Basal cell adenoma

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A Case of Basal Cell Adenoma of the Upper Lip

A Case of Basal Cell Adenoma of the Upper Lip

Basal cell adenoma is a rare type of benign salivary gland tumor found most commonly in the parotid gland. We present a rare case of basal cell adenoma arising in the minor salivary gland of the upper lip. The patient was a 59-year-old Japanese man who visited our department in December 2012 with a chief complaint of a mass in the upper lip, which had increased in size over several years. A mobile, elastic, and relatively soft mass without tenderness was palpable in the upper lip region. The mucosa of the upper lip covering the mass was normal. Tumor extirpation was performed under local anesthesia. Histologically, the tumor had a capsule and was composed of islands of relatively uniform, monotonous cells. Immunohistochemically, the inner tumor comprised tubuloductal structures that showed strong staining for CK7, while the outer tumor showed weak staining for CK7. The outer tumor cells also stained positively for CD10 and p63. The MIB-1 (Ki-67) labeling index was extremely low. Basal cell adenoma was diagnosed based on these results. The postoperative course was uneventful 12 months after surgery and there has been no recurrence.
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Basal Cell Adenoma in the Parotid Gland: CT and MR Findings

Basal Cell Adenoma in the Parotid Gland: CT and MR Findings

The patient underwent left total parotidectomy on the 2nd hospital day. The mass was located in the deep lobe of parotid gland and was firmly adhered to the posterior belly of left digastric muscle. Grossly, it was round, well demarcated, and relatively hard. On gross resection, a cystic mass contained a round solid lesion protruding into the lumen, filled with blood- tinged, brownish fluid (Fig 2E). Microscopically, the solid le- sion showed epithelial nests and tubular structure composed of uniform cells with peripheral palisade. No mitosis was found. The histology was compatible with basal cell adenoma with cystic change (Figs 2F and G).
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Basal Cell Adenoma of the Parotid Gland: A Case Report and Review of the Literature

Basal Cell Adenoma of the Parotid Gland: A Case Report and Review of the Literature

2.Ogawa I, Nikai H, Takata T, Miyauchi M, Ito H, Ijuhin N. The cellular composition of basal cell adenoma of parotid gland: An Immunohistochemical analysis. Oral Surg Oral Med Oral Pathol1990;70(5):619-26. 3.González-García R1, Nam-Cha SH, Muñoz-Guerra MF, Gamallo-Amat C. Basal cell adenoma of the pa- rotid gland. Case report and review of the literature. Med Oral Patol Oral Cir Bucal 2006;11(2):E206-9 4.Chakravarthi S, Rao V.T, Prasad L.K, Kalyan, Kat- timani V.S. Basal Cell Adenoma – A Rare Presentation of Parotid Swelling – A Case Report and Review of The Literature. Jr.of Orofac. Scie. 2009;1(2):13-16. 5.Chawla AJ, Tan TY, Tan GJ. Basal cell adenoma of parotid gland: CT scan features Eur J Radiol 2006;58(2):260-5.
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Basal Cell Adenoma of Palate, a Rare Occurrence with Review of Literature

Basal Cell Adenoma of Palate, a Rare Occurrence with Review of Literature

Kleinsasser and Klein (1967) first used the term basal cell adenoma to describe an encapsulated, slow growing, merely epithelial neoplasm composed of dis- cernible basal cells arranged in the form of solid sheets or nests and trabecular/ tubular cord like pattern. [3] The most common site of occurrence is the parotid gland [4- 5] followed by upper lip with a decreasing incidence in palate, buccal mucosa and lower lip. [4] It usually oc- curs in patients over 50 years of age with slight female predilection. [6] Concerning its Clinical presentation, it exhibits as a slow growing, asymptomatic, movable, round or oval, normal-colored sub mucosal mass meas- uring less than 3 cm in diameter. [4]
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Original Article Basal cell adenoma of the parotid gland: clinical and pathological findings in 29 cases

Original Article Basal cell adenoma of the parotid gland: clinical and pathological findings in 29 cases

The surgical method was the same as that used for other benign parotid gland tumors. Facial nerve function was impaired (HB grade Figure 2. Representative images of tumors in the three study groups. A and B: A 45-year-old man with a basal cell adenoma in the upper part of the superficial lobe of the left parotid gland. B: CT shows a round, well-defined homo- geneously enhancing lesion (white arrow). C and D: A 60-year-old woman with a basal cell adenoma in the lower part of the superficial lobe of the left parotid gland (white arrow). D: The tumor shows slight heterogeneous enhance- ment (white arrow) on contrast-enhanced CT. E and F: A 76-year-old woman with a basal cell adenoma in the deep lobe of the left parotid gland. F: CT shows a round, well-defined, homogeneously enhancing lesion in the deep lobe of the left parotid gland (white arrow).
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Basal cell adenocarcinoma of the salivary gland: a morphological and immunohistochemical comparison with basal cell adenoma with and without capsular invasion

Basal cell adenocarcinoma of the salivary gland: a morphological and immunohistochemical comparison with basal cell adenoma with and without capsular invasion

invasion that showed focal positivity for CK5/6, all 26 remaining BCNs expressed CK5/6 with a diffuse pattern (Table 4). Some cases expressed CK5/6 more strongly in peripherally located cells. Although all 10 ACCs also expressed CK5/6, the positivity was mostly focal, and mainly in the inner epithelial cells. This is interesting be- cause CK5/6 is a myoepithelial/basal marker. The BCNs not only differed from the ACCs in terms of CK5/6 ex- pression, they also differed in nuclear β-catenin and S100P protein expression. Thus, nuclear β-catenin was expressed by 70–100% of the BCNs (Figure 2D) and 0% of the ACCs, and S100P protein was expressed by 0–10% of the BCNs but by 50% of the 10 ACCs (Figure 2E). With regard to CD117, 57%, 60%, 100%, and 100% of the BCAC, BCA with capsular invasion, BCA without capsu- lar invasion, and ACC cases expressed this marker, re- spectively (Figure 2F). However, this marker exhibited focal CD117 expression in most BCNs whereas all ACCs diffusely expressed CD117. In terms of p53, while only 3 of the 27 BCNs (11%) were focally positive for this marker, 6 of 10 ACCs (60%) were positive for it. Moreover, in all ACCs, the Ki-67 labeling index exceeded 5% whereas most BCNs had a low ki-67 labeling index (< 5%). All BCNs and ACCs expressed VEGF, while none expressed c-erbB2.
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Basal Cell Adenoma of the Parotid Gland: MR Imaging Findings with Pathologic Correlation

Basal Cell Adenoma of the Parotid Gland: MR Imaging Findings with Pathologic Correlation

Few imaging findings of BCA of the parotid gland have been reported. 6-9 In our cases, the morphology of BCAs was a well-defined margin and rounded contour, as with cases in previous reports. High-grade malignant tumors can easily be differentiated from BCAs by the infiltrative margins of malig- nant tumors. The differential diagnosis of BCA includes pleo- morphic adenoma, Warthin tumor, and low-grade malignant tumors. Most pleomorphic adenomas have an area containing abundant fibromyxoid stroma, which shows bright SI on T2WI as well as marked enhancement on postcontrast images. These areas show delayed enhancement on dynamic study. In addition, pleomorphic adenomas show lobulated contours and typically have a thick capsule. 9-11 These characteristic MR
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CT and Ultrasound Features of Basal Cell Adenoma of the Parotid Gland: A Report of 22 Cases with Pathologic Correlation

CT and Ultrasound Features of Basal Cell Adenoma of the Parotid Gland: A Report of 22 Cases with Pathologic Correlation

A 55-year-old man with type 1 BCA in the right parotid gland A, and B, CT shows a round, well-defined, homogeneously enhancing lesion in the superficial region of the right parotid super[r]

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A Study on Knowledge, Perceptions and Attitudes about Screening and Diagnosis of Diabetes in Saudi Population

A Study on Knowledge, Perceptions and Attitudes about Screening and Diagnosis of Diabetes in Saudi Population

A 45 year female presented with firm left parotid mass for last 6 months. Aspirated smears revealed cohesive benign epithelial cells with fragments of myxoid matrix and occasional spindle cells, diagnosed as PSA in cytology. In histology it was diagnosed as basal cell adenoma. Basal cell adenomas have high rate of erroneous diagnosis in cytology and main differential diagnosis is epithelial rich PSA. 26,27 We have missed the streaming palisaded

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Basal cell lesions of maxillofacial region

Basal cell lesions of maxillofacial region

BCAC found in the parotid gland and account for 0.6% of parotid tumors. (Nagao et al., 1998) This tumor accounts for 1.6% of all salivary gland tumors and 2.9% of malignant salivary gland tumors. (Ellis and Auclair, 1996) No gender predilection and occurs in third to tenth decades of life. BCAC usually shows the features same as the solid or tubulo- trabecular type of BCA. Microscopically basic growth pattern same as solid and tubule-trabecular type of BCA, the solid type is most common and show a mosaic-like pattern. This tumor shows pushing borders or frank infiltration. The bulk of solid aggregates contain small dark staining basaloid cells. Some ductal structures also present. Nuclei are small, irregular and vary in size. Peripheral palisaded tumor cells are less as compared to BCA. Mitotic figures are present. Poorly differentiated variant show more nuclear and cytoplasmic pleomorphism and increased mitotic activity. Infiltration occurs into peri-glandular fat, muscle, and dermis. Perineural invasion is seen and intravascular invasion is rare. The eosinophilic hyaline material is seen. Necrosis and hemorrhage can also be seen. (Salivary gland tumor pathology. Irving Dardick) Differential diagnosis consists of basal cell adenoma, adenoid cystic carcinoma, polymorphous low-grade adenocarcinoma, and small cell undifferentiated carcinoma. Invasion and the increased mitotic activity is the differentiating factor between BCA and BCAC. Hyaline droplets are absent in ACC. BCA show another form of intercellular basal lamina than ACC. polymorphous low-grade adenocarcinoma does not show regular and mosaic-like growth pattern. And also shows the single type of tumor cells. Peripheral palisading is absent in polymorphous low-grade adenocarcinoma. In small cell undifferentiated carcinoma ductal differentiation and mosaic- like growth with or without peripheral palisading are not seen. Foci of tumor cells are very infiltrative in small cell undifferentiated carcinoma. (Salivary gland tumor pathology. Irving Dardick)
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Original Article Expression of MYB protein and its clinicopathological significance in adenoid cystic carcinoma of salivary gland

Original Article Expression of MYB protein and its clinicopathological significance in adenoid cystic carcinoma of salivary gland

LB et al [13] found MYB-positive expression in 14% (16/113) of non-ACC tumors, with a higher expression in basal-like squamous cell carci- noma (4/5), as well as in individual polymorphic adenoma and basal cell adenoma. Similar results were observed in this study. In the study of West et al [2], tissue microarray was used to detect MYB expression. In 65% (24/37) of the ACC cases studied, a strong MYB expression was observed, and mostly in neoplastic myo- epithelial cells. The expression was weakly pos- itive in 9% (10/115) of the non-ACC tumors in salivary gland. The tumors included carcinoma in pleomorphic adenoma, myoepithelial carci- noma, myoepithelial tumor, pleomorphic ade- noma, mucoepidermoid carcinoma, but the expression rate was below 50%. In this study of 98 cases diagnosed with ACC of the salivary gland, 87 were positive, accounting for 88.8%. Among the positive cases, the expression of MYB protein was strong in 58 cases, account- ing for 59.2%, and was weak in 29 cases, accounting for 29.6%. Among the 68 cases of non-ACC tumors, it was weakly positive in only Figure 6. Overall survival curves of ACC in salivary gland. A. Positive and
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An Analysis of Clinical and
Histopathological Correlation of Skin Tumours.

An Analysis of Clinical and Histopathological Correlation of Skin Tumours.

keratinocytic tumours and 6% of all skin tumours. All these tumours were observed as single lesions in the head and neck regions. 47 % were found in females and 53 % in males. They all belong to the age group of 40 to 60 years. Histologically, the tumours showed nests and islands of basaloid cells with pallisading at the periphery. Characteristic retraction artifact was observed between the pallisading cells and the stroma due to increase in basal lamina material. In a patient with nodule in face, FNAC was performed and reported as Basal Cell carcinoma with follicular differentiation. On biopsy the lesion was found to be Basal cell hamartoma
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Neonatal Islet Cell Adenoma: Case Report and Literature Review

Neonatal Islet Cell Adenoma: Case Report and Literature Review

Campbell, Eugene Neonatal Islet Cell Adenoma: Case Report and Literature Review. http://pediatrics.aappublications.org/content/53/5/753[r]

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Lethal (2) Giant Larvae: An Indispensable Regulator of Cell Polarity and Cancer Development

Lethal (2) Giant Larvae: An Indispensable Regulator of Cell Polarity and Cancer Development

Hugl-2 is also associated with cancer progression and suppression. It has been found that Snail, an EMT inducer, downregulate Hugl-2 expression in cells. However, when Hugl-2 expression is induced in Snail-expressing cells, Hugl-2 overrides Snail tumor- igenesis and induces mesenchymal to epithelial tran- sition (MET) [85]. Another research has also found that ZEB1, an EMT-inducing transcriptional re- pressor, suppresses the expression of Hugl-2 in colo- rectal and breast cancers [86]. ZEB1 and Snail have the ability of regulating the expression of the cellcell adhesion molecule and thereby controlling EMT pro- gression. Increased ZEB1 and Snail expression levels, involving with dedifferentiation and invasion of tu- mor cells, can be observed in different human cancers, correlating with dedifferentiation and invasion of tumor cells [87-89]. These findings indicate that loss of Hugl-2 is associated with EMT, and EMT-related fac- tors have negative effects on the expression of Hugl-2. Moreover, Hugl-1 and Hugl-2 are both essential for maintenance of polarity, proliferation and morphol- ogy of human mammary epithelial cells [90]. Aberrant localization or deletion of Lgl2 contributes to gastric epithelial dysplasia and gastric adenocarcinoma as well as pancreatic intraepithelial neoplasia and pan- creatic ductal adenocarcinoma [91-93]. Apical mem- brane localization of Hugl-2, combined with aPKC, is associated with lymphatic invasion and lymph node metastasis in human lung adenocarcinoma [94]. However, roles of Hugl-2 in regulation of other cancer types need to be studied in future works. Taken to- gether, the expression changes of Hugl-1/-2 in vari- ous cancers suggest their tumor-suppressive roles (Table 1).
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Keratotic and Pigmented Basal Cell Carcinoma

Keratotic and Pigmented Basal Cell Carcinoma

BCC compromises 60% - 80% of basal cell carcinomas and is most common over the skin of the forehead. Such tumours of the face have the propensity to invade the skull, nares, orbit or temporal bone thus leading to lethal meningitis. BCC may have solid, cystic, adenoid, keratotic, pigmented, infiltrating and sclerosing patterns. Pig- mented BCC contains functional melanocytes producing melanin whereas keratotic BCC shows a pronounced squamous differentiation. The presence of melanophages does not influence the functional behavior of the tu- mours.

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Morphometric characteristics of basal cell carcinoma peritumoral stroma varies among basal cell carcinoma subtypes

Morphometric characteristics of basal cell carcinoma peritumoral stroma varies among basal cell carcinoma subtypes

In addition to biochemical factors, some morphometric characteristics of BCCs have been explored. Studies performed by Dixon et al. [26] and Jacobs et al. [24] have investigated the relationship between tumour nest mor- phology and tumour aggressiveness. Significant relation- ships were found between non-circular nests, smaller degrees of peripheral palisading, and tumour aggressive- ness. Dixon et al. [26] and Jacobs et al. [27] also found that fibrous stroma was associated with less aggressive tumours, and that hyalinization was present in the stromas of more aggressive tumours. A couple of studies have also explored the relationship between nuclear cell morphome- try and tumour aggressiveness [28,29]. De Rosa et al. [28] claimed that higher nuclear areas and perimeters were associated with increased aggressiveness; however Appel
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ANGIOGENESIS ASSESSMENT IN BASAL CELL CARCINOMA

ANGIOGENESIS ASSESSMENT IN BASAL CELL CARCINOMA

In addition to angiogenesis assessment, several dif­ ferent methods including quantitative assay of AgNOR,3 extracellular matrix analysis, myofibroblastic markers4 and morphometric assessment5 may bring significant contribution in the prediction of outcome of basal cell carcinoma. Finally, among the endothelial markers, CD3 1 is the best for microvessel highlighting because of its high sensitivity and specificity, but as reported in sev­ eral articles, factor VIII related antigen is also a perfect marker and has reliable prognostic significance. 13·15
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Cardiac Tumors and the Nevoid Basal Cell Carcinoma Syndrome

Cardiac Tumors and the Nevoid Basal Cell Carcinoma Syndrome

The syndrome of multiple cysts of the jaws, basal cell carcinomata, and skel- etal anomalies. Nevoid basal cell carcinoma syndrome.[r]

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Safety and efficacy of vismodegib in patients with basal cell carcinoma nevus syndrome: pooled analysis of two trials

Safety and efficacy of vismodegib in patients with basal cell carcinoma nevus syndrome: pooled analysis of two trials

First described in patients with basal cell carcinoma (BCC) nevus syndrome (BCCNS), aberrant activation of the Hedgehog (Hh) pathway is a key pathogenic driver in BCC [1, 2]. The majority of genetic alterations in the Hh pathway are loss-of-function mutations in the tumor-suppressor gene PTCH1 [2, 3]. Patients with BCCNS develop dozens of BCCs over their lifetimes [4], including unresectable advanced BCCs (aBCCs) that are either locally advanced (laBCC) or metastatic (mBCC).

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Basal Cell Carcinoma in a 12-Year-Old Boy

Basal Cell Carcinoma in a 12-Year-Old Boy

Nevoid basal cell carcinoma syndrome Numerous basal cell carcinomas (mean Autosomal dominant; numerous basal onset: 15 y) on sun-exposed and non- cell nevi, jaw cysts, planter and palmar[r]

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