Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The myoepithelial cell (MC) is a component of various secretory glands, including salivary glands. Besides its function, a tumor suppressor and a tumor facilitating functions have been attributed to this cell. We investigated the immunoprofile of benign MC in intraductal areas of carcinoma ex-pleomorphic adenoma (CXPA), comparing them with the MC in duct-like areas of pleomorphic adenoma, origin of the malignant tumor. Antibodies against myoepithelial markers-CK14, alpha-SMA, calponin, P63, CD10, and D2-40-plus laminin and maspin was applied in four selected cases of intracapsular and minimal invasive CXPA with only luminal differentiation presenting areas of intraductal carcinoma. The immunohistochemical reactions of all the antibodies showed stronger staining in benign MC surrounding the malignant epithelial cells than in benign MC in duct-like areas of pleomorphic adenoma, thus revealing that in the malignization process the benign MC become differentiated and produce important proteins related to the tumor suppressor function.
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PMID:Immunoprofile of reactive salivary myoepithelial cells in intraductal areas of carcinoma ex-pleomorphic adenoma. 1675 5

Embryonal sarcoma of the liver is a rare, aggressive malignant tumor that typically occurs in children and teenagers. Microscopic features include spindle, oval, or stellate cells with poorly defined cell borders, nuclear pleomorphism and multinucleation, and variable immunoreactivity to cytokeratin, vimentin, and alpha-1-antitrypsin. Intracellular and extracellular PAS-positive, diastase-resistant hyaline globules are commonly present. The authors evaluated a panel of IHC stains to better define the pattern of immunoreactivity in this tumor. Embryonal sarcomas of the liver were identified from archival files and were immunostained with antibodies: cytokeratin AE1/3, hepatocyte, SMMS, myogenin, calponin, h-caldesmon, desmin, S100, vimentin, CD34, C-kit (CD117), CD10, ALK-1, PE10, Bcl2, p53, and Ki-67. Six cases were identified. Patient age ranged from 6 to 24 years. Tumors ranged from 10 to 20 cm and contained spindled and epithelioid areas with PAS-positive, diastase-resistant globules and atypical cells with focal multinucleation. All cases showed immunoreactivity with vimentin and five showed immunoreactivity with Bcl2. Focal immunoreactivity was seen with cytokeratin AE1/3 in three cases, CD10 in four, calponin in two, desmin in one, and p53 in four. All tumors were negative with hepatocyte, myogenin, CD34, SMMS, h-caldesmon, PE10, ALK-1, and S100. No cytoplasmic staining was seen with C-kit. The proliferation index ranged from 30% to 95%. The diagnosis of embryonal sarcoma is based on typical morphologic features in a large liver tumor occurring in a young patient. The most useful IHC stains help to exclude tumors such as hepatoblastoma, hepatocellular carcinoma, embryonal rhabdomyosarcoma, and other sarcomas.
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PMID:Immunohistochemical analysis of embryonal sarcoma of the liver. 1678 89

Intracystic papillary carcinomas (IPC) of the breast have traditionally been considered to be variants of ductal carcinoma in situ (DCIS). However, it is not clear if all lesions categorized histologically as IPC are truly in situ carcinomas, or if some such lesions might represent circumscribed or encapsulated nodules of invasive papillary carcinoma. Given that the demonstration of a myoepithelial cell (MEC) layer around nests of carcinoma cells is a useful means to distinguish in situ from invasive carcinomas of the breast in problematic cases, assessment of the presence or absence of a MEC layer at the periphery of the nodules that comprise these lesions could help resolve this issue. We studied the presence and distribution of MEC at the periphery of the nodules of 22 IPC and, for comparison, 15 benign intraductal papillomas using immunostaining for 5 highly sensitive markers that recognize various MEC components: smooth muscle myosin heavy chain, calponin, p63, CD10, and cytokeratin 5/6. All 22 lesions categorized as IPC showed complete absence of MEC at the periphery of the nodules with all 5 markers. In contrast, a MEC layer was detected around foci of conventional DCIS present adjacent to the nodules of IPC. Furthermore, all benign intraductal papillomas, including those of sizes comparable to those of IPC, showed a MEC layer around virtually the entire periphery of the lesion with all 5 MEC markers. In conclusion we could not detect a MEC layer at the periphery of the nodules of any of 22 lesions categorized histologically as IPC. One possible explanation for this observation is that these are in situ lesions in which the delimiting MEC layer has become markedly attenuated or altered with regard to expression of these antigens, perhaps due to their compression by the expansile growth of these lesions within a cystically dilated duct. Alternatively, it may be that at least some lesions that have been categorized as IPC using conventional histologic criteria actually represent circumscribed, encapsulated nodules of invasive papillary carcinoma. Regardless of whether these lesions are in situ or invasive carcinomas, available outcome data indicate that they seem to have an excellent prognosis with adequate local therapy alone. Therefore, we believe it is most prudent to continue to manage patients with these lesions as they are currently managed (ie, similar to patients with DCIS) and to avoid categorization of such lesions as frankly invasive papillary carcinomas. Given our observations, we favor the term "encapsulated papillary carcinoma" over "intracystic papillary carcinoma" for circumscribed nodules of papillary carcinoma surrounded by a fibrous capsule in which a peripheral layer of MEC is not identifiable.
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PMID:Intracystic papillary carcinomas of the breast: a reevaluation using a panel of myoepithelial cell markers. 1686 72

Endometrial stromal sarcomas are rare malignant mesenchymal tumors that usually develop in the uterine corpus and occasionally arise at various extrauterine sites. This report describes the first case of primary extrauterine endometrial stromal sarcoma arising in the extraperitoneal portion of the round ligament presenting as a solitary inguinal mass in a 46-year-old woman. The patient presented gradually growing tumor in the right inguinal region. Local tumor resection was performed and no recurrence or metastasis was found at 15 months after the operation. Histological examination revealed that the tumor comprised uniform, spindle-shaped cells with blunt nuclear figure and scattered small arteries, and infiltrated into adjacent tissue. No endometriosis was morphologically identified in the lesion. Immunohistochemically, the tumor cells were positive for CD10, estrogen receptor, progesterone receptor, alpha-smooth muscle actin, and calponin. We confirmed JAZF1/JJAZ1 fusion by reverse transcription-polymerase chain reaction and the corresponding chromosomal translocation by interphase fluorescence in situ hybridization on paraffin sections. It is essential that the inguinal region should be recognized as a possible primary site of endometrial stromal sarcoma, and the detection of a JAZF1/JJAZ1 fusion can be useful when the diagnosis is not confirmed by microscopic observation or immunohistochemistry for the tumor arising in extrauterine sites.
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PMID:Extrauterine endometrial stromal sarcoma with JAZF1/JJAZ1 fusion confirmed by RT-PCR and interphase FISH presenting as an inguinal tumor. 1723 69

It has been shown that stromal-vascular fraction isolated from adipose tissues contains an abundance of CD34+ cells. Histological analysis of adipose tissue revealed that CD34+ cells are widely distributed among adipocytes and are predominantly associated with vascular structures. The majority of CD34+ cells from freshly isolated stromal-vascular fraction were CD31-/CD144- and could be separated from a distinct population of CD34+/CD31+/CD144+ (endothelial) cells by differential attachment on uncoated plastic. The localization of CD34+ cells within adipose tissue suggested that the nonendothelial population of these cells occupied a pericytic position. Analysis of surface and intracellular markers of the freshly isolated CD34+/CD31-/CD144- adipose-derived stromal cells (ASCs) showed that >90% coexpress mesenchymal (CD10, CD13, and CD90), pericytic (chondroitin sulfate proteoglycan, CD140a, and CD140b), and smooth muscle (alpha-actin, caldesmon, and calponin) markers. ASCs demonstrated polygonal self-assembly on Matrigel, as did human microvascular endothelial cells. Coculture of ASCs with human microvascular endothelial cells on Matrigel led to cooperative network assembly, with enhanced stability of endothelial networks and preferential localization of ASCs on the abluminal side of cords. Bidirectional paracrine interaction between these cells was supported by identification of angiogenic factors (vascular endothelial growth factor, hepatocyte growth factor, basic fibroblast growth factor), inflammatory factors (interleukin-6 and -8 and monocyte chemoattractant protein-1 and -2), and mobilization factors (macrophage colony-stimulating factor and granulocyte/macrophage colony-stimulating factor) in media conditioned by CD34+ ASCs, as well a robust mitogenic response of ASCs to basic fibroblast growth factor, epidermal growth factor, and platelet-derived growth factor-BB, factors produced by endothelial cells. These results demonstrate for the first time that the majority of adipose-derived adherent CD34+ cells are resident pericytes that play a role in vascular stabilization by mutual structural and functional interaction with endothelial cells.
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PMID:A population of multipotent CD34-positive adipose stromal cells share pericyte and mesenchymal surface markers, reside in a periendothelial location, and stabilize endothelial networks. 1796 85

Papillary neoplasms of the breast represent a complex spectrum ranging from benign to malignant lesions. The myoepithelial cell (MEC) layer is generally continuous in papillomas and increasingly discontinuous to absent in atypical and malignant counterparts. Identification of MECs can be difficult on morphological grounds and currently relies on immunomarkers. We investigated the potential role of p63 and CD10 in 20 papillary lesions and compared them with 1A4 and calponin. In 18 cases, adjacent normal breast tissue was available for study. All four markers were diffusely positive in all samples of normal tissue and benign papillomas indicating similar sensitivity in the identification of MECs. Intense positivity was found in 100% of the cases with 1A4 and CD10, but in only 76% with calponin and in 60.5% with p63 (differences statistically significant, p < 0.05), suggesting that the former two render more reproducible results. The most specific markers were p63 and CD10 which showed cross-reactivity in 0% and in up to 33% of the cases respectively. 1A4 and calponin showed diffuse cross-reactivity in all cases. When assessing benign versus atypical papillomas, the best parameters were diffuse positivity using CD10 or p63, and continuous MEC layer, mainly using CD10. When comparing benign papillomas to carcinomas all parameters were equally useful with 1A4 and CD10. Regardless of the marker, intense positivity was the only parameter that could distinguish atypical papillomas from papillary carcinomas. p63 staining, which renders a nuclear and mostly discontinuous reactivity, was not as useful as the other markers when the parameter continuous MEC layer was evaluated. Although CD10 seems to combine the highest specificity and reproducibility with a good sensitivity, reproducibility of 1A4 is higher. Thus, a minimum panel to assess papillary lesions should include both markers. Although p63 is the most specific, its nuclear and discontinuous pattern may lead to erroneous diagnosis, especially in the differentiation between benign papillomas and atypical/malignant lesions.
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PMID:Use of p63 and CD10 in the differential diagnosis of papillary neoplasms of the breast. 1808 74

Basaloid carcinoma of the breast (BCB) is an unusual neoplasm composed of basal-type neoplastic cells similar to those found in adenoid cystic carcinoma (ACC), although lacking distinctive features such as a cribriform pattern, a dual neoplastic population (epithelial-myoepithelial/basaloid), and stromal deposits of basement membrane-like material. In this article, we present 9 cases of breast cancer showing overall/predominant basaloid morphology. Patients' ages ranged from 47 to 75 years (mean, 61.4 years). Surgical treatment included mastectomy or quadrant excision with or without axillary dissection. Most tumors had a circumscribed outline and ranged in size from 1.3 to 5.5 cm (mean, 2.5 cm). Microscopically, they featured sheets, nests, and cords of proliferating basaloid tumor cells with ovoid, hyperchromatic nuclei with inconspicuous nucleoli and scant cytoplasm. No foci with characteristics of ACC were found in any of the tumors. Transition into pleomorphic basaloid carcinoma with foci of high-grade ductal carcinoma in situ plus infiltrating ductal carcinoma (IDC) and admixture with grade 3 ductal and sarcomatoid carcinoma was seen in 2 cases. Tumor cells were positive for wide-spectrum keratins and epithelial membrane antigen (9/9) and high-molecular-weight keratins (7/9). They were negative for smooth muscle actin, p63, calponin, and CD10 in all tested cases. Estrogen receptor, progesterone receptor, and HER-2 were negative. Axillary lymph node metastases were seen in 3 cases. At follow-up (range, 10-169 months), 5 patients were alive, 1 with evidence of contralateral breast cancer. Three patients died: one of disseminated BCB metastases, another of liver cirrhosis, and one of disseminated estrogen receptor/progesterone receptor-positive contralateral IDC. One patient was lost to follow-up. We concluded that BCB has some phenotypic and immunohistochemical features enabling its distinction from ACC or IDC. It appears to be a morphological and possibly a clinical entity. Compared with ACC, BCB appears to be more aggressive and may entail a more guarded prognosis.
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PMID:Basaloid carcinoma of the breast: a review of 9 cases, with delineation of a possible clinicopathologic entity. 1816 8

Human uterine fibroblasts (HuF) isolated from the maternal part (decidua parietalis) of a term placenta provide a useful model of in vitro cell differentiation into decidual cells (decidualization, a critical process for successful pregnancy). After isolation, the cells adhere to plastic and have either a small round or spindle-shaped morphology that later changes into a flattened pattern in culture. HuF robustly proliferate in culture until passage 20 and form colonies when plated at low densities. The cells express the mesenchymal cell markers fibronectin, integrin-beta1, ICAM-1 (CD54), and collagen I. Flow cytometry of HuF has detected the presence of CD34, a marker of the hematopoietic stem cell lineage, and an absence of CD10, CD11b/Mac, CD14, CD45, and HLA type II. Furthermore, they also express the pluripotency markers SSEA-1, SSEA-4, Oct-4, Stro-1, and TRA-1-81 as detected by confocal microscopy. Treatment for 14-21 days with differentiation-inducing media leads to the differentiation of HuF into osteoblasts, adipocytes, and chondrocytes. The presence of alpha-smooth muscle actin, calponin, and myosin light-chain kinase in cultured HuF implies their similarity to myofibroblasts. Treatment of the HuF with dimethyl sufoxide causes reversion to the spindle-shaped morphology and a loss of myofibroblast characteristics, suggesting a switch into a less differentiated phenotype. The unique abilities of HuF to exhibit multipotency, even with myofibroblast characteristics, and their ready availability and low maintenance requirements make them an interesting cell model for further exploration as a possible tool for regenerative medicine.
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PMID:Multipotent properties of myofibroblast cells derived from human placenta. 1840 96

The clinicopathologic and immunohistochemical features of 69 pediatric examples of infantile digital fibroma/fibromatosis (IDF) were analyzed. Thirty males, 26 females, and 1 child (sex unstated) ranging from newborn to 120 months of age (median, 12 mo) manifested 74 lesions (5 identified in follow-up) involving the toe or finger (n=71) and the hand or foot (n=3). Tumors ranged in size from 3 to 35 (median, 10) mm. All but 4 study members presented with a solitary lesion. Metachronous IDFs developed in 7 patients within 17 to 82 months. Microscopically, a cytologically bland, fibroproliferative lesion was observed forming a dome-shaped/polypoid nodule directly beneath the epidermis and invading dermal adnexa. Mitotic figures per 20 high-powered fields ranged from 0 to 7 (median, 1). Paranuclear cytoplasmic inclusions were identified in 57 tumors. Tumor cells immunohistochemically expressed calponin (11 of 11 tumors), desmin (9/9), alpha-smooth muscle actin (11/11), CD99 (11/11), CD117 (6/8), heavy caldesmon (2/11 and scattered cytoplasmic inclusions in 4 tumors), CD10 (1/9), nuclear beta-catenin (2/11), and CD34 (1/11), but not muscle actin (HUC1-1), keratins, estrogen/progesterone receptor proteins, or activated caspase-3. Twenty-eight of 38 patients (74%) experienced recurrent/persistent disease (single in 22; multiple in 6) (median, 4 mo after surgery). One recurrent tumor spontaneously regressed and the size of another remained unchanged for almost 17 years before reexcision. All 23 patients with >5 years follow-up are currently disease free (median disease-free interval, 23 y). Minor postoperative functional/cosmetic complaints were reported in 47%. No patient with adequate clinical data developed the digitocutaneous dysplasia syndrome or a conventional fibromatosis, or relayed a family history of IDF/conventional fibromatosis. Our results indicate that IDF is a unique myofibroblastic process separable from conventional fibromatoses and from histologic mimics. Conservative excision or observation after biopsy (with additional surgery employed as necessary) are recommended treatment options.
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PMID:Infantile digital fibroma/fibromatosis: a clinicopathologic and immunohistochemical study of 69 tumors from 57 patients with long-term follow-up. 1883 Jan 28

Recent molecular studies have indicated that ductal carcinoma in situ (DCIS)-associated myoepithelial cells (MECs) show differences from MECs in normal breast tissue. Such alterations may influence the progression of DCIS to invasive cancer. The purpose of this study was to investigate further phenotypic alterations in DCIS-associated MECs. Paraffin sections of 101 cases of DCIS (56 without and 45 with associated invasive carcinoma) were immunostained for 7 MEC markers: smooth muscle actin, smooth muscle myosin heavy chain (SMMHC), calponin, p63, cytokeratin (CK) 5/6, CD10, and p75. In each case, the distribution and intensity of staining for each marker in DCIS-associated MECs was compared with that in MECs surrounding normal ductal-lobular structures on the same slide. In 85 cases (84.2%), DCIS-associated MECs showed decreased expression of one or more MEC markers when compared with normal MECs. The proportion of cases that showed reduced expression was 76.5% for SMMHC, 34.0% for CD10, 30.2% for CK5/6, 17.4% for calponin, 12.6% for p63, 4.2% for p75, and 1% for smooth muscle actin. Reduced MEC expression of SMMHC was significantly more frequent in high grade than in non-high-grade DCIS (84.8% vs. 61.5% of cases, P=0.01). We conclude that DCIS-associated MECs show immunophenotypic differences from MECs surrounding normal mammary ductal-lobular structures. The biologic significance of this remains to be determined. However, these results indicate that the sensitivity of some MEC markers is lower in DCIS-associated MECs than in normal MECs. This observation should be taken into consideration when selecting MEC markers to help distinguish in situ from invasive breast carcinomas.
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PMID:Phenotypic alterations in ductal carcinoma in situ-associated myoepithelial cells: biologic and diagnostic implications. 2110 98


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