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Adenosquamous Carcinoma of the Pancreas: a Clinicopathologic Series of 25 Cases David E

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Adenosquamous Carcinoma of the Pancreas: a Clinicopathologic Series of 25 Cases David E Adenosquamous Carcinoma Of The Pancreas: A Clinicopathologic Series Of 25 Cases David E. Kardon, M.D., Lester D.R. Thompson, M.D., Ronald M. Przygodzki, M.D., Clara S. Heffess, M.D. Department of Endocrine and Otorhinolaryngic-Head & Neck Pathology (DEK, LDRT, CSH), and Department of Cellular Pathology (RMP), Molecular Division, Armed Forces Institute of Pathology, Washington, DC months after diagnosis (range, 1 to 33 months). Background: Adenosquamous carcinoma is a Conclusions: Adenosquamous carcinoma of the rare aggressive subtype of pancreatic adenocar- pancreas represents a distinct clinical and cinoma. We describe the clinical, pathologic, pathologic entity, demonstrating the expected and molecular characteristics of 25 of these le- immunoprofile and k-ras oncogene mutation of sions, the largest series to date. Methods: a ductal origin, with a worse prognosis than Twenty-five cases of adenosquamous carcinoma ductal adenocarcinoma. of the pancreas diagnosed between 1961 and 1994 were retrieved from the files of the Endo- KEY WORDS: Pancreas, Adenosquamous carci- crine Registry of the Armed Forces Institute of noma, Mucoepidermoid carcinoma, Adenoacan- Pathology. Histologic features were reviewed, thoma, Histology, Immunohistochemistry, K-ras. histochemical, immunohistochemical, and mo- Mod Pathol 2001;14(5):443–451 lecular (k-ras) studies were performed, and pa- tient follow-up was obtained. Results: The pa- Carcinoma of the pancreas has an incidence of 7.5 tients included 17 men and eight women, aged to 10 per 100,000 person years and is one of the 28 to 82 years (mean, 65.4 y). The patients usu- more lethal malignancies in humans, accounting or painless (17 ؍ ally experienced weight loss (n while also presenting with for the fourth highest cause of cancer deaths in the ,(11 ؍ jaundice (n other abdominal symptoms. The tumors af- United States (1). Adenosquamous carcinoma, fol- which has been called adenoacanthoma (2, 3) and ,(17 ؍ fected the head most frequently (n ,Five mucoepidermoid carcinoma (4), is a rare subtype .(4 ؍ or body (n (9 ؍ lowed by the tail (n cases involved more than one anatomic region accounting for 1 to 4% of exocrine malignancies of the pancreas. Microscopically, all tumors (5–7), and is characterized by the histologic pat- demonstrated dual differentiation toward ade- terns of both ductal adenocarcinoma and squa- nocarcinoma and squamous cell carcinoma. All mous carcinoma within the same tumor. Despite cases tested were immunoreactive with keratin isolated case reports or small series published on (AE1:AE3 and CK1), whereas other keratin this tumor type (3, 5, 8, 9) and statistical inclusion markers were variably expressed: CK5/6 (88%), in general studies of pancreatic exocrine neoplasms CK7 (68%), Cam5.2 (41%), and CK20(26%). CA- (2, 6), there is no large clinicopathologic series to 19–9 (84%) and CEA (74%) were positive in the date, and no series that specifically addresses the majority of the cases. K-ras oncogene mutations histochemical, immunohistochemical, and molec- were identified in seven of 13 cases. All patients ular profile of these uncommon tumors. Further- died from their disease an average of 5.8 more, there is no correlation of these results with the clinical presentation and patient outcome. We describe a series of 25 patients with adenosqua- Copyright © 2001 by The United States and Canadian Academy of mous carcinoma to specify the clinical findings as- Pathology, Inc. VOL. 14, NO. 5, P. 443, 2001 Printed in the U.S.A. sociated with these tumors, illustrate their patho- Date of acceptance: October 10, 2000. logic features, document their immunophenotype, The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of present their K-ras oncogene profile, and analyze the Department of Defense. these data as they relate to patient outcome in a Address reprint requests to: Clara S. Heffess, M.D., Department of Endocrine and Otorhinolaryngic-Head & Neck Pathology, Building 54, single comprehensive study. Our results are ana- Room G066-09, Armed Forces Institute of Pathology, 6825 16th Street, lyzed in comparison with a review of the English N.W., Washington, DC 20306-6000; e-mail: [email protected]; fax: 202-782-3130. literature (MEDLINE 1966–2000). 443 MATERIALS AND METHODS was considered sufficient for the diagnosis of ade- nosquamous carcinoma. Squamous differentiation Twenty-five cases of adenosquamous carcinoma was defined as solid nests or sheets of cells with of the pancreas were selected from the files of the abundant cytoplasm, distinct cellular borders, and Endocrine Tumor Registry of the Armed Forces In- intercellular bridges, with or without extracellular stitute of Pathology, Washington, DC, between 1961 keratin production. Mucicarmine stains were used and 1994. The cases were recovered from a search to confirm mucin production by the adenocarci- of 8,372 (0.3%) benign and malignant primary pan- noma fraction of the tumors. Fifteen of the consults creatic neoplasms seen in consultation during this were autopsies, and 10 were surgical specimens, time. Twenty-four of the specimens were from hos- either resections or biopsies. pitals within the United States, and one was from a Immunophenotypic analysis was performed in 19 military base in Europe. Ten cases were obtained cases with suitable material. The standardized from military hospitals, 10 from Veterans Adminis- avidin-biotin method of Hsu et al. (10) was em- tration medical centers, and five from civilian ␮ sources including four community hospitals and ployed, using 4- m thick, formalin-fixed, paraffin- one university hospital. Four additional cases were embedded sections taken from a single representa- identified by the search, but were excluded because tive block. In five cases immunophenotypic of a significant component of anaplastic carcinoma expression was determined on the primary tumor within the primary lesion. as well as the metastatic deposit. Table 1 docu- Adequate follow-up was a prerequisite for inclu- ments the panel of commercially available immu- sion in the study. Materials within the AFIP files nohistochemical antibodies used. When required, were supplemented by a review of the patient de- proteolytic antigen retrieval was performed by pre- mographics, symptoms at presentation, medical digestion for 3 minutes with 0.05% protease VIII history including radiation exposure, surgical pa- (Sigma Chemical Co., St. Louis, MO) in a 0.1 M thology and operative reports, cancer registry phosphate buffer at a pH of 7.8 at 37°C. Antigen records, and by written questionnaires or oral enhancement (recovery) was performed, as re- communication with the treating physician(s). quired, using formalin-fixed, paraffin-embedded Follow-up data included the exact location of tissue treated with a buffered citric acid solution the primary, the pattern of metastatic spread, the and heated for 20 minutes in a calibrated micro- specific treatment modalities used, and the wave oven (11). After this, the sections were allowed length of survival. We were unable to obtain ac- to cool at room temperature in a citric acid buffer curate staging information on the cases due to solution for 45 minutes before the procedure was the referral nature of our practice. This clinical continued. Standard positive controls were used investigation was conducted in accordance and throughout, with serum used as the negative con- compliance with all statutes, directives, and trol. A positive reaction was determined by moder- guidelines of the Code of Federal Regulations, ate to heavy chromogen deposition within the cy- Title 45, Part 46, and the Department of Defense toplasm of the tumor cells. Directive 3216.2 relating to human subjects in Point mutations in K-ras-2 were sought in 15 research. cases. In five of the cases, metastatic lesions were Hematoxylin and eosin-stained slides from all analyzed as well as the primary carcinomas. Muta- cases were reviewed to confirm that histopatho- tional analysis was performed by topographic mi- logic criteria for the diagnosis of adenosquamous crodissection as previously described (12–14). This carcinoma were met. Any degree of definitive squa- type of sampling specifically selects areas of tumor mous differentiation within an adenocarcinoma from 5-␮m thick paraffin-embedded tissue sec- TABLE 1. Immunohistochemical Panel Primary Antigen/Antibody Company Dilution Antigen Recovery Antibody Cytokeratin (AE1/ mm Boehringer Mannheim Protease treatment AE3 and CK1) Biochemicals, Indianapolis, IN, 1:50 and Dako, Carpinteria, CA 1:200 Cam 5.2 (CK 8/18) mm Becton Dickinson, San Jose, CA 1:50 Protease treatment CK 5/6 mm Dako Microwave CK 7 mm Dako 1:40 Protease treatment CK 20 mm Dako 1:100 Protease treatment CA 19-9 mm Signet Labs, Dedham, MA Neat Enzyme digestion pCEA rp Dako 1:2650 — Chromogranin rp Dako 1:640 — mm, mouse monoclonal; rp, rabbit polyclonal 444 Modern Pathology tions, which will yield the highest concentration of ranged from 1 to 27 months, with a mean duration tumor cells and the lowest number of “back- of 5.4 months. The patients with the longest dura- ground” normal cells. No differentiation between tion of symptoms had nonspecific symptoms of the glandular and squamous components was bloating and nausea. made in the sampling of the tumors for molecular analysis, as the frequent mingling of the tumor elements precluded this type of separation. PCR Pathology amplification for the K-ras-2 exon 1 gene was per- Macroscopic formed using flanking intron primers (12–14). Cycle sequencing was performed using the BigDye termi- The tumors occurred in the head of the pancreas ϭ ϭ ϭ nator cycle sequencing approach (Perkin-Elmer, (n 17), the tail (n 9), and the body (n 4). Foster City, CA) with one of the amplifying primers, Among these, five tumors encompassed multiple and subsequently run on an ABI Prism 377 auto- anatomic segments of the pancreas, with one case mated sequencer (Perkin-Elmer) using a 6% dena- involving the entire pancreas.
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