Solid blue dot tumour: minor salivary gland acinic cell carcinoma.

Acinic cell adenocarcinoma (ACC) is a low-grade malignant salivary neoplasm that constitutes approximately 17% of all primary salivary gland malignancies. In the head and neck region, the parotid gland is the predominant site of origin and ACC is usually more frequent in women than men. Previous radiation exposure and familial predisposition are some of the risk factors for ACC. ACCs rarely involve minor salivary glands constituting only 13-17% of all minor salivary gland tumours. Generally, a slowly enlarging mass lesion in the tail of the parotid gland is the most frequent presentation. ACC has a significant tendency to recur, metastasise and may have an aggressive evolution. Therefore, a long-term follow-up is mandatory after treatment. Here we report the case of a woman in her 60s with an ACC in association with the labial minor salivary gland, presenting in the post-treatment period of squamous cell carcinoma of the tongue.

Influence of cigarette smoking on histological subtypes of stage I lung adenocarcinoma.

BACKGROUND: The purpose of this study was to examine the association between cigarette smoking and histological subtypes of lung adenocarcinoma. METHODS: We reviewed a total of 320 consecutive patients with stage I adenocarcinoma who underwent complete resections with systematic node dissections from January 2004 to December 2006 at the National Cancer Center Hospital East. RESULTS: A statistically significant difference was observed in recurrence-free probabilities between never smokers and ever smokers (3-year recurrence-free probabilities of 95.6% and 88.6%, respectively, p = 0.034). Among adenocarcinoma histological subtypes, only a solid component was significantly more frequent in ever smokers than in never smokers (p < 0.001). Among patients with solid components, significantly more cases had lymphatic permeation (p = 0.007), intratumoral vascular invasion (p < 0.001), and visceral pleural invasion (p < 0.001). Multivariate analysis revealed that ever-smoking history was the only statistically significant independent clinical predictor for a solid component (p < 0.001). Among ever smokers, smoking extent in pack-years of patients with solid components was significantly greater than that of those without solid components (p < 0.001). With respect to predominant subtypes, smoking extent in pack-years of patients with predominantly solid adenocarcinomas was significantly greater than that of patients with predominantly bronchioloalveolar carcinoma, papillary, or acinar adenocarcinomas (all p < 0.001). CONCLUSION: A greater smoking extent was associated with the presence of adenocarcinoma solid components, which may have more aggressive biological features resulting in poorer outcomes.

Parotid acinar cell carcinoma in a long-term survivor of childhood acute lymphoblastic leukemia.

Secondary malignancies are an important cause of morbidity and mortality in childhood cancer survivors. Salivary gland tumors account for about 6% of the second cancers. The majority of these are mucoepidermoid carcinomas (MEC) of the parotid gland. We report the clinical and pathological features of a rarer histological type, acinic cell carcinoma (ACC), in a childhood acute lymphoblastic leukemia (ALL) survivor. The behavior of secondary ACC appears similar to primary tumor and similar treatment may be adopted. Early recognition and complete resection is important for achieving a good outcome. Careful monitoring for recurrence or a third malignancy is needed.

Acinar cell carcinoma arising from an ectopic pancreas.

We herein report a rare case of ectopic pancreatic acinar cell carcinoma (ACC) which presented as a submucosal tumor of the pylorus. A 73-year-old man came to our hospital presenting with epigastralgia. Esophago-gastroduodenal endoscopy showed no mucosal lesions, but a submucosal tumor was observed around the pylorus. Abdominal computed tomography revealed two round masses. One was located in the pylorus, while the other was found between the portal vein and the inferior vena cava. An examination of a biopsy specimen was inconclusive. We diagnosed a gastrointestinal stromal tumor or malignant lymphoma preoperatively, and decided to perform an operation in order to confirm the diagnosis and select the optimal treatment. Intraoperatively, the mass in the pylorus invaded the pancreatic head, and the lymph node in the hepatoduodenal ligament was swollen. We performed a pancreaticoduodenectomy as a radical excision. The resected specimen showed the 7.6 x 4.9-cm size tumor to mainly originate from the pylorus. Histopathologically, the tumor was identified as pancreatic ACC with lymph node metastasis. The tumor cells were labeled by immunohistochemical staining for alpha1-antitrypsin. Because of the tumor location, we considered the tumor to have originated from the ectopic pancreatic tissue in the stomach. This is only the second case of ACC originating from an ectopic pancreas reported in the literature.

[Differential genetic pathway of duct and acinar carcinomas of the pancreas].

Genetic pathways of various types of pancreatic carcinoma are described. There are many differences in the genetic pathway between duct carcinogenesis and acinar carcinogensis. K-ras mutation is a key event in the early stage of pancreatic duct carcinogenesis and various gene alterations accumulate from precancerous ductal lesions until the development of carcinomas. Therefore, inhibition of K-ras gene mutation might be important for the prevention, and the combination of therapeutic agents against some target genes might be needed for therapy of ductal carcinomas.

Transgenic expression of CCK2 receptors sensitizes murine pancreatic acinar cells to carcinogen-induced preneoplastic lesions formation.

In humans, initial events of pancreatic carcinogenesis remain unknown, and the question of whether this cancer, which has a ductal phenotype, exclusively arises from duct cells has been raised. Previous studies have demonstrated that transgenic expression of the CCK2 receptor in acinar cells of ElasCCK2 mice plays a role in the development of pancreatic neoplasia. The aim of our study was to examine initial steps of carcinogenesis in ElasCCK2 mice, adding a supplementary defect by using a chemical carcinogen, azaserine. Results of posttreatment sequential immunohistochemical examinations and quantifications demonstrate that mice responded to azaserine. Transition of acinar cells into duct-like cells expressing Pdx1 and gastrin, as well as proliferation of acinar cells, were transiently observed in both transgenic and control mice. The carcinogen also induced formation of preneoplastic lesions, adenomas, exhibiting properties of autonomous growth. Importantly, expression of the CCK2 receptor increased the susceptibility of pancreas to azaserine. Indeed, treated ElasCCK2 mice exhibited larger areas of pancreatic acinar-ductal transition, increased cellular proliferation as well as larger adenomas areas vs. control mice. These amplified responses may be related to auto/paracrine stimulation of CCK2 receptor by gastrin expressed in newly formed duct-like cells. Our results demonstrate that activation of CCK2 receptor and azaserine result in cumulative effects to favor the emergence of a risk situation that is a potential site for initiation of carcinogenesis.

Potential utility of p53 immunopositivity in differentiation of adenocarcinomas from reactive epithelial atypias of the lung.

Reactive atypia of alveolar epithelium occurs in many types of lung injury and may sometimes raise suspicions of adenocarcinoma or bronchioloalveolar carcinoma. To assess whether there is sufficient difference in the frequency of p53 protein immunopositivity in these lesions to provide a practical basis for differentiating malignancy from reactive atypia, we immunostained 110 malignant and inflammatory/fibrotic lung specimens for p53 protein. Paraffin-embedded sections were immunostained with p53 protein antibody (clone BP53-12; BioGenex, San Ramon, CA) and standard capillary gap (Microprobe; Fisher Scientific, Fairlawn, NJ) avidin- biotin complex technique with antigen retrieval solution. Percent of immunopositive cells was semiquantitatively categorized as follows: 0%, less than 1%, 1% to 10%, 10% to 50%, more than 50%. Of reactive atypias, 94% are negative or show p53 immunopositivity in less than 10% of cells. Of p53 positive malignancies, 86% are positive in more than 10% of cells. When p53 immunopositivity occurs in more than 10% of atypical cells, the lesion is usually a malignancy, primarily adenocarcinoma. Most reactive atypias are immunopositive in less than 10% of atypical cells. Important caveats were noted. Rare reactive atypias are p53 immunopositive in greater than 10% of cells. Bronchioloalveolar carcinomas are infrequently p53 immunopositive. Therefore, this approach would be less useful in their differentiation from reactive atypias.

Acinic cell carcinoma arising in a parotid lymph node.

The case of a 37-year-old woman with primary acinic cell carcinoma arising in an intraparotid lymph node is presented. The patient is free of disease 20 months after superficial parotidectomy. This is probably the first histologically documented case of acinic cell carcinoma arising from intranodal salivary gland tissue. Awareness of possible malignant alteration of ectopic salivary gland tissue in lymph nodes is essential.