Acinic Carcinoma Research Articles

Molecular and clinical features of pancreatic acinar cell carcinoma: A single institutional experience.

e16335 Background: Acinar Cell Carcinoma (ACC) accounts for around 1% of pancreatic cancer. The molecular and clinical features of acinar cell carcinoma are less characterized. We sought to evaluate the clinical and molecular features of patients with ACC at MD Anderson Cancer Center. Methods: Patients with ACC who had germline and/or somatic molecular testing at MD Anderson Cancer Center from 2008 to 2022 were identified retrospectively. After obtaining approval of approval of the institutional review board genomic alterations including germline or somatic BRCA mutations, KRAS mutation, demographic, clinical, and pathological information were extracted from institutional databases using the Palantir Foundry software platform (Syntropy); this included natural language processing with subsequent validation by manual chart review. Overall Survival (OS) was calculated from the date of diagnosis to death or last follow-up. The Kaplan-Meier method was used for survival analysis. Results: 16 patients were identified with molecular testing results available. There were 13 males and 3 females. The median age of diagnosis was 62.5 years (range 49 -72). 14/16 patients (87.5%) had metastatic disease, one (6.25%) patient had borderline resectable disease and one (6.25%) had localized resectable disease at initial diagnosis. Median OS was for 24 months for patients with metastatic disease. There were 2 patients with mixed pathology, 1 with acinar cell carcinoma with neuroendocrine features and the 2nd had mixed acinar cell-ductal carcinoma. 15/16 (93.75%) patients were tested for KRAS and all 15 were KRAS wildtype. Somatic mutations in DNA damage repair genes (BRCA2, PALB2) were present in 3 patients (25%) and 2 patients had germline mutation (BRCA and ATM) (16%) out of 12 patients tested for those genes. 6/16 (37.5%) patients were treated with FOLFIRINOX at first line. 3/6 (50%) of these patients had partial response, 2/6 (33%) had stable disease and only 1/6 (16%) had progression. 5 patients were treated with FOLFOX based regimen and 1/5 (20%) had response, 2/5 (40%) had stable disease and 2/5 (40%) had progression of disease. 5 patients were treated with gemcitabine-based regimen and only 1 had response which received gemcitabine/nab-paclitaxel combined with cisplatin. Conclusions: ACC were KRAS wild type and had higher rates of germline/somatic mutations in DNA damage repair genes. Better treatment outcome of FOLFIRNIOX/ platinum-based regimens was suggested based on this limited patient dataset. Larger studies are needed to further understand the molecular features of ACC and guide the treatment of this rare entity of pancreatic cancer.

An NCDB demographic and socioeconomic analysis of mixed acinar ductal carcinoma.

An NCDB demographic and socioeconomic analysis of mixed acinar ductal carcinoma.

PRIMARY MALIGNANT MELANOMA OF THE PAROTID GLAND, A RARE ENTITY: A CASE REPORT

The prevalence of primary malignant tumors of the salivary gland is 1 per 100,000 people. Most salivary gland tumors originate in the parotid gland (80%), of which 25% are malignant. Adenoid cystic carcinoma, mucoepidermoid carcinoma and acinar duct carcinoma are among the most common types of salivary gland cancer [1]. Around 25% of parotid tumors are metastatic, originating mainly in the head and neck region. The main metastatic tumors of the parotid gland are squamous cell carcinoma and malignant melanoma [2]. Parotid melanoma is generally secondary to a primary location on the skin of the head and neck. When its primary site cannot be found, we speak of primary melanoma of the parotid gland, an even rarer entity. Here, we report the case of a primary malignant melanoma of parotid gland in a 66-year-old male subject.

Morphologic Features of Invasion in Lung Adenocarcinoma: Diagnostic Pitfalls.

Reproducibility of pulmonary invasive adenocarcinoma diagnosis is poor when applying the World Health Organization (WHO) classification. In this article, we aimed first to explain by 3-dimensional morphology why simple pattern recognition induces pitfalls for the assessment of invasion as applied in the current WHO classification of pulmonary adenocarcinomas. The underlying iatrogenic-induced morphologic alterations in collapsed adenocarcinoma in situ overlap with criteria for invasive adenocarcinoma. Pitfalls in seemingly acinar and papillary carcinoma are addressed with additional cytokeratin 7 and elastin stains. In addition, we provide more stringent criteria for a better reproducible and likely generalizable classification.

Intraductal mixed acinar ductal carcinoma of pancreas: report of a case

Intraductal mixed acinar ductal carcinoma of pancreas: report of a case

A patient with pancreatic acinar carcinoma a - a rare clinical case report

A patient with pancreatic acinar carcinoma a - a rare clinical case report

Analysis of association between new-onset type 2 diabetes mellitus and pancreatic cancer: retrospective research

Introduction. Pancreatic cancer is characterized by an extremely unsatisfactory prognosis, despite the development of technologies for the treatment of this pathology. In more than 80 % of patients at the time of the initial request for medical care, the disease is represented by a locally advanced or metastatic stage. Currently used methods of treatment of this nosology are most effective at the early stages of the disease. The absence of characteristic clinical, instrumental and laboratory symptoms, as well as organizational measures for the early detection of this neoplasia creates certain difficulties for effective treatment. Type 2 diabetes is probably one of the risk factors for the development of pancreatic cancer. Epidemiological studies have shown that newly diagnosed type 2 diabetes is associated with a 1.5–2.0-fold increased risk of developing pancreatic cancer in patients over 50 years of age. Insulin resistance and its associated hyperglycemia, hyperinsulinemia, and inflammation are thought to be the main mechanisms contributing to the development of diabetes-related pancreatic cancer. New-onset type 2 diabetes mellitus may be a preclinical sign of pancreatic cancer, and patients with newly diagnosed diabetes may constitute a population in which pancreatic cancer can be detected at an early stage, that will significantly improve the results of treatment.
 Objective. To analyze the relationship between new-onset type 2 diabetes mellitus and the development of pancreatic cancer.
 Material and methods. A retrospective analysis of the medical records of patients with a confirmed diagnosis of pancreatic cancer, who were treated at the Academician A.M. Granov Russian Scientific Center of Radiology and Surgical Technologies from 2019 to 2022, was carried out. As a source of information, data from medical records of inpatient and outpatient treatment cards were used. In total, the data of 203 persons were studied: morphologically confirmed pancreatic ductal adenocarcinoma was diagnosed in 172 patients (group I), in 31 patients pancreatic tumors had a different histological structure: acinar carcinoma, neuroendocrine tumors (group II). Group I excluded 8 patients without diabetes mellitus who were taking medications, which affect the blood glucose levels. The frequency of occurrence of type 2 diabetes mellitus in the groups was analyzed and then the statistical significance was assessed using the calculation of Fisher's exact test. Group I was analyzed by sex and age, then patients from group I aged 50–75 years were divided into 3 subgroups depending on the glycemic profile: 1) patients with long-term type 2 diabetes mellitus (anamnesis more than 3 years); 2) patients with new-onset type 2 diabetes mellitus (anamnesis less than 3 years); 3) patients without disorders of glucose metabolism. In the subgroup of patients with a long history of type 2 diabetes mellitus, the fact of disease decompensation was additionally assessed.
 Results. Type 2 diabetes mellitus was more common in patients with pancreatic ductal adenocarcinoma (p 0.01, Fisher's exact test p = 0.0012) than in other pancreatic neoplasms. The age of patients in group I ranged from 36 to 81 years. The average age of men was 61 ± 8.5 years. The average age of women was 58.9 ± 8.2 years. Among patients of group I aged 50–75 years, new-onset type 2 diabetes mellitus occurred in 78 (68.4 %) persons, type 2 diabetes mellitus with an anamnesis of more than 3 years was detected in 19 (16.6 %) patients, normal metabolism of glucose was observed in 17 (14 %) patients. Of 19 patients with a long anamnesis of type 2 diabetes mellitus (more than 3 years), decompensation in the form of impaired glycemic control was observed in 12 (63.2 %) patients before the diagnosis of pancreatic cancer, in 7 (36.8 %) patients no signs of decompensation of the course of type 2 diabetes mellitus were registered.
 Conclusions. New-onset type 2 diabetes mellitus occurred in 78 (64.4 %) patients over 50 years of age with pancreatic ductal adenocarcinoma. The data obtained indicate the feasibility of conducting studies to identify patients aged 50–70 years with newly diagnosed type 2 diabetes in the risk group for the development of pancreatic cancer and examine this contingent at the stage of primary health care. Further retrospective as well as prospective multicenter studies on the association between newly diagnosed type 2 diabetes mellitus and the risk of developing pancreatic cancer are required.

Genomic classifier aligns most pancreatic acinar carcinoma with pancreatic ductal adenocarcinoma

Genomic classifier aligns most pancreatic acinar carcinoma with pancreatic ductal adenocarcinoma

A novel GLCC1::BRAF fusion with independent MYCN and MYC amplifications in primary tumor and metastasis in pediatric pancreatic acinar carcinoma

Abstract Introduction/Objective Pediatric pancreatic acinar cell carcinoma (PACC) is a rare malignancy, comprising 5-15% of pediatric pancreatic tumors. BRAF rearrangement is found in 20-30% of PACC cases, most commonly an inversion in chromosome 7. We report a case of PACC with GLCC1::BRAF fusion. Methods/Case Report A 10-year-old male presented with six months of weight loss, back pain, and loose stools. Imaging demonstrated concentric soft tissue thickening around the celiac axis and superior mesenteric artery, clinically interpreted as vasculitis. Follow-up imaging showed extension of the soft tissue thickening, prompting biopsy of a periaortic lymph node showing metastatic PACC. Pancreaticduodenectomy revealed a 3.8 cm pancreatic neck mass with perineural invasion and metastatic deposits in multiple lymph nodes and retroperitoneal soft tissue. Fluorescence in situ hybridization of both specimens demonstrated BRAF gene rearrangement, with the partner identified as GLCC1 by next generation sequencing and fusion assays. Microarray on the lymph node demonstrated amplification of MYC on chromosome 8, but not in the resection specimen, which showed gain of chromosome 2 and amplification of MYCN. Results (if a Case Study enter NA) NA Conclusion The GLCC1::BRAF fusion has previously been reported once in a case of pheochromocytoma with peritoneal seeding. The MYC gene family members, c-MYC and MYCN, are involved many cancer types; amplifications are often associated with unfavorable prognosis in tumors such as neuroblastoma. However, the amplification of both genes in the same tumor at different loci has not been reported. The combination of the primary GLCC1::BRAF fusion with secondary amplification of MYC and MYCN is likely to drive the aggressive behavior and metastasis in this case of PACC. Treatment for PACC includes chemoradiation and BRAF inhibition. However, BRAF rearrangements without the V600E mutation show variable response to BRAF inhibitors. Potential alternatives include inhibitors to other targets within the BRAF signaling pathway. Further investigation is needed to determine the clinicopathologic impact of these novel genetic aberrancies.

Differential expression of LLGL2 in prostate ductal adenocarcinoma and acinar adenocarcinoma and its significance

Objective: To investigate the expression differences of LLGL2 between prostatic ductal adenocarcinoma (PDA) and prostatic acinar adenocarcinoma, and its potential clinical significance. Methods: Eighteen patients diagnosed of PDA or prostatic acinar adenocarcinoma with PDA component by histopathology during January 2015 and December 2019 in the Beijing Hospital, China were retrospectively studied. The transcriptome analysis was conducted using the tissue of PDA and prostatic acinar adenocarcinoma. Differentially expressed genes and the differences in expression profiles were identified. Further, differentially expressed proteins were verified by immunohistochemistry. Results: The tissue from 8 of the 18 patients were used for transcriptome analysis, the results of which were compared with data from public databases. 129 differentially expressed genes were identified. 45 of them were upregulated while 84 were downregulated. The results of gene enrichment analysis and gene oncology (GO) analysis revealed that the differentially expressed genes were mostly enriched in the hypertrophic cardiomyopathy and interleukin-17 related pathways. GPAT2, LLGL2, MAMDC4, PCSK9 and SMIM6 were differentially expressed between PDA and prostatic acinar adenocarcinoma. Moreover, LLGL2 was more likely expressed in the cytoplasm (P=0.04) than the nucleus (P<0.01) in PDA, compared with prostatic acinar adenocarcinoma. Conclusions: The gene expression profiling indicates that PDA are very similar to prostatic acinar adenocarcinoma. Among the differentially expressed proteins screened and verified in this study, the expression of GPAT2, LLGL2, MAMDC4 and PCSK9 is increased in PDA, while that of SMIM6 is reduced in PDA. The expression of LLGL2 shows significantly different patterns between PDA and prostatic acinar carcinoma, and thus may help differentiate PDA from prostatic acinar adenocarcinoma in clinical practice.

Evaluation of annexin A1 expression in lung, breast, colon, and prostatic adenocarcinomas and in tumor microenvironment

Objectives: Annexin A1 (ANXA1) which plays a role in tumor development and metastasis has been reported to be an effective regulator for tumor stroma and interacts with different components in the tumor microenvironment. The role of ANXA1 in tumorigenesis has not been fully understood. One of the main reasons for this is the great variability of ANXA1 expression in malignant tumors across different tumor types. Materials and Methods: Archived hematoxylin-eosin stained preparations of lung adenocarcinoma, breast invasive ductal carcinoma, colonic adenocarcinoma, and prostatic acinar carcinoma were re-evaluated and tumor regions to be analyzed with the tissue microarray method were determined. The ANXA1 expressions between the tumors and tumor microenvironment were evaluated immunohistochemically. Results: ANXA1 expression was decreased in the lung, breast, colon, and prostate adenocarcinomas. The most prominent staining was seen in lung adenocarcinoma cases. There was no statistically significant difference between the tumors in terms of ANXA1 staining (P &gt; 0.05). ANXA1 was shown to be a more stained tumor microenvironment than in the tumor. Statistically significant staining with ANXA1 between within tumor and tumor microenvironment was observed in breast adenocarcinomas (P &lt; 0.05). Our study showed differences between ANXA1 expression in different cancers, in tumor cells, and tumor microenvironment. Conclusion: Considering the effects of ANXA1 on tumor development and metastasis, a potential use as a biomarker may be suggested. Particularly, in breast adenocarcinomas, the high expression of ANXA1 in the tumor microenvironment supports the notion that it could induce the tumor stroma response.

Analysis of survival and prognostic factors of clear cell adenocarcinoma of the prostate: a case–control study for a rare cancer entity

Clear cell adenocarcinoma of the prostate (CCPC) is a rare entity compared to acinar carcinoma of the prostate (APC). The survival rate and prognostic factors of CCPC are still unclear and deserve further study. We downloaded data on prostate cancer from the Surveillance, Epidemiology, and End Results database for 1975–2019. After inclusion and exclusion criteria, we compared APC and analyzed cancer-specific mortality (CSM) and overall mortality (OM) in CCPC patients and prognostic risk factors using a propensity score matching (PSM) study and multivariate Cox regression. We included 408,004 cases of APC as a control group and 130 cases of CCPC as a case group. Compared with APC patients, the incidence of CCPC was extremely low, and the median age of diagnosis was older (72.00 years vs. 69.00 years, p < 0.01). In addition, more rates were diagnosed at an earlier stage (1975–1998, 93.1% vs. 50.2%, p < 0.001), more unstaged or unknown stage ratios (87.7% vs. 42.7%, p < 0.001), and more surgical treatments (66.2% vs. 47.6%, p < 0.001), but the prognosis of CCPC patients was worse. After PSM, the median survival time of CCPC patients was shorter (57.50 month vs. 88.00 month, p < 0.01), the rate of CSM was higher (41.5% vs. 27.7%, p < 0.05), and the rate of OM was higher (99.2% vs. 90.8%, p < 0.01). In the adjusted model 2 after PSM, the CSM risk of CCPC patients reached HR 1.76 (95%CI 1.13–2.72), which was 76% higher than that of APC patients (p < 0.05). It was further found that surgical treatment might benefit CSM in CCPC patients (HR 0.39, 95%CI 0.18–0.82, p < 0.05) in Univariate analysis, but it was insignificant in further multivariate analysis. This is the first large-scale case–control report on the survival risk and prognostic factors of CCPC patients. We found that the prognosis of CCPC patients was significantly worse than that of APC. Surgery might be an effective treatment that may improve its prognosis. Clear cell adenocarcinoma, prostate, acinar carcinoma, survival rate, rare cancer, propensity score matching, case–control study.

Pathological and immunohistochemical characterization of pancreatic carcinoma in cats

The aim of this study was to characterize the pathological and immunohistochemical aspects of pancreatic carcinoma in cats, through a retrospective study. From January 2010 to December 2021, 1,908 cat necropsies were performed, in which 20 cases of exocrine pancreatic neoplasia were diagnosed (1.04%). Affected cats were mature adults and seniors, except for one 1-year-old cat. In 11 cases the neoplasm was a soft, focal nodule on the left (8/11) or right (3/11) lobe. In nine cases there were multifocal nodules throughout the pancreatic parenchyma. The size of the single masses ranged from 2 to 12 cm, and the multifocal masses from 0.5 to 2 cm. The most frequent tumour type was acinar carcinoma (11/20), followed by ductal carcinoma (8/20), undifferentiated carcinoma (1/20) and carcinosarcoma (1/20). On immunohistochemical evaluation, all the neoplasms were remarkably reactive to pancytokeratin antibody. The ductal carcinomas were strongly reactive for cytokeratins 7 and 20, which proved to be a good marker for pancreatic ductal carcinoma in cats. The main form of metastasis was abdominal carcinomatosis, with a marked invasion of blood and lymphatic vessels by neoplastic cells. Our findings reinforce the fact that pancreatic carcinoma should be rated highly in the differential diagnosis in mature adult and senior cats with abdominal masses, ascites and/or jaundice.

Mixed Acinar Neuroendocrine Carcinoma of the Pancreas: Comparative Population-Based Epidemiology of a Rare and Fatal Malignancy in The United States.

Mixed acinar neuroendocrine carcinoma of the pancreas (MANEC-P) is an extremely rare malignancy with a poor prognosis. However, epidemiological estimates of MANEC-P remain unknown. This study aimed to estimate and compare the incidence, prevalence, and cancer-specific survival (CSS) of MANEC-P in the United States (US). Patients with MANEC-P were identified through the Surveillance, Epidemiology, and End Results (SEER) and National Program of Cancer Registries databases between 2000-2017. The primary outcomes included age-adjusted incidence rate, limited-duration prevalence, and CSS. A total of 630 patients were identified for the incidence analysis and 149 for the prevalence and CSS analyses. The MANEC-P incidence rate was 0.011 per 100,000 individuals, which was the lowest among pancreatic cancer histologic subtypes. The incidence rate was significantly higher in men and Black races and peaked at 75-79 years of age. The incidence rate was the lowest in the midwestern region (0.009) and the highest in the northeastern US (0.013). The 17-year prevalence was 0.00005%, indicating that 189 patients were alive in the United States at the beginning of 2018. The median CSS of MANEC-P was estimated to be 41 (23, 69) months. In conclusion, MANEC-P is very rare, and its incidence rate has been steady in the US over the last two decades. MANEC-P has a poor prognosis and is the 5th leading cause of pancreatic cancer-related death in the US.

Ulcerated, tender nodules of the lower extremities

Ulcerated, tender nodules of the lower extremities

Relevance of detection of RAF fusion in pan-negative melanoma in routine practice.

e21500 Background: Pan-negative melanomas (i.e. without MAPK kinase pathway alteration and C-kit wild type) account for 30% of melanomas (according to the AACR GENIE database). In case of immunotherapy failure, therapeutic options are limited. Oncogene fusions represent a target of interest in many solid cancers (NSCLC, Cholangiocarcinoma, Glioma, GIST, pancreatic acinar carcinoma, thyroid, and prostate cancers). In melanoma, the frequency of oncogene fusion is not well documented and not routinely investigated. Methods: We conducted a single-center retrospective study. The objective was to determine the frequency of oncogene fusion detected by RNA sequencing (Archer Fusion pLex) performed in routine practice, in patients with advanced or metastatic pan negative melanoma. Data on clinical, pathological, and molecular characteristics and patient outcomes were collected. Analysis was carried out on the genetic material available for the diagnosis of the disease except for 1 patient who benefited from a new anatomopathological sample during an unfavorable evolution. In parallel, an extended molecular alteration search was performed using extended targeted NGS (OncoMine Comprehensive Assay panel). Results: We identified 48 patients with an advanced pan negative melanoma between January 2021 and January 2022 with a median age at diagnosis of 63 years. It was a cutaneous melanoma in 72,9 % (35/48) of the cases, a mucous melanoma in 14,5% (7/48) of the cases and a melanoma of unknown primary site in 12,5% (6/48) of the cases. The detection of fusion transcript was made in 89,5 % (43/48) of the cases. We identified 6 patients with a RAF fusion, including 4 BRAF gene fusion (MKLN1-BRAF, AGK-BRAF, SNX29-BRAF, PTPRJ-BRAF) and 2 RAF1 fusion (MAP4-RAF1, EFCC1-RAF1). Of the other molecular alterations, NF1 mutation was the most frequent molecular alteration identified (25 % (12/48) of patients). At lower frequencies, 6,8 % (3/48) of patients had a PI3K mutation, and 8,3 % (4/48) of patients had NOTCH, PTCH1, GNAQ mutations. Among the 6 patients with RAF fusions, all the patients initially received treatment with anti-PD1+/- anti-CTLA4 immunotherapy. After immunotherapy failure, 4 patients benefited from second-line targeted therapy (2 with BRAF and MEK inhibitors combination, 2 MEK inhibitors alone). One patient presented an objective imaging response, the other three patients have not yet benefited from reassessment imaging. Conclusions: In a population of pan negative melanoma, we detected 12,5 % (6/48) of RAF fusion. Fusion detection allowed the introduction of a second line of targeted therapy, in the absence of a validated therapeutic option in 66,6 % (4/6) of cases This study suggests the relevance of detecting RAF fusion in a selected population.

Spatial Whole Transcriptome Profiling of the Tumor Microenvironment in Prostate Carcinomas

BackgroundDespite years of studies and effort, the best strategies for treating prostate cancer and minimizing the complications of treatment remain unanswered questions. This gap in knowledge is partially due to the inability to dissect the complex heterogeneous tumor microenvironment (TME) and immune compartment. Spatially resolved molecular profiling of tumor sections will enhance our understanding of these complexities; However, it has been particularly challenging to do spatial molecular profiling in formalin‐fixed paraffin‐embedded (FFPE) tissues due to RNA degradation associated with this tissue‐embedding method, which is routinely used in oncology workflows.The 10x Genomics Visium Spatial Gene Expression Solution for FFPE tissue overcomes these limitations, enabling spatial gene expression analysis of FFPE tissues combined with classical histology staining techniques such as Hematoxylin &amp; Eosin (H&amp;E) staining and immunofluorescence.MethodsWe used the 10x Genomics Visium Spatial Gene Expression Solution for FFPE tissue to analyze and resolve tumorigenic profiles in sections of normal and adenocarcinoma prostate samples. This assay incorporates ~5,000 molecularly barcoded, spatially encoded capture probes in spots over which the tissue is placed, imaged, and permeabilized. Imaging and sequencing data are processed together, resulting in a spatially resolved transcriptional readout.ResultsWe profiled the whole transcriptome in normal, invasive adenocarcinoma, and acinar cell carcinoma FFPE human prostate tissues.Unsupervised clustering of the whole transcriptome data from normal, invasive adenocarcinoma, and acinar cell prostate carcinoma FFPE sections enabled the identification of 2 different regions, which had a well defined spatial distribution within the tissues. Well known prostate gland and prostate‐cancer markers were over‐expressed in the corresponding healthy and cancerous portions of the tissue, validating the performance of this method. We found that, while in healthy tissues basal cells and luminal cells are spatially organized, this pattern is lost in tumor samples, where luminal cells are greatly expanded in the invasive carcinoma region and do not colocalize with basal cells. Moreover, T lymphocytes are dispersed throughout the whole tissue section in the adenocarcinoma, while plasma B cells are located in the peritumoral region which could impact prognosis.ConclusionsSpatial whole transcriptome analysis opens new opportunities for better understanding the TME which can not only help discover novel predictive tumor biomarkers, but also enable identifying cell type and tumor region specific drug targets.

Small cell-like change in prostatic adenocarcinoma and intraductallesions \u2013 neuroendocrine or not?

BackgroundSmall cell-like change in prostatic neoplasia (both invasive adenocarcinoma and intraepithelial lesions) is described in three previous reports. None of them to date proved to be associated with overt prostate neuroendocrine carcinoma.Case presentationWe report findings from a radical prostatectomy of 80-year-old patient (adenocarcinoma GG5 pT3b with 10% involvement of the gland) with small cell-like change in intraductal carcinoma and in the invasive component. An additional 3.5-mm focus of poorly differentiated carcinoma was observed (PSA, TTF1, chromogranin and CD56 negative; synaptophysin positive in scattered cells; and a Ki67 label index of 50%).ConclusionOur case expands the data accumulated on small cell-like change in prostate neoplasia. As most of other reported cases, there was no expression of neuroendocrine markers or high proliferative index in small-cell like areas. On the other hand, for the first time, a transition morphology between acinar adenocarcinoma and neuroendocrine carcinoma was observed in a prostate with small cell-like change.

Survival after Pancreatic Resection in Older Patients with Pancreatic Malignancy

Introduction: Pancreatic malignancies have among the highest mortality rates of solid organ cancers, and there has been a global trend towards an increasing incidence. In the context of an aging population, more older patients will present for consideration of curative resection. Although mortality and morbidity associated with pancreatic resection has improved, there are mixed outcomes reported in the literature regarding survival outcomes for older patients undergoing pancreatectomy. Methods: A retrospective cohort study was performed including patients ≥75 years of age undergoing pancreatic resection for primary pancreatic malignancy, identified using a prospectively maintained database of a single surgeon’s experience. The primary outcomes were median survival and 5-year overall survival. Secondary outcomes included hospital length of stay, peri-operative morbidity and mortality, patterns of recurrence and disease-free survival. Results: 41 patients aged ≥75 years were identified from a total of 497 major pancreatic resections for malignancy between 2007 and 2020. The mean age was 80.6 (range 75 - 88) Of these patients, patients underwent pancreacitoduodectomy (n=36), distal pancreatectomy (n=3), total pancreatectomy (n=2) for pancreatic adenocarcinoma (n=34), ampullary adenocarcinoma (n=5), pancreatic acinar carcinoma (n=1) and invasive microcystic cystadenoma (n=1). 21 patients (51%) had concurrent major vascular resection. The median survival was 24 months, and the 5-year overall survival rate 37%. 30-day and 90-day mortality was 0% and 4.9% (n=2), respectively. Conclusion: Pancreatic resection for malignancy in appropriately selected older adults is safe and confers comparable survival outcomes to the general population. Age alone should not be a contraindication to pancreatectomy.

Malignant pancreatic tumor other than solid pseudopapillary tumor in pediatric patients: A single-center experience.

Pancreatic tumors, except solid pseudopapillary tumors (SPTs), are rare in pediatric patients. Herein, we report various types of pancreatic tumors in pediatric patients and review the literature regarding their treatments and prognosis.We retrospectively reviewed the data of pediatric patients who underwent surgery for pancreatic tumors, excluding SPTs, between January 2009 and December 2019 at Seoul National University Children's Hospital. A total of 35 pediatric patients were identified as having undergone surgery for pancreatic tumors. Of these patients, 30 were excluded because the tumor was identified as an SPT.The diagnoses of the five remaining (non-SPT) pancreatic tumors were pancreatic neuroendocrine tumor, mixed acinar neuroendocrine carcinoma, kaposiform hemangioendothelioma, and intraductal papillary mucinous neoplasm. All five patients survived; however, recurrence and liver metastasis were observed in one patient. The detailed demographics, treatments, and prognosis of each patient were reviewed.Despite the rarity and low incidence of pancreatic tumors in pediatric patients, four types of non-SPT tumors are reported here. Hence, the possibility of these should not be overlooked, especially since the diagnosis and adjuvant treatment differ vastly between the tumor types.