of tumorigenesis and metastasis, as revealed by functional studies in mouse models of pancreatic neuroendocrine and luminal breast cancer, complemented by experimental metastasis assays. Activation in neoplastic cells of the ALK7 signaling pathway by its principal ligand activinB induces apoptosis. During tumorigenesis, cancer cells use two different approaches to evade this barrier, either downregulating activin B and/or downregulating ALK7. Suppressing ALK7 expression additionally contributes to the capability for metastatic seeding. ALK7 is associated with shorter relapse-free survival of various human cancers and distant-metastasis-free survival of breast cancer patients. This study introduces mechanistic insights into primary and metastatic tumor development, inthe form of a protective barrier that triggers apoptosis in cells that are not "authorized" to proliferate within a particular tissue, by virtue of those cellsexpressing ALK7 in a tissue microenvironment bathed in its ligand.

Y90 Clinical Data Update: Cholangiocarcinoma, Neuroendocrine Tumor, Melanoma, and Breast Cancer Metastatic Disease

While the most compelling levels of evidence for the use of Yttrium-90 (90Y) radioembolization are in patients with hepatocellular carcinoma and hepatic metastases from colorectal cancer, a growing body of literature supports its use in other primary and secondary hepatic malignancies. This includes intrahepatic cholangiocarcinoma, as well as hepatic metastases from neuroendocrine cancer, ocular melanoma, and breast cancer. While is it not feasible to conduct prospective, randomized trials for radioembolization in the setting of these malignancies due to the low overall prevalence of liver-only disease, numerous single-arm studies in the last several years make a compelling argument for its use in select situations. This clinical update summarizes those findings.

Abstract P3-06-08: Mucinous and neuroendocrine breast cancers: A spectrum of genetically-related lesions distinct from common forms of estrogen receptor-positive breast cancers

Abstract Introduction: Mucinous (MBCs) and neuroendocrine breast carcinomas (NBCs) are special histologic types of estrogen receptor (ER)-positive breast cancers. Together, MBCs and NBCs account for approximately 5% of invasive breast cancers. NBCs are defined by the expression of neuroendocrine markers (i. e., chromogranin and/ or synaptophysin), whereas MBCs consist of nests of cancer cells floating in pools of extracellular mucin and can be either hypocellular/type A (MBC-A) or hypercellular/type B (MBC-B). MBC-B may display neuroendocrine differentiation. We compared the repertoire of somatic genetic alterations in MBCs-A and MBCs-B, and in NBCs, and evaluated whether they differ from ER-positive/ HER2-negative invasive ductal carcinomas of no special type (IDC-NSTs). Materials and methods: Reanalysis of the targeted capture or whole exome sequencing data of 22 MBCs (12 MBCs-A and 10 MBCs-B), and of 15 NBCs was performed. The BAM files were retrieved and somatic mutations were detected with MuTect, indels with Strelka, Varscan2, Scalpel and Lancet, and copy number alterations using FACETS. The mutational repertoire of MBCs-A and MCBs-B was compared to that of NBCs, and of ER-positive/ HER2-negative IDC-NSTs from The Cancer Genome Atlas (TCGA) breast cancer study (n=310). Results: The most frequently mutated genes in MBCs-A were SF3B1 and FRG1B (17%, each); in MBCs-B were GATA3 and KMT2C (30%, each), and in NBCs were FOXA1 and TBX3 (20%, each) and KMT2C (20%). No significant differences were observed in single gene comparisons between MBCs-A, MBCs-B and NBCs (Fisher's exact tests, p>0.05). When compared with ER-positive/HER2-negative IDC-NSTs from TCGA, NBCs harbored a higher frequency of mutations targeting FOXA1 (20% vs 2.9%, Fisher's exact test, p<0.05) and TBX3 (20% vs 2.9%, Fisher's exact test, p<0.05), and a lower frequency of TP53 mutations (0% vs 23.9%; Fisher's exact test, p<0.05). We observed a lower frequency of PIK3CA mutations in both MBCs-A (8.3% vs 40%, Fisher's exact test, p<0.05) and MBCs-B (0% vs 40%; Fisher's exact test, p<0.01) compared to ER-positive/HER2-negative IDC-NSTs. Although not statistically significant, PIK3CA mutations were numerically less frequent in NBCs than in ER+/HER2- IDC-NSTs (13.3% vs 40%; Fisher's exact test, p>0.05). Concurrent 1q gains and 16q losses, the hallmark copy number alterations of ER-positive/HER2-negative breast cancer were found in 47% of the ER-positive/HER2-negative IDC-NSTs from TCGA, but only present in 20% of NBCs and in none of the MBCs-A or MBCs-B. Conclusion: Type A MBCs, type B MBCs and NBCs harbor similar patterns of genetic alterations, including a low frequency of PIK3CA mutations and of concurrent 1q gains/ 16q deletions. Taken together, our data suggest that both MBCs and the vast majority of NBCs constitute a spectrum of histologically and genomically related subtypes, distinct from ER-positive/HER2-negative IDC-NSTs. Citation Format: Pareja F, Da Cruz Paula A, Selenica P, Lee JY, Marchio C, Brown D, Geyer FC, Brogi E, Vincent-Salomon A, Weigelt B, Reis-Filho JS. Mucinous and neuroendocrine breast cancers: A spectrum of genetically-related lesions distinct from common forms of estrogen receptor-positive breast cancers [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P3-06-08.

Paraneoplastic syndrome in neuroendocrine breast cancer: A case report

AbstractBackgroundParaneoplastic syndromes are rare manifestations of underlying malignancies, most commonly small cell lung cancer and invasive ductal carcinoma of the breast.CaseWe present a case of anti‐AMPA receptor paraneoplastic limbic encephalitis, a specific paraneoplastic syndrome, in a woman with neuroendocrine breast cancer. Her condition improved with surgical resection and chemotherapy.ConclusionThis is the first known case of anti‐AMPA receptor paraneoplastic limbic encephalitis in a patient with primary neuroendocrine breast cancer.

Somatostatin receptor SSTR2A and SSTR5 expression in neuroendocrine breast cancer

Neuroendocrine breast cancer (NEBC) is a group of rare tumors, which could benefit from therapy targeting the somatostatin receptors (SSTRs). In particular, SSTR2A and SSTR5 are potential targets given their consistent expression in gastrointestinal and pancreatic primary and metastatic neuroendocrine cancers. Currently, there are no studies describing the expression of SSTRs in NEBC. The purpose of our study was to characterize the immunohistochemical expression of SSTR2A and SSTR5 in a cohort of NEBC.Thirty-one primary NEBC cases were analyzed, and SSTR2A and SSTR5 immunohistochemistry performed and scored using the modified immunoreactive score proposed by Remmele and Stanger.All patients were females with a mean age of 66.6 years (SD = 14). 77% of cases were histological grade 2. SSTR2A showed a weak positivity in 11 cases (35.5%), moderate positivity in 6 cases (19.4%) and strong positivity in 5 cases (16.1%). Nine cases were negative for SSTR2A (29%). SSTR5 showed a weak positivity in 16 cases (51.6%), moderate positivity in 6 cases (19.4%), while no cases showed strong positivity. Nine cases were negative for SSTR5 (29%). Five cases were negative for both SSTR2A and SSTR5.A weak to moderate SSTR2A and SSTR5 expression was observed in 50–70% of the cases. A subset of NEBCs with strong SSR2A expression may benefit from SSTRs targeted therapy. These results need further validation in a larger series including metastatic NEBC, to provide potential therapeutic targets for patients with advanced disease.

PO15 Neuroendocrine Breast Carcinoma – Could surgery be avoided?

Background & purpose: Neuroendocrine breast cancer (NEBC) is a rare variant of breast cancer. International experience and understanding of this condition are limited and guidelines on management non-existent. We present our case of NEBC, which showed a pathologic complete response (PCR) to neo-adjuvant chemotherapy and question whether surgery could be avoided in this condition.

Primary small cell carcinoma of the breast: a case report

BackgroundNeuroendocrine breast cancer is a rare entity that was defined in 2003 by the World Health Organization as a separate breast cancer subtype. The diagnosis of neuroendocrine breast cancer requires the presence of neuroendocrine features in at least 50% of malignant cells, the exclusion of non-mammary primary tumors, as well as the presence of an in situ component in breast histology. The treatment and prognosis of neuroendocrine breast cancer are still not well established. Small cell carcinoma of the breast is a subtype of neuroendocrine cancer, resembling small cell carcinoma of the lung. It has a very poor prognosis and warrants treatment with platinum-based chemotherapy.Case presentationWe herein report the case of a 47-year-old white woman with a left breast mass that was found to be an early-stage, high-grade small cell carcinoma of the breast. Positron emission tomography-computed tomography imaging excluded any other primary disease. Our patient underwent a left total mastectomy with sentinel lymph node biopsy and received cisplatin-based adjuvant chemotherapy. Our patient remains free of disease to date.ConclusionsThis case report sheds light on a rarely described disease and provides a comprehensive approach to diagnosis and management. Neuroendocrine carcinoma of the breast is a well-defined histologic subtype of breast cancer. Small cell carcinoma of the breast is a rare subtype of neuroendocrine breast cancer. Due to the rarity of this entity, prognosis has still not been well established, and treatment has not been standardized, cisplatin-based treatment has been used in this case similar to small cell carcinoma of the lung.

MEN4 and CDKN1B mutations: the latest of the MEN syndromes.

Multiple endocrine neoplasia (MEN) refers to a group of autosomal dominant disorders with generally high penetrance that lead to the development of a wide spectrum of endocrine and non-endocrine manifestations. The most frequent among these conditions is MEN type 1 (MEN1), which is caused by germline heterozygous loss-of-function mutations in the tumor suppressor gene MEN1 MEN1 is characterized by primary hyperparathyroidism (PHPT) and functional or nonfunctional pancreatic neuroendocrine tumors and pituitary adenomas. Approximately 10% of patients with familial or sporadic MEN1-like phenotype do not have MEN1 mutations or deletions. A novel MEN syndrome was discovered, initially in rats (MENX), and later in humans (MEN4), which is caused by germline mutations in the putative tumor suppressor CDKN1B The most common phenotype of the 19 established cases of MEN4 that have been described to date is PHPT followed by pituitary adenomas. Recently, somatic or germline mutations in CDKN1B were also identified in patients with sporadic PHPT, small intestinal neuroendocrine tumors, lymphoma and breast cancer, demonstrating a novel role for CDKN1B as a tumor susceptibility gene for other neoplasms. In this review, we report on the genetic characterization and clinical features of MEN4.

Mouse mammary tumour virus (MMTV) and human breast cancer with neuroendocrine differentiation

BackgroundMouse mammary tumour viruses (MMTVs) may have a role in a subset of human breast cancers. MMTV positive human breast cancers have similar histological characteristics to neuroendocrine breast cancers and to MMTV positive mouse mammary tumours. The purpose of this study was to investigate the expression of neuroendocrine biomarkers – synaptophysin and chromogranin, to determine if these histological characteristics and biomarker expression were due to the influences of MMTV.MethodsImmunohistochemistry analyses to identify synaptophysin and chromogranin were conducted on a series of human breast cancers in which (i) MMTV had been previously identified and had similar histological characteristics to MMTV positive mouse mammary tumours and (ii) MMTV positive mouse mammary tumours.ResultsThe expression of synaptophysin and chromogranin in MMTV positive mouse mammary tumors were all positive (7 of 7 specimens – 100% positive). The expression of synaptophysin and chromogranin in MMTV positive human breast cancers was much less prevalent (3 of 22 – 14%). There was no expression of synaptophysin and chromogranin in the normal breast tissue control specimens.DiscussionIt is not possible to draw any firm conclusions from these observations. However, despite the small numbers of MMTV positive mouse mammary tumours in this study, the universal expression in these specimens of synaptophysin and chromogranin proteins is striking. This pattern of synaptophysin and chromogranin expression is very different from their expression in MMTV positive human breast cancers. The reason for these differences is not known.ConclusionsThe high prevalence of positive expression of synaptophysin and chromogranin in MMTV positive mouse mammary tumours and low expression of synaptophysin and chromogranin in MMTV positive human breast cancers indicates that MMTV is not usually associated with neuroendocrine human breast cancers.

Bcl-xL promotes metastasis independent of its anti-apoptotic activity.

Bcl-xL suppresses mitochondria-mediated apoptosis and is frequently overexpressed in cancer to promote cancer cell survival. Bcl-xL also promotes metastasis. However, it is unclear whether this metastatic function is dependent on its anti-apoptotic activity in the mitochondria. Here we demonstrate that Bcl-xL promotes metastasis independent of its anti-apoptotic activity. We show that apoptosis-defective Bcl-xL mutants and an engineered Bcl-xL targeted to the nucleus promote epithelial–mesenchymal transition, migration, invasion and stemness in pancreatic neuroendocrine tumour (panNET) and breast cancer cell lines. However, Bcl-xL proteins targeted to the mitochondria or outside of the nucleus do not have these functions. We confirm our findings in spontaneous and xenograft mouse models. Furthermore, Bcl-xL exerts metastatic function through epigenetic modification of the TGFβ promoter to increase TGFβ signalling. Consistent with these findings, we detect nuclear Bcl-xL in human metastatic panNETs. Taken together, the metastatic function of Bcl-xL is independent of its anti-apoptotic activity and its residence in the mitochondria.

The Spectrum of Microvasculature Basal Microvilli in Human Solid Tumors: A Pilot Study

In our pervious study, we had reported that basal microvilli with cellular trafficking ability exist in pancreatic ductal adenocarcinoma (PDAC) and murine PDAC models, which a remarkable example of how endothelial plasticity in tumor blood vessels feed tumor cells. As human solid tumors in different organs are driven by similar oncogenic mutations, basal microvilli may exist in other human solid tumors. Here we have done a small pilot study in human solid tumors to see whether other solid tumors take this approach, and surprisingly found that basal microvilli-like structure observed in human cholangiocarcinoma, metastatic nonfunctional pancreatic neuroendocrine tumor (panNET) and breast cancer, but not human hepatocellular carcinoma, glioblastoma, renal clear cell carcinoma and oral squamous cell carcinoma. Consistent with characteristics of basal microvilli in PDAC, immuno-staining results showed that the expression of VEGFR2 was down-regulate in the microvasculature with basal microvilli in panNET. This finding indicates that basal microvilli might be a common way to get nutrients from or clear waste to the microvasculature in aggressive and metastatic tumors.

Neuroendocrine breast cancer: A single center experience.

e12037 Background: Neuroendocrine cancer of the breast is rarely seen and grouped into small cell, large cell and carsinoid like carcinoma variants. In our study demographic features of neuroendocr...