Pleomorphic lipoma with pseudopapillary structures: a pleomorphic counterpart of pseudoangiomatous spindle cell lipoma.
Explore the source record for details and available documents.
Biomarkers, Tumor↗
SEARCH · Search PubMed
Results for “pleomorphic”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
On the Pleomorphism of Bacteria: I. On the Pleomorphism of B. Paratyphi B.
Explore the source record for details and available documents.
Journal Article↗
Pleomorphic soft tissue myogenic sarcomas of adulthood. A reappraisal in the mid-1990s.
325 diverse sarcomas, 39 rhabdomyosarcomas (RMS), including all histologic variants, and 135 leiomyosarcomas (LMS) were identified. Within these two groups, 18 (46%) of the RMS and 14 (10%) of the LMS represented pleomorphic variants. These neoplasms were studied by morphology (histology and ultrastructure) and by immunohistochemical methods employing antibodies to intermediate filaments (vimentin and desmin) and actin isoforms [alpha-smooth (sm) and alpha-sarcomeric (sr) actins]. Twenty-four pleomorphic malignant fibrous histiocytomas (MFH) and eight pleomorphic liposarcomas (LS) were examined in a similar fashion. By light microscopy, the pleomorphic RMS, LMS, and MFH were indistinguishable, as each was dominated by pleomorphic cells disposed in a haphazard growth pattern; moreover, many featured fascicular, storiform, and sclerotic zones. The distinction between these neoplasms became apparent only following immunohistochemistry and/or ultrastructural study. All pleomorphic RMS disclosed rudimentary sarcomeres and exhibited the following cytoskeletal profile: vimentin (+) (18 of 18), desmin (+) (14 of 18), alpha-sr actin (+) (18 of 18) and alpha-sm actin (+) (five of 18). All the pleomorphic LMS featured smooth-muscle differentiation of variable degrees in the form of cytoplasmic bundles of microfilaments and associated dense bodies; their cytoskeletal profile was vimentin (+) (14 of 14), desmin (+) (seven of 14), alpha-sr actin (+) (none of 14), and alpha-sm actin (+) (eight of 14). The latter was demonstrated in all moderately differentiated, but absent or only focally expressed in poorly differentiated variants. All pleomorphic MFH and LS were devoid of myogenic (skeletal or smooth) ultrastructural features and expressed vimentin solely. This combined morphological and immunohistochemical study illustrates the following: First, these pleomorphic sarcomas are often indistinguishable by histologic growth pattern alone; thus, an accurate diagnosis requires study with all of these techniques. Second, pleomorphic myogenic sarcomas are restricted to adults and are not uncommon neoplasms among pleomorphic sarcomas: RMS (28%), LMS (21%), MFH (38%), and LS (13%). Third, the study defines desmin-negative and alpha-sm actin-positive pleomorphic RMS, and desmin-negative and alpha-sm-actin-negative pleomorphic LMS.
Actins↗
An immunohistochemical study of bizarre neoplastic cells in pleomorphic adenoma: its cytological nature and proliferative activity.
The cytological nature and proliferative activity of bizarre neoplastic cells, widely scattered in pleomorphic adenomas of salivary gland origin were studied. Pleomorphic adenomas containing numerous bizarre neoplastic cells were found in four cases, and were equal to 2.9% of all pleomorphic adenomas examined. All four cases presented as well-circumscribed, firm masses measuring less than 1.5 cm in size, located in the palate, and were of 7 months to 4 years duration. Histopathologically, these pleomorphic adenomas were cell rich type, and were well demarcated from surrounding tissues, although their fibrous capsules were partially defective. In addition to characteristic histopathological findings of pleomorphic adenoma, numerous neoplastic cells with bizarre appearance were scattered throughout the lesion, excepting for tubuloductal structures. These bizarre neoplastic cells had irregular-shaped and large nuclei with or without hyperchromatism, although their nucleoli were small and mitotic figures were few. Furthermore, there were many multinucleated giant cells, some of which showed multilobulated nuclei. Neither necrosis nor infarct was seen in the tumors. Immunohistochemically, bizarre neoplastic cells scattered in solid-proliferating areas and myxoid areas were neoplastic myoepithelial cells in nature. There was no statistical significance of MIB-1 labeling indices between pleomorphic adenomas with bizarre neoplastic cells and usual pleomorphic adenomas. The p53 labeling indices were quite low. Although the benign nature of pleomorphic adenomas with numerous bizarre neoplastic cells and hypercellularity, distinguishing such pleomorphic adenomas from various stages of malignant transformation in pleomorphic adenomas and other carcinomas should be made by histological section of submitted biopsy specimen or aspirated content for cytological diagnosis. The present paper suggests that the term 'bizarre cell pleomorphic adenoma' is an appropriate name for this neoplasm, in that it is distinguished from the usual benign pleomorphic adenoma which is easily diagnosed by routinely prepared histological or cytological stainings.
Adenoma, Pleomorphic↗
c-myc, ras p21 and p53 expression in pleomorphic adenoma and its malignant form of the human salivary glands.
Using an immunohistochemical study and an immunoblot analysis, the expression of cellular oncogenes of the human salivary glands such as c-myc, ras p21, and p53 tumor-suppressor gene in pleomorphic adenomas and its malignant form, carcinoma in pleomorphic adenomas was examined to evaluate a differential biological significance, in comparison with that in normal salivary gland tissues. Immunohistochemically, the c-myc product was detected in 42% of the pleomorphic adenomas and in 56% of the carcinomas in pleomorphic adenoma. The ras p21 expression was observed in 24% of pleomorphic adenomas, and in 50% of carcinomas in pleomorphic adenoma. The p53 protein was detected in 18% of the pleomorphic adenomas and in 67% of the carcinomas in pleomorphic adenoma. Although there was no significant difference between the benign and malignant forms for the expression of c-myc, a statistical significance in ras p21 and p53 expression was found between the pleomorphic adenoma and its malignant form (P < 0.05) and P < 0.001, respectively). An immunoblotting assay clearly demonstrated the expression of c-myc and p53 gene products in both the benign and malignant forms of the pleomorphic adenoma, and that of ras p21 in the malignant form. These results indicate that activation of c-myc and ras p21 proto-oncogenes and the involvement of p53 mutation may play important roles in the malignant transformation of salivary gland pleomorphic adenoma.
Adenoma, Pleomorphic↗
Differential diagnosis of adenoid cystic carcinoma from pleomorphic adenoma of the salivary gland on fine needle aspiration cytology.
OBJECTIVE: To evaluate the distinguishing morphologic features of pleomorphic adenoma and adenoid cystic carcinoma on fine needle aspiration cytology. STUDY DESIGN: A retrospective study was undertaken to compare the cytomorphology of 9 adenoid cystic carcinomas with that of 12 pleomorphic adenomas of the salivary gland among histologically proven cases. RESULTS: The most consistent finding for differentiating adenoid cystic carcinoma from pleomorphic adenoma in our study was the amount of cytoplasm of individual tumor cells. Plasmacytoid appearance is a reliable finding for pleomorphic adenoma, and it enables us to rule out adenoid cystic carcinoma. All 12 cases of pleomorphic adenoma showed tumor cells containing abundant cytoplasm in clusters and isolated cells, with plasma cell-like appearance in 9 cases, especially in isolated cells. In contrast with pleomorphic adenoma, most adenoid cystic carcinomas showed little cytoplasm. Hyaline spherical globules were found in four of nine adenoid cystic carcinomas but were not found in any case of pleomorphic adenoma. It was specific but not sensitive to adenoid cystic carcinoma. Fibrillary chondromyxoid ground substance and a mixture of epithelial cells with stroma were found in two-thirds of the pleomorphic adenomas in our cases. The pattern of cell clusters was helpful to differentiate pleomorphic adenoma from adenoid cystic carcinoma. Large, loose clusters with a spindle cell core suggested pleomorphic adenoma. Small, dense trabeculae with a smooth margin and dense clusters containing clear, round spaces were more suggestive of adenoid cystic carcinoma. Overall cellularity, proportion of isolated cells, orientation of cellular clusters and degree of cellular overlapping gave almost no help in making the distinction between the lesions. CONCLUSION: A plasmacytoid appearance of individual tumor cells with abundant cytoplasm was a reliable finding in pleomorphic adenoma for differentiating it from adenoid cystic carcinoma. Practically, nuclear features were not enough to distinguish the two lesions in isolated cases.
Adenoma, Pleomorphic↗
[The expression of matrix metalloproteinases and their tissue inhibitors in pleomorphic adenoma].
OBJECTIVE: To examine the expression of MMPs and TIMPs in pleomorphic adenoma of salivary gland and to investigate the relationship between the expression and the biological behaviour of the tumor. METHODS: Twenty-three cases of pleomorphic adenoma were divided into active type and common type according to their biological behavior. Immunohistochemistry for MMP-2, MMP-9, TIMP-1, TIMP-2 and gelatin zymography analysis were performed in these 23 cases and in 6 malignant and 6 benign salivary gland tumors. RESULTS: The immunoreactivity of MMP-2 protein and MMP-2/TIMP-1, 2 ratio were significantly higher in active pleomorphic adenoma than in common pleomorphic adenoma (P = 0.028, P = 0.009, P = 0.045). The expression of active MMP-2, proMMP-9 and active MMP-9 were significantly higher in active pleomorphic adenoma than in common pleomorphic adenoma (P = 0.034, P = 0.021, P = 0.001). There was no significant difference in expression of MMP-2, MMP-9, TIMP-1 and TIMP-2 between the salivary malignant tumor and active pleomorphic adenoma, also between the salivary benign tumor and common pleomorphic adenoma. CONCLUSIONS: The expression of MMPs and TIMPs in active pleomorphic adenoma is similar to that in salivary carcinomas, and the expression in common pleomorphic adenoma also resembled to that in salivary adenoma. The expression of MMP-2, 9 and TIMP-1, 2 is related to the biological behavior of pleomorphic adenoma of salivary gland.
Adenoma, Pleomorphic↗
Role of fine needle aspiration cytology in diagnosis of pleomorphic adenomas.
This retrospective study was carried out to review the cases diagnosed as pleomorphic adenoma in major or minor salivary glands and determine the difficulties encountered on typing this tumour on fine needle aspiration cytology (FNAC). Over a 19-year period (1982-2000) 488 pleomorphic adenomas were diagnosed on FNAC from different sites (parotid - 372 cases, submandibular - 95 cases; oral cavity - 21 cases). Histology was available in 232 cases. Twenty-nine cases where a histological diagnosis of pleomorphic adenoma was made but the cytological diagnosis was variable were also reviewed. In 216 of the 232 cases a good cytohistological correlation was available. On review only 4 of the 16 cases initially diagnosed as pleomorphic adenoma on FNAC where the histology revealed a different tumour were categorized as pleomorphic adenoma, while 3 each were classified as adenoid cystic carcinoma and benign tumour ?type, and 2 each were diagnosed to be muco-epidermoid carcinoma, monomorphic adenoma and acinic cell carcinoma. On review of the FNAC smears from 29 cases where a histological diagnosis of pleomorphic adenoma was available while the cytological diagnosis was variable, only 11 (38%) were categorized as pleomorphic adenoma. In the majority of the remaining cases the cytological diagnosis did not alter markedly, 7 of 10 cases where the tumour could not be typed on cytology initially could not be typed even on review. In conclusion, FNAC is an ideal, fairly accurate preoperative procedure for the diagnosis of pleomorphic adenomas. Certain diagnostic problems occur in differentiating pleomorphic adenomas from adenoid cystic carcinoma, monomorphic adenoma and mucoepidermoid carcinoma. Carcinoma ex-pleomorphic adenoma is difficult to identify on FNAC and in our series all 4 such cases on histology were considered benign on cytology.
Adenoma, Pleomorphic↗
[Immunohistological investigation of the histological origin and differentiation of pleomorphic adenoma of the parotid gland].
Immunohistological expressions of the cytokeratin (CK) subclass, vimentin, glial fibral antigen protein (GFAP), alpha-smooth muscle actin, and S-100 protein were investigated in pleomorphic adenoma of the parotid gland. In addition, the correlation between immunohistological findings in the normal parotid gland and those in pleomorphic adenoma was examined. Vimentin, S-100 protein, and GFAP, which were not detected in the normal parotid gland, were observed in pleomorphic adenoma. Only CK-1, which was not detected in the normal parotid gland, was expressed intensely in squamous metaplastic lesions of pleomorphic adenoma. All other CK detected in pleomorphic adenoma were also expressed in the normal parotid gland. Therefore, the expression of vimentin, S-100 protein, GFAP, and CK-1 in pleomorphic adenoma is related to oncogenesis. Since most types of CK expression were observed in solid pleomorphic adenoma lesions and all types of CK expression detected in other lesions were included, cellular differentiation between solid and nonsolid lesions was elucidated. According to the pattern of CK subclass expression, the following sequence of differentiation was suggested; solid lesion-->myxoid lesion-->chondroid lesion, solid lesion-->tubular lesion, solid lesion-->myoepithelioid lesion, and solid lesion-->squamous metaplastic lesion. In normal parotid glands, satellite cells around the ductal cells showed all types of CK subclass expression detected in myoepithelial cells, acinus cells, and ductal cells. Since the types and patterns of CK expression in solid lesions of pleomorphic adenoma are the same as those in satellite cells in the normal parotid gland, pleomorphic adenoma seems to originate from satellite cells. If satellite cells in the normal parotid gland are considered to be so-called reserve cells in the bicellular theory, the origin and cellular differentiation of pleomorphic adenoma can be explained in relation to CK subclass expression.
Actins↗
Pleomorphic carcinoma of the pancreas: reappraisal of surgical resection.
Pleomorphic carcinoma is a rare variant of pancreatic exocrine carcinoma. The aim of this communication is to reappraise surgical resection of pleomorphic carcinoma of the pancreas. Clinicopathological findings of four Japanese patients with pleomorphic carcinoma of the pancreas were reviewed and compared with those of 24 Japanese patients with adenocarcinoma of the pancreas to clarify possible surgical implications of pleomorphic carcinoma. Of the four patients, three were female and one male, aged 64, 65, 66, and 74 yr, respectively. Two carcinomas were located in the head of the pancreas, one in the body, and the other in the tail. Ultrasonography demonstrated a well defined hypoechoic mass measuring 5-10 cm, with central necrotic area in all of the patients. Computed tomography showed a low density tumor with sharp margin and heterogeneous internal structure in all. On angiography, three tumors were hypervascular and another was hypovascular. Extensive vascular encasement was observed in all. Pancreatoduodenectomy was done in two patients and distal pancreatectomy in the other two. Multiple liver metastases occurred 1 month after surgical resection in two patients and local recurrence 1 month in one and 2 months in the other, leading to death either 2 (2 patients) or 3 months (2 patients) after pancreatectomy. Significantly differentiating features of the four pleomorphic carcinomas of the pancreas and the 24 adenocarcinomas of the pancreas were the mean diameter (6.6 +/- 1.3 cm vs 3.5 +/- 0.3 cm, p = 0.0007), margin of the tumor (expansive in the four pleomorphic carcinomas versus infiltrative in 21 of the 24 adenocarcinomas, p = 0.003) and vascularity on angiography (hypervascular in three of the four pleomorphic carcinomas versus hypovascular in 21 of the 23 adenocarcinomas, p = 0.013). The 1-yr and 3-yr survival rates of the four patients with pleomorphic carcinoma were 0% and 0%, whereas those of the 24 patients with adenocarcinoma of the pancreas were 42% and 13%, respectively (p < 0.0001). These findings suggest that the clinical course of patients with pleomorphic carcinoma of the pancreas is so poor even after surgical resection that pleomorphic carcinoma of the pancreas is not a candidate for pancreatectomy despite its locally expansive growth.
Adenocarcinoma↗
Benign metastasizing pleomorphic adenoma of the parotid gland: a clinicopathologic puzzle.
BACKGROUND: Pleomorphic adenoma constitutes the most common benign parotid gland tumor. Local recurrence after surgical treatment (lateral or total parotidectomy) has been described in 1% to 5% of cases. Malignant degeneration has been reported in 2% to 9% of cases of pleomorphic adenoma of salivary gland origin. Metastasizing pleomorphic adenomas without histologic evidence of malignancy have rarely been reported. Metastatic lesions have been discovered in bone, lymph nodes, the lung, oral cavity, pharynx, skin, liver, retroperitoneum, kidney, calvarium, and central nervous system. To the best of our knowledge, we hereby report the first case of pleomorphic adenoma of the parotid gland metastasizing to the ipsilateral maxilla. METHODS: We simultaneously examined apoptosis-related protein expression and markers of cell-proliferation activity in our case of benign pleomorphic adenoma metastasis and compared outcome with a control group of primary parotid pleomorphic adenomas. RESULTS: Analysis of p53, Bcl-2, MIB1, CD 105, p27, and p21 expression did not reveal significant differences between metastasizing pleomorphic adenoma of the salivary gland and the control group of primary parotid pleomorphic adenomas. CONCLUSIONS: Clinical rather than pathologic evidence seems to justify inclusion of metastasizing salivary pleomorphic adenoma in the group of low-grade malignant salivary tumors.
Adenoma, Pleomorphic↗
Comparison of proliferating cell nuclear antigen index in benign and malignant salivary pleomorphic adenoma.
The expression of proliferating cell nuclear antigen (PCNA) was studied in benign and malignant pleomorphic adenomas by using monoclonal antibody to PCNA. Carcinoma in pleomorphic adenoma (n = 8), cell-rich variant (n = 6) and typical pleomorphic adenoma (n = 6) were selected in this study. The PCNA index in carcinoma in pleomorphic adenoma showed a higher index of nuclear staining (mean 22.9%, S.D. 6.2) than in typical pleomorphic adenoma (mean 6.9%, S.D. 3.4) or a cell-rich variant of pleomorphic adenoma (mean 8.8%, S.D. 3.3). A significant difference in PCNA index was found between benign and malignant pleomorphic adenoma (P < 0.05). The present study suggests that PCNA index significantly differs between pleomorphic adenoma and carcinoma in pleomorphic adenoma, but in the prediction of malignant transformation potential it should be combined with routine histopathological examination.
Adenoma, Pleomorphic↗
Microsatellite alterations at chromosome 8q loci in pleomorphic adenoma.
OBJECTIVE: To determine the extent, localization, and clinical significance of microsatellite loci alterations at sites of reported cytogenetic abnormalities in pleomorphic adenomas. BACKGROUND: Pleomorphic adenoma is a benign salivary gland tumor with a propensity for recurrence and potential for malignant conversion. Although its cause remains unclear, clonal cytogenetic abnormalities have been reported consistently. DESIGN: DNA extracted from paired normal and tumor tissue specimens from 1 patient with carcinoma ex pleomorphic adenoma and 17 patients with pleomorphic adenoma (3 contained foci of carcinoma ex pleomorphic adenoma) was evaluated for loss of heterozygosity at microsatellite loci with a multiplex polymerase chain reaction-based analysis. Correlation with clinical and pathologic features was performed. RESULTS: Overall 10 (56%) of 18 cases manifested loss of heterozygosity at the loci tested. The frequency of loss of heterozygosity noted on 3p, 6q, 8p, 8q, and 12q microsatellite loci was 17%, 12%, 8%, 47%, and 27% of informative cases, respectively. Specimens from patients with carcinoma ex pleomorphic adenoma showed a similar loss of heterozygosity incidence at these loci. No apparent association between molecular abnormalities and clinical-pathologic features was observed in this cohort. CONCLUSIONS: Loss of heterozygosity at microsatellite loci on 8q, a breakpoint at which translocations have been previously documented in pleomorphic adenoma, is a frequent event in this tumor. The incidence is not increased in patients with focal carcinoma ex pleomorphic adenoma, suggesting that loss of heterozygosity at 8q is an early event in tumorigenesis. Further evaluation at these loci is needed to identify potential tumor suppressor genes that may be associated with the initiation and progression of pleomorphic adenomas.
Adenoma, Pleomorphic↗
Immunohistochemical localization of members of the transforming growth factor (TGF)-beta superfamily in normal human salivary glands and pleomorphic adenomas.
Although pleomorphic adenoma is the most common type of salivary gland epithelial tumor, it frequently contains "mesenchymal"-like components, including myxoid or chondroid tissues. We reported previously that chondroid tissue formation in pleomorphic adenoma was associated with overexpression of bone morphogenetic proteins (BMPs) by neoplastic myoepithelial cells. BMPs belong to the transforming growth factor (TGF)-beta superfamily, so we hypothesized that pleomorphic adenoma may express TGF-betas and that these molecules may regulate mesenchymal-like tissue formation. To evaluate this hypothesis, we immunohistochemically examined TGF-beta1, -beta2 and -beta3 expression and localization in normal salivary glands and in 43 cases of pleomorphic adenomas. There was no evidence of TGF-beta1 expression in normal salivary glands or pleomorphic adenomas. Signals for TGF-beta2 in the normal salivary glands were observed in the intercalated ducts, while in pleomorphic adenomas they were observed in the inner ductal cells of the tubulo-glandular structures. Signals for TGF-beta3 in the normal salivary glands were observed in mucous cells, whereas in pleomorphic adenomas they were observed in the solid nests of neoplastic myoepithelial cells, in the portion showing squamous metaplasia, and in the inner ductal cells of tubulo-glandular structures. TGF-betas induce ectopic cartilage formation in vivo, but chondroid tissues in pleomorphic adenomas showed only weak TGF-beta3 expression. TGF-beta may be related to differentiation of the inner ductal cells and the neoplastic myoepithelial cells. In conclusion, pleomorphic adenomas expressed TGF-beta2 and -beta3, which may be associated with differentiation of the inner ductal cells and neoplastic myoepithelial cells.
Adenoma, Pleomorphic↗
[The relationship of abnormal expression of cell glucoprotein with recurrence of pleomorphic adenoma in salivary gland].
OBJECTIVE: To study the relationship of expression of mucin 1 and E-cadherin with recurrence of pleomorphic adenoma in salivary gland, and to investigate the signal to predict the recurrence potential of the tumor. METHODS: ; The capsule of tumor was observed by microscope. The expression of mucin 1 and E-cadherin in 33 cases of primary adenoma, 12 cases of recurrent pleomorphic adenomas and 7 cases of malignant pleomorphic adenomas were detected by immunohistochemistry. RESULTS: There was no significant difference about the status of capsule and the positive rate of mucin 1 expression between primary and recurrent pleomorphic adenoma (P > 0.05). The abnormal distribution of mucin 1 expression was observed in recurrent pleomorphic adenoma (6/8), which was characterized by the positive staining of the whole cytomembrane. On the other hand, positive staining of the primary pleomorphic adenoma was observed on the top of the membrane (19/21). The difference was statistically significant (P < 0.05). The staining pattern in malignant pleomorphic adenoma was similar with the recurrent ones except higher ratio of positive expression. No significant different was observed among the three kind of tumors on the expression rate of E-cadherin (P > 0.05). CONCLUSION: The status of capsule didn't have much actual usage in predicting the recurrence of pleomorphic adenoma. There was no significant relationship between the expression of E-cd and the recurrence of the tumor. The abnormal distribution of mucin 1 expression contributes to the invasiveness of the tumor and can be used as the predictive signal for recurrence of pleomorphic adenoma.
Adenocarcinoma↗
Pleomorphic variant of invasive lobular carcinoma of the breast.
Infiltrating lobular carcinoma (ILC) of the classic type is well recognized; less well appreciated is a group of variant forms of ILC, which includes solid, alveolar, mixed, apocrine, signet-ring, histiocytoid, and tubulolobular variants. In addition, Page et al (Diagnostic Histopathology of the Breast, Churchill Livingstone, 1987, pp 219-226) recently have emphasized the pleomorphic variant of ILC, which demonstrates the infiltrating pattern of classic ILC; however, the nuclei are more pleomorphic and have features that may overlap with those of infiltrating duct carcinoma. To determine whether pleomorphic ILC shows significant prognostic differences from classic ILC, we reviewed the clinical courses of 25 patients with classic ILC and compared them with 16 patients with pleomorphic ILC. The major determinant in placing ILC into the pleomorphic category was the presence of nuclei of nuclear grade 2 or 3. All classic ILCs had nuclei of grade 1 by the Scarff-Bloom-Richardson criteria. Survival to recurrence was significantly worse (P less than or equal to .05) for the patients with pleomorphic ILC at lengths of survival greater than 30 months. In addition, node-negative patients with pleomorphic ILC were four times more likely to experience recurrence than node-negative patients with classic ILC; those with positive nodes and pleomorphic histology were 30 times more likely to experience recurrence. Although there appeared to be a trend toward decreased overall length of survival for those patients with pleomorphic ILC when compared with patients with classic ILC, this difference was not statistically significant.
Adult↗
Pleomorphic basal cell carcinoma.
BACKGROUND: A variant of basal cell carcinoma (BCC) with scattered large, pleomorphic cells has previously been reported as "basal cell epithelioma with giant tumor cells" and "basal cell carcinoma with monster cells." OBJECTIVE: Our purpose was to describe the clinical, histologic, and DNA ploidy findings in BCCs with these cytologic features. METHODS: Nineteen pleomorphic BCCs from 15 patients were prospectively collected, and other BCCs in these patients were retrospectively reviewed by light microscopy. One lesion was recurrent. Seven of the pleomorphic BCCs and one nonpleomorphic BCC were studied by image analysis. RESULTS: These pleomorphic BCCs ranged from 2.8 to 12.5 mm in greatest diameter and were most commonly located on the head and neck. Five BCCs were present on the face and scalp of a patient with basal cell nevus syndrome. There have been no subsequent recurrences of the pleomorphic BCCs (follow-up from 3 to 32 months; median, 20 months). All 19 pleomorphic BCCs displayed characteristic features of BCC: peripheral palisading, stromal retraction, mucin production, and apoptosis. All 19 also showed huge pleomorphic mononucleated and multinucleated giant tumor cells. The nuclei of these large cells were often hyperchromatic with prominent nucleoli and abundant cytoplasm, and occasionally with intranuclear cytoplasmic protrusions. In addition, there were frequent and atypical mitoses in 47% of the cases. All pleomorphic BCCs studied by cell image analysis of formalin-fixed, paraffin-embedded tissue were aneuploid. The DNA content of the giant tumor cells was not a multiple of a single DNA value. CONCLUSION: Pleomorphic BCCs clinically present as typical BCCs. Despite their striking focal cellular atypia, these lesions seem to behave as ordinary BCCs.
Adult↗
Subungual pleomorphic fibroma.
BACKGROUND: Pleomorphic fibroma is a benign fibroblastic tumor characterized by pleomorphic, hyperchromatic cells or giant multinucleated cells embedded in a collagenous stroma. These cytologic features may lead to an incorrect diagnosis of malignancy. Most cases reported in the literature are located on trunk or extremities; the presentation as a subungual mass is rare. METHODS: We report an unusual case of a subungual pleomorphic fibroma in 66-year-old woman. Clinical information was obtained. Histologic examination and immunohistochemical studies were performed. RESULTS: A 66-year-old woman presented with a longstanding (40 years), subungual mass that deformed the nail of the left middle finger. Microscopic examination revealed a paucicellular tumor composed of hyperchromatic spindled, pleomorphic, floret-like giant cells embedded in haphazardly arranged collagen bundles in the dermis. No mitotic figures were seen. The tumor cells were vimentin-positive but did not stain with antibodies to S-100, cytokeratin, smooth muscle actin, factor XIIIa or CD34 negative. The diagnosis of a pleomorphic fibroma was made. Follow-up shows no evidence of tumor, 36 months after excision. CONCLUSION: Pleomorphic fibroma of the subungual region is an unusual cutaneous tumor with histologic features that may cause confusion with true sarcomas. This is only the second case reported of a subungual pleomorphic fibroma. Pleomorphic fibroma should be considered in the differential diagnosis of pleomorphic subungual tumors.
Aged↗