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Southern Medical Journal:
doi: 10.1097/SMJ.0b013e3181ebadbd
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Adenosquamous Carcinoma of the Pancreas: A Distinct Clinicopathologic Entity

Trikudanathan, Guru MD; Dasanu, Constantin A. MD, PhD

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Continued Medical Education
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Author Information

From the Department of Internal Medicine, University of Connecticut Medical Center, Farmington, CT; and Department of Hematology-Oncology, St. Francis Hospital and Medical Center, Hartford, CT.

Reprint requests to Constantin A. Dasanu, MD, PhD, Gothic Park, 43 Woodland Street, G-80, Hartford, CT 06105. Email: c_dasanu@yahoo.com

Dr. Guru Trikudanathan and Dr. Dasanu have no financial disclosures to declare and no conflicts of interest to report.

We certify that we do not have any affiliation with or financial involvement in any organization or entity with a direct financial interest in the subject matter or materials discussed in the manuscript (e.g., employment, consultancies, stock ownership, honoraria, and expert testimony). We do not have any commercial or proprietary interest in any drug, device, or equipment mentioned in the article below. No financial support was used for this work. No previously published figures or tables were used in this article. We certify sufficient participation of each author in the conception, design, analysis, interpretation, writing, revising, and approval of the manuscript.

Accepted February 26, 2010.

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Abstract

Among exocrine pancreatic tumors, adenosquamous carcinoma (ASC) is a rare, aggressive subtype with a worse prognosis and a higher potential for metastases compared to its more conventional glandular counterpart, adenocarcinoma. The disease distribution shows an approximately 1:1 male/female ratio and a median survival of circa five months. Although such features as central necrosis and hypervascularity are suggestive of pancreatic ASC, more research is necessary to identify other, more specific markers for this tumor subtype. Humoral hypercalcemia of malignancy has also been described with ASC of the pancreas, likely as a result of PTHrP production by the squamous component of the tumor. Similar to the therapeutics of pancreatic adenocarcinoma, adjuvant chemotherapy or chemoradiotherapy is currently indicated for resectable ASC of the pancreas, while gemcitabine or gemcitabine combinations are used for a more advanced disease. Both pathologic and molecular features of pancreatic ASC characterize it as a distinct subtype of pancreatic cancer. As a result, its molecular and genetic makeup could be exploited for both diagnostic and therapeutic quests in the future.

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Key Points

* Adenosquamous carcinoma (ASC) of the pancreas is rare and portends poor prognosis.

* ASC should be considered in the differential diagnosis in subjects with large tumor size, widely metastatic disease, and/or paraneoplastic hypercalcemia.

* Central necrosis and hypervascularity may represent important features of pancreatic ASC.

* Adjuvant chemoradiotherapy has been shown to improve the outcome in resected pancreatic ASC.

* Gemcitabine, alone and in combination with other agents, is used for the treatment of advanced/metastatic disease.

Pancreatic cancer with an incidence of 7.5 to 10 per 100,000 person years is the tenth most common cancer in North America.1,2 It is the fourth leading cause of cancer mortality in the United States, with a five-year survival of less than 5%.2 Among the exocrine pancreatic tumors, adenosquamous carcinoma (ASC) represents a rare aggressive subtype with a worse overall prognosis. Of historical interest, the first report of ASC in the literature belongs to Herxheimer and was published over a century ago.3 Since then, there has been moderate progress in the categorization, diagnosis, and management of this rare entity.

Histologically, ASC of the pancreas is defined as a neoplasm with 30% or more malignant squamous cell carcinoma admixed with ductal adenocarcinoma (Fig.).4 However, it is still unknown whether the degree of squamous-cell differentiation in pancreatic ASC (eg, <30% versus >30%) is clinically relevant.5 Although the proportion of squamous-cell differentiation necessary to diagnose pancreatic ASC has been somewhat arbitrarily set at 30% or more of the carcinoma, some authors claim that evaluating the proportion of squamous-cell component in tumor specimens is too subjective and argue that pancreatic adenocarcinoma with any degree of squamous differentiation should be diagnosed as adenosquamous carcinoma.5,6 The presence of varying proportions of typical, often mucin-producing, columnar, glandular cells, admixed with keratinized squamous epithelium in this neoplasm, has led to the use of numerous nomenclatures to portray this distinct entity, including adenoacanthoma, adenocancroid, adenocarcinoma with squamous metaplasia, mixed squamous and adenocarcinoma, and muco-epidermoid carcinoma of the pancreas (Fig.).

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Adenosquamous cancers are commonly seen at the sites where adenocarcinoma typically occurs (stomach, intestine, and uterus).7–9 They are also known to occur at such sites as the esophagus, anus, and vagina, where squamous-cell carcinomas are encountered.10–12 Interestingly, it has been reported that the prognosis of ASC was somewhat better in the carcinomas affecting stomach and lung, while it was dismal in the uterine, gallbladder, and pancreatic locations.13

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Materials and Methods

To identify relevant articles, a search in the PubMed® and MEDLINE® databases from 1950 to 2009 through the Ovid interface was performed using the medical subject heading terms “pancreatic” and “adenosquamous carcinoma.” We included all the accessible case series from the Centers of Excellence with clearly presented data, involving pancreatic ASC (>3 cases only) for our current review. From the 14 identified case series, only nine presented detailed clinical data on ASC of the pancreas and hence were used for this review (Tables 1 and 2).

Table 1
Table 1
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Table 2
Table 2
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Epidemiology

The true incidence of pancreatic ASC is difficult to establish, as many of these lesions are large and inoperable. Hence, analysis limited to surgical cases may not be totally indicative of the real incidence, since many of these patients may have not undergone subsequent surgery or autopsy.14 The estimates from review and classification of pancreatic tumors from autopsy and/or surgical specimens have revealed that the incidence ranges from 0.3% to 11.1% (Table 1), although the latter estimates are from a series of only 27 patients. It has also been argued that ASC could be more common than one would suspect from the number of cases reported, as a more careful study might disclose the existence of small foci of one histologic tumor type in the other.15 In the series we reviewed, there were 63 males and 57 females, implying an almost 1:1 ratio. The age of patients ranged from 28 to 89 years (Table 2). Interestingly, many of these studies originate from Japan. Data regarding the racial predisposition was available only from two case series.5,16 Both studies report Caucasians to represent the most commonly affected ethnic group by pancreatic ASC—92% reported by Kardon et al5 and 87% according to Voong et al.16 This is in contrast to the ethnic distribution of pancreatic cancer in general, where patients of African descent are thought generally to be at higher risk when compared to Caucasians.1 Old age, tobacco smoking, obesity, long-standing diabetes mellitus, chronic pancreatitis, peptic ulcer disease, diets high in various meats and fat, and low serum folate levels have been associated with pancreatic cancer in general and could also increase the risk for ASC of the pancreas.17 Survival has been uniformly poor with the median duration reported to be circa five months (Table 2).

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Clinical Presentation

Major symptoms at presentation of pancreatic ASC were similar to those of the usual invasive neoplastic ductal lesions of the pancreas (Table 3). Other symptoms at presentation included dull back pain, low-grade fever, fatigue, malaise, pruritis, nausea, and bloating.5,13 At the time of presentation, common clinical associations included diabetes, upper GI bleeding secondary to tumor invasion of the duodenum, complications of neoplasia-induced coagulopathy such as pulmonary embolism, and deep vein thrombosis.5,13 Humoral hypercalcemia of malignancy as a result of PTHrP secretion was reported in two patients.30,31 In both cases, hypercalcemia responded transiently to bisphosphonates; however, it recurred later in the course and did not respond to repeated therapy with bisphosphonates.

Table 3
Table 3
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More than half (55.8%) of the tumors arise from the head of the pancreas, consistent with the data reported by Okabayashi and Hanazaki,32 where 76.9% of the tumors were located in the pancreatic head. Sizes ranged from 1.5 to 14.5 cm, with an average size being 5 cm at diagnosis (Table 3). Therefore, they are generally larger than the size of ductal adenocarcinoma at diagnosis.31 Consequently, physicians should consider this fact in the differential diagnosis of pancreatic adenocarcinoma, when the patients present with severe abdominal symptoms and/or large tumor size.32 Large metastatic retroperitoneal lesions were also reported with pancreatic ASC, often larger than the primary pancreatic tumor itself.33 Such an unusual growth pattern of pancreatic ASC is worth noting, as it could lead to the misdiagnosis of primary tumor sites.33

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Diagnostic Evaluation

Accurate preoperative diagnosis of ASC of the pancreas is challenging, since there are no specific investigations or defining image characteristics that would facilitate differentiation from the more common exocrine pancreatic tumors. In combination with the CT/MRI scans, the cytological examination of exocrine pancreatic secretion may be useful to make a preoperative diagnosis. Although the diagnostic accuracy of cytological examination is not very high (30–79% in pancreatic adenocarcinoma), it has gradually evolved with the advent of endoscopic retrograde pancreatic juice aspiration over the last years.34 Although some authors describe the usefulness of preoperative fine needle aspiration cytology (FNAC),35 this procedure is generally not recommended because of the alleged risk of peritoneal seeding with malignant cells caused by this procedure.

After clinicopathological analysis of two cases of ASC of the pancreas, Nabae et al36 concluded that the presence of central necrosis could be indicative of adenosquamous carcinoma or squamous carcinoma of the pancreas. They have also suggested pancreatic ASC to be considered in the differential diagnosis of any hypervascular pancreatic tumor. Anecdotal reports of peripancreatic vascular invasion analysis on color Doppler concluded that the peripancreatic vessels should be carefully observed in ASC of the pancreas.33 Other research suggests that T2-weighted MRI images show a characteristic high intensity signal in this tumor.30 ASC of the pancreas can also selectively take up gallium-67 (Ga-67) and be visualized by nuclear scanning, which could be utilized in detecting this tumor type. ASC cells have a high affinity for Ga-67 citrate, and this substance accumulates at the inflammation sites caused by the cancer invasion. Thus, Ga-67 scintigraphy may be useful in diagnosing pancreatic cancer with malignant squamous-cell elements.37 However, caution is necessary as increased Ga-67 uptake has been noted in other inflammatory conditions such as pancreatitis or infected pseudocysts.38

Tumor markers for adenocarcinoma such as CA-19-9 and CEA have been shown not only to identify the glandular component, but also to display focal immunoreactivity in squamous-cell areas.5 Nevertheless, elevated serum CEA and CA-19-9 have been identified in approximately 70–100% of subjects with pancreatic ASC, which is similar to the situation in ductal adenocarcinoma of the pancreas.39 Therefore, further research is needed in order to identify new, more specific tumor markers for the pancreatic ASC.

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Management

Although ASC of the pancreas has distinct characteristics, the adopted treatment strategy is similar to that of patients with adenocarcinoma. Smoot et al40 conducted a retrospective review of all pancreatic ASC cases diagnosed at Mayo Clinic in Rochester, Minnesota, between 1985–2003. Of the 23 patients entering that study, 12 had a curative surgical resection, whereas 11 had been treated with palliative care only. The median survival was eight months in the curative resection group and 4.8 months in the palliative care only group. The authors further concluded that completed surgical resection offers the only possibility for improved survival in resectable tumors.40

Okabayashi and Hanazaki32 analyzed 39 single-institution pancreatic ASC cases reported to undergo surgery between 1980–2007. The surgical procedures included pancreaticoduodenectomy (PD) including pylorus-preserving PD (76.9%), distal pancreatectomy (20.5%), and total pancreatectomy (2.6%). The overall 1-, 2- and 3-year survival after pancreatic resection was 25.5%, 14% and 14%. Univariate analysis of the different prognostic factors that predicted the outcome of the surgery concluded that the tumor location was the main adverse risk factor. The overall survival was four months for the tumors located in the pancreatic body/tail as compared to eight months for tumors located in the head of the pancreas. The authors attributed this prognostic difference to the tumor size, as the distal pancreatic tumor averaged 7.3 cm compared with the proximal tumor size averaging 4.7 cm. Nonetheless, they concluded that surgical resection was better suited for proximal tumors as it was the most significant prognostic factor impacting the surgical outcome.32

Voong et al16 evaluated the impact of adjuvant chemoradiation on the outcome of resected pancreatic ASC and examined the clinicopathologic features associated with prognosis in their series of 39 patients from Johns Hopkins University, Baltimore, MD. They were able to demonstrate a statistically significant improvement in survival of the patients who received such agents as fluorouracil (5-FU), gemcitabine or capecitabine, and radiotherapy at the median dose of 5040 cGy (range 4500–5000 cGy), compared with the survival data in the group not treated with adjuvant therapy. They showed that a tumor size of 3 cm or larger, poor tumor differentiation, nodal metastasis, and the presence of perineural/vascular invasion were associated with a worse outcome.16 However, Voong et al were unable to correlate the proportion of squamous differentiation with the overall survival. Nevertheless, they suggested that the presence of any squamous component in the pathologic specimen renders the tumor biologically more aggressive and appears to portend a worse prognosis.

For advanced unresectable or metastatic pancreatic ASC tumors, the current standard of care is similar to the one of pancreatic adenocarcinoma where gemcitabine can be used either alone or in combination with such agents as 5-FU, capecitabine, platinum agents, or erlotinib. Concerted efforts are being made to test many available targeted agents, either emerging or already in clinical use. While the rarity of this pancreatic cancer subtype is an inherent limitation, clinical trials are encouraged for the patients with good performance status in order to open new avenues to the understanding and the management of this aggressive disease entity.

In the analyzed literature, we found only anecdotal reports on the alleged ability of chemotherapy to debulk larger, inoperable ASC pancreatic tumors and make them amenable for resection.41 Further research will hopefully provide more information regarding the etiopathogenesis of pancreatic ASC and, as a result, more effective therapeutic solutions.

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Existing Theories on the Origins of ASC of the Pancreas

Several theories speculate the genesis of the adenosquamous carcinoma. In the first one, the squamous metaplasia theory, it has been proposed that squamous metaplasia occurs as a result of ductal inflammation due to chronic pancreatitis or obstruction by an adenomatous tumor.15 It is thought to ultimately transform into a malignant adenosquamous pancreatic tumor. The second theory is the collision theory, suggesting that the two histologically distinct tumors, adenocarcinoma and squamous-cell carcinoma, arise independently from different sites and ultimately join or coalesce.42 There is no clear evidence to confirm this theory, but squamous-cell tumor components have been demonstrated to be intermingled in the body of the predominant adenocarcinoma type. The electron microscopy has clearly demonstrated two distinct cell types as chief components of pancreatic ASC. The adenocarcinoma cell is characterized by an abundant endoplasmic reticulum, a well-developed Golgi apparatus, and secretory vesicles. The malignant squamous cell has a scanty endoplasmic reticulum but prominent bundles of tonofilaments, similar to the cells seen in squamous-cell carcinoma.42 Other researchers endorse the third theory, the differentiation theory, suggesting that ASC arises as a result of malignant differentiation from a pluripotential duct cell into the two distinct histologic types.25 Immunohistochemical studies have demonstrated positive stains for carbohydrate antigenic determinant 19-9 (CA 19-9), ST-439, and keratin of varying degrees in both squamous and adenomatous cells of pancreatic ASC, giving further impetus to this theory.25

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Molecular Pathogenesis

Scientific advances in the past couple of decades enriched our understanding of the pathogenesis of pancreatic cancer. The most important emerging paradigm is that pancreatic cancer represents a disease of inherited and acquired genetic mutations. The frequently mutated genes that have been identified in pancreatic ductal adenocarcinoma include K-ras2, p16/CDKN2a, TP53 and DPC4/MAD4.17

With regard to pancreatic ASC, Kardon et al5 performed a limited K-ras2 oncogene mutational analysis in 13 of the 25 cases with amplifiable genomic DNA. They found six of the 13 cases to have a heterozygous mutation at codon 12. This mutation changed the amino acid product of codon 12 from a glycine to a valine or an aspartate residue. There was no appreciable correlation between the presence of K-ras mutations and the proportion of squamous and adenocarcinomatous elements. However, these researchers suggested that K-ras mutation may correlate with survival in ASC of pancreas, as the patients with K-ras oncogene mutation survived for an average of eight months in comparison to those with the wild phenotype who survived only seven months.5 The presence of K-ras point mutation was also reported by Murakami et al in their small case series6 and by Campman et al43 in their peculiar ASC arising in a mucinous cystadenoma of the pancreas. Thus, the presence of K-ras gene mutation might confer a modest survival advantage in pancreatic ASC.

More recently, Brody et al29 studied the pattern of genetic alterations on microdissected tissue samples of a series of ASC of the pancreas. They reported the loss of the tumor suppressor genes p16/CDKN2a (also known as INK4A) and TP53 in 100% and 60% of the cases, respectively. This is similar to the 90% and, respectively, 60% loss of the above genes seen in pancreatic adenocarcinoma. Furthermore, they detected K-ras2 gene mutations at codon 12 in all analyzed cases, affecting both squamous and adenocarcinomatous portions. They concluded that this mutation is critical for tumorigenesis and suggested a common precursor cell of origin for both squamous and adenocarcinomatous components. DPC4 gene (deleted in pancreatic carcinoma genes 4) on chromosome 18q21, missing only rarely in extrapancreatic malignancies, was lost in five of the eight pancreatic ASC cases. Moreover, the analysis showed strong nuclear p53 positivity. This was comparable to the molecular signature of advanced unresectable pancreatic adenocarcinoma and could reflect the more aggressive nature of ASC of the pancreas.

Furthermore, Brody et al29 demonstrated a reduced and/or absent E-cadherin expression in seven out of eight pancreatic ASC patients, which could also contribute to the aggressive nature of this tumor via its central role in the epithelial to mesenchymal transition. Reduced E-cadherin expression is also associated with resistance to EGFR inhibition, thus having potential therapeutic implication as well. These investigators finally suggested that p63, a member of the p53 family which is positive in all pancreatic ASC cases, is a useful marker for identification of squamous differentiation in cancers with growth patterns not clearly identified as adenosquamous carcinoma of the pancreas.29 Future studies of the common molecular and pathologic features of this rare aggressive tumor may provide further insights for finding novel molecular markers and subsequently using them as diagnostic and/or therapeutic targets for this disease.

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Conclusion

Despite its rarity worldwide, ASC of the pancreas is increasingly recognized and reported. It has a worse prognosis and a higher potential for metastasis compared to the more common pancreatic adenocarcinoma. Although thought to be encountered more frequently, the currently reported incidence ranges from 0.3 to 11.1%, with no gender disparity. Often, pancreatic ASC features larger tumors, arising from the head of the pancreas, and produces more severe abdominal symptoms. Besides the common symptoms associated with any pancreatic neoplasm, paraneoplastic hypercalcemia should be anticipated, likely through the PTHrP production by the squamous component of the tumor. The presence of such radiologic features as central necrosis, peripancreatic vascular invasion and increased Ga-67 uptake may be helpful in making the diagnosis. Similar to the situation in pancreatic adenocarcinoma, a complete surgical resection of pancreatic ASC, along with adjuvant chemotherapy or chemoradiotherapy, are critical for the extended survival. Nevertheless, survival in patients with ASC of the pancreas has been uniformly poor, with a median duration of only five months. Concerted efforts of basic scientists and clinicians are necessary in order to improve the clinical outcome of this cancer subtype. Combination of various chemotherapy agents or incorporation of novel molecularly targeted agents in the chemotherapeutic scheme of advanced, unresectable ASC of the pancreas is increasingly being used in an attempt to further improve its clinical outcome.

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References

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2. American Cancer Society. Facts and Figures, Atlanta, GA, American Cancer Society, Inc, 2006.

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6. Murakami Y, Yokoyama T, Yokoyama Y, et al. Adenosquamous carcinoma of the pancreas: preoperative diagnosis and molecular alterations. J Gastroenterol 2003;38:1171–1175.

7. Mori M, Fukuda T, Enjoji M. Adenosquamous carcinoma of the stomach. Histogenetic and ultrastructural studies. Gastroenterology 1987;92:1078–1082.

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11. Morson BC, Volkstädt H. Muco-epidermoid tumors of the anal canal. J Clin Pathol 1963;16:200–205.

12. Sheets JL, Dockerty MB, Decker DG, et al. Primary epithelial malignancy in the vagina. Am J Obstet Gynecol 1964;89:121–129.

13. Yamaguchi K, Enjoji M. Adenosquamous carcinoma of the pancreas: a clinicopathologic study. J Surg Oncol 1991;47:109–116.

14. Madura JA, Jarman BT, Doherty MG, et al. Adenosquamous carcinoma of the pancreas. Arch Surg 1999;134:599–603.

15. Cihak RW, Kawashima T, Steer A. Adenoacanthoma (adenosquamous carcinoma) of the pancreas. Cancer 1972;29:1133–1140.

16. Voong KR, Davison J, Pawlik TM, et al. Resected pancreatic adenosquamous carcinoma: clinicopathologic review and evaluation of adjuvant chemotherapy and radiation in 38 patients. Hum Pathol 2010;41:113–122.

17. Maitra A, Hruban RH. Pancreatic cancer. Annu Rev Pathol 2008;3:157–188.

18. Halpert B, Makk L, Jordan GLJ. A retrospective study of 120 patients with carcinoma of the pancreas. Surg Gynecol Obstetr 1965;121:91–96.
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25. Motojima K, Tomioka T, Kohara N, et al. Immunohistochemical characteristics of adenosquamous carcinoma of the pancreas. J Surg Oncol 1992;49:58–62.

26. Hsu JT, Chen HM, Wu RC, et al. Clinicopathologic features and outcomes following surgery for pancreatic adenosquamous carcinoma. World J Surg Oncol 2008;6:95.
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28. Rahemtullah A, Misdraji J, Pitman MB. Adenosquamous carcinoma of the pancreas: cytologic features in 14 cases. Cancer 2003;99:372–378.

29. Brody JR, Costantino CL, Potoczek M, et al. Adenosquamous carcinoma of the pancreas harbors KRAS2, DPC4 and TP53 molecular alterations similar to pancreatic ductal adenocarcinoma. Mod Pathol 2009;22:651–659.

30. Inoue T, Nagao S, Tajima H, et al. Adenosquamous pancreatic cancer producing parathyroid hormone-related protein. J Gastroenterol 2004;39:176–180.

31. Kobayashi N, Higurashi T, Iida H, et al. Adenosquamous carcinoma of the pancreas associated with humoral hypercalcemia of malignancy (HHM). J Hepatobiliary Pancreat Surg 2008;15:531–535.

32. Okabayashi T, Hanazaki K. Surgical outcome of adenosquamous carcinoma of the pancreas. World J Gastroenterol 2008;14:6765–6770.

33. Komatsuda T, Ishida H, Konno K, et al. Adenosquamous carcinoma of the pancreas: report of two cases. Abdom Imaging 2000;25:420–423.

34. Nakaizumi A, Tatsuta M, Uehara H, et al. Cytologic examination of pure pancreatic juice in the diagnosis of pancreatic carcinoma. The endoscopic retrograde intraductal catheter aspiration cytologic technique. Cancer 1992;70:2610–2614.

35. Lozano MD, Panizo A, Sola IJ, et al. FNAC guided by computed tomography in the diagnosis of primary pancreatic adenosquamous carcinoma. A report of three cases. Acta Cytol 1998;42:1451–1454.

36. Nabae T, Yamaguchi K, Takahata S, et al. Adenosquamous carcinoma of the pancreas: report of two cases. Am J Gastroenterol 1998;93:1167–1170.

37. Kuji I, Sumiya H, Taki J, et al. Intense Ga-67 uptake in adenosquamous carcinoma of the pancreas. Ann Nucl Med 1997;11:41–43.

38. Kennedy TD, Martin NL, Robinson RG, et al. Identification of an infected pseudocyst of the pancreas with 67Ga-citrate: case report. J Nucl Med 1975;16:1132–1134.

39. Hsu JT, Yeh CN, Chen YR, et al. Adenosquamous carcinoma of the pancreas. Digestion 2005;72:104–108.

40. Smoot RL, Zhang L, Sebo TJ, et al. Adenosquamous carcinoma of the pancreas: a single-institution experience comparing resection and palliative care. J Am Coll Surg 2008;207:368–370.

41. Tanaka N, Ohoida J, Matuno T, et al. Response of adenosquamous carcinoma of the pancreas to interferon-alpha, tumor necrosis factor-alpha and 5-fluorouracil combined treatment. Anticancer Res 1994;14:2739–2742.

42. Kovi J. Adenosquamous carcinoma of the pancreas: a light and electron microscopic study. Ultrastruct Pathol 1982;3:17–23.

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Product Code: SMJ09-10B

Adenosquamous Carcinoma of the Pancreas

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September 2010 CME Questions

1. As opposed to the more common ductal adenocarcinoma, the adenosquamous carcinoma of the pancreas is characterized by all of the following except:

A. Paraneoplastic hypercalcemia

B. Higher metastatic potential

C. Lack of central necrosis

D. Hypervascularity

2. A 65-year-old male presented with a new onset of upper abdominal pain, progressive jaundice, and nausea. An abdominal ultrasound suggested the presence of a suspicious 5-cm mass with central necrosis located in the head of the pancreas. Which of the following would not be part of the initial evaluation?

A. Abdominal CT scan with contrast

B. ERCP with cytology examination

C. Fine needle aspiration (FNA) biopsy

D. Ga67 nuclear scanning

3. You are seeing a 56-year old woman with a newly diagnosed metastatic adenosquamous carcinoma of the pancreas. Which of the following represents an acceptable pharmacotherapeutic option?

A. Gemcitabine alone

B. Gemcitabine in combination with capecitabine

C. Gemcitabine in combination with erlotinib

D. All of the above

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http://www.sma.org/medallion-level-cmece/cme-credit-form?pcode=SMJ09-10B

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Figure. 2010
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CME Questions - Answer Key

1. C, 2. D, 3. B

Keywords:

adenocarcinoma; adenosquamous carcinoma; central necrosis; pancreas; squamous cell

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