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PubMed1976

Parotid neoplasms: a report of 250 cases and review of the literature.

A 25-year experience with parotid tumors was reviewed. From a total of 250 neoplasms, 173 were histologically benign and 77 were malignant. Benign mixed tumors accounted for 59% of all lesions. Clinical parameters used to diagnose parotid neoplasms were found to be unreliable in determining whether a given tumor was benign or malignant. The mean age for malignant lesions was 10 years greater than for benign lesions. The phenomenon of malignant transformation of a benign tumor was considered in four patients. Complete surgical excision is the safest and preferred method for diagnosis. Preoperative needle or incisional biopsy are associated with a high degree of local recurrence. The appropriate management of any parotid tumor is predicated on special histological type. Local excision or enucleation no longer have a place in the surgical management of benign parotid tumors. Postoperative tumor recurrence and morbidity are directly related to awareness of surgical anatomy and pursuit of correct surgical techniques for adequate resection. The five-year recurrence rate for 102 benign mixed tumors was 6%. Recurrence in malignant tumors varied with specific histological types but was generally high. Five-year survival for all malignant parotid tumors was 48%.

Adolescent↗
PubMed1983

ABO (H) cell surface antigens in benign and malignant parotid neoplasms.

Twenty-two inflammatory, benign, or malignant parotid lesions were studied by means of the specific red cell adherence test (SRCA), a modification of the Coombs' mixed cell agglutination reaction. In 22 normal parotid tissues the acinar structures were devoid of red cell agglutination, but it was present in ductal epithelium. Findings were similar in 2 cases of parotitis, 11 benign mixed tumors, and 1 malignant mixed tumor. All lacked red cell agglutination in areas of neoplastic change. Benign Warthin's tumors (4 cases) demonstrated antigenicity in the columnar epithelial component of the tumor, but lacked red cell agglutination in areas of the lymphoid component. One malignant Warthin's tumor showed agglutination in areas of normal columnar epithelium but not in areas of malignant dedifferentiation. Undifferentiated carcinoma (1 case) and adenoid cystic carcinoma (2 cases) did not possess detectable ABO (H) antigens in neoplastic areas of the gland. The absence of ABO antigens in normal acinar glands supports their suggested myoepithelial or mesenchymal derivation, as the absence of antigen in benign and malignant mixed tumors supports their proposed mesenchymal derivation. Ductular epithelium and the epithelial components of benign Warthin's tumors have ABO (H) antigens, while the loss of antigen in the epithelial portion of the malignant Warthin's tumor is characteristic of epithelial neoplastic dedifferentiation. Loss of antigen in adenoid cystic and undifferentiated carcinomas of the parotid supports the concept that antigen is absent in epithelially derived malignant neoplasms.

ABO Blood-Group System↗
PubMed1988

Amylase expression in human parotid neoplasms: evidence by in situ hybridization for lack of transcription of the amylase gene.

Salivary alpha-amylase (EC 3.2.1.1) is the major protein component of human parotid gland secretion. We studied amylase gene structure and expression in tissue from a series of normal and neoplastic parotid glands by Southern blot analysis, in situ hybridization, and immunohistochemistry. Thirty-two tumors were examined. Southern blot analysis of DNA extracted from a Warthin tumor, an adenoid cystic carcinoma, and a mucoepidermoid carcinoma showed no evidence of structural rearrangement of amylase genes. Eleven parotid Warthin tumors were negative for amylase protein and mRNA by immunocytochemistry and in situ hybridization. One pleomorphic adenoma in the group of 10 examined showed focal staining for amylase protein, although amylase mRNA could not be demonstrated in the same population of cells by in situ hybridization in serial tissue sections. Five mucoepidermoid carcinomas and three acinar cell carcinomas were devoid of amylase protein and mRNA. Normal parotid tissue obtained from all patients studied revealed abundant acinar cell amylase mRNA and protein. In situ hybridization, in conjunction with immunocytochemistry, allows precise cellular localization of mRNA and protein, thereby establishing the site of production of specific transcripts. We conclude that the interruption in amylase gene expression in parotid gland neoplasms occurs at the transcriptional level.

Amylases↗
PubMed1992

[Concerning diagnosis and treatment of parotid neoplasms].

This study is a review of 57 patients with tumours in the parotid glands who underwent surgery at the ORL Clinic in Białystok. Malignant tumours constituted 17.5% of all parotid tumours and adenoid cystic carcinoma was the dominant type in this group. Pleomorphic adenomas were the most common benign tumour. The role of fine needle aspiration biopsy in diagnosis of parotid tumours is discussed. Superficial parotidectomy was the predominant form of treatment (47 cases). Total parotidectomy was done in 7 cases. The results of treatment are presented.

Adolescent↗
PubMedDate not supplied

[The intraoperative color lymphosialography of patients with parotid neoplasms].

Intraoperative color lymphosialography was carried out in 56 patients with benign tumors of the parotid salivary gland. A characteristic staining of the gland distinguishing it from the tumor was seen during surgery in all the cases. Peripheral branches of the facial nerve were well seen too. Employment of this technique has helped reduce by half the number of x-ray contrast examinations and resulted in a lower incidence (only 5 percent) of postoperative complications.

Adenoma↗
PubMedDate not supplied

Solitary fibrous tumor: report of a case with an unusual presentation as a spindle cell parotid neoplasm.

BACKGROUND: Initially described as a pleural tumor, solitaryfibrous tumor of the parotid gland (SFT) is rare and has been reported at a wide range ofanatomic sites. Although cases of SFT arising in the parotid gland have been previously described, a review of the literature failed to reveal cytology-based reports of this entity. CASE: A 42-year-old man presented with a right parotid mass that had gradually enlarged over 3 years. He was otherwise asymptomatic. Fine needle aspiration biopsy of the mass showed a hypercellular smear composed of spindle cells in both clusters and isolated forms, with ovoid nuclei, evenly distributed chromatin, inconspicuous nucleoli and scant to moderate cytoplasm with focally wispy, collagenous, intercellular material. The background was hemorrhagic, without chondromyxoid matrix or inflammatory cells. There was no evidence of a myoepithelial component. A diagnosis of spindle cell neoplasm was rendered. Histologic examination of the total parotidectomy specimen revealed a SFT arising in the parotid gland. The diagnosis was supported by immunohistochemical studies. CONCLUSION: SFT is a well-circumscribed neoplasm composed of short, spindled, plump cells with scanty cytoplasm growing in a haphazard or "patternless" pattern. Tumor cells are intimately admixed with collagenous stroma. Hemangiopericytomalike vessels are frequently seen. Although SFT rarely occurs in the salivary gland and a definitive diagnosis based on cytologic preparations alone is difficult, the diagnosis of SFT can be considered when cytologic examination reveals a hypercellular smear composed of isolated, cohesive clusters of spindled, fibroblastlike cells associated with a collagenous component in ahemorrhagic background. The preoperative magnetic esonance image findings of a highly vascular neoplasm support the diagnosis.

Adult↗