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1. Antoine M, Khitrik-Palchuk M, Saif MW: Long-term survival in a patient with acinar cell carcinoma of pancreas. A case report and review of literature. JOP; 2007;8(6):783-9
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  • [Title] Long-term survival in a patient with acinar cell carcinoma of pancreas. A case report and review of literature.
  • CONTEXT: Acinar cell carcinoma of the pancreas is a rare malignancy that may have acinar and endocrine differentiation.
  • However, treatment protocols for acinar cell carcinoma of the pancreas have not been standardized.
  • CASE REPORT: We describe a case of a 44-year-old woman presenting with low grade fever and mid-abdominal tenderness secondary to a pancreatic mass with acinar and endocrine differentiation metastatic to the liver.
  • The patient received multiple lines of conventional and investigational chemotherapy regimens.
  • The patient developed Clostridium difficile colitis and septic shock resulting in death 37 months after the diagnosis of acinar cell carcinoma of the pancreas.
  • CONCLUSION: This is a case of acinar cell carcinoma of the pancreas with an endocrine component, treated with multiple chemotherapeutic agents, in which the patient survived 37 months after diagnosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Fatal Outcome. Female. Humans. Survival Analysis. Treatment Outcome

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  • (PMID = 17993731.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 28
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2. Erkan M, Kleeff J, Esposito I, Giese T, Ketterer K, Büchler MW, Giese NA, Friess H: Loss of BNIP3 expression is a late event in pancreatic cancer contributing to chemoresistance and worsened prognosis. Oncogene; 2005 Jun 23;24(27):4421-32
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  • In the present study, the hypoxia-inducible proapoptotic gene, BNIP3, was analysed in terms of expression, effect on patient survival, and chemo-responsiveness in pancreatic cancer cell lines. cDNA microarray, real-time light cycler quantitative polymerase chain reaction, laser-capture microdissection, and immunohistochemistry analyses were used to evaluate BNIP3 expression in normal and diseased pancreatic specimens.
  • BNIP3 mRNA levels were 3.0- and 6.3-fold lower in chronic pancreatitis and pancreatic cancer compared to the normal pancreas, respectively.
  • Microdissection analysis confirmed the reduction of BNIP3 expression in pancreatic cancer cells compared to normal duct cells.
  • By immunohistochemistry, BNIP3 was predominantly expressed in the acinar cells of the normal and diseased pancreas.
  • Hypoxia induced BNIP3 expression in four out of eight pancreatic cancer cell lines, while it was absent under normoxic and hypoxic conditions in the remaining four.
  • In conclusion, loss of BNIP3 expression occurs late in pancreatic cancer, contributes to resistance to chemotherapy, and correlates with a worsened prognosis.
  • [MeSH-major] Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Membrane Proteins / deficiency. Membrane Proteins / genetics. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins / deficiency. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Fluorouracil / pharmacology. Humans. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Survival Rate

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  • (PMID = 15856026.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BNIP3 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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3. Coyne JD, Dervan PA: Primary acinic cell carcinoma of the breast. J Clin Pathol; 2002 Jul;55(7):545-7
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  • [Title] Primary acinic cell carcinoma of the breast.
  • This paper describes an additional case, the first following chemotherapy, which in addition had an unfavourable prognosis.
  • It also describes alterations in cell morphology, immunohistochemistry, and ultrastructure following chemotherapy.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Acinar Cell / pathology. Neoplasms, Second Primary / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fatal Outcome. Female. Humans. Middle Aged. Prognosis

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  • [Cites] Histopathology. 2000 Mar;36(3):286-9 [10809602.001]
  • [Cites] Virchows Arch. 2000 Jul;437(1):74-81 [10963383.001]
  • [Cites] Am J Surg Pathol. 1998 Feb;22(2):221-30 [9500224.001]
  • [Cites] Hum Pathol. 1990 Feb;21(2):192-8 [2155174.001]
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  • [Cites] J Pathol. 1986 Apr;148(4):307-20 [3701496.001]
  • (PMID = 12101208.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1769684
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4. Mori S, Kondoh S, Ryozawa S, Urayama N, Satake M, Kitoh H, Yamashita H, Nakashima T, Gondo T, Okita K: [A case of AFP producing pancreatic acinar cell carcinoma diagnosed by EUS FNA and treated by intraarterial injection chemotherapy]. Nihon Shokakibyo Gakkai Zasshi; 2004 Feb;101(2):177-82
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  • [Title] [A case of AFP producing pancreatic acinar cell carcinoma diagnosed by EUS FNA and treated by intraarterial injection chemotherapy].
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / ultrasonography. Pancreas / pathology. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / ultrasonography. alpha-Fetoproteins / biosynthesis
  • [MeSH-minor] Adult. Biopsy, Fine-Needle. Cisplatin / administration & dosage. Drug Administration Schedule. Endosonography. Fluorouracil / administration & dosage. Humans. Injections, Intra-Arterial. Male

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  • (PMID = 15011443.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / alpha-Fetoproteins; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; CF regimen
  • [Number-of-references] 8
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5. Seki Y, Okusaka T, Ikeda M, Morizane C, Ueno H: Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent. Jpn J Clin Oncol; 2009 Nov;39(11):751-5
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  • [Title] Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent.
  • Pancreatic acinar cell carcinoma (ACC) is a comparatively rare tumor and account for approximately 1% of all cases of pancreatic cancer.
  • Clinical presentation is usually related to either local spread or metastasis.
  • The clinical features, especially those related to the prognosis and treatment outcomes, have not yet been fully clarified.
  • There are no established treatments for unresectable pancreatic ACC.
  • We administered gemcitabine monotherapy to four patients with ACC; however, the results were not satisfactory.
  • Disease control without obvious tumor shrinkage was observed in one patient.
  • On the other hand, fluoropyrimidine-based chemotherapy may have some activity against this tumor, because one of the three patients who received S-1 as second-line chemotherapy showed a partial response.
  • Prospective clinical trials are necessary to confirm the effectiveness of fluoropyrimidine for the treatment of pancreatic ACC.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Deoxycytidine / analogs & derivatives. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / drug therapy. Tegafur / therapeutic use
  • [MeSH-minor] Aged. Disease-Free Survival. Drug Combinations. Female. Humans. Male. Middle Aged. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19666905.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
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6. Shet T, Ramadwar M, Sharma S, Laskar S, Arora B, Kurkure P: An eyelid sialoblastoma-like tumor with a sarcomatoid myoepithelial component. Pediatr Dev Pathol; 2007 Jul-Aug;10(4):309-14
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  • [Title] An eyelid sialoblastoma-like tumor with a sarcomatoid myoepithelial component.
  • Nonround cell tumors are rare in children and often difficult to diagnose.
  • This article describes an 18-month-old child who presented with a mass on the outer aspect of the left eyelid.
  • Histologically, the tumor had nests of basaloid and relatively round cells with immature acinar or ductular structures similar to those seen in a conventional sialoblastoma, but these nests were embedded in a malignant spindle cell stroma.
  • This stroma on immunohistochemistry was marked with S-100 and cytokeratin, which, in combination with the pertinent ultrastructural evidence, indicated a myoepithelial differentiation.
  • Overall histologic features suggested a tumor similar to a sialoblastoma with sarcomatoid transformation of the myoepithelial component, hitherto not described in literature.
  • This tumor probably arose from the palpebral lobe of the lacrimal gland.
  • Postsurgery, the patient received chemotherapy (6 cycles of ifosfamide, vincristine, and doxorubicin hydrochloride [Adriamycin]) and local radiotherapy in view of residual disease.
  • Three months after completion of the treatment (1 year after surgery), the patient is well, without any local disease.
  • Awareness of this unusual histology of sialoblastoma will help in avoiding misdiagnosis and also refine treatment-related issues on this rare tumor.
  • [MeSH-major] Eyelid Neoplasms / pathology. Myoepithelioma / pathology. Sarcoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Combined Modality Therapy. Desmosomes / ultrastructure. Disease-Free Survival. Humans. Immunohistochemistry. Infant. Treatment Outcome

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  • (PMID = 17638426.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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7. Holen KD, Klimstra DS, Hummer A, Gonen M, Conlon K, Brennan M, Saltz LB: Clinical characteristics and outcomes from an institutional series of acinar cell carcinoma of the pancreas and related tumors. J Clin Oncol; 2002 Dec 15;20(24):4673-8
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  • [Title] Clinical characteristics and outcomes from an institutional series of acinar cell carcinoma of the pancreas and related tumors.
  • PURPOSE: Acinar cell carcinoma is a rare tumor of the exocrine pancreas.
  • Clinical features such as prognostic information, survival, and treatment outcomes are unknown.
  • PATIENTS AND METHODS: Thirty-nine patients with pathologically confirmed acinar neoplasms of the pancreas were identified between August 1981 and January 2001.
  • Demographic data, tumor characteristics, and treatment information were obtained by chart review.
  • Survival probabilities were estimated by using the Kaplan-Meier method and compared using the log-rank test.
  • On the basis of a univariate analysis, the patients' stage of disease correlated significantly with survival.
  • The median survival of patients with localized disease was 38 months, versus 14 months for those presenting with metastases (P = 0.03).
  • Patients who could be treated with surgery as first-line therapy had a longer survival time (36 months) compared with those who did not have surgery (14 months).
  • Two of 18 patients who received chemotherapy and three of eight patients who received radiation had a major response.
  • CONCLUSION: The survival curves suggest a more aggressive cancer than pancreatic endocrine neoplasms but one that is less aggressive than ductal adenocarcinoma of the pancreas.
  • Those patients who present with localized disease have a much better prognosis than those who present with metastases.
  • There is a high recurrence rate after complete surgical resection, suggesting that micrometastases are present even in localized disease and that adjuvant therapies may be indicated.
  • Chemotherapy and radiation afford disappointing results, however, and novel therapies are needed.
  • [MeSH-major] Carcinoma, Acinar Cell / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 12488412.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Dall'igna P, Cecchetto G, Bisogno G, Conte M, Chiesa PL, D'Angelo P, De Leonardis F, De Salvo G, Favini F, Ferrari A, TREP Group: Pancreatic tumors in children and adolescents: the Italian TREP project experience. Pediatr Blood Cancer; 2010 May;54(5):675-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • INTRODUCTION: Malignant pancreatic tumors are exceedingly rare in pediatric age and their clinical features and treatment usually go unappreciated by most pediatric oncologists and surgeons.
  • RESULTS: Tumor types were 4 pancreatoblastomas, 2 pancreatic carcinomas, 3 neoplasms of the endocrine pancreas, and 12 solid pseudopapillary tumors.
  • Three of the four patients with pancreatoblastoma had advanced disease at diagnosis and were given chemotherapy; at the time of this report, three patients were alive in first remission, while one died due to treatment toxicity.
  • Both the cases of pancreatic carcinoma had the acinar cell subtype and successfully underwent pancreaticoduodenectomy with complete tumor resection, remaining without evidence of disease at the time of this analysis.
  • The histological diagnoses of the three endocrine tumors were a malignant islet cell tumor, a gastrinoma, and a well-differentiated tumor.
  • All 12 patients with solid pseudopapillary tumors underwent complete tumor resection and were given no adjuvant treatment; 11 were alive in first remission, while one experienced a local and distant relapse 5 years after diagnosis.
  • CONCLUSIONS: Surgery remains the keystone of treatment for pancreatic tumors in pediatric age as in adults.
  • [MeSH-major] Pancreatic Neoplasms / epidemiology. Rare Diseases / epidemiology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Italy / epidemiology. Male. Prospective Studies. Treatment Outcome

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  • [CommentIn] Pediatr Blood Cancer. 2010 May;54(5):659-60 [20063425.001]
  • (PMID = 19998473.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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9. Cavallini A, Falconi M, Bortesi L, Crippa S, Barugola G, Butturini G: Pancreatoblastoma in adults: a review of the literature. Pancreatology; 2009;9(1-2):73-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Pancreatoblastoma is a very uncommon neoplasm in adults and its management represents a great challenge with regards to different treatment options.
  • Given the rarity of the disease, the aim of this study was to review our personal experience with adult pancreatoblastoma as well as the cases reported in the literature in order to support clinicians observing this entity.
  • After a search on the Medline database, a review of all cases was performed as well, focusing on clinical, radiological and hystopathological features and treatment options.
  • RESULTS: At our Institution, 2 adult males, 26 and 69 years old, underwent successful pancreatic resection for pancreatoblastoma.
  • In general, despite aggressive treatment, pancreatoblastoma in adults is associated with poorer outcome than in children, with a median survival time of 18.5 months.
  • Both our patients are disease free after 15 months (case 2) and 51 months (case 1).
  • The latter represents the most successful result in long-term disease-free survival.
  • CONCLUSION: Pancreatoblastoma is a rare neoplasm in adults.
  • The differential diagnosis includes nonfunctional pancreatic endocrine tumor, acinar cell carcinoma, solid pseudopapillary tumor and adenocarcinoma.
  • Surgical resection is the only treatment associated with long-term survival.
  • Chemotherapy may play a role as palliative treatment in advanced disease.
  • [MeSH-major] Carcinoma, Neuroendocrine. Pancreatic Neoplasms
  • [MeSH-minor] Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Humans. Male. Pancreaticoduodenectomy

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  • [Copyright] Copyright 2008 S. Karger AG, Basel and IAP.
  • (PMID = 19077457.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 36
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10. Kataoka Y, Nio Y, Yano S, Koike M, Hashimoto K, Itakura M, Itagaki T, Nishi T, Endo S, Higami T: [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin]. Gan To Kagaku Ryoho; 2006 Apr;33(4):525-8
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  • [Title] [Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin].
  • Pancreatic acinar cell carcinomas are rare, and little is reported on their chemotherapy.
  • We report a 49-year old male patient with pancreatic acinar cell carcinoma and multiple liver metastases, which responded to oral TS-1 and hepatic arterial infusion of cisplatin.
  • The patient underwent a partial hepatectomy, MCT abrasions and excision of the pancreatic tumor.
  • Postoperative pathological studies revealed metastases of acinar cell carcinoma to the liver and lymph nodes; the primary lesion was undetermined.
  • Abdominal CT one year after surgery revealed a pancreatic body tumor, which was surgically removed.
  • Pathological studies showed primary pancreatic acinar cell carcinoma, while previous metastases remained under control.
  • To summarize, TS-1 and cisplatin can be effective treatments for pancreatic acinar cell carcinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Cisplatin / administration & dosage. Combined Modality Therapy. Drug Administration Schedule. Drug Combinations. Hepatectomy. Humans. Infusions, Intra-Arterial. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Male. Middle Aged. Oxonic Acid / administration & dosage. Pyridines / administration & dosage. Tegafur / administration & dosage

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  • (PMID = 16612167.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Pyridines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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11. Morishima K, Hyodo M, Nihei Y, Sata N, Yasuda Y: [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1]. Gan To Kagaku Ryoho; 2010 Jan;37(1):127-9
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  • [Title] [A case of acinar cell carcinoma of pancreas with liver metastases treated effectively by S-1].
  • A 65-year-old man underwent a total gastrectomy and distal pancreatectomy for acinar cell carcinoma of the pancreas.
  • Multiple metastatic liver lesions were found one year postoperatively.
  • He was treated with S-1 chemotherapy over 34 months, and the tumors significantly reduced in size without severe side effects.
  • Four years after surgery, the liver metastases increased in size, associated with pain especially in the right upper quadrant.
  • Acinar cell carcinoma of the pancreas is a rare and highly malignant tumor, and there are few reports regarding treatment with chemotherapy.
  • Herein, we report a case with multiple liver metastases which were controlled by systemic chemotherapy using S-1.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / therapy. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / therapy. Tegafur / therapeutic use
  • [MeSH-minor] Aged. Drug Combinations. Gastrectomy. Hepatectomy. Humans. Male. Pancreatectomy

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  • (PMID = 20087046.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid
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12. Mueller SB, Micke O, Herbst H, Schaefer U, Willich N: Alpha-fetoprotein-positive carcinoma of the pancreas: a case report. Anticancer Res; 2005 May-Jun;25(3A):1671-4
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  • [Title] Alpha-fetoprotein-positive carcinoma of the pancreas: a case report.
  • We report on the case of a 19-year-old male with an alpha-fetoprotein (AFP)-producing acinar cell carcinoma of the pancreas.
  • Tumour markers other than AFP were normal.
  • Because of inoperability, a combined radiochemotherapy was initiated with a hyperfractionated dose of 44.8 Gy.
  • Initially, the tumour showed a good response to irradiation and 5-fluorouracil (5-FU) application, and therapy showed sufficient local control.
  • After combined radio-chemotherapy, AFP levels declined from about 3000 ng/ml (reference area: 0-7 ng/ml) to 18 ng/ml, but increased when widespread metastasis appeared.
  • The patient died 18 months after the initial therapy due to general tumour progression.
  • Originally, AFP was thought to be specific to hepatocellular carcinoma and germ cell tumours.
  • Rare cases of acinar cell carcinomas of the pancreas were found to express AFP.
  • When present, AFP expression is useful for diagnosis and as a marker for monitoring therapeutic response and recurrence of the disease.
  • [MeSH-major] Pancreatic Neoplasms / metabolism. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Humans. Male

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  • (PMID = 16033080.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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13. Kebir FZ, Lahmar A, Arfa N, Manai S, El Ouaer MA, Bouraoui S, Gouttalier C, Mezabi-Regaya S: Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis. Hepatobiliary Pancreat Dis Int; 2010 Feb;9(1):103-6
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  • [Title] Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis.
  • BACKGROUND: Acinar cell carcinoma (ACC) is a rare malignancy of the pancreas arising from acinar cells.
  • Unlike ductal adenocarcinoma, this tumor rarely presents with pancreatitis.
  • METHODS: We present a case of ACC associated with chronic calcifying pancreatitis, and a review of the literature focusing on diagnosis and management.
  • RESULTS: A 43-year-old man was proposed for Wirsungojejunal derivation for chronic pancreatitis.
  • Histopathological examination of the tissue extracted revealed an ACC.
  • Six months post-operatively, the patient developed hepatic metastasis and was treated with gemcitabine as palliative chemotherapy.
  • CONCLUSIONS: The clinical presentation of ACC of the pancreas is not specific and the tumor can be under-diagnosed when associated with chronic pancreatitis.
  • Data regarding course, treatment, and prognosis of this tumor are generally lacking.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatitis, Chronic / complications
  • [MeSH-minor] Adult. Humans. Male. Prognosis

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  • (PMID = 20133240.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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14. Diegel CR, Cho KR, El-Naggar AK, Williams BO, Lindvall C: Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma. Cancer Res; 2010 Nov 15;70(22):9143-52
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  • [Title] Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma.
  • Cross-talk between the canonical Wnt and mammalian target of rapamycin (mTOR) signaling pathways occurs at multiple levels in the cell and likely contributes to the oncogenic effects of these pathways in human cancer.
  • To gain more insight into the interplay between Wnt and mTOR signaling in salivary gland tumorigenesis, we developed a mouse model in which both pathways are constitutively activated by the conditional inactivation of the Apc and Pten tumor suppressor genes.
  • Loss of either Apc or Pten alone did not cause tumor development.
  • However, deletion of both genes resulted in the formation of salivary gland tumors with 100% penetrance and short latency that showed a remarkable morphologic similarity to human acinic cell carcinoma.
  • Treatment of tumor-bearing mice using the mTOR inhibitor rapamycin led to complete regression of tumors, indicating that tumor growth was dependent on continued mTOR signaling.
  • Importantly, we found that human salivary gland acinic cell carcinomas also express markers of activated mTOR signaling.
  • Together, these results suggest that aberrant activation of mTOR signaling plays a pivotal role in acinar cell neoplasia of the salivary gland.
  • Because rapamycin analogues are approved for treating other types of human malignancies, our findings suggest that rapamycin therapy should be evaluated for treating patients with salivary gland acinic cell carcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / deficiency. Carcinoma, Acinar Cell / metabolism. PTEN Phosphohydrolase / deficiency. Salivary Glands / metabolism. TOR Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Female. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Mice, 129 Strain. Mice, Knockout. Salivary Gland Neoplasms / genetics. Salivary Gland Neoplasms / metabolism. Salivary Gland Neoplasms / pathology. Signal Transduction / drug effects. Sirolimus / pharmacology. Tumor Burden / drug effects


15. Way D, Smith S, Sivendran S, Chie L, Kanovsky M, Brandt-Rauf PW, Chung DL, Michl J, Pincus MR: A protein kinase C inhibitor induces phenotypic reversion of ras-transformed pancreatic cancer cells and cooperatively blocks tumor cell proliferation with an anti- ras peptide. Cancer Chemother Pharmacol; 2002 Jun;49(6):429-37
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  • [Title] A protein kinase C inhibitor induces phenotypic reversion of ras-transformed pancreatic cancer cells and cooperatively blocks tumor cell proliferation with an anti- ras peptide.
  • We sought to determine whether CGP 41 251 blocks proliferation of ras-transformed mammalian cells and whether it synergistically exerts this effect with a ras-p21 peptide (residues 96-110) that interferes with the interaction of ras-p21 with JNK.
  • METHODS: We incubated ras-transformed rat pancreatic cancer TUC-3 cells and their normal counterpart pancreatic acinar BMRPA1 cells with CGP 42 251 alone and in the presence of the ras-p21 96-110 peptide, both in pre- and post-monolayer phases and determined cell counts and morphology and, for TUC-3 cells, their ability to grow on soft agar.
  • RESULTS: CGP 41 251, but not its inactive analogue, CGP 42 700, blocked pre-monolayer growth and reduced post-monolayer cell counts of both TUC-3 and BMRPA1 cells (IC(50) 0.28 and 0.35 micro M, respectively).
  • After 2 weeks of treatment, all the remaining TUC-3 cells exhibited the untransformed phenotype.
  • CONCLUSIONS: CGP 41 251 strongly blocks growth of ras-transformed pancreatic cancer cells by causing cell death and by induction of phenotypic reversion.
  • These findings suggest the possibility of using these two agents in anticancer therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Acinar Cell / pathology. Cell Transformation, Neoplastic / drug effects. Enzyme Inhibitors / pharmacology. Mitogen-Activated Protein Kinases / physiology. Oncogene Protein p21(ras) / physiology. Pancreatic Neoplasms / pathology. Peptide Fragments / pharmacology. Protein Kinase C / physiology. Staurosporine / pharmacology
  • [MeSH-minor] Cell Division / drug effects. Cells, Cultured / cytology. Cells, Cultured / drug effects. Humans. JNK Mitogen-Activated Protein Kinases. Phenotype. Protein Binding. Signal Transduction

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  • (PMID = 12107546.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 42500
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Peptide Fragments; 120685-11-2 / 4'-N-benzoylstaurosporine; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.2 / Oncogene Protein p21(ras); H88EPA0A3N / Staurosporine
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16. Santos-García D, Prieto JM, Lema M: [Clinical course of multiple sclerosis in patients treated with cytostatic drugs for cancer]. Rev Neurol; 2009 Jan 16-31;48(2):71-4
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  • [Title] [Clinical course of multiple sclerosis in patients treated with cytostatic drugs for cancer].
  • [Transliterated title] Evolución clínica de pacientes con esclerosis múltiple tratados con citostáticos por cáncer.
  • INTRODUCTION: The risk of side effects secondary to global and non-specific immune suppression has limited the systematic application of immunosuppressive therapy in multiple sclerosis (MS).
  • However, when a patient with MS develops a cancer, cytostatic drugs as treatment for the neoplastic process may induce improvement not only of the cancer but also of MS.
  • CASE REPORTS: We present a series of four women with clinically defined MS and subjected to cytostatic therapy (cisplatin, 5-fluorouracil, leukovorin, adriamycin, tamoxifen and anastrozole) after the development of cancer: two presented breast cancer, one colon cancer, and the fourth parotid gland malignancy.
  • Their clinical and neuroimaging course is described, following chemotherapy for the malignant disease.
  • The four women have improved and remain clinically stable after neoplastic treatment.
  • At the present one patient receives weekly intramuscular interferon-beta 1a, whereas the other did not received any treatment.
  • Immunosuppressive therapy could be a therapeutic option among patients with an aggressive clinical course.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Brain / pathology. Cytostatic Agents / therapeutic use. Multiple Sclerosis, Chronic Progressive / pathology. Multiple Sclerosis, Relapsing-Remitting / pathology. Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / complications. Adenocarcinoma / drug therapy. Adenocarcinoma / surgery. Adult. Breast Neoplasms / complications. Breast Neoplasms / drug therapy. Breast Neoplasms / radiotherapy. Breast Neoplasms / surgery. Carcinoma, Acinar Cell / complications. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Ductal, Breast / complications. Carcinoma, Ductal, Breast / drug therapy. Carcinoma, Ductal, Breast / radiotherapy. Carcinoma, Ductal, Breast / surgery. Cisplatin / administration & dosage. Colonic Neoplasms / complications. Colonic Neoplasms / drug therapy. Colonic Neoplasms / surgery. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Leucovorin / administration & dosage. Magnetic Resonance Imaging. Methylprednisolone / adverse effects. Methylprednisolone / therapeutic use. Nitriles / administration & dosage. Parotid Neoplasms / complications. Parotid Neoplasms / drug therapy. Parotid Neoplasms / radiotherapy. Parotid Neoplasms / surgery. Tamoxifen / administration & dosage. Triazoles / administration & dosage

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  • (PMID = 19173204.001).
  • [ISSN] 1576-6578
  • [Journal-full-title] Revista de neurologia
  • [ISO-abbreviation] Rev Neurol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytostatic Agents; 0 / Immunosuppressive Agents; 0 / Nitriles; 0 / Triazoles; 094ZI81Y45 / Tamoxifen; 2Z07MYW1AZ / anastrozole; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; X4W7ZR7023 / Methylprednisolone
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17. Chilosi M, Murer B: Mixed adenocarcinomas of the lung: place in new proposals in classification, mandatory for target therapy. Arch Pathol Lab Med; 2010 Jan;134(1):55-65
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  • [Title] Mixed adenocarcinomas of the lung: place in new proposals in classification, mandatory for target therapy.
  • CONTEXT: Lung cancer is one of the most frequent and lethal malignant neoplasms, but knowledge regarding the molecular basis of its pathogenesis is far from complete due to the striking diversity of different forms.
  • The current lung cancer classification (World Health Organization 2004) can efficiently distinguish clinically relevant major subtypes (small cell and non-small cell carcinomas), but its results are partly inadequate when facing prognostic and therapeutic decisions for non-small cell carcinomas, especially for the group of tumors classified as adenocarcinoma.
  • Lung adenocarcinoma comprises a heterogeneous group of tumors characterized by diverse morphologic features and molecular pathogenesis.
  • The category of mixed adenocarcinomas includes most adenocarcinomas (approximately 80%) and, according to World Health Organization criteria, is defined by the occurrence of a mixed array of different patterns (acinar, papillary, bronchioloalveolar, solid with mucin).
  • The histologic recognition of mixed adenocarcinoma is subjective and cannot consistently discriminate between responders and nonresponders to new targeted therapies (eg, tyrosine kinase inhibitors).
  • Diagnostic problems are mainly related to the poor reproducibility of histologic criteria, especially when applied in small biopsies and cytology, and to the difficulty in assigning each form to a precisely defined entity, as needed by updated therapeutic approaches.
  • In this evolving scenario, pathologists face new challenging diagnostic roles that include not only the precise morphologic definition of carcinoma subtypes but also their molecular characterization.
  • OBJECTIVE: To use a comprehensive critical analysis reconciling the overwhelming variety of biologic, morphologic, molecular, and clinical data to define new classification schemes for lung adenocarcinoma.
  • CONCLUSIONS: A new classification approach should redefine lung adenocarcinoma heterogeneity reconciling classic morphology, immunophenotypic and molecular features of neoplastic cells, and also relevant information provided by stem cell biology.
  • This approach, which has been already successfully applied in World Health Organization classification of other tumors, could improve the recognition of new reproducible profiles for adenocarcinomas, more closely and reproducibly related to clinical features and response to specific therapies, limiting the use of "wastebasket" categories such as mixed adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / classification. Adenocarcinoma / pathology. Lung Neoplasms / classification. Lung Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Cell Differentiation. Drug Therapy. Humans. Stem Cells / pathology. World Health Organization

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  • (PMID = 20073606.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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18. Fujii M, Sato H, Ogasawara T, Ando T, Tsujii S, Nagahori J, Komatsu Y, Matsuoka A: [A case of liver metastasis of pancreatic acinar cell carcinoma treated with S-1 and intra-arterial CDDP combination therapy]. Gan To Kagaku Ryoho; 2010 Oct;37(10):1987-90
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  • [Title] [A case of liver metastasis of pancreatic acinar cell carcinoma treated with S-1 and intra-arterial CDDP combination therapy].
  • A 55-year-old man underwent a pylorus-preserving pancreatoduodenectomy in August 2006 because of acinar cell carcinoma of the head of the pancreas.
  • Since abdominal CT revealed multiple liver metastases, we started systemic chemotherapy with gemcitabine (1,400 mg/body, day 1, 8, 15/q4w) in October 2006.
  • At the beginning of this treatment, it seemed to be a stable disease, but CT revealed tumor progression in January 2007.
  • Despite the change to oral chemotherapy with S-1 (100 mg/body, day 1-14/q3w), tumors were markedly enlarged in March 2007.
  • Therefore, we selected combination chemotherapy with oral S-1 and hepatic arterial infusion of CDDP (50 mg/body) as third-line.
  • After 6 months of treatment, abdominal CT revealed marked shrinkage of tumors, accompanied by a decrease in AFP level.
  • Though the patient died of hepatic failure in July 2009 (33 months after recurrence), he spent most of his time at home and worked as usual.
  • We suggest that combination chemotherapy with oral S-1 and intra-arterial CDDP can be effective treatments for pancreatic acinar cell carcinoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Cisplatin / therapeutic use. Liver Neoplasms / drug therapy. Oxonic Acid / therapeutic use. Pancreatic Neoplasms / drug therapy. Tegafur / therapeutic use
  • [MeSH-minor] Drug Combinations. Fatal Outcome. Humans. Infusions, Intra-Arterial. Male. Middle Aged. Recurrence. Tomography, X-Ray Computed

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  • (PMID = 20948270.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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19. Dobashi Y, Suzuki S, Matsubara H, Kimura M, Endo S, Ooi A: Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas. Cancer; 2009 Jan 1;115(1):107-18
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  • [Title] Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas.
  • One representative cascade is the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin (mTOR) pathway.
  • In AC, the frequency of p-mTOR staining was higher in the well differentiated subtype, in particular, in the acinar structure.
  • Conversely, in squamous cell carcinomas, mTOR activation was associated with a significantly higher frequency of lymph node metastasis.
  • First, mTOR may function not only in the proliferation of tumor cells as an effector molecule downstream of EGFR but also possibly in the morphogenesis of AC.
  • Second, the activation of mTOR may play a key role in metastasis in squamous cell carcinoma.
  • Overall, the current results demonstrated the potential for the application of rapamycin, an mTOR inhibitor, as an additional novel component of chemotherapy for a defined subset of patients with lung carcinoma.
  • [MeSH-major] Lung Neoplasms / metabolism. Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Humans. Neoplasm Metastasis. Neoplasms, Squamous Cell / metabolism. Neoplasms, Squamous Cell / pathology. Phosphorylation. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction. TOR Serine-Threonine Kinases


20. Grundmann O, Fillinger JL, Victory KR, Burd R, Limesand KH: Restoration of radiation therapy-induced salivary gland dysfunction in mice by post therapy IGF-1 administration. BMC Cancer; 2010 Aug 10;10:417
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  • [Title] Restoration of radiation therapy-induced salivary gland dysfunction in mice by post therapy IGF-1 administration.
  • Currently there are few xerostomia treatment approaches that provide long-term results without significant side effects.
  • To address this problem we investigated the potential for post-therapeutic IGF-1 to reverse radiation-induced salivary gland dysfunction.
  • METHODS: FVB mice were treated with targeted head and neck radiation and significant reductions in salivary function were confirmed 3 days after treatment.
  • On days 4-8 after radiation, one group of mice was injected intravenously with IGF-1 while a second group served as a vehicle control.
  • Stimulated salivary flow rates were evaluated on days 30, 60, and 90 and histological analysis was performed on days 9, 30, 60, and 90.
  • RESULTS: Irradiated animals receiving vehicle injections have 40-50% reductions in stimulated salivary flow rates throughout the entire time course.
  • Mice receiving injections of IGF-1 have improved stimulated salivary flow rates 30 days after treatment.
  • Parotid tissue sections were stained for amylase as an indicator of functioning acinar cells and significant reductions in total amylase area are detected in irradiated animals compared to unirradiated groups on all days.
  • Post-therapeutic injections of IGF-1 results in increased amylase-positive acinar cell area and improved amylase secretion.
  • Irradiated mice receiving IGF-1 show similar proliferation indices as untreated mice suggesting a return to tissue homeostasis.
  • CONCLUSIONS: Post-therapeutic IGF-1 treatment restores salivary gland function potentially through normalization of cell proliferation and improved expression of amylase.
  • These findings could aid in the rational design of therapy protocols or drugs for the treatment of radiation-induced salivary gland dysfunction in patients who have completed their anti-cancer therapies.

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  • (PMID = 20698985.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / K22 DE016096-01A1; United States / NIDCR NIH HHS / DE / DE16096; United States / NIDCR NIH HHS / DE / R01 DE018888; United States / NIDCR NIH HHS / DE / DE016096-01A1; United States / NIDCR NIH HHS / DE / K22 DE016096; United States / NIDCR NIH HHS / DE / DE018888-01A1; United States / NIDCR NIH HHS / DE / R01 DE018888-01A1; United States / NIDCR NIH HHS / DE / DE18888
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I
  • [Other-IDs] NLM/ PMC3087323
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21. Valentich MA, Eynard AR, Barotto NN, Díaz MP, Bongiovanni GA: Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced pancreatic tumors in rats. Food Chem Toxicol; 2006 Dec;44(12):2101-5
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  • We have previously shown that a single i.p. injection of nitrosomethylurea (NMU) in 3-day-old rats orally treated with the pesticide mancozeb (MZ), the flavonoid quercetin (Q) or in combination (MZ-Q) induces hyperplasia, atypical acinar cell proliferation and carcinoma in situ (CIS) in the pancreas.
  • The animals were fed on a diet supplemented by MZ or/and Q from the 10th day of pregnancy, thorough lactation and as pups after weaning until being sacrificed at week 24.
  • Saline injection with non-supplemented diet was used for the control group (SAL).
  • The experimental groups were (1) SAL (control), (2) SAL-PB, (3) NMU, (4) NMU-PB, (5) MZ-NMU, (6) MZ-NMU-PB, (7) Q-NMU, (8) Q-NMU-PB, (9) MZ-Q-NMU and (10) MZ-Q-NMU-PB.
  • Acinar cell hyperplasia was found in all groups of NMU-treated rats.
  • Dysplastic foci (DYS) were seen in groups 3-10 at the following percentages: 19, 48, 71, 27, 71, 35, 100 and 30, respectively.
  • CIS were recorded in groups 4 to 10 at percentages: 4, 36, 13, 11, 0, 16, 5, respectively.
  • CONCLUSION: Although PB, Q or MZ given alone enhance DYS lesions in NMU-treated rats, the MZ/Q/PB combined treatments may increase (mainly in males) or decrease (mainly in female) the DYS and CIS proportion.
  • [MeSH-major] Carcinogens / pharmacology. Carcinoma in Situ / chemically induced. Fungicides, Industrial / toxicity. Maneb / toxicity. Pancreatic Neoplasms / chemically induced. Phenobarbital / pharmacology. Quercetin / pharmacology. Zineb / toxicity
  • [MeSH-minor] Alkylating Agents / toxicity. Animals. Animals, Newborn. Disease Models, Animal. Drug Interactions. Drug Therapy, Combination. Female. Hyperplasia / chemically induced. Hyperplasia / pathology. Maternal Exposure. Maternal-Fetal Exchange. Methylnitrosourea / toxicity. Pregnancy. Rats. Rats, Wistar

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  • (PMID = 16965848.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Carcinogens; 0 / Fungicides, Industrial; 12427-38-2 / Maneb; 684-93-5 / Methylnitrosourea; 9IKM0I5T1E / Quercetin; R0HY55EB9E / mancozeb; X1FSB1OZPT / Zineb; YQE403BP4D / Phenobarbital
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22. Haas M, Laubender RP, Stieber P, Holdenrieder S, Bruns CJ, Wilkowski R, Mansmann U, Heinemann V, Boeck S: Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer. Tumour Biol; 2010 Aug;31(4):351-7
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  • [Title] Prognostic relevance of CA 19-9, CEA, CRP, and LDH kinetics in patients treated with palliative second-line therapy for advanced pancreatic cancer.
  • The objective of this study was to define prognostic serum biomarkers that could serve as surrogate survival endpoints during second-line treatment for advanced pancreatic cancer.
  • This retrospective single-center study included patients treated with second-line therapy for advanced exocrine pancreatic cancer.
  • A pretreatment value and at least one serial measurement during the first two cycles of second-line chemotherapy for CA 19-9, CEA, CRP, and LDH had to be available in order to evaluate the prognostic role of kinetics on overall survival.
  • A cutoff of a >20% increase from baseline during treatment was defined in order to form groups with suspected different outcomes.
  • The effect of serial biomarker changes on survival was modeled by Cox proportional hazards regression in univariate and multivariate analyses.
  • Overall, 70 patients treated with second-line therapy for advanced disease were included; 94% had distant metastases at treatment initiation.
  • Median time to progression was 2.7 months and median survival 5.4 months.
  • Univariate analysis found that an increase of >20% during treatment was significantly associated with a worse overall survival for CA 19-9 (HR 2.00, p = 0.018), CEA (HR 2.38, p = 0.004), and CRP (HR 3.06, p < 0.001).
  • These associations remained significant within multivariate analysis for CEA (HR 2.86, p = 0.001) and CRP (HR 3.20, p = 0.001).
  • Serum biomarker kinetics might serve as useful prognostic tools during second-line chemotherapy in advanced pancreatic cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. C-Reactive Protein / metabolism. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. L-Lactate Dehydrogenase / blood. Palliative Care. Pancreatic Neoplasms / blood
  • [MeSH-minor] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Biomarkers, Tumor / blood. Bone Neoplasms / blood. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Carcinoma, Acinar Cell / blood. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / pathology. Female. Humans. Kinetics. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / blood. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Peritoneal Neoplasms / blood. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Prognosis. Retrospective Studies. Survival Rate

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  • (PMID = 20480409.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 9007-41-4 / C-Reactive Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
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23. Park CC, Zhang H, Pallavicini M, Gray JW, Baehner F, Park CJ, Bissell MJ: Beta1 integrin inhibitory antibody induces apoptosis of breast cancer cells, inhibits growth, and distinguishes malignant from normal phenotype in three dimensional cultures and in vivo. Cancer Res; 2006 Feb 1;66(3):1526-35
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  • Current therapeutic approaches to cancer are designed to target molecules that contribute to malignant behavior but leave normal tissues intact. beta(1) integrin is a candidate target well known for mediating cell-extracellular matrix (ECM) interactions that influence diverse cellular functions; its aberrant expression has been implicated in breast cancer progression and resistance to cytotoxic therapy.
  • The addition of beta(1) integrin inhibitory agents to breast cancer cells at a single-cell stage in a laminin-rich ECM (three-dimensional lrECM) culture was shown to down-modulate beta(1) integrin signaling, resulting in malignant reversion.
  • To investigate beta(1) integrin as a therapeutic target, we modified the three-dimensional lrECM protocol to approximate the clinical situation: before treatment, we allowed nonmalignant cells to form organized acinar structures and malignant cells to form tumor-like colonies.
  • We then tested the ability of beta(1) integrin inhibitory antibody, AIIB2, to inhibit tumor cell growth in several breast cancer cell lines (T4-2, MDA-MB-231, BT474, SKBR3, and MCF-7) and one nonmalignant cell line (S-1).
  • We show that beta(1) integrin inhibition resulted in a significant loss of cancer cells, associated with a decrease in proliferation and increase in apoptosis, and a global change in the composition of residual colonies.
  • In contrast, nonmalignant cells that formed tissue-like structures remained resistant.
  • Moreover, these cancer cell-specific antiproliferative and proapoptotic effects were confirmed in vivo with no discernible toxicity to animals.
  • Our findings indicate that beta(1) integrin is a promising therapeutic target, and that the three-dimensional lrECM culture assay can be used to effectively distinguish malignant and normal tissue response to therapy.

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  • (PMID = 16452209.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 64786-09; United States / NCI NIH HHS / CA / R37 CA064786; United States / NCI NIH HHS / CA / P50 CA 58207-08; United States / NCI NIH HHS / CA / R01 CA124891; United States / NCI NIH HHS / CA / P50 CA058207; United States / NCI NIH HHS / CA / U54 CA112970; United States / NCI NIH HHS / CA / U54 CA112970-01; United States / NCI NIH HHS / CA / P50 CA 112970-01; United States / NCI NIH HHS / CA / CA064786-09; United States / NCI NIH HHS / CA / CA112970-01; United States / NCI NIH HHS / CA / R01 CA064786; United States / NCI NIH HHS / CA / R01 CA064786-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD29; 0 / Integrins; P188ANX8CK / Trastuzumab
  • [Other-IDs] NLM/ NIHMS225828; NLM/ PMC2933188
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24. Dudeja V, Vickers SM, Saluja AK: The role of heat shock proteins in gastrointestinal diseases. Gut; 2009 Jul;58(7):1000-9
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  • By virtue of this protective function, HSPs have been shown to prevent acinar cell injury in acute pancreatitis.
  • Further, inhibition of HSPs has been shown to induce apoptotic cell death in cancer cells suggesting that inhibition of HSPs has a potential to emerge as novel anti-cancer therapy, either as monotherapy or in combination with other chemotherapeutic agents.
  • The anti-apoptotic function and mechanism of various subtypes of HSPs as well as the current status of anti-HSP therapy are discussed in this review.

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  • (PMID = 19520890.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA124723-02; United States / NCI NIH HHS / CA / CA-131663; United States / NCI NIH HHS / CA / CA-124723; United States / NCI NIH HHS / CA / R21 CA131663; United States / NIDDK NIH HHS / DK / DK-58694; United States / NCI NIH HHS / CA / R01 CA124723; United States / NCI NIH HHS / CA / R01 CA124723-02; United States / NIDDK NIH HHS / DK / R01 DK058694
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Heat-Shock Proteins
  • [Number-of-references] 89
  • [Other-IDs] NLM/ NIHMS131974; NLM/ PMC2896385
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25. Rajpal S, Warren RS, Alexander M, Yeh BM, Grenert JP, Hintzen S, Ljung BM, Bergsland EK: Pancreatoblastoma in an adult: case report and review of the literature. J Gastrointest Surg; 2006 Jun;10(6):829-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatoblastoma in an adult: case report and review of the literature.
  • A 50-year-old man presented with progressive gastrointestinal symptoms.
  • An abdominal computed tomography scan demonstrated a 12 x 12-cm pancreatic mass involving the greater curvature of the stomach and multiple hypervascular hepatic metastases.
  • An initial fine needle aspiration of the pancreatic mass was nondiagnostic, and a subsequent fine needle aspiration of a liver mass was read as metastatic acinar cell carcinoma.
  • The patient underwent a palliative resection for tumor-associated pain and gastrointestinal hemorrhage that revealed a large pancreatic tumor invading through the full thickness of the colon at the splenic flexure and adherent to the posterior gastric wall.
  • The pathology from the distal pancreatectomy, splenectomy, partial gastrectomy, partial colectomy, and cholecystectomy unexpectedly supported a diagnosis of pancreatoblastoma with evidence for squamoid corpuscles as well as areas of acinar formation.
  • Despite multiple chemotherapy regimens, the patient's disease continued to progress in the liver and the lungs.
  • During the course of his therapy, the patient's serum alpha-fetoprotein levels and serum lipase levels rose concurrently, suggesting tumor-associated production of both of these factors.
  • Seventeen months after the diagnosis of metastatic pancreatoblastoma, the patient died from his disease.
  • Our case illustrates the fact that pancreatoblastomas are extremely difficult to diagnosis preoperatively.
  • In addition, our case demonstrates that pancreatoblastomas can be alpha-fetoprotein producing, hormone producing, and enzyme producing when it occurs in adults.
  • [MeSH-major] Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Abdominal Pain / etiology. Biopsy, Fine-Needle. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / secondary. Disease Progression. Humans. Immunohistochemistry. Liver Neoplasms / secondary. Male. Middle Aged. Nausea / etiology. Neoplasm Invasiveness. Satiety Response. Splenic Vein / diagnostic imaging. Splenic Vein / pathology. Stomach / pathology. Tomography, X-Ray Computed. Vomiting / etiology

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  • (PMID = 16769539.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
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26. Distler M, Rückert F, Dittert DD, Stroszczynski C, Dobrowolski F, Kersting S, Grützmann R: Curative resection of a primarily unresectable acinar cell carcinoma of the pancreas after chemotherapy. World J Surg Oncol; 2009;7:22
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  • [Title] Curative resection of a primarily unresectable acinar cell carcinoma of the pancreas after chemotherapy.
  • BACKGROUND: Acinar cell carcinoma (ACC) represents only 1-2% of pancreatic cancers and is a very rare malignancy.
  • At the time of diagnosis only 50% of the tumors appear to be resectable.
  • Reliable data for an effective adjuvant or neoadjuvant treatment are not available.
  • CASE PRESENTATION: A 65-year old male presented with obstructive jaundice and non-specific upper abdominal pain.
  • MRI-imaging showed a tumor within the head of the pancreas concomitant with Serum-Lipase and CA19-9.
  • During ERCP, a stent was placed.
  • Endosonographic fine needle biopsy confirmed an acinar cell carcinoma.
  • Laparotomy presented an locally advanced tumor with venous infiltration that was consequently deemed unresectable.
  • Chemotherapy was well tolerated, and no severe complications were observed.
  • Twelve months later, the patient was in stable condition, and CT-scanning showed an obvious reduction in the size of the tumor.
  • Histopathological examination gave evidence of a diffuse necrotic ACC-tumor, all resection margins were found to be negative.
  • Eighteen months later, the patient showed no signs of recurrent disease.
  • Therefore, neoadjuvant chemotherapy could be an option to reduce a primarily unresectable ACC to a point where curative resection can be achieved.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Acinar Cell / drug therapy. Carcinoma, Acinar Cell / surgery. Fluorouracil / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Aged. Combined Modality Therapy. Humans. Magnetic Resonance Imaging. Male. Neoplasm Staging. Prognosis. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19239719.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2657786
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27. Kitagami H, Kondo S, Hirano S, Kawakami H, Egawa S, Tanaka M: Acinar cell carcinoma of the pancreas: clinical analysis of 115 patients from Pancreatic Cancer Registry of Japan Pancreas Society. Pancreas; 2007 Jul;35(1):42-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas: clinical analysis of 115 patients from Pancreatic Cancer Registry of Japan Pancreas Society.
  • OBJECTIVES: Acinar cell carcinoma (ACC) of the pancreas is a rare tumor, and many aspects remain unclear because no large-scale clinical studies have been conducted.
  • METHODS: The present study investigated the clinical characteristics, treatment, and therapeutic outcomes of 115 patients registered in the Pancreatic Cancer Registry of the Japan Pancreas Society, and therapeutic plans were reviewed.
  • RESULTS: Although ACC has been associated with advanced stage and poor prognosis, this tumor was resectable in 76.5% of the patients, and the 5-year survival rate after resection was favorable, being 43.9%.
  • If ACC is unresectable or recurrent, chemotherapy is likely to prove useful.
  • Multidisciplinary therapy centering on the role of surgery will need to be established.
  • [MeSH-major] Carcinoma, Acinar Cell / mortality. Pancreatic Neoplasms / mortality. Registries / statistics & numerical data
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Female. Humans. Japan / epidemiology. Male. Middle Aged. Neoplasm Staging / statistics & numerical data. Prognosis. Survival Rate. Treatment Outcome

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  • (PMID = 17575544.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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