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PubMed1999

Fluorescence in situ hybridization mapping of breakpoints in pleomorphic adenomas with 8q12-13 abnormalities identifies a subgroup of tumors without PLAG1 involvement.

Recently, we identified the PLAG1 gene as the target gene in pleomorphic adenomas with chromosome abnormalities involving 8q12. The majority of breakpoints were shown to reside within the 5' noncoding region of the gene. We now report three pleomorphic adenomas with breakpoints located distal to PLAG1 in band 8q13. These tumors had the following chromosome 8 abnormalities: ins(8;12)(q12-13;q14q15), t(8;12)(q13;q15), and t(6;8)(p21.3-22;q13). Fluorescence in situ hybridization mapping of the chromosome 8 breakpoints revealed a yeast artificial chromosome clone spanning the breakpoints in two tumors. In none of the cases was PLAG1 activated and/or disrupted. Three candidate genes, N8, HMGIC, and HMGIY, were analyzed for rearrangements and/or abnormal expression by using reverse transcriptase-polymerase chain reaction, rapid amplification of 3' cDNA ends, and Northern blot analyses.

Adenoma, Pleomorphic↗
PubMed1978

Glycosaminoglycan-synthetic activity of pleomorphic adenoma. Adenoid cystic carcinoma and nonneoplastic tubuloacinar cells of the salivary gland.

An analysis was carried out on glycosaminoglycan produced in pleomorphic adenoma, adenoid cystic carcinoma, sialadenitis and normal tissue of the salivary gland. After incubation of the tissue segments in a medium containing 35SO4, a radioautograph of the tissue section was made to observe the localization of 35SO4 incorporation, and 35S-labelled materials were purified from the tissues, and analyzed. High 35S-radioactivity was observed in the ductal cells of the inflammatory gland tissue and in the acinar cells of normal palatinal gland, but little radioactivity was observed in the interstitial components in these tissues, and the amount of 35SO4 incorporated in the tumor cells was also significant. Eighty to 90% of the 35S-radioactivity incorporated could be detected as 35S-glycosaminoglycans in all tissues except for the normal palatinal gland, which contained a large amount of 35S-sulfated glycoprotein. No significant difference in the synthetic activity of 35S-glycosaminoglycans and in their components were observed between nonneoplastic and neoplastic cells. These results suggest that glycosaminoglycan-producing cells in pleomorphic adenoma as well as in adenoid cystic carcinoma are derived from the tubuloacinar cells of the salivary gland.

Adenoma, Pleomorphic↗
PubMed1980

A myoepithelial cell line established from a human pleomorphic adenoma arising in minor salivary gland.

Transformed cells were isolated by using tissue culture techniques from a human pleomorphic adenoma. They revealed ultrastructurally myoepithelial and intercalated ductal cells as the neoplastic cell components that arose in the minor salivary gland of the palate. All transformed clones were demonstrated by electron microscopic examination to be only one type of cells having fine structures similar to myoepithelial cells with typical myofibrils in the cytoplasm. Of five clones isolated, one clone with stable growth was inoculated into nude mice, resulting in a production of myoepithelioma with mucinous substance. In addition, these cloned cells and myoepithelioma cells derived from one clone were found to express viral particles in the intercellular spaces. These findings indicate that a human myoepithelial cell line carrying tumorigenicity is established from the pleomorphic adenoma.

Adenoma, Pleomorphic↗
PubMed1992

Characterization of a novel cell line from pleomorphic adenoma of the parotid gland with myoepithelial phenotype and producing interleukin-6 as an autocrine growth factor.

A cell line was obtained from a primary culture of a pleomorphic adenoma of the parotid gland in a 24-year-old woman. The cells of the line (PA 16/23) grew spontaneously in minimal culture conditions and showed stable morphologic characteristics over 30 passages. PA 16/23 cells had immunophenotypic and ultrastructural features similar to those of transformed myoepithelial cells, which are regarded as the precursors of pleomorphic adenomas. Furthermore, these cells have been demonstrated immunocytochemically to contain interleukin-6 (IL-6) on light and electron microscopic examination. IL-6 also has been found by enzyme-linked immunosorbent assay in the culture supernatant and has been proven to be capable of stimulating growth of the PA 16/23 cells.

Adenoma, Pleomorphic↗
PubMed1982

The treatment of pleomorphic adenomas by formal parotidectomy.

We reviewed 100 patients who underwent formal parotidectomy. Seventy-two were new patients in whom a parotid lump proved to be a pleomorphic adenoma. Twenty-eight were patients in whom a tumour had recurred after treatment for pleomorphic adenoma by local excision (with or without irradiation) elsewhere. After a follow-up of 1--15 years (median 4 years), there were no recurrences in the primary group but 5 recurrences among the secondary cases. Permanent facial nerve damage was not seen in the primary group, but 11 patients undergoing secondary parotidectomy were left with some permanent facial weakness. Malignant change occurred in 4 patients in the secondary group.

Adenoma, Pleomorphic↗
PubMed1992

Benign metastasizing pleomorphic adenoma of salivary gland: diagnosis of bone lesions by fine-needle aspiration biopsy.

Two cases of benign salivary gland pleomorphic adenomas metastatic to bone (benign-metastasizing pleomorphic adenomas) diagnosed by fine-needle aspiration biopsy are presented. Both primary tumors were slightly atypical cytologically but neither case demonstrated features of carcinoma. The metastatic lesions contained benign epithelial, myoepithelial, and stromal components. In both cases the clinical history was either not known by the radiologist or not communicated to the cytopathologist interpreting the case, and a primary tumor of bone was the leading clinical diagnosis. Obtaining pertinent clinical history and comparing the cytomorphology of the bone aspirate with the primary parotid tumor allowed for an accurate diagnosis in both cases. The differential diagnosis with primary bone tumors is discussed and the importance of clinical history is emphasized.

Adenoma, Pleomorphic↗
PubMed1993

Pleomorphic adenoma of the breast: cytology of fine-needle aspiration and its differential diagnosis.

The cytologic findings of a case of pleomorphic adenoma of the breast are presented. This rare tumor appeared identical to pleomorphic adenoma of salivary glands. It presented diagnostic difficulties, however, because of its rarity and the fact that its associated clinical findings suggested a malignancy. The cytologic differential diagnosis includes a phyllodes tumor, fibroadenoma, and metaplastic carcinoma. Awareness of this entity should permit a definitive diagnosis by aspiration biopsy.

Adenoma, Pleomorphic↗
PubMed1995

Detection of hidden structural rearrangements by FISH in pleomorphic adenomas.

Previous cytogenetic analysis of pleomorphic adenomas of the salivary glands has revealed a subgroup of tumors with interstitial deletions of 8q with breakpoints at q12 and q21-23. In this paper we have re-examined four adenomas with confirmed or suspected deletions of 8q by FISH. Painting of interphase nuclei and metaphase chromosomes with whole chromosome libraries revealed that in each of the four cases the deleted chromosome 8 material was found inserted or translocated onto other chromosomes. In two of the cases we were also able to resolve several other complex rearrangements. Our FISH data thus suggest that gross deletions of 8q do not occur in pleomorphic adenomas. These observations are of crucial importance for the molecular interpretations of the 8q12 rearrangements. The fact that all rearrangements with breakpoints at 8q12 seem to be translocations or insertions strongly indicates that they involve a similar molecular mechanism. Our findings illustrate that chromosome painting is a valuable and useful adjunct to conventional cytogenetic analysis of solid tumors.

Adenoma, Pleomorphic↗
PubMed1995

Regional fine mapping of the multiple-aberration region involved in uterine leiomyoma, lipoma, and pleomorphic adenoma of the salivary gland to 12q15.

Cytogenetic aberrations involving 12q13-15 are frequently observed in a variety of benign solid tumors. Using a chromosome walking approach combined with fluorescence in situ hybridization analysis, we were able to show that the chromosome 12 breakpoints involved in uterine leiomyoma, pleomorphic adenoma of the salivary gland, and lipoma cluster to the same chromosomal region, which we therefore designated MAR (multiple-aberration region). By comparing the G-banding pattern of prometaphase chromosomes of amniotic fluid cells and lymphocytes to the position of hybridization signals obtained with a cosmid pool encompassing this breakpoint hot spot region, MAR was assigned to 12q15. We conclude that, despite the cytogenetic breakpoint assignment to the three bands 12q13-15 in individual uterine leiomyomas, lipomas, and pleomorphic adenomas of the salivary glands in the past, most likely 12q15 is the only 12q breakpoint site in these three distinct solid tumor types.

Adenoma, Pleomorphic↗
PubMed2001

Surgical treatment of recurrent pleomorphic adenoma of the parotid gland: a clinical analysis of 52 patients.

BACKGROUND: Surgical management of recurrent pleomorphic adenoma of the parotid gland has a considerable risk of facial nerve injury and a high re-recurrence rate. To obtain more insight into this issue we evaluated our experiences. METHODS: Medical records and histologic material of all these patients (31 women and 21 men), who had been treated from 1976-1995 were reviewed. Median interval between initial treatment and commencement of recurrences was 3 (0.8-18) years. Last surgery consisted of parotidectomy in 48 patients (92%), including 19 (40%) total procedures and wide local excision with involved skin in four patients. RESULTS: At a median follow-up of 9 years, eight patients (8/52; 15%) had re-recurrences develop, including 4 of 21 patients (19%) after a previous parotidectomy (group I) and 4 of 31 patients (13%) without prior parotidectomy (group II). The chance of re-recurrence in a group of patients with a minimal follow-up of 10 years after salvage surgery was 17% (4 of 24). The risk of a new relapse was, respectively, 4% and 8% at 1 and 5 years after treatment of recurrent disease. Acceptable N.VII function was preserved in 45 of the 49 (92%) nerves at risk. The risk of N.VII injuy was higher and more serious in group I (29% vs 10% in group II). The function of four of the five (80%) reconstructed zygomaticotemporal branches of the N.VII was adequate. CONCLUSION: Surgical treatment of recurrent pleomorphic adenoma of the parotid gland, usually consisting of a parotidectomy with wide extent and eventually facial nerve reconstruction, demonstrates favorable results with acceptable morbidity. The risk of new relapse and N.VII injury was higher after previous parotidectomy.

Adenoma, Pleomorphic↗
PubMedDate not supplied

Relationship of intraoperative rupture of pleomorphic adenomas to recurrence: an 11-25 year follow-up study.

BACKGROUND: Intraoperative rupture of the capsule of a pleomorphic adenoma is reported to be associated with an increased recurrence rate. For many years, we have noted few recurrences among patients who experienced rupture of the capsule during surgery. Therefore, we asked "How often has surgical rupture of the capsule of a mixed parotid tumor resulted in recurrence among our patients?" This study is a summary of our clinical observations and not a methodologic one. METHODS: The medical records of 346 patients operated on between 1965 and 1981 were reviewed. The surgical notes and histopathologic descriptions were examined with special reference to the relationship between surgical margins and tumor capsule. Satisfactory follow-up was obtained from 238 patients primarily operated on in our department. The average observation time was 18 years. None of our patients received postoperative irradiation. RESULTS: Six (2.5%) patients had a recurrence 7 to 18 years postoperatively (mean 11.8 years). This recurrence rate is of the same order of magnitude as other reports. Rupture of the capsule with macroscopic spillage of tumor cells occurred in 26 patients and two (8%) of them developed recurrent tumors. Surgical dissection close to the capsule was performed in 87 cases, with one recurrence. In the remaining 121 patients the surgical dissections were done without visualizing the tumor capsule. Three (2.5%) of these cases developed recurrent tumor. The 8% recurrence rate after capsule rupture is not statistically different from the 2% for the other patients. There was also no difference in recurrence rate between patients with microscopic positive or negative surgical resection margins. CONCLUSIONS: We question whether spillage of tumor cells from a pleomorphic adenoma plays such an important role in the development of recurrent tumors as has been previously postulated. We also question the justification and benefit of postoperative radiotherapy for patients with this benign disease.

Adenoma, Pleomorphic↗
PubMed1985

Immunocytochemical identification of cell types in pleomorphic adenoma, with particular reference to myoepithelial cells.

An immunocytochemical study was carried out on normal salivary gland tissue and ten salivary gland pleomorphic adenomas. Antibodies to myosin were used to stain myoepithelial cells. Duct cells were stained using an antibody to total keratin and a subpopulation of basal duct cells with an antibody to 45/46K keratins. Basement membranes were stained with anti-type IV collagen. The results demonstrated that myoepithelial cells are relatively rare in the majority of pleomorphic adenomas and that many of the cells which have been classically described as myoepithelial in routine histological preparations do not clearly show this type of differentiation. However, the tumors presented a spectrum of differentiation patterns from those that were mainly ductal to the rare tumour which was largely myoepithelial. It is further suggested that the 45/46K keratin antibody is capable of identifying a subpopulation of cells which could possibly be important in the histogenesis of this tumour.

Adenoma, Pleomorphic↗
PubMed1997

A 2-Mb YAC contig and physical map covering the chromosome 8q12 breakpoint cluster region in pleomorphic adenomas of the salivary glands.

Pleomorphic adenomas are benign epithelial tumors originating from the major and minor salivary glands. Extensive cytogenetic studies have demonstrated that they frequently show chromosome abnormalities involving chromosome 8, with consistent breakpoints at 8q12. In previous studies, we have shown that these breakpoints are located in a 9-cM interval between MOS/D8S285 and D8S260. Here, we describe directional chromosome walking studies starting from D8S260 as well as D8S285. Using the CEPH and ICRF YAC libraries, these studies resulted in the construction of two nonoverlapping YAC contigs of about 2 and 5 Mb, respectively. Initial fluorescence in situ hybridization (FISH) analysis suggested that the majority of 8q12 breakpoints clustered within the 2-Mb contig, which was mapped to the centromeric part of chromosome band 8q12. This contig has at least double coverage and consists of 34 overlapping YAC clones. The localization of the YACs was confirmed by FISH analysis. On the basis of mapping data of landmarks with an average spacing of 65 kb as well as restriction enzyme analysis, a long-range physical map was established for the chromosome region spanned by the 2-Mb contig. The relative positions of various known genes and expressed sequence tags within this contig were also determined. Subsequent FISH analyses of pleomorphic adenomas using YACs as well as cosmids revealed that all but two of the 8q12 breakpoints in the primary tumors tested mapped within a 300-kb interval between the MOS proto-oncogene and STS EM156. The target gene affected by the chromosome aberrations mapping within this interval was recently shown to be the PLAG1 gene, which encodes a novel zinc finger protein.

Adenoma, Pleomorphic↗
PubMed1990

Two-colour immunofluorescence marker study of pleomorphic adenomas.

Extensive use of two-colour immunofluorescence staining for various cell markers in pleomorphic adenoma, revealed three consistent phenotypic features: (1) keratin polypeptide No. 14, which was virtually restricted to myoepithelial cells (MEC) in normal salivary glands, appeared in a large fraction of the tumour cells, suggesting that the principal neoplastic element is derived from MEC or their immediate precursors; (2) a complex co-expression pattern of various cell markers was found, with extensive concurrence of keratin and vimentin in strands of MEC-like and myxoid tumour cells, probably reflecting different degrees of tumour cell differentiation; and (3) two phenotypically distinctive dendritic cell populations were identified, one consisting of keratin positive tumour cells and the other of HLA-DR positive but keratin negative stromal cells. The significance of these findings with regard to the histogenesis and complex morphology of pleomorphic adenoma is discussed.

Adenoma, Pleomorphic↗
PubMed1984

A cytochemical study on the salivary gland pleomorphic adenoma (mixed tumor) and the fetal and adult salivary gland.

We studied the pleomorphic adenoma of the salivary gland ultrastructurally and cytochemically [Mg2+-activated adenosine triphosphatase (Mg2+-ATPase)], compared it with normal human fetal and adult salivary glands, and evaluated the histogenesis of this tumor. In the adult salivary gland, reaction products shows Mg2+-ATPase activity were localized in the plasma membranes of myoepithelial cells adjacent to the acinar cells or intercalated duct cells. However, in the salivary gland of the 16-week fetus, they were seen along all adjoining plasma membranes of the cells of terminal buds and duct-like structures. The present case of pleomorphic adenoma comprised two histological components: solid and myxomatous areas. Reaction products were seen along adjoining plasma membranes of both light and dark cells in solid areas.

Adenoma, Pleomorphic↗
PubMed1988

A causal relationship between chromosomal rearrangements and the genesis of salivary gland pleomorphic adenomas.

The results of chromosome analyses performed on 50 pleomorphic salivary gland adenomas in Germany are summarized herein and compared with those obtained on 100 adenomas studied in Sweden. In both series, characteristic or even specific structural chromosomal rearrangements involving either chromosome 8 or 12 were found that allowed the cytogeneticist to distinguish between subgroups. However, the significantly higher percentage of tumors with chromosome abnormalities in the adenomas examined in Germany is particularly noteworthy. In the near future, cytogenetic investigations together with molecular methods will allow investigators to describe basic mechanisms for the development of pleomorphic adenomas in terms of oncogenetics.

Adenoma, Pleomorphic↗
PubMed1984

Immunofluorescence study of secretory epithelial markers in pleomorphic adenomas.

Amylase (Am), lactoferrin (Lf), lysozyme (Ly), secretory component (SC), epithelial IgA, and epithelial IgM were traced by paired immunofluorescence staining in ethanol-fixed specimens from 15 pleomorphic adenomas of the parotid gland. Epithelial elements positive for some of the markers were detected in a variable number of the specimens (Am, 0; Lf, 11, Ly, 2; CEA, 6; SC, 11; IgA, 9; and IgM, 6); their expression seemed to depend on a certain degree of glandular differentiation. Variable co-expression of secretory epithelial markers probably reflected different degrees of differentiation, indicating that clonal diversification may explain the histological complexity of pleomorphic adenomas. The most consistent expression (in almost 75% of the specimens) shown by Lf and SC might further reflect histogenetic relationship to intercalated ducts in which these antigens are normally found in largest amounts.

Adenoma, Pleomorphic↗
PubMed1989

Ultrastructural observations on luminal structures of pleomorphic adenoma of parotid and submandibular salivary glands of man.

Luminal structures found in salivary pleomorphic adenomas consisted of lumina surrounded by epithelial cells that varied from being packed together to being widely separated except at the luminal margin. Communication between lumina and the surrounding stroma was occasionally seen. Secretory material and cellular debris were seen in lumina, invaginations of the luminal surfaces of periluminal cells, associated vesicles, and vacuoles. Secretory granules, lysosomes and lipofuscin were seen in periluminal cells. Secretory material and debris from necrotic periluminal cells appear to accumulate in lumina, and to be endocytosed and degraded lysosomally by periluminal cells. The finding of communications between lumina and the surrounding stroma suggests that the stromalization of the epithelium includes the luminal structures. The present investigation supports the hypothesis that many of the cellular features of the pleomorphic adenoma relate to the microenvironment.

Adenoma, Pleomorphic↗