Apocrine Adenocarcinoma of the Bilateral Axillae

A case of apocrine adenocarcinoma arising in the bilateral axillae is reported. The patient was an 88 year old Japanese male who complained of a mass lesion and puslike discharge in the right axilla. Another mass was also noticed in the left axilla. No other neoplastic lesion was found in other sites of the body. The histologic appearances of the bilateral axillary tumors were almost identical. Both were adenocarcinoma with varying degrees of differentiation, composed of glands and nests of atypical epithelial cells with abundant eosinophilic cytoplasm. Some neoplastic cells exhibited cytoplasmic projections on their apical surface. Foci of in situ carcinoma were observed within the neoplastic tissue in the bilateral axillae. The neoplastic cells were immunohistochemically positive for epithelial membrane antigen (EMA) and gross cystic disease fluid protein (GCDFP-15), but negative for carcinoembryonic antigen (CEA). On the basis of their histologic and immunohistochemical features and distinctive location, the tumors were diagnosed as apocrine adenocarcinoma. Acta Pathol Jpn 41: 927-932, 1991.     

Apocrine adenocarcinoma of the bilateral axillae.

A case of apocrine adenocarcinoma arising in the bilateral axillae is reported. The patient was an 88-year-old Japanese male who complained of a mass lesion and pus-like discharge in the right axilla. Another mass was also noticed in the left axilla. No other neoplastic lesion was found in other sites of the body. The histologic appearances of the bilateral axillary tumors were almost identical. Both were adenocarcinoma with varying degrees of differentiation, composed of glands and nests of atypical epithelial cells with abundant eosinophilic cytoplasm. Some neoplastic cells exhibited cytoplasmic projections on their apical surface. Foci of in situ carcinoma were observed within the neoplastic tissue in the bilateral axillae. The neoplastic cells were immunohistochemically positive for epithelial membrane antigen (EMA) and gross cystic disease fluid protein (GCDFP-15), but negative for carcinoembryonic antigen (CEA). On the basis of their histologic and immunohistochemical features and distinctive location, the tumors were diagnosed as apocrine adenocarcinoma.     

Molecular cytogenetic comparison of apocrine hyperplasia and apocrine carcinoma of the breast

The relationship of apocrine metaplasia to invasive breast cancer is controversial. Different authors have reported that apocrine differentiation in proliferative lesions may be a risk factor, a precursor lesion, or have no association with malignancy. The aim of this study was to compare the genetic alterations in benign apocrine hyperplasia with apocrine ductal carcinoma in situ (DCIS) and invasive apocrine carcinomas of the breast using comparative genomic hybridization. The mean number of alterations in apocrine hyperplasia was 4.1 (n = 10) compared to 10.2 in apocrine DCIS (n = 10) and 14.8 (n = 4) in invasive carcinoma. The most common alterations in apocrine hyperplasia were gains of 2q, 13q, and 1p and losses of 1p, 17q, 22q, 2p, 10q, and 16q. Apocrine DCIS and invasive carcinomas showed gains of 1q, 2q, 1p, and losses of 1p, 22q, 17q, 12q, and 16q as their most common DNA copy number changes. Apocrine hyperplasia is considered to be a benign lesion and its relationship to invasive carcinoma remains unclear. Our data suggest that some apocrine hyperplasias may be clonal proliferations. The mean number of alterations are lower in apocrine hyperplasia, however the changes show considerable overlap with those identified in in situ and invasive apocrine carcinoma. These alterations are also commonly seen in nonapocrine breast cancer. The data are consistent with apocrine hyperplasia as a putative nonobligate precursor of apocrine carcinoma.     

Immunohistochemical analysis of the distribution of a breast tumor associated antigen recognized by a monoclonal antibody.

A new monoclonal antibody (MoAb), MM 1-80, recognizing a tumor associated epitope of a breast high molecular weight mucin molecule was tested, using the avidin biotin immunoperoxidase method on normal and pathological mammary tissues. The normal mammary ducts and lobules were negative. Fibroadenomas showed a strong intracytoplasmic staining. In apocrine metaplasia, adenosis, and papillomatosis, scattered cells showed intracytoplasmic, luminal border or secretion reactivity. In lobular and ductal hyperplasia the cells showed intracytoplasmic immunoreactivity which, however, became more intense and homogeneous in atypical lesions, i.e. lobular and ductal in-situ carcinomas. The infiltrating carcinomas of different histotype expressed positivity on 98% of the cases (113/115) and axillary metastatic lymph nodes were always positive (20/20). The MoAb was tested on 175 human neoplasias of different origin which were in the majority of the cases negative with the exception of adenocarcinomas of the lung, ovary and bladder. MM1-80 appears to react preferentially with mammary cells undergoing hyperplastic, metaplastic and neoplastic processes. The 1-80 epitope distribution is different in these lesions starting with a predominant luminal expression in benign lesions and becoming strong and cytoplasmic in the malignant breast cell.     

Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study

AIMS: Prolactin plays an important role in the proliferation and differentiation of normal breast epithelium, and possibly in the development of breast carcinoma. The effects of prolactin are mediated by its receptor; thus, alteration in the expression of this receptor could be important in studying the biology of breast cancer. This investigation was aimed at comparing the expression of prolactin receptors in normal, benign, and malignant breast tissue. MATERIAL/METHODS: The expression of prolactin receptors was studied in paraffin wax embedded sections of 102 breast biopsies (93 female and nine male), using the monoclonal antibody B6.2, and the avidin-biotin immunoperoxidase technique. Six biopsies were normal, 34 had benign lesions, and 62 were malignant. RESULTS: In normal cases, prolactin receptor positivity was seen only on the luminal borders of the epithelial cells lining ducts and acini. In most benign lesions, variable degrees of luminal and cytoplasmic staining were seen. Cells showing apocrine metaplasia and florid regular ductal epithelial hyperplasia were mostly negative. In malignant cases, the staining pattern was mostly cytoplasmic and heterogeneous. Forty one of the 59 carcinomas in women showed a degree of positivity involving 10-100% of the tumour cells. A significant direct correlation was found between prolactin receptor and oestrogen receptor staining when only cases that scored more than 100/300 for the latter receptor, using the H scoring system, were considered (p = 0.0207). No correlation was found between prolactin receptors and progesterone receptors, patient's age, tumour size, tumour grade, or axillary lymph node status. CONCLUSIONS: Prolactin receptors seem to be expressed at different cellular sites in normal, benign, and malignant breast epithelial cells. The receptor is expressed in more than two thirds of female breast carcinomas, suggesting that it may play a role in the pathogenesis of the disease. The positivity is correlated with moderate and strong staining for oestrogen receptors in tissue sections, but not with other prognostic factors.     

Bilateral apocrine carcinoma of the breast Molecular and immunocytochemical evidence for two independent primary tumours

Apocrine carcinoma is an uncommon variant of breast cancer. The frequency of bilaterality in patients who have apocrine carcinoma in one breast is not significantly different from that for bilateral mammary carcinomas in general, but bilateral apocrine carcinomas are very uncommon. We report on a bilateral apocrine carcinoma of the breast in a 74-year-old woman. The apocrine differentiation in both tumours was confirmed by the positivity of the cytoplasmic granules for PAS after diastase digestion and immunoreactivity for GCDFP-15 and sialyl-Tn. The tumour in the right breast showed immunohistochemical expression of p53, and a mutation was demonstrated by PCR-SSCP; the tumour in the left breast was negative for p53 on immunohistochemistry, and no mutation was found at the molecular level. c-erbB2 expression was not detected in the right tumour but there was overexpression (at the cell membrane) in the left tumour. Both tumours were aneuploid: the right tumour displayed multiple stemlines, whereas the left tumour had a triploid profile. Using the fluorescence in situ hybridization technique we demonstrated that both tumours displayed chromosome 17 polysomy and numerical abnormalities of chromosome 1, polysomy in the right and monosomy in the left tumour. We conclude that the two tumours are probably independent, as are most bilateral carcinomas of the breast.     

CD10 and calretinin staining of endocervical glandular lesions,endocervical stroma and endometrioid adenocarcinomas of the uterine corpus: CD10 positivity is characteristic of,but not specific for,mesonephric lesions and is not specific for endometrial stroma

AIMS: In the female genital tract CD10 has been used to assist in the evaluation of mesenchymal tumours of the uterus and in determining whether endometrial stroma is present. CD10 positivity has also been shown in cervical mesonephric remnants and this antibody has been suggested as a useful immunohistochemical marker of mesonephric lesions in the female genital tract. Calretinin has also been shown to be positive in mesonephric lesions. In this study the specificity of these two antibodies in evaluating cervical and uterine glandular lesions and the value of CD10 in determining whether stroma is endometriotic or not were investigated. METHODS AND RESULTS: Cases of cervical tubo-endometrial metaplasia (TEM) (n = 11), microglandular hyperplasia (MGH) (n = 10), endometriosis (n = 8), mesonephric remnants/hyperplasia (n = 12), endocervical adenocarcinoma, usual type (n = 15), mucinous variant of minimal deviation adenocarcinoma (MDA) (n = 7) and mesonephric adenocarcinoma (n = 3) were stained with antibodies against CD10 and calretinin. Nine cases of endometrial adenocarcinoma of endometrioid type were also stained. In all the cervical cases normal endocervical glands were negative with both antibodies except for one case with strong positive luminal staining with CD10. All cases of TEM, MGH and endometriosis were negative with CD10 and calretinin except for focal staining with CD10 in one case each of MGH (cytoplasmic staining) and endometriosis (luminal staining). Most usual endocervical adenocarcinomas were negative with both antibodies, although one exhibited focal cytoplasmic staining with calretinin and five exhibited limited luminal positivity with CD10. All MDAs were negative with both antibodies. Ten of 12 mesonephric remnants/hyperplasia showed luminal positivity with CD10 and one exhibited cytoplasmic and nuclear staining with calretinin. Two of three mesonephric adenocarcinomas showed luminal positivity with CD10 and nuclear and cytoplasmic positivity with calretinin. Seven of nine endometrial adenocarcinomas were positive with CD10 (four cytoplasmic, two membranous and cytoplasmic, one luminal and cytoplasmic) and three with calretinin (two cytoplasmic, one nuclear and cytoplasmic). Positive staining of endometriotic stroma with CD10 was present in all endometriosis cases but normal cervical stroma was also strongly positive, especially around glands. Endometriotic stroma and cervical stroma were negative with calretinin. CONCLUSIONS: We conclude that most endocervical glandular lesions, including mesonephric remnants/ hyperplasia, are negative with calretinin. However, the focal nuclear and cytoplasmic positivity with calretinin in two of three mesonephric adenocarcinomas suggests that this may be a useful indicator of a mesonephric origin of a cervical adenocarcinoma. Most mesonephric remnants/hyperplasias exhibit luminal positivity with CD10, although this is not invariable and staining is usually focal. Positive luminal staining of a benign endocervical glandular lesion with CD10 may help confirm mesonephric remnants. Although positive staining with CD10 was found in two of three mesonephric adenocarcinomas, the observed immunoreactivity of several conventional cervical adenocarcinomas limits the diagnostic value of CD10 in confirming a mesonephric origin for an adenocarcinoma. Since all cervical MDAs were negative with CD10, positivity with this antibody may be of value in distinguishing mesonephric hyperplasia from MDA, although this distinction rarely necessitates immunohistochemistry. Most endometrial adenocarcinomas of endometrioid type stain with CD10 and thus positivity with this antibody is not specific for a mesonephric origin of an endometrial adenocarcinoma. Positivity of normal cervical stroma limits the value of CD10 staining in confirming a diagnosis of cervical endometriosis.     

The diagnostic utility of EZH2 H-score and Ki-67 index in non-invasive breast apocrine lesions

In diagnostic breast pathology, there is no reliable applicable immunostain to help discern atypical and in situ apocrine lesions from benign apocrine tissue. At present, the diagnosis of non-invasive apocrine lesions remains challenging with current diagnoses rendered based on discrete morphologic characteristics on conventional hematoxylin and eosin staining. Interobserver variability is significant even among subspecialists partly due to lack of adjuvant diagnostic immunohistochemical stains. Herein, we set to elucidate the potential utility of EZH2 and Ki-67 immunostains as tangible tools in non-invasive apocrine proliferations. A cohort of apocrine breast lesions [Benign apocrine hyperplasia (BAH), n = 10; Atypical apocrine hyperplasia (AAH), n = 16; Apocrine ductal carcinoma in situ (ADCIS), n = 12] were subjected to EZH2 immunostaining and analyzed via H-scoring of nuclear expression. Mean H-scores for EZH2 progressively increased from BAH (23.5), to AAH (47.4) and ADCIS (196.4), and showed a significant difference utilizing the Kruskal-Wallis test (p < 0.0001). Further interrogation of Ki-67 demonstrated incremental expression from BAH to AAH and ADCIS at 1.6 %, 4.7 % and 24.7 %, respectively (p < 0.0001, Kruskal-Wallis test), suggesting an association with increased proliferation. Our results demonstrate that a combination of EZH2 and Ki-67 immunostaining may be employed in differentiating among challenging apocrine breast lesions and suggest a putative diagnostic utility for EZH2 and Ki-67 in non-invasive apocrine breast lesions.     

Apocrine adenosis: a precursor of aggressive breast cancer?

AIM--To investigate overexpression of c-erbB2, expression of the p53 protein product and proliferation rates in benign breast lesions with specific reference to apocrine adenosis. METHODS--Twenty one cases of apocrine adenosis were stained with monoclonal antibodies to p185, the protein product of the c-erbB2 oncogene, the protein product of the p53 tumour suppressor gene and to the cell cycle related protein Ki67. Three cases were associated with concomitant ductal carcinoma in situ of large cell type and two were associated with invasive tubular or cribriform carcinoma. RESULTS--Twelve (57.1%) cases showed membrane staining for c-erbB2 oncoprotein of apocrine cells within sclerosing adenosis and six (28.6%) had occasional p53 protein positive cells. One case not associated with carcinoma showed extensive staining of apocrine metaplasia outside the area of apocrine adenosis. The proliferation rate, as measured by Ki67 staining, was increased in some of the lesions and all lesions showed at least some of the cells to be in the cell cycle. CONCLUSIONS--The expression of abnormal oncogene products and increased proliferation in some of these apocrine lesions questions the supposed degenerative nature of the atypia seen in such cases and suggests that there may be an association between these lesions and large cell ductal carcinoma in situ and hence invasive carcinoma.     

Apocrine (cutaneous) sweat gland carcinoma of axilla with signet ring cells: a diagnostic dilemma on fine-needle aspiration cytology

Carcinoma arising in the apocrine sweat glands is rare and there are few reports describing the cytological features of this neoplasm. We describe the cytological features of a histologically confirmed apocrine carcinoma occurring in a 55-year-old man who presented with an ulcerated mass in the right axilla. Fine-needle aspiration cytology revealed features of a signet ring adenocarcinoma. The significance of this infrequently encountered neoplasm lies in its potential for diagnostic confusion with more common lesions containing signet ring cells. In an axillary mass lesion, cytological features along with clinical correlation are essential to distinguish primary apocrine carcinoma from mammary neoplasms with signet ring cells and other metastatic adenocarcinomas.     

The spectrum of apocrine lesions of the breast

Apocrine change is seen in a wide spectrum of breast lesions, ranging from microscopic cysts to invasive carcinoma. This article reviews the range of apocrine lesions and discusses the clinical significance of these lesions. Although apocrine change in many cases does not present any diagnostic difficulty, apocrine proliferations demonstrating cytologic atypia can be particularly challenging. The histologic criteria that have been proposed to foster reproducibility in categorizing such lesions are reviewed. This review attempts to clarify the terminology that has been applied to a range of benign lesions, including sclerosing adenosis and complex sclerosing lesions, containing foci of apocrine change. Malignant apocrine lesions, including both in situ and invasive carcinoma, are also discussed.     

The enigmatic nature of apocrine breast lesions

Epithelial cells of fetal breast glandular structures, at the third trimester of pregnancy (28 weeks), produce GCDFP-15, in the absence of specific apocrine morphology. Apocrine epithelium of the breast may be a normal process of differentiation rather than a result of metaplasia, and it has been demonstrated that it is estrogen-receptor, progesterone-receptor and bcl-2 negative, but androgen-receptor (AR) positive. The significance of AR expression in apocrine epithelium is uncertain. Apocrine epithelium is seen in a wide spectrum of breast entities, ranging from benign lesions to invasive carcinoma. Breast cancer accounts 32% of all cancer cases among women and is the most common type of cancer in women. Little is known about breast carcinogenesis. Widely, it is accepted that breast cancer, like most other type of cancer, is being developed through the accumulation of genetic aberrations. Apocrine epithelium may reflect instability of the breast epithelium, creating an environment favouring further oncogenic alterations. In the last decade, several lines of evidence support the idea that some breast benign epithelial apocrine lesions are clonal lesions and may be considered as truly pre-malignant or precursors of breast carcinoma. Apocrine changes in many cases do not present any diagnostic difficulty; on the other hand, apocrine proliferations with cytologic atypia can be particularly difficult and challenging. The purpose of this study is to collect and highlight the areas of consensus in the literature as well as the controversial areas concerning the apocrine epithelium of the breast.     

Immunohistochemical expression of epidermal growth factor receptor in salivary gland tumours

Summary Immunohistochemical localization of epidermal growth factor receptor (EGFR) in normal salivary glands and tumours (108 cases) was studied using a monoclonal antibody. In the normal salivary glands, EGFR was occasionally detected in ductal segments of intercalated, striated, and excretory ducts, but not in acinar cells. The frequency of positive EGFR staining in salivary gland tumours was not high: pleomorphic adenoma, 33.8%; mucoepidermoid tumour, 25.0%; adenolymphoma, 44.4%; and sialoadenocarcinoma, 66.6%. Pleomorphic adenomas showed positive staining for EGFR on the luminal side of luminal cells and in squamous metaplastic cells of tumour tissue. Some modified myoepithelial cells were also reactive whereas outer spindle tumour cells were unstained. Adenolymphomas regularly exhibited positive EGFR staining in the cell membrane; mucoepidermoid carcinoma displayed positive staining in cell membranes in epidermoid tumour cells and cytoplasmic staining in mucous-secreting tumour cells. Sialocarcinomas revealed cell membrane staining and whole cytoplasmic staining for EGFR. The immunohistochemical localization of EGFR could be classified into two types, one the cell membrane-positive type found in epithelial tumour cells, and the second the cytoplasmic positive type seen in normal ductal cells, the luminal tumour cells of pleomorphic adenomas and mucous-secreting tumour cells.     

A case of intracystic apocrine papillary tumor: Diagnostic pitfalls for malignancy

Intraductal/intracystic papillary carcinoma (IPC) of the breast is defined as a malignant non-invasive papillary tumor arising from the ductal–lobular system. Based on the presence of myoepithelial cells in the cystic wall, IPC is distinguished from encapsulated papillary carcinoma (EPC). Here, we report a case of an intracystic apocrine papillary tumor in the breast of a 49-year-old woman. Histopathologic examination revealed that the entire papillary structures and cyst wall were comprised of apocrine cells, some of which showed nuclear atypia with macronucleoli. Immunohistochemical examination revealed a lack of myoepithelial cells in the papillary fronds and cyst wall. Although the dense proliferation of apocrine cells mimicked a cribriform pattern, detailed examination identified a delicately intermingled interstitium in the cribriform-like growth area in the present case. We judged the current case to be benign apocrine papilloma. Only a few apocrine variants of IPC or EPC have been reported to be malignant or potentially malignant. Since even benign apocrine lesions are known to lack myoepithelial cells, histopathologic evaluation regarding malignant potential requires caution in apocrine variants. The detection of clearly benign areas and knowledge of the “pseudo-cribriform” pattern should provide clues to distinguish between benign and malignant apocrine papillary tumors.     

Immunoreactive prolactin in lesions and tumours of salivary glands

The prolactin binding in obstructive lesions and tumours of salivary glands was described by use of the immunohistochemical PAP technique. Normal salivary glands had prolactin binding cells in the striated ducts only. Chronic obstructive lesions of submandibular glands showed negative immunoreaction for prolactin binding in ductal cells, but positive staining of the luminal surface of ductal segments. In pleomorphic adenomas, occasional neoplastic cells located along the luminal borders of tubular, ductal, or of duct-like epithelial structures were strongly reactive with anti-prolactin and 26.5% of cases pleomorphic adenoma were positive for anti-prolactin. Adenoid cystic carcinoma exhibited positive prolactin binding on the luminal surface of some of tumour foci, but not in the rest of the tumour. Warthin's tumour was devoid of detectable prolactin binding.     

Expression of c-erbB2, p53, Bcl-2, Bax,c-myc and Ki-67 in apocrine metaplasia and apocrine change within sclerosing adenosis of the breast

Molecular evidence has recently suggested a number of different pathways leading to the development of ductal carcinoma of the breast. The links between atypical ductal hyperplasia and low-grade ductal carcinoma in situ and lobular neoplasia and lobular carcinoma are well known pathologically, but high-grade in situ and invasive carcinomas appear to have a different biological oncogenetic pathway. Morphologically there is a similarity between apocrine cells and some cases of high-grade ductal carcinoma. In order to investigate this possibility a number of different biological markers known to occur in high-grade breast carcinomas were assessed in both apocrine metaplasia (APM) and a putative premalignant lesion called apocrine change within sclerosing adenosis (AA). In 64 cases of APM and 18 cases of AA we examined for expression of c-erbB2, p53, Bcl-2, Bax, c-myc and Ki-67 proteins using immunocytochemistry. c-erbB2 expression was seen in 55.6% of AA cases and in 10.9% of APM cases. p53 expression was detected in 27.8% of AA cases but only 1.6% of APM cases. All cases of AA and APM were negative for the anti-apoptotic protein Bcl-2, but all the APM and 33.3% of AA cases showed cytoplasmic positivity for Bax, a pro-apoptotic protein. All the cases of AA and APM were positive for c-myc oncoprotein, however, the mean percentage of nuclear positivity was 50% in AA and 37% in cases of APM cases. The mean percentage positivity for Ki-67, a proliferation associated antigen, was 3.6% in AA and 1.3% in APM. The results indicate that a subset of breast lesions containing APM epithelium show abnormal oncoprotein and apoptosis-related protein expression and have a higher proliferation rate.     

细胞角蛋白34βE12在鉴别乳腺良、恶性病变中的意义

目的 探讨高分子量细胞角蛋白34βE12作为良性病变的标记物对鉴别乳腺病变的意义。方法收集90例有随访活检和组织病理学诊断对照的乳腺细针吸取细胞学(FNAC)资料：良性病变50例,包括非增生性病变30例和增生性病变20例、导管内癌10例和浸润癌30例,对其FNAC涂片和相应的石蜡切片作34βE12的抗生物素蛋白-生物素-过氧化酶复合(ABC)法免疫组织化学分析。利用SPSS10．0软件进行统计学分析。结果 (1)34βE12在良性非增生和增生性病变组中的表达差异无显著性。(2)34βE12在良性病变和癌组中的表达差异具显著性,34βE12在癌组中,FNAC涂片和相应的石蜡切片分别为66．7％和63．3％的病例表现为完全阴性或散在1 的肿瘤细胞胞质阳性;在良性病变组中,FNAC涂片和相应的石蜡切片分别为100％和78％的病例表现为2 至3 的细胞阳性,且在石蜡切片中34βE12表现为完整的细胞膜和细胞质的强阳性,与癌中阳性标本之细胞质颗粒状阳性为主的表达特点不同。(3)34βE12在细胞分化较好的筛孔型、乳头型和实性型导管内癌中为完全阴性和散在细胞胞质阳性,而在细胞分化较差的粉刺型导管内癌中为阴性至3 的细胞阳性。结论 34βE12可作为乳腺病变鉴别诊断中良性病变的标记物,上皮细胞出现34βE12表达缺失时高度提示为癌;大量上皮细胞表达34βE12,且为细胞膜强阳性时,则应多考虑为良性病变。     

Distribution of epithelial membrane antigen in benign and malignant lesions of the salivary glands

Summary An antiserum against epithelial membrane antigen has been used to stain a variety of lesions arising in the salivary glands. In normal major and minor glands staining was localised to the ductal systems. There was no evidence of myoepithelial cell staining. The mucous elements of the submandibular and sublingual glands were negative, but in the mucous elements of the minor glands there was focal cytoplasmic positivity. There was no cytoplasmic staining of serous elements in major or minor salivary glands. In pleomorphic adenomas the luminal membrane of ductal elements was strongly positive, with focal cytoplasmic positivity in some myxoid areas. In mucoepidermoid tumours both adjacent cell membranes and cytoplasm were strongly positive. The ductal structure of adenoid cystic carcinomas were clearly delineated while the pseudoducts produced by enclosed areas of stroma were negative. All mesenchymally derived tumours were negative and a tumour previously considered as a chondroma was strongly positive. The results are discussed in relation to phenotypic heterogeneity and the histogenesis of salivary gland tumours.     

Morphological heterogeneity of esophageal carcinoma

To clarify the morphological heterogeneity of esophageal carcinoma, the adenocarcinomatous, basaloid, and sarcoma-like components of 178 esophageal carcinomas were studied with regard to histopathology, mucin histochemistry, immunohistochemistry, and ultrastructure. Adenocarcinomatous components with mucicarminophilic cells and/or glandular structures, basaloid components, and sarcoma-like components were found in 55 lesions (30.9%), 17 lesions (9.3%), and five lesions (2.8%) respectively. Carcinoembryonic antigen staining was positive in 52 lesions (29.2%), secretory component staining was positive in 15 (8.4%), and lactoferrin staining was positive in 12 (6.7%). Eight intraepithelial carcinomas were found to have no adenocarcinomatous components, and two intramucosal carcinomas had adenocarcinomatous components in the invasive portions. These findings strongly suggest that the adenocarcinomatous components do not arise from the ductal epithelium, but occur during the process of invasion. There were no significant clinicopathological differences between the carcinomas with adenocarcinomatous components and those without. Ultrastructurally, the adenocarcinomatous components were seen to possess intracellular microcysts, intercellular lumina, and bundles of tonofilaments, having features of both glandular and squamous epithelia. On the basis of the concept that the basaloid components are histological variants of squamous cell carcinoma and that sarcoma-like components arise from mesenchymal metaplasia of squamous cell carcinoma, it is possible that the three components may originate from the squamous component. The present study thus demonstrated a high incidence of histological variation among esophageal carcinomas.     

Immunohistochemistry of a gross cystic disease fluid protein (GCDFP-15) of the breast. A marker of apocrine epithelium and breast carcinomas with apocrine features.

Gross cystic disease fluid is a pathologic secretion from breast composed of several glycoproteins, including a unique 15,000-dalton monomer protein, GCDFP-15. By the immunoperoxidase technique, GCDFP-15 was localized in the apocrine metaplastic epithelium lining breast cysts and in apocrine glands in the axilla, vulva, eyelid, and ear canal. In normal breast tissue, a few individual epithelial cells within lobules and small ducts were focally positive for GCDFP-15. Fourteen of 30 breast carcinomas stained positively for GCDFP-15. Of 16 carcinomas with apocrine features, 12 stained positively. Benign and malignant lesions from other tissues, including lung, colon, ovary, endometrium, stomach, prostate, liver, esophagus, and kidney, revealed no immunoreactivity. The only cells of "non-apocrine" tissues that contained GCDFP-15 were serous cells of the submandibular salivary gland, submucosal glands of the bronchi, and accessory lacrimal glands. Phylogenetically, these tissues have biologic features in common with apocrine glands. This report is the first to characterize GCDFP-15 as a specific tissue marker of apocrine epithelium.