scholarly journals Acinar Cell Cystadenocarcinoma of the Pancreas

2017 ◽  
Vol 11 (2) ◽  
pp. 504-510 ◽  
Author(s):  
Keita Aoto ◽  
Tatsuo Shimura ◽  
Yasuhide Kofunato ◽  
Ryo Okada ◽  
Rei Yashima ◽  
...  
Keyword(s):  
Distal Pancreatectomy ◽  
Tumor Cells ◽  
Acinar Cell ◽  
Transverse Colon ◽  
Partial Resection ◽  
Pancreatic Acinar Cells ◽  
Total Resection ◽  
Residual Stomach ◽  
Pubmed Search ◽  
Pancreatic Exocrine

Acinar cell cystadenocarcinoma is a rare malignant epithelial neoplasm of the pancreas with a diffusely cystic, gross architecture in which the cysts are lined with neoplastic epithelial cells that demonstrate evidence of pancreatic exocrine enzyme production. This is the 10th case that has been reported in the literature. A 77-year-old male complaining of left hypochondrial pain was referred to our hospital for treatment of a pancreatic tumor. A huge, honeycomb-structured tumor was detected in the pancreatic tail. Distal pancreatectomy with total resection of the residual stomach and partial resection of the transverse colon were performed. Microscopically, there were variably sized cystic lesions in the tumor. Immunohistochemical examinations revealed that tumor cells were positive for alpha 1-antichymotrypsin and alpha 1-trypsin, showing that tumor cells had features of pancreatic acinar cells. Thus, the tumor was diagnosed as acinar cell cystadenocarcinoma. Herein, we report a rare case with acinar cell cystadenocarcinoma, which is the 10th case reported in the literature based on a PubMed search. We managed to resect the tumor completely by distal pancreatectomy with total resection of the residual stomach and partial resection of the transverse colon. The patient is still alive 26 months after surgery without any recurrence after 1 year of adjuvant chemotherapy with S-1.

scholarly journals Extent of resection in glioblastoma: a 10-year local survival analysis

2021 ◽  
Vol 23 (Supplement_4) ◽  
pp. iv19-iv19
Author(s):  
Theodore Hirst ◽  
Patrick McAleavey ◽  
Tom Flannery
Keyword(s):  
Neurological Deficit ◽  
Survival Benefit ◽  
Extent Of Resection ◽  
Cox Proportional Hazards ◽  
Partial Resection ◽  
Gross Total Resection ◽  
Molecular Profile ◽  
Total Resection ◽  
Local Survival ◽  
The Impact

Abstract Aims The impact on extent of resection (EOR) in glioblastoma has been well documented. It is clear that gross-total resection (GTR) confers best overall survival (OS), however the minimum EOR required to confer a survival benefit over biopsy is debated. Recent studies favour partial resection (PR) over biopsy for IDH-wildtype, MGMT-unmethylated tumours. We describe our experiences locally with these principles in mind. Method Retrospective evaluation of a single surgeon cohort. All patients over 18 years old, undergoing a surgical treatment for histologically confirmed GBM in the stated period were included. We collected information on demographics, tumour volume, EOR, complications, adjuvant therapies, molecular profile, and OS. We used log rank tests and Cox Proportional Hazards Models to identify factors associated with OS. Results The patient and tumour characteristics of our cohort were similar to those documented in the literature. The mean age was 56.6 years. 72 patients underwent biopsy and 202 had debulking surgery. Median OS was 11 months. Of those debulked, gross-total resection was achieved in 41 patients (20%); associated median OS was 29 months. Patients receiving partial resection (defined as EOR <80%) had no clear survival benefit over patients undergoing biopsy (median OS 6 vs 5 months) but had a higher rate of post-op neurological deficit (3% vs 12%). Tumour molecular profile appeared to influence survival outcome in a manner comparable to worldwide experience. Conclusion In our experience, partial resection is not a justifiable surgical aim in the typical glioblastoma cohort. The limited benefit that it may confer over biopsy appears to be outweighed by the risk of neurological deficit that affects quality and probably quantity of life. This finding applies to our glioblastoma population in general as well as those specifically with an MGM-unmethylated tumour.

scholarly journals Endoscopic Endonasal Resection of Symptomatic Rathke Cleft Cysts: Total Resection or Partial Resection

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiejun Zhang ◽  
Jihu Yang ◽  
Yan Huang ◽  
Yufei Liu ◽  
Lei Chen ◽  
...  
Keyword(s):  
Cyst Wall ◽  
Partial Resection ◽  
Csf Leak ◽  
Cerebrospinal Fluid Leakage ◽  
Total Resection ◽  
Endoscopic Endonasal ◽  
Clinical Prognosis ◽  
Electrolyte Disturbance ◽  
Operative Complications ◽  
Post Operative Complications

Objective: Rathke cleft cysts (RCC) are benign sellar lesions, and endoscopic endonasal surgery (EES) for symptomatic RCC is becoming increasingly popular, but total resection or partial resection (TR or PR) of the cyst wall is still inconclusive. The aim of this study was to review the complications and clinical prognoses associated with total and partial resection of the cyst wall by EES.Methods: We retrospectively analyzed a series of 72 patients with symptomatic RCC treated by EES from -January 2011 to June 2019 at Shenzhen University First Affiliated Hospital. For these 72 cases, 30 were treated with TR and 42 were treated with PR. Intra- and post-operative complications and clinical prognosis were investigated.Results: All 72 patients underwent a pure EES. In the TR group, 10 patients (33.3%) had intraoperative cerebrospinal fluid leakage (CSF leak), three patients (10%) had postoperative CSF leak, eight patients (26.7%) had postoperative diabetes insipidus (DI), eight patients (26.7%) had postoperative electrolyte disturbance, and 12 patients (40%) had temporary hypopituitarism postoperatively. While in the PR group, three patients (7.1%) had intraoperative CSF leak, two patients (4.8%) had postoperative DI, three patients (7.1%) had postoperative electrolyte disturbance, four patients (9.5%) had temporary hypopituitarism postoperatively, and no cases experienced postoperative CSF leak. The intra- and post-operative complications were significantly higher in TR group then PR group (P IntraoperativeCSFleak = 0.004, P Post−operativeCSFleak =0.036, P TransientDI = 0.008, P Temporaryhypopituitarism = 0.002, P Permanenthypopituitarism = 0.036, P Electrolytedisturbance = 0.023). No significant differences in post-operative improvement and recurrence.Conclusions: EES is a safe and effective approach for the treatment of symptomatic RCC. Complete sucking out the cyst contents and partial resection of the cyst wall may be sufficient for treatment, and total resection of the cyst wall is associated with a higher incidence of complications.

scholarly journals HNF1A recruits UTX to activate a differentiation program that suppresses pancreatic cancer

2019 ◽  
Author(s):  
Mark Kalisz ◽  
Edgar Bernardo ◽  
Anthony Beucher ◽  
Miguel Angel Maestro ◽  
Natalia del Pozo ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Pancreatic Acinar Cells ◽  
Ductal Adenocarcinoma ◽  
Molecular Phenotype ◽  
Mesenchymal Transition ◽  
A Cell ◽  
Pancreatic Exocrine ◽  
Direct Genetic Evidence

AbstractDefects in transcriptional regulators of pancreatic exocrine differentiation have been implicated in pancreatic tumorigenesis, but the molecular mechanisms are poorly understood. The locus encoding the transcription factor HNF1A harbors susceptibility variants for pancreatic ductal adenocarcinoma (PDAC), while KDM6A, encoding the histone demethylase UTX, carries somatic mutations in PDAC. Here, we show that pancreas-specific Hnf1a null mutations phenocopy Utx deficient mutations, and both synergize with KrasG12D to cause PDAC with sarcomatoid features. We combine genetic, epigenomic and biochemical studies to show that HNF1A recruits UTX to genomic binding sites in pancreatic acinar cells. This remodels the acinar enhancer landscape, activates a differentiation program, and indirectly suppresses oncogenic and epithelial-mesenchymal transition genes. Finally, we identify a subset of non-classical PDAC samples that exhibit the HNF1A/UTX-deficient molecular phenotype. These findings provide direct genetic evidence that HNF1A-deficiency promotes PDAC. They also connect the tumor suppressive role of UTX deficiency with a cell-specific molecular mechanism that underlies PDAC subtype definition.

scholarly journals Solitary Pancreatic Metastasis From Breast Matrix-Producing Carcinoma: A First Case Report

2017 ◽  
Vol 102 (7-8) ◽  
pp. 294-298
Author(s):  
Yoshiyuki Kiyasu ◽  
Ken Hayashi ◽  
Go Miyahara ◽  
Makoto Narita
Keyword(s):  
Distal Pancreatectomy ◽  
Tumor Cells ◽  
Pancreatic Metastasis ◽  
Axillary Lymph ◽  
Histopathologic Examination ◽  
Axillary Metastasis ◽  
Epithelial Tumor ◽  
Tumor Biopsy ◽  
Pancreatic Metastases ◽  
First Case

Introduction: Breast matrix-producing carcinoma (MPC) is a rare histologic type. Pancreatic metastases from breast cancers are also rare. We report the first case of solitary pancreatic metastasis from breast MPC, treated with distal pancreatectomy. Case presentation: A 56-year-old woman presented with a 56-mm mass in her right breast and a swollen right axillary lymph node. Both lesions had characteristic early ring enhancement on dynamic magnetic resonance imaging (MRI). Tumor biopsy revealed MPC. She underwent total mastectomy and axillary clearance. On histopathologic examination, the tumor was composed of extracellular matrix with areas of osseous and chondroid differentiation without spindle cells or osteoclasts, surrounded by a dense population of glandular epithelial tumor cells. On immunohistochemical analysis, the tumor cells were positive for AE1/AE3 and cytokeratin 5/6. The final diagnosis was breast MPC with axillary metastasis. Two years later, dynamic MRI displayed a mass in the pancreatic body with early ring enhancement, suspicious for solitary breast MPC metastasis. Distal pancreatectomy was performed. Histopathologic examination revealed bone and cartilaginous matrix with necrosis, surrounded by pleomorphic sarcomatous tumor cells. Tumor cells showed less cytokeratin positivity than the primary breast lesion. These findings were compatible with breast MPC metastasis. Conclusion: Solitary pancreatic metastasis from breast MPC has not yet been reported. Surgical resection of malignant pancreatic metastases is controversial; however, considering that breast MPC has limited responsiveness to radiotherapy and chemotherapy, curative resection would be important in this case. The histopathologic features of MPC may reflect enhancement and calcification on radiologic studies.

scholarly journals Mechanism and regulation of folate uptake by pancreatic acinar cells: effect of chronic alcohol consumption

2010 ◽  
Vol 298 (6) ◽  
pp. G985-G993 ◽  
Author(s):  
Hamid M. Said ◽  
Lisa Mee ◽  
V. Thillai Sekar ◽  
Balasubramaniem Ashokkumar ◽  
Stephen J. Pandol
Keyword(s):  
Acinar Cells ◽  
Pancreatic Acinar Cell ◽  
Pancreatic Acinar Cells ◽  
Exocrine Function ◽  
Acid Uptake ◽  
Human Pancreas ◽  
Chronic Alcohol ◽  
Transport Inhibitors ◽  
Pancreatic Exocrine ◽  
One Carbon Metabolism

Folate plays an essential role in one-carbon metabolism, and a relationship exists between methyl group metabolism and pancreatic exocrine function. Little, however, is known about the mechanism(s) and regulation of folate uptake by pancreatic acinar cells and the effect of chronic alcohol use on the process. We addressed these issues using the rat-derived pancreatic acinar cell line AR42J and freshly isolated primary rat pancreatic acinar cells as models. We found [3H]folic acid uptake to be 1) temperature and pH dependent with a higher uptake at acidic than at neutral/alkaline pH; 2) saturable as a function of substrate concentration at both buffer pH 7.4 and 6.0; 3) inhibited by folate structural analogs and by anion transport inhibitors at both buffer pH 7.4 and 6.0; 4) trans-stimulated by unlabeled folate; 5) adaptively regulated by the prevailing extracellular folate level, and 6) inhibited by modulators of the cAMP/PKA-mediated pathway. Both the reduced folate carrier (RFC) and the proton-coupled folate transporter (PCFT) were found to be expressed in AR42J and in primary pancreatic acinar cells, as well as in native human pancreas with expression of RFC being higher than PCFT. Chronic alcohol feeding of rats (4 wk; 36% of calories from ethanol) led to a significant decrease in folate uptake by freshly isolated primary pancreatic acinar cells compared with cells from pair-fed controls; this effect was associated with a parallel decrease in the level of expression of RFC and PCFT. These studies reveal that folate uptake by pancreatic acinar cells is via a regulated carrier-mediated process which may involve RFC and PCFT. In addition, chronic alcohol feeding leads to a marked inhibition in folate uptake by pancreatic acinar cells, an effect that is associated with reduction in level of expression of RFC and PCFT.

Crambene induces pancreatic acinar cell apoptosis via the activation of mitochondrial pathway

2006 ◽  
Vol 291 (1) ◽  
pp. G95-G101 ◽  
Author(s):  
Yang Cao ◽  
Sharmila Adhikari ◽  
Abel Damien Ang ◽  
Marie Véronique Clément ◽  
Matthew Wallig ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Fas Ligand ◽  
Annexin V ◽  
Acinar Cells ◽  
Mitochondrial Pathway ◽  
Pancreatic Acinar Cell ◽  
Pancreatic Acinar Cells ◽  
Pancreatic Acini

We investigated the apoptotic pathway activated by crambene (1-cyano-2-hydroxy-3-butene), a plant nitrile, on pancreatic acinar cells. As evidenced by annexin V-FITC staining, crambene treatment for 3 h induced the apoptosis but not necrosis of pancreatic acini. Caspase-3, -8, and -9 activities in acini treated with crambene were significantly higher than in untreated acini. Treatment with caspase-3, -8, and -9 inhibitors inhibited annexin V staining, as well as caspase-3 activity, pointing to an important role of these caspases in crambene-induced acinar cell apoptosis. The mitochondrial membrane potential was collapsed, and cytochrome c was released from the mitochondria in crambene-treated acini. Neither TNF-α nor Fas ligand levels were changed in pancreatic acinar cells after crambene treatment. These results provide evidence for the induction of pancreatic acinar cell apoptosis in vitro by crambene and suggest the involvement of mitochondrial pathway in pancreatic acinar cell apoptosis.

Multiple isoforms of the ryanodine receptor are expressed in rat pancreatic acinar cells

2000 ◽  
Vol 351 (1) ◽  
pp. 265-271 ◽  
Author(s):  
Timothy J. FITZSIMMONS ◽  
Ilya GUKOVSKY ◽  
James A. McROBERTS ◽  
Edward RODRIGUEZ ◽  
F. Anthony LAI ◽  
...  
Keyword(s):  
Western Blot ◽  
Ryanodine Receptor ◽  
Acinar Cell ◽  
Acinar Cells ◽  
Protein Band ◽  
Pancreatic Acinar Cell ◽  
Pancreatic Acinar Cells ◽  
Rt Pcr ◽  
Pancreatic Acini ◽  
Cell Functions

Regulation of cytosolic Ca2+ is important for a variety of cell functions. The ryanodine receptor (RyR) is a Ca2+ channel that conducts Ca2+ from internal pools to the cytoplasm. To demonstrate the presence of the RyR in the pancreatic acinar cell, we performed reverse transcriptase (RT)-PCR, Western blot, immunocytochemistry and microscopic Ca2+-release measurements on these cells. RT-PCR showed the presence of mRNA for RyR isoforms 1, 2 and 3 in both rat pancreas and dispersed pancreatic acini. Furthermore, mRNA expression for RyR isoforms 1 and 2 was demonstrated by RT-PCR in individual pancreatic acinar cells selected under the microscope. Western-blot analysis of acinar cell immunoprecipitates, using antibodies against RyR1 and RyR2, showed a high-molecular-mass (> 250kDa) protein band that was much less intense when immunoprecipitated in the presence of RyR peptide. Functionally, permeablized acinar cells stimulated with the RyR activator, palmitoyl-CoA, released Ca2+ from both basolateral and apical regions. These data show that pancreatic acinar cells express multiple isoforms of the RyR and that there are functional receptors throughout the cell.

Primary extraskeletal osteosarcoma in the pineal region

2004 ◽  
Vol 101 (6) ◽  
pp. 1061-1064 ◽  
Author(s):  
Prajak Saesue ◽  
Ekawut Chankaew ◽  
Orasa Chawalparit ◽  
Nollaporn Sudasna Na Ayudhya ◽  
Sorranart Muangsomboon ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Bone Structure ◽  
Postoperative Radiotherapy ◽  
Obstructive Hydrocephalus ◽  
Pineal Region ◽  
Partial Resection ◽  
Tumor Control ◽  
Extraskeletal Osteosarcoma ◽  
Content Type ◽  
Imaging Results

✓ Primary extraskeletal osteosarcoma occurring in the brain parenchyma is distinctly uncommon, with only five cases having been reported. The authors describe the case of a 45-year-old man who presented with progressive headache and diplopia. Computerized tomography scanning and magnetic resonance imaging results revealed a pineal region tumor with obstructive hydrocephalus. The patient underwent partial resection of the tumor. The histological examination showed large pleomorphic tumor cells embedded in osteoid matrix. Immunohistochemical analysis was negative for various antibodies and thus excluded a glial, germ cell, epithelial, and lymphoid tumor origin. Only vimentin showed strong positivity in most of the tumor cells. Ultrastructurally, the tumor cells were rich in dilated rough endoplasmic reticula. Clear zones between tumor cells and osteoid matrix were observed. The osteoid matrix was made up of small collagen fibrils and hydroxyapatite deposits. The tumor was not attached to the bone structure of the skull. These findings are consistent with the features of extraskeletal osteosarcoma. Data from complete medical and radiological studies excluded a metastatic origin for this tumor. Partial resection and postoperative radiotherapy had provided tumor control at 11 months after the onset of symptoms. This is the first reported case of a primary extraskeletal osteosarcoma occurring in the pineal region.

scholarly journals SEC23B is required for pancreatic acinar cell function in adult mice

2017 ◽  
Vol 28 (15) ◽  
pp. 2146-2154 ◽  
Author(s):  
Rami Khoriaty ◽  
Nancy Vogel ◽  
Mark J. Hoenerhoff ◽  
M. Dolors Sans ◽  
Guojing Zhu ◽  
...  
Keyword(s):  
Acinar Cell ◽  
Cell Function ◽  
Acinar Cells ◽  
Cell Loss ◽  
Normal Function ◽  
Pancreatic Acinar Cell ◽  
Pancreatic Acinar Cells ◽  
Total Protein Content ◽  
Pancreatic Cell ◽  
Adult Mice

Mice with germline absence of SEC23B die perinatally, exhibiting massive pancreatic degeneration. We generated mice with tamoxifen-inducible, pancreatic acinar cell–specific Sec23b deletion. Inactivation of Sec23b exclusively in the pancreatic acinar cells of adult mice results in decreased overall pancreatic weights from pancreatic cell loss (decreased pancreatic DNA, RNA, and total protein content), as well as degeneration of exocrine cells, decreased zymogen granules, and alterations in the endoplasmic reticulum (ER), ranging from vesicular ER to markedly expanded cisternae with accumulation of moderate-density content or intracisternal granules. Acinar Sec23b deletion results in induction of ER stress and increased apoptosis in the pancreas, potentially explaining the loss of pancreatic cells and decreased pancreatic weight. These findings demonstrate that SEC23B is required for normal function of pancreatic acinar cells in adult mice.

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