Salivary adenocarcinoma, not otherwise specified: A collection of orphans
ABSTRACT Salivary adenocarcinoma, not otherwise specified, refers to gland-forming malignancies that do not satisfy the diagnostic requirements of other "named" malignancies.
To review the features of 11 patients with salivary adenocarcinoma, not otherwise specified. To also compare the diagnostic frequencies of 2 databases, one from the Mount Sinai Medical Center (New York, NY), the other from the Shanghai Ninth People's Hospital (Shanghai, People's Republic of China).
Pathology files were searched to establish a database of salivary tumors. All available hematoxylin-eosin- stained slides from the resection specimens diagnosed as either adenocarcinoma, not otherwise specified, or with vague or unusual diagnoses (eg, probable carcinoma-ex-pleomorphic adenoma) were pulled from our files and reexamined. Dates of death were confirmed with the Social Security Death Index.
We identified 11 patients with salivary adenocarcinoma, not otherwise specified, ranging in age from 49 to 80 years (median, 67 years), with a male preponderance. The parotid gland was the most common site of tumor origin. Ten of these tumors were high grade, and 1 was intermediate grade. Two patients were diagnosed at stage II, while the remaining patients were diagnosed at stage III or IV. Histologically, all tumors were invasive, with variable glandular differentiation and diverse architectural patterns. The diverse cytologic tumor cell types included cuboidal, columnar, epithelioid, polygonal, oncocytoid, clear, melanoma-like, mucinous, sebaceous, and plasmacytoid. Four patients died after 4 to 27 months (mean, 15 months), 1 patient is alive with disease at 12 months, 1 patient is disease-free at 14 years, and 3 patients remain disease-free after short follow-ups (10, 12, and 12 months). One patient had surgery just recently, and the remaining patient had no follow-up.
Salivary adenocarcinoma, not otherwise specified, is an aggressive, high-grade malignancy, with a predisposition for the parotid gland. It is characterized by cytologic and architectural diversity and an invasive growth pattern.
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ABSTRACT: Major salivary gland cancers are rare, with many histologic types and subtypes. The low incidence and heterogeneity of primary parotid carcinomas makes their outcome difficult to evaluate. Treatment remains primarily surgical, but optimal therapeutic regimens have yet to be fully realized. The present study reviews the experience of three Italian institutions in the treatment of primary parotid carcinomas in order to describe the clinicopathological presentation and treatment options with emphasis on radiotherapy and to analyze the factors influencing survival. The records of 110 patients with primary parotid neoplastic lesions treated at three Italian institutions from 1993 to 2004 were retrospectively reviewed. Six patients were excluded from the study: 3 received surgery alone and 3 were not assessable, for a total of 104 assessable patients. Acute and late toxicity of radiotherapy was quantified following the recommendations of the RTOG/EORTC. Survival was analyzed by the actuarial Kaplan-Meier product-limit method. The influence of selected factors on 10-year disease-specific survival was analyzed. The 104 assessable patients were treated as follows: 11 patients received radiotherapy as their only treatment (3 with a palliative purpose) and 93 had postoperative radiotherapy. Thirty-two patients underwent neck dissection: neck lymph node metastases were found in all them. Their mean age was 60 years (range, 14-92). According to the UICC/2002 TNM Classification, 8 patients were stage I, 19 stage II, 34 stage III, 25 stage IVA, 5 stage IVB, 3 recurrent and 10 not assessable (Tx). The most frequent histologies were adenoid cystic carcinoma (n = 16), mucoepidermoid carcinoma (n = 15), and acinic cell carcinoma (n = 15). Twenty-three patients had recurrences: 10 had local recurrences, 3 neck recurrences, 9 distant metastases, and 1 patient had both local recurrence and distant metastases. No factors were observed that would negatively influence the prognosis. Actuarial 10-year disease-specific survival was 71% and actuarial 10-year local control 82%. The treatment of salivary gland malignancies remains primarily surgical. Our study confirms the results of the literature with surgery and adjunctive radiotherapy in patients with advanced-stage disease. No variables were observed to influence the prognosis.Tumori 02/2007; 95(4):442-8. DOI:10.1016/S0167-8140(07)80211-8 · 1.09 Impact Factor
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ABSTRACT: Parotid gland carcinoma is an infrequent tumor, and series that report on these neoplasms are relatively scarce in the literature. The objective of the current study was to identify prognostic factors in patients with parotid gland carcinoma and to develop a method for defining the probability of recurrence. Patients with parotid gland carcinoma who were treated at the authors' institution from January 1981 through December 2004 and who completed treatment constituted the study group. Disease-free survival was calculated by using the Kaplan-Meier method. Logistic regression analysis was employed to define the recurrence-associated prognostic factors. One hundred twenty-seven patients were included (64 men and 63 women); their mean age was 53 years. Mucoepidermoid carcinoma was diagnosed in 34.6% of patients, adenoid cystic was diagnosed in 15.7% of patients, adenocarcinoma was diagnosed in 14.3% of patients, and acinic cell carcinoma was diagnosed in 9.4% of patients. The median disease-free survival was 8.3 years (95% confidence interval [95% CI], 4.3-12.2 years). Logistic regression analysis confirmed tumor classification, facial nerve palsy, grade of tumor differentiation, patient age, and surgical margins as recurrence-associated factors (P < .00001). Using this model, 3 postoperative risk groups were defined-high-risk, intermediate-risk, and low-risk-that had recurrence frequencies of 71.4%, 43.1%, and 8.8%, respectively (P = .0001). The 5-year disease-free survival rates for these groups were 18.7%, 53.9%, and 99.9%, respectively (P = .00001). In this study, the authors identified several significant prognostic factors. Consequently, they have proposed a prognostic score categorization that allows for a straightforward calculation of the risk of recurrence for a given patient that may help to define therapeutic strategies, target patient counseling, and design future trials.Cancer 05/2007; 109(10):2043-51. DOI:10.1002/cncr.22647 · 4.90 Impact Factor
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ABSTRACT: BACKGROUND.The role of promoter methylation in the inactivation of E-cadherin (E-cad) in salivary gland adenoid cystic carcinoma (ACC) is unknown. The objective of this study was to determine the role and potential clinical implications of promoter methylation of E-cad in salivary gland ACC.METHODS.The promoter methylation status of E-cad was determined by using methylation-specific polymerase chain reaction (PCR) analysis in 60 primary salivary gland ACC tissues and 3 ACC cell lines. The level of E-cad protein expression was determined by immunohistochemical analysis of each tumor. E-cad protein and messenger RNA (mRNA) expression levels were examined by immunohistochemical analysis and reverse transcriptase-PCR in 3 ACC cell lines. Associations between molecular alterations and patients' clinicopathologic characteristics were analyzed statistically. E-cad mRNA expression was examined in a 5-azacytidine-treated ACC-2 cell line.RESULTS.Promoter methylation of E-cad was detected in 34 of 60 tumors (57%). Of those 34 tumors, 18 tumors (53%) showed no E-cad protein expression, whereas only 5 of the remaining 26 tumors (19%) without E-cad promoter methylation showed no E-cad protein expression (P = .01). Tumors that had E-cad promoter methylation had a significantly higher histologic grade (P = .01) and more perineural invasion (P = .02) compared with tumors that did not have methylation. All 3 ACC cell lines exhibited E-cad promoter methylation and a lack of E-cad mRNA and protein expression, whereas 5-azacytidine restoredE-cad mRNA expression in the ACC-2 cell line.CONCLUSIONS.E-cad frequently is inactivated in salivary gland ACC through promoter methylation, and E-cad promoter methylation may play a role in tumor cell differentiation and perineural invasion. Cancer 2007. © 2007 American Cancer Society.Cancer 07/2007; 110(1):87 - 95. DOI:10.1002/cncr.22758 · 4.90 Impact Factor