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1. Poggi G, Villani L, Bernardo G: Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma. Rare Tumors; 2009;1(1):e6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma.
  • Glucagonomas are pancreatic islet cell tumors arising from the alpha cells which belong to neuroendocrine tumors.
  • We report the case of a 52- year old man with a pancreatic glucagonoma with synchronous multiple liver metastases treated by surgery, transarterial chemoembolization, percutaneous radiofrequency thermal ablation and long-acting octreotide.
  • Our report confirms that a multimodal approach is very effective in patients with unresectable liver metastases from pancreatic endocrine tumors providing long-lasting palliation and probably prolonging survival.

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  • (PMID = 21139900.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2994425
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2. Okauchi Y, Nammo T, Iwahashi H, Kizu T, Hayashi I, Okita K, Yamagata K, Uno S, Katsube F, Matsuhisa M, Kato K, Aozasa K, Kim T, Osuga K, Nakamori S, Tamaki Y, Funahashi T, Miyagawa J, Shimomura I: Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS). Intern Med; 2009;48(12):1025-30
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  • [Title] Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS).
  • To identify the location of pancreatic endocrine tumors, arterial stimulation and venous sampling (ASVS) is known to be useful for insulinoma and gastrinoma, but its usefulness for glucagonoma has not been verified to date.
  • Here we report a case of glucagonoma that was diagnosed by ASVS with calcium loading, in which an approximately 6-fold increase of glucagon was observed in the splenic artery territory.
  • MEN1 gene analysis verified the presence of a mutation and the glucagonoma was confirmed after operation.
  • In conclusion, ASVS could be useful for the diagnosis of glucagonoma.
  • [MeSH-major] Glucagon / blood. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19525592.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9007-92-5 / Glucagon; SY7Q814VUP / Calcium
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3. Marko PB, Miljković J, Zemljic TG: Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors. Acta Dermatovenerol Alp Pannonica Adriat; 2005 Dec;14(4):161-4, 166
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors.
  • The computed tomographic scan of the abdomen revealed multiple hepatic tumors.
  • Histopathological examination of ultrasound-guided needle biopsy from a hepatic lesion demonstrated a neuroendocrine tumor.
  • Somatostatin-receptor scintigraphy with radio-labelled octreotide confirmed the likelihood of the neuroendocrine nature of the hepatic tumors and excluded the presence of other such lesions throughout the rest of the body, including the pancreas.
  • The serum glucagon level was markedly increased.
  • The diagnosis of necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors was made and therapy with the long-acting somatostatin analogue octreotide was started.
  • Having reached the final stage of the disease, which was further complicated by congestive heart failure, the patient died one year later.
  • As no autopsy was performed, we were unable to establish whether the hepatic tumors represented a metastatic process of previously undetected pancreatic glucagonoma or if they were extra-pancreatic glucagon-secreting tumors.
  • The correct diagnosis of necrolytic migratory erythema is important, since it might be the clue for early detection of glucagonoma or of extra-pancreatic glucagon-secreting tumors.
  • [MeSH-major] Dermatitis / etiology. Erythema / etiology. Liver Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Male. Middle Aged. Octreotide / therapeutic use

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  • (PMID = 16435046.001).
  • [ISSN] 1318-4458
  • [Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • [ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovenia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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4. Docherty HM, Hay CW, Ferguson LA, Barrow J, Durward E, Docherty K: Relative contribution of PDX-1, MafA and E47/beta2 to the regulation of the human insulin promoter. Biochem J; 2005 Aug 1;389(Pt 3):813-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Of these, the homoeodomain protein PDX-1 (pancreatic duodenal homeobox factor-1), the basic leucine zipper protein MafA and the basic helix-loop-helix heterodimer E47/BETA2 (beta-cell E box transactivator 2; referred to here as beta2) bind to important regulatory sites.
  • Mutagenesis of the PDX-1, MafA and E47/beta2 binding sites reduced promoter activity by 60, 74 and 94% respectively, in INS-1 beta-cells.
  • In the islet glucagonoma cell line alphaTC1.6, overexpression of PDX-1 and MafA separately increased promoter activity approx.
  • In HeLa cells, PDX-1 stimulated the basal promoter by approx.
  • PDX-1 was shown further to activate the endogenous insulin 1 gene in alphaTC1.6 cells, whereas MafA activated the insulin 2 gene.

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  • (PMID = 15862113.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / MAFA protein, human; 0 / Maf Transcription Factors, Large; 0 / NEUROD1 protein, human; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Tcf7l1 protein, rat; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein
  • [Other-IDs] NLM/ PMC1180732
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5. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • Those two would probably result in discovery of more glucagonomas and other neuroendocrine tumours without characteristic clinical syndromes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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6. Doi AM, Hill G, Seely J, Hailey JR, Kissling G, Bucher JR: alpha 2u-globulin nephropathy and renal tumors in national toxicology program studies. Toxicol Pathol; 2007 Jun;35(4):533-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] alpha 2u-globulin nephropathy and renal tumors in national toxicology program studies.
  • Chemically induced renal neoplasms in male rats, developed coincident with alpha(2u)-globulin nephropathy, are not considered predictive of risk to humans by the International Agency for Research on Cancer (IARC) and the U.S.
  • Criteria have been defined to establish the role of alpha(2u)-globulin nephropathy in renal carcinogenesis, based on a proposed mode of action involving sustained tubular cell proliferation resulting from alpha(2u)-induced nephropathy, with consequent development of neoplastic lesions.
  • Recent NTP studies demonstrated inconsistencies with this proposed mechanism, including in some cases, far weaker kidney tumor responses than expected based on the extent of alpha(2u)-globulin nephropathy.
  • NTP studies with decalin, propylene glycol mono-t-butyl ether and Stoddard solvent IIC included extended evaluations of alpha(2u)-related nephropathy, and were thus used in assessing the linkage between key events in 90-day studies with renal tumors in 2-year studies.
  • This review revealed no or at best weak associations of tumor responses with renal alpha(2u)-globulin concentrations, indices of cell turnover, or microscopic evidence of alpha(2u)-associated nephropathy in prechronic studies.
  • While tumor responses corresponded somewhat with a measure of cumulative alpha(2u)-associated nephropathy (linear mineralization of the papilla) at the end of the 2-year studies, the severity of chronic nephropathy was generally in best agreement with the pattern of tumor response.
  • These results suggest that while alpha(2u)-globulin nephropathy may contribute to the renal tumor response, the critical component(s) of the nephropathy most closely associated with the development of tumors could not be clearly identified in this review.
  • [MeSH-major] Alpha-Globulins / toxicity. Kidney Diseases / chemically induced. Kidney Neoplasms / chemically induced
  • [MeSH-minor] Animals. Carcinogens / toxicity. Cyclohexenes / toxicity. Databases, Factual. Endpoint Determination. Hydrocarbons / toxicity. Immunohistochemistry. Male. Naphthalenes / toxicity. Proliferating Cell Nuclear Antigen / metabolism. Propylene Glycols / toxicity. Rats. Rats, Inbred F344. Retrospective Studies. Terpenes / toxicity

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  • Hazardous Substances Data Bank. LIMONENE .
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  • (PMID = 17562486.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 ES999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / Carcinogens; 0 / Cyclohexenes; 0 / Hydrocarbons; 0 / Naphthalenes; 0 / Proliferating Cell Nuclear Antigen; 0 / Propylene Glycols; 0 / Terpenes; 0 / alpha 2u globulin; 57018-52-7 / propylene glycol mono-t-butyl ether; 8052-41-3 / Stoddard solvent; 88451Q4XYF / decalin; 9MC3I34447 / limonene
  • [Other-IDs] NLM/ NIHMS33523; NLM/ PMC2104517
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7. Choi YS, Hoory T, Monie A, Wu A, Connolly D, Hung CF: alpha-Galactosylceramide enhances the protective and therapeutic effects of tumor cell based vaccines for ovarian tumors. Vaccine; 2008 Oct 29;26(46):5855-63
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  • [Title] alpha-Galactosylceramide enhances the protective and therapeutic effects of tumor cell based vaccines for ovarian tumors.
  • In the current study, we characterized the therapeutic effect of tumor cell-based vaccines combined with the adjuvant, alpha-galactosylceramide (alpha-GalCer) using two different mouse models.
  • Our data suggests that treatment with alpha-GalCer led to an increase in the IFN-gamma serum levels in the presence or absence of irradiated mouse ovarian surface epithelial tumor cells (MOSEC).
  • Furthermore, administration of irradiated MOSEC tumor cells with adjuvant alpha-GalCer generated significant protective and therapeutic antitumor effects against MOSEC tumors in vaccinated C57BL/6 mice.
  • In addition, immune cells expressing CD4, CD8 or NK1.1 markers were found to be important for the protective antitumor effects generated by irradiated tumor cell-based vaccines combined with adjuvant alpha-GalCer.
  • We also found that treatment of a spontaneous ovarian cancer murine model, the Müllerian inhibiting substance type II receptor T antigen (TgMISIIR-TAg) transgenic mice with ovarian tumor cell-based vaccines combined with adjuvant alpha-GalCer led to prolonged survival as well as increased numbers of tumor-specific CD8+ T cells.
  • Therefore, irradiated tumor cell-based vaccines in combination with alpha-GalCer are capable of breaking immune tolerance and generating significant antitumor effects in two different mouse tumor models.

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  • (PMID = 18771701.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA113341-04; United States / NCI NIH HHS / CA / U19 CA113341; United States / NCI NIH HHS / CA / 1U19 CA113341-01; United States / NCI NIH HHS / CA / U19 CA113341-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cancer Vaccines; 0 / Cytokines; 0 / Galactosylceramides; 0 / alpha-galactosylceramide; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ NIHMS77539; NLM/ PMC2597163
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8. Williams LE, DeNardo GL, Meredith RF: Targeted radionuclide therapy. Med Phys; 2008 Jul;35(7Part1):3062-3068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Targeted radionuclide therapy (TRT) seeks molecular and functional targets within patient tumor sites.
  • A number of agents have been constructed and labeled with beta, alpha, and Auger emitters.
  • Lymphoma (B-cell) has been the primary clinical application.
  • Extension to solid tumors will require raising the macroscopic absorbed dose by several-fold over values found in present technology.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28513035.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Anatomy / Auger effect / Cancer / Computed tomography / Conformal radiation treatment / Dosimetry / Medical imaging / Positron emission tomography / Positron emission tomography (PET) / Proteins / Single photon emission computed tomography / Single photon emission computed tomography (SPECT) / Tissue engineering / Tissues / absorbed dose / alpha-particle sources / antibodies / beta-ray sources / blood / cellular biophysics / positron emission tomography / radiation therapy / radioisotopes / radionuclide therapy / single photon emission computed tomography / tumours
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9. Zhu X, Palmer MR, Makrigiorgos GM, Kassis AI: Solid-tumor radionuclide therapy dosimetry: New paradigms in view of tumor microenvironment and angiogenesis. Med Phys; 2010 Jun;37(6Part1):2974-2984

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solid-tumor radionuclide therapy dosimetry: New paradigms in view of tumor microenvironment and angiogenesis.
  • PURPOSE: The objective of this study is to evaluate requirements for radionuclide-based solid tumor therapy by assessing the radial dose distribution of beta-particle-emitting and alpha-particle-emitting molecules localized either solely within endothelial cells of tumor vasculature or diffusing from the vasculature throughout the adjacent viable tumor cells.
  • METHODS: Tumor blood vessels were modeled as a group of microcylindrical layers comprising endothelial cells (one-cell thick, 10μm diameter), viable tumor cells (25-cell thick, 250μm radius), and necrotic tumor region (>250μm from any blood vessel).
  • Sources of radioactivity were assumed to distribute uniformly in either endothelial cells or in concentric cylindrical 10μm shells within the viable tumor-cell region.
  • The EGSnrc Monte Carlo simulation code system was used for beta particle dosimetry and a dose-point kernel method for alpha particle dosimetry.
  • The radioactive decays required to deposit cytocidal doses (≥100Gy) in the vascular endothelial cells (endothelial cell mean dose) or, alternatively, at the tumor edge [tumor-edge mean dose (TEMD)] of adjacent viable tumor cells were then determined for six beta (P32, P33, C67u, Y90, I131, and R188e) and two alpha (A211t and B213i) particle emitters.
  • RESULTS: Contrary to previous modeling in targeted radionuclide therapy dosimetry of solid tumors, the present work restricts the region of tumor viability to 250μm around tumor blood vessels for consistency with biological observations.
  • For delivering ≥100Gy at the viable tumor edge (TEMD) rather than throughout a solid tumor, energetic beta emitters Y90, P32, and R188e can be effective even when the radionuclide is confined to the blood vessel (i.e., no diffusion into the tumor).
  • Furthermore, the increase in tumor-edge dose consequent to beta emitter diffusion is dependent on the energy of the emitted beta particles, being much greater for lower-energy emitters I131, C67u, and P33 relative to higher-energy emitters Y90, P32, and R188e.
  • Compared to alpha particle emitters, a ∼150-400 times higher number of beta-particle-emitting radioactive atoms is required to deposit the same dose in tumor neovasculature.
  • However, for the alpha particle emitters A211t and B213i to be effective in irradiating viable tumor-cell regions in addition to the vasculature, the carrier molecules must diffuse substantially from the vasculature into the viable tumor.
  • CONCLUSION: The presented data enable comparison of radionuclides used for antiangiogenic therapy on the basis of their radioactive decay properties, tumor neovasculature geometry, and tumor-cell viability.
  • For alpha particle emitters or low-energy beta particle emitters, the targeting carrier molecule should be chosen to permit the radiopharmaceutical to diffuse from the endothelial wall of the blood vessel, while for long-range energetic beta particle emitters that target neovasculature, a radiopharmaceutical that binds to newly formed endothelial cells and does not diffuse is preferable.
  • The work is a first approximation to modeling of tumor neovasculature that ignores factors such as pharmacokinetics and targeting capability of carrier molecules.
  • The calculations quantify the interplay between irradiation of neovasculature, the surrounding viable tumor cells, and the physical properties of commonly used radionuclides and can be used to assist estimation of radioactivity to be administered for neovasculature-targeted tumor therapy.

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  • [Copyright] © 2010 American Association of Physicists in Medicine.
  • (PMID = 28512969.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Alpha particles / Beta particles / Cancer / Cell growth / Cell processes / Diffusion / Dose-volume analysis / Dosimetry / Monte Carlo methods / Nutrients / Radiation treatment / Radioactivity / Radiopharmaceuticals / alpha particle emitter / blood vessels / cellular biophysics / dosimetry / electron emitter / neovasculature targeting / radiation therapy / targeted radionuclide therapy / tumor targeting / tumor vascularity / tumours
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10. Lobo I, Carvalho A, Amaral C, Machado S, Carvalho R: Glucagonoma syndrome and necrolytic migratory erythema. Int J Dermatol; 2010 Jan;49(1):24-9
Hazardous Substances Data Bank. GLUCAGON .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma syndrome and necrolytic migratory erythema.
  • The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.
  • The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.
  • The dermatologic and endocrine approach to this syndrome is discussed here.
  • Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Skin / pathology
  • [MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
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  • (PMID = 20465606.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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11. Yoshida M, Hayashi K, Ohara H, Miyabe K, Okumura F, Naitoh I, Tanaka H, Ando T, Nakazawa T, Takahashi S, Joh T: A case of pancreatic glucagonoma with erythema. Nihon Shokakibyo Gakkai Zasshi; 2010 Jun;107(6):930-6
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of pancreatic glucagonoma with erythema.
  • Full-body computed tomography (CT) scanning revealed a tumor mass in the tail of the pancreas; CT and magnetic resonance imaging (MRI) scans confirmed the presence of a spherical mass.
  • In contrast CT scans, although the contrast was gradually increased, no strong contrast differences were observed between the tumor and the surrounding tissue.
  • Blood test results revealed that the patient had a high glucagon level.
  • We diagnosed glucagonoma syndrome on the basis of the above results and resected the tail of the pancreas.
  • Pathological analysis revealed that the tumor cells had proliferated in ribbon-like, cord-like structures.
  • Immunostaining results were positive for glucagon, which confirmed our diagnosis.
  • [MeSH-major] Erythema / etiology. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20530930.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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12. Simonenko VB, Dulin PA, Beliaev LB, Makanin MA, Dem'ianenko AV, Zykova AA, Zhuravleva SI, Kolesnikova VN: [A case of pancreatic glucagonoma]. Klin Med (Mosk); 2007;85(8):67-70
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of pancreatic glucagonoma].
  • Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).
  • This functionally active, usually malignant tumor has typical clinical manifestations.
  • Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.
  • By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.
  • Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).
  • [MeSH-major] Glucagonoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17926496.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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13. Technau K, Renkl A, Norgauer J, Ziemer M: Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma. Eur J Dermatol; 2005 Mar-Apr;15(2):110-2
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.
  • Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.
  • However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.
  • Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.
  • In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.
  • We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications


14. Krysiak R, Okopień B, Herman ZS: [Rare pancreatic endocrine tumors]. Przegl Lek; 2008;65(4):209-16
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Rare pancreatic endocrine tumors].
  • [Transliterated title] Rzadkie guzy endokrynne trzustki.
  • Functional pancreatic endocrine tumors other than gastrinoma and insulinoma are quite rare.
  • Some of these tumors may be part of multiple endocrine neoplasia type one (MEN-1) syndrome or phakomatoses.
  • Depending on their cell type, functional pancreatic endocrine tumors may cause distinct clinical endocrine syndromes, such as the 'glucagonoma syndrome', Verner-Morrison syndrome and the 'somatostatinoma syndrome'.
  • Currently, the only curative treatment for islet cell tumors is complete surgical resection.
  • The medical treatment of endocrine pancreatic tumours consists of somatostatin analogues, chemotherapy, and interferon-alpha.
  • The purpose of this manuscript is to provide an overview of the contemporary etiopathogenesis, diagnosis and treatment of rare pancreatic endocrine tumors.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Somatostatinoma / diagnosis. Somatostatinoma / therapy. Vipoma / diagnosis. Vipoma / therapy
  • [MeSH-minor] Humans. Rare Diseases / diagnosis. Rare Diseases / therapy

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  • (PMID = 18724549.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 47
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15. Cruz-Bautista I, Lerman I, Perez-Enriquez B, Padilla LS, Torres CL, Lopez A, Cabrera T, Mehta RP, Gómez-Pérez FJ, Rull JA, Orozco-Topete R: Diagnostic challenge of glucagonoma: case report and literature review. Endocr Pract; 2006 Jul-Aug;12(4):422-6
Genetic Alliance. consumer health - Glucagonoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic challenge of glucagonoma: case report and literature review.
  • OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma.
  • METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma.
  • The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected.
  • Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures.
  • After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously.
  • The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma.
  • Subsequently, all related symptoms resolved, and the glucagon levels normalized.
  • CONCLUSION: The diagnosis of glucagonoma is often delayed.
  • Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / diagnosis
  • [MeSH-minor] Erythema / etiology. Humans. Hyperpigmentation / etiology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / ultrasonography. Pancreatic Neoplasms / ultrastructure. Regional Blood Flow. Tomography, X-Ray Computed. Wound Healing

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  • (PMID = 16901799.001).
  • [ISSN] 1530-891X
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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16. Pollak MN, Blouin M, Zakikhani M, Zhao Y, Algire C: Dependence of malignant proliferation associated with loss of PTEN on glucose concentration in the hyperglycemic range: Relevance to population studies linking hyperglycemia to unfavorable cancer prognosis. J Clin Oncol; 2009 May 20;27(15_suppl):11113

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 11113 Background: Loss of function of the tumor suppressor PTEN enhances malignant proliferation, but effects on cellular energy metabolism are less well characterized.
  • Population studies show that the metabolic syndrome (characterized by hyperglycemia, hyperinsulinism, and obesity) is increasingly prevalent in affluent societies and is associated with adverse outcome of many cancers, but the molecular basis for this is poorly understood.
  • METHODS: We used a tetracycline-inducible PTEN expression vector in the PTEN-null U251 glioma cell line to characterize effects of PTEN on cellular energy metabolism.
  • RESULTS: Forced expression of PTEN led to decreased phospho-AKT<sup>Ser473</sup>, decreased hexokinase II and HIF-1 alpha levels, and increased p53 levels.
  • While proliferation of PTEN-positive cells was insensitive to variation in glucose concentration at levels higher than 2.5 mM, PTEN-null cells significantly increased proliferation with increasing glucose concentration across normal physiologic range to ∼10 mM.
  • PTEN-null cells consumed more glucose than PTEN-positive cells (17.2 ± 2.0 vs. 8.8 ± 1.5 mM/million cells/48 hrs) and produced more lactate (35.9 ± 4.8 vs. 10.7 ± 2.3 mM/million cells/48 hrs).
  • When cells were incubated in presence of 2-deoxy-glucose (2-DG), growth inhibition was greater for PTEN-null cells (47.4% inhibition relative to control without 2-DG) compared with PTEN-positive cells (10.8% inhibition relative to control without 2-DG).
  • The data also suggest that PTEN status is relevant to selection of tumors likely to respond to experimental therapies that exploit glucose dependency.

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  • (PMID = 27963493.001).
  • [ISSN] 1527-7755
  • [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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17. Heinrich MC, Carden R, Griffith D, Liang C, Marino-Enriquez A, McKinley A, Presnell A, Fletcher JA: In vitro activity of sorafenib against imatinib- and sunitinib-resistant kinase mutations associated with drug-resistant GI stromal tumors. J Clin Oncol; 2009 May 20;27(15_suppl):10500

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro activity of sorafenib against imatinib- and sunitinib-resistant kinase mutations associated with drug-resistant GI stromal tumors.
  • : 10500 Background: Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are targets of imatinib (front-line therapy) or sunitinib (second-line therapy).
  • METHODS: Kinase mutants were biochemically profiled for SOR, SU, and IM sensitivity by measuring inhibition of kinase phosphorylation after drug treatment in mutant-expressing CHO cells.
  • We also tested the biochemical and cellular activity of SOR and IM against GIST cells derived from IM-resistant tumor clones.
  • To confirm these observations in a GIST cellular context, we tested the relative potency of IM and SU against two previously described IM-resistant GIST cell lines (GIST430: exon 11 + V654A, GIST48: exon 11 + D820A).
  • SOR was significantly more potent than IM against KIT in these cell lines.

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  • (PMID = 27963686.001).
  • [ISSN] 1527-7755
  • [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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18. Wagner AJ, Von Hoff DH, LoRusso PM, Tibes R, Mazina KE, Ware JA, Yan Y, Derynck MK, Demetri GD: A first-in-human phase I study to evaluate the pan-PI3K inhibitor GDC-0941 administered QD or BID in patients with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):3501

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A first-in-human phase I study to evaluate the pan-PI3K inhibitor GDC-0941 administered QD or BID in patients with advanced solid tumors.
  • GDC-0941 is a potent and selective oral inhibitor of the class I PI3K with 3 nM IC50 for the p110-alpha subunit in vitro and 28 nM IC50 in a cell-based pAKT assay and demonstrates broad activity in breast, ovarian, lung, and prostate cancer models.
  • METHODS: A Phase I dose escalation study using a 3+3 design was initiated in patients (pts) with solid tumors.
  • Potential signs of anti-tumor activity have been observed with a soft tissue sarcoma pt on-study for >176 days with stable disease (30 mg qd), an ovarian cancer pt with an on-study 2.8-fold decrease in CA-125 response to normal levels (30 mg bid) and a pt with endometrial cancer with a decrease in tumor FDG-PET uptake (80 mg qd).
  • CONCLUSIONS: GDC-0941 is generally well-tolerated with potential signs of anti-tumor activity.

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  • (PMID = 27961289.001).
  • [ISSN] 1527-7755
  • [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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19. Boyle H, You B, Fronton L, Ribba B, Girard P, Tranchand B, Tod M, Coquelin H, Droz J, Flechon A: Major prognostic value of modeled AUC&lt;sub&gt;hCG-AFP&lt;/sub&gt;, a dynamic kinetic marker characterizing tumor marker decline of nonseminomatous germ cell tumors (NSGCT) intermediate-poor-risk patients according to the IGCCCG. J Clin Oncol; 2009 May 20;27(15_suppl):5085

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Major prognostic value of modeled AUC<sub>hCG-AFP</sub>, a dynamic kinetic marker characterizing tumor marker decline of nonseminomatous germ cell tumors (NSGCT) intermediate-poor-risk patients according to the IGCCCG.
  • : 5085 Background: The level of human chorionic gonadotrophin (hCG) and alpha-foetoprotein (AFP) serum tumor marker is well established in NSGCT as prognostic factor, the relevance of marker kinetic analysis under treatment is still unclear.
  • AUC<sub>hCG-AFP</sub> was a significant prognostic factor in the univariate analysis on the 2 year PFS (100% vs 73.8% vs 67.7%, p = 0.035) as well as IGCCCG score (poor/intermediate risk groups), primary site (mediastinal/other) and HL<sub>hCG-AFP</sub>.

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  • (PMID = 27964275.001).
  • [ISSN] 1527-7755
  • [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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20. Massard C, Huguet H, Kramar A, Beyer J, Hartmann JT, Lorch A, Pico J, Rosti G, Droz J, Fizazi K: Cross-validation of a new prognostic index integrating tumor marker decline in patients with relapsed disseminated germ cell tumors. J Clin Oncol; 2009 May 20;27(15_suppl):5086

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cross-validation of a new prognostic index integrating tumor marker decline in patients with relapsed disseminated germ cell tumors.
  • : 5086 Background: Early serum tumor marker decline during chemotherapy was previously shown to be prognostic for progression-free survival (PFS) and overall survival (OS) in patients with relapsed GCT in an analysis of the IT94 phase III trial, which compared conventional chemotherapy versus high dose chemotherapy (Massard C, ASCO 2008.
  • METHODS: Data on tumor site, response to first line chemotherapy, serum tumor markers at baseline and after two cycles of chemotherapy were obtained from 235 patients accrued in the IT94 trial (training set) and from 181 patients included in phase III prospective trials of high-dose chemotherapy conducted by the German GCT group (Lorch et al, J Clin Oncol.
  • The change from baseline of serum alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCG) was assessed and classified into 'favorable marker decline' and 'unfavorable marker decline' group, as previously described (ASCO 2008.
  • In multivariate analysis of the IT94 trial, an unfavorable AFP decline and a mediastinal primary site were adverse prognostic factors for both PFS and OS, and this was confirmed in the validation set.
  • Among patients from the good prognostic group (favorable AFP decline and non-mediastinal primary site), those who were treated with high-dose chemotherapy had a better PFS (2-year PFS rate: 54% vs 37%; HR = 0.62; p = 0.017), and a trend for a better OS (2-year OS rate: 68% vs. 58%; HR = 0.77; p = 0.29) as compared to patients who were treated with conventional chemotherapy.
  • In contrast, there was no difference in outcome in patients from the poor prognostic group (unfavourable AFP decline and/or mediastinal primary site), whether they received conventional chemotherapy or high-dose chemotherapy.
  • CONCLUSIONS: AFP decline during the first 6 weeks of salvage chemotherapy and a mediastinal primary tumor site predict for PFS and OS in patients with relapsed disseminated GCT.

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  • (PMID = 27964274.001).
  • [ISSN] 1527-7755
  • [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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21. Lopez R, Gallardo E, Ruibal A, Leon L, Sanchez-Salmon A, Abdulkader I, Gude F, Curiel T, Barandela J, Gayoso L: HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients. J Clin Oncol; 2009 May 20;27(15_suppl):e22010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients.
  • : e22010 Background: Tumor hipoxia induces the up-regulation of several genes via the hipoxia-inducible transcription factors (HIF) 1 and 2.
  • HIF-2 alpha (HIF-2 α) and HIF-1 alpha (HIF-1α) are associated with the prognosis of operable NSCLC patients.
  • Sections were scored as positive if >10% of cells stained positively.
  • RESULTS: HIF- 1α expression was observed in 84/96 patients (34/39 adenocarcinomas and 50/57 squamous cell carcinomas), however it did not correlate with clinical stage (I-II: 41/45 vs III-IV: 44/51).
  • The maxSUV values of 18F-FDG-PET were higher (p:0,039) in HIF-1α -positive (17,1±8,6) than in negative tumors (11,8±4,4).
  • HIF-2 α expression was observed in 60/103 cases (27/42 adenocarcinomas and 33/61 squamous cell carcinomas) and it did not correlate with clinical stage ((I-II: 28/45 vs III-IV: 32/57).

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  • (PMID = 27963184.001).
  • [ISSN] 1527-7755
  • [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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22. Kamai T, Tomosugi N, Abe H, Yoshida K: Protein profiling of tumor tissues by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to discriminate between localized and metastatic renal cell carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e16098

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Protein profiling of tumor tissues by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to discriminate between localized and metastatic renal cell carcinoma.
  • : e16098 Background: We previously reported that mRNA of interferon-alpha receptor type 2 (IFNAR2) was upregulated in metastatic and IFN-a resistant renal cell carcinoma (RCC) in comparison to localized RCC or metastatic tumors with good response to IFN-a (BMC Cancer, 2007).
  • Protein profiling using human tumor tissues may give insight into cellular pathways leading to carcinogenesis and metastasis in RCC.
  • METHODS: We examined mRNAs expression for IFNAR2 in paired tumor and non-tumor samples from the surgical specimens of Japanese patients with RCC using a real-time reverse transcription polymerase chain reaction.
  • Then we selected representative five IFNAR2 upregulated clear cell carcinomas cases with metastatic tumor, five IFNAR2 upregulated metastatic sarcomatoid carcinomas, and five normal expression clear cell carcinomas with localized tumor.
  • We investigated protein profiling in the tumor tissues of above three groups using surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS) coupled with IMAC-Cu chips.
  • The heat map analysis based on the clustering distinguished completely metastatic tumors with IFNAR2 upregulated groups from localized tumors with IFNAR2 normal expression group.
  • Furthermore, the heat map discriminated metastatic sarcomatoid carcinomas from metastatic clear cell carcinomas with a sensitivity of 100% and a specificity of 80%.
  • CONCLUSIONS: SELDI-TOF MS profiling of tumor tissues can be applied to differentiate patients with three types of RCCs.

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  • (PMID = 27963090.001).
  • [ISSN] 1527-7755
  • [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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23. Oberkirchner U, Linder KE, Zadrozny L, Olivry T: Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide. Vet Dermatol; 2010 Oct;21(5):510-6
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  • [Title] Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide.
  • Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas.
  • In humans with glucagonoma-associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release.
  • In this report an 11-year-old golden retriever dog with pancreatic glucagonoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME.
  • The dog was later euthanized because of progressive metastatic disease.
  • In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma-associated NME.
  • This somatostatin analogue could be a valuable option to treat canine patients with non-resectable or relapsing pancreatic glucagonoma-associated NME.
  • [MeSH-major] Dog Diseases / drug therapy. Glucagonoma / veterinary. Necrolytic Migratory Erythema / veterinary. Octreotide / therapeutic use. Pancreatic Neoplasms / veterinary
  • [MeSH-minor] Animals. Anorexia / chemically induced. Anorexia / veterinary. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Dogs. Dose-Response Relationship, Drug. Lymph Nodes / pathology. Male. Paraneoplastic Syndromes / pathology. Paraneoplastic Syndromes / veterinary

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  • [Copyright] © 2010 The Authors. Journal compilation © 2010 ESVD and ACVD.
  • (PMID = 20500495.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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24. Gogacz M, Bogusiewicz M, Putowski L, Adamiak A, Wertel I, Jakowicki JA, Rechberger T: [Expression of tumor necrosis factor-alpha (TNF-alpha) on peritoneal fluid mononuclear cells in women with endometriosis]. Ginekol Pol; 2008 Jan;79(1):31-5
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  • [Title] [Expression of tumor necrosis factor-alpha (TNF-alpha) on peritoneal fluid mononuclear cells in women with endometriosis].
  • [Transliterated title] Ekspresja receptorów dla czynnika martwicy guza-alpha (TNF-alpha) na jednojadrzastych komórkach immunokompetentnych płynu otrzewnowego u kobiet z endometrioza.
  • OBJECTIVES: Tumor necrosis factor-alpha (TNF-alpha) plays a key role in the processes underlying the development of pelvic endometriosis.
  • TNF-alpha acts on target cells via two receptors: TNFR1(p55) and TNFR2(p75).
  • Depending on cell type and its activation state, ligand binding to TNF-alpha may induce activation and proliferation of the cells or promote apoptosis.
  • 14 patients with benign, non-inflammatory ovarian tumors composed the reference group.
  • Mononuclear cells have been isolated from peritoneal fluid, obtained during laparoscopy.
  • CONCLUSION: Higher percentage of peritoneal fluid macrophages expressing TNFR1 and TNFR2 proteins in endometriosis suggests dependence of these cells on TNF-alpha stimulation.
  • [MeSH-major] Ascitic Fluid / metabolism. Endometriosis / metabolism. Macrophages, Peritoneal / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism. T-Lymphocytes / metabolism

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  • (PMID = 18510047.001).
  • [ISSN] 0017-0011
  • [Journal-full-title] Ginekologia polska
  • [ISO-abbreviation] Ginekol. Pol.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II
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25. Werther M, Schmelz HU, Schwerer M, Sparwasser C: [Sclerosing Sertoli cell tumor of the testis: a rare tumor. Case report and review of the literature on the subtypes of Sertoli-cell tumor]. Urologe A; 2007 Nov;46(11):1551-6
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  • [Title] [Sclerosing Sertoli cell tumor of the testis: a rare tumor. Case report and review of the literature on the subtypes of Sertoli-cell tumor].
  • [Transliterated title] Sklerosierender Sertoli-Zell-Tumor des Hodens - ein seltener Tumor : Fallvorstellung und Literaturübersicht über die Subtypen des Sertoli-Zell-Tumors.
  • Sertoli cell tumors of the testis are extremely rare (0.4-1.5% of all testicular neoplasms) and have a heterogeneous pathology.
  • Histopathologically classic, large cell calcifying and sclerosing subtypes are differentiated.Up to now, 14 cases of sclerosing Sertoli cell tumor are known.
  • While no cases of sclerosing Sertoli cell tumor with a malignant course have been reported, both other subtypes have been found to be potentially malignant.
  • In the case of malignancy the prognosis is very poor, and it is difficult to select the best treatment because there is so little experience with this type of tumor.
  • Once the diagnosis of a Sertoli cell tumor has been confirmed, exact determination of the histological subtype is essential to allow appropriate risk-adapted therapy.
  • [MeSH-major] Sertoli Cell Tumor / diagnosis. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biomarkers, Tumor / blood. Biopsy. Diagnosis, Differential. Fatty Liver, Alcoholic / blood. Humans. Male. Neoplasm Staging. Sclerosis. Testis / pathology. Ultrasonography. alpha-Fetoproteins

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  • (PMID = 17898983.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
  • [Number-of-references] 20
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26. Peros G, Sakorafas GH, Konstantoudakis G, Giannopoulos GA, Petropoulou K, Parasi A: Duodeno-pancreatic neuroendocrine tumours. Eur J Cancer Care (Engl); 2010 May;19(3):393-402
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  • [Title] Duodeno-pancreatic neuroendocrine tumours.
  • Duodeno-pancreatic neuroendocrine tumours (DP-ETs) are increasingly diagnosed today due to the widespread use of modern imaging methods.
  • Duodeno-pancreatic endocrine tumours should be treated by radical surgical resection, which offers a high chance for cure when the disease is localized.
  • A high index of suspicion is required in these patients for the presence of a multiple endocrine neoplasia type syndrome.
  • Histological/immunohistochemical diagnosis was somatostatin-producing tumour in the first patient, oncocytic endocrine tumour positive for neurone-specific enolase and focally for chromogranin in the second patient, glucagonoma and pancreatic polypeptide-producing endocrine pancreatic tumour in the third patient, and gastrin, somatostatin, calcitonin, insulin and adrenocorticotropic hormone (ACTH)-producing tumour in the fourth.
  • The second patient died 6.5 years following surgery due to disseminated disease.
  • [MeSH-major] Duodenal Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biopsy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Proteins / metabolism. Treatment Outcome

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  • (PMID = 19708940.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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27. Kovács RK, Korom I, Dobozy A, Farkas G, Ormos J, Kemény L: Necrolytic migratory erythema. J Cutan Pathol; 2006 Mar;33(3):242-5
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  • The classical symptoms are associated with alpha-cell pancreatic islet cell tumor or 'glucagonoma'.
  • Generally, extracutaneous hallmarks of this disease include weight loss, diabetes, anaemia and diarrhoea.
  • OBSERVATION: We report a case of a 39-year-old woman with a 3-year history of recalcitrant psoriasiform eruption, who had no other associated symptoms on routine examination.
  • Abdominal computer tomography was performed, which revealed a tumor in the tail of the pancreas.
  • After distal resection of the pancreas her skin symptoms resolved in a few days time.
  • Histology was consistent with glucagonoma.
  • CONCLUSIONS: It is infrequent to have only necrolytic migratory erythema, hyperglucagonaemia and islet-cell tumor but no other extracutaneous symptoms in glucagonoma syndrome.
  • Skin symptoms are important, often they are the clue to the diagnosis of glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Glucagonoma / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Female. Humans. Necrosis. Paraneoplastic Syndromes. Treatment Outcome

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  • (PMID = 16466513.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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28. Kindmark H, Sundin A, Granberg D, Dunder K, Skogseid B, Janson ET, Welin S, Oberg K, Eriksson B: Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years. Med Oncol; 2007;24(3):330-7
Hazardous Substances Data Bank. GLUCAGON .

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  • [Title] Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years.
  • BACKGROUND: Glucagon-secreting endocrine pancreatic tumor is a rare disease, hence controlled studies on clinical management are lacking.
  • In an attempt to assess the efficacy of diagnostic and therapeutic measures in patients with glucagonoma, a retrospective study was performed using the archives of a tertiary care center.
  • PATIENTS AND METHODS: Records from 340 patients with endocrine pancreatic tumors were reassessed and 23 patients with malignant endocrine pancreatic tumor and elevated plasma glucagon levels were identified.
  • RESULTS: About 7% of patients with histologically verified tumors fullfilled our criteria for glucagonoma.
  • Only 22% of these patients had developed diabetes prior to the diagnosis of glucagonoma.
  • Seventy eight percent had metastatic disease to the liver at diagnosis.
  • During the study period, 11 patients died at a median of 80 months from diagnosis whereas 11 patients are still alive after a median follow up of 52 months.
  • CONCLUSIONS: Glucagonomas represent 7% of our comprehensive referral material of endocrine pancreatic tumors.
  • Necrolytic migratory erythema was a common finding (52%) and diabetes less frequent at presentation than previously reported.
  • Tumors were positive on somatostatin receptor scintigraphy and objective responses were seen to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Erythema / complications. Glucagonoma / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Glucagon / blood. Humans. Interferons. Liver Neoplasms / secondary. Male. Middle Aged. Receptors, Somatostatin / metabolism. Retrospective Studies. Sex Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 17873310.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 9007-92-5 / Glucagon; 9008-11-1 / Interferons
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29. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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30. McCluggage WG, Young RH: Ovarian sertoli-leydig cell tumors with pseudoendometrioid tubules (pseudoendometrioid sertoli-leydig cell tumors). Am J Surg Pathol; 2007 Apr;31(4):592-7
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  • [Title] Ovarian sertoli-leydig cell tumors with pseudoendometrioid tubules (pseudoendometrioid sertoli-leydig cell tumors).
  • The propensity for ovarian endometrioid adenocarcinomas to morphologically mimic Sertoli, Sertoli-Leydig, and granulosa cell tumors, is well known.
  • The converse situation, mimicry of an endometrioid neoplasm by a sex cord-stromal tumor, has not been emphasized.
  • In this report, we describe 9 ovarian Sertoli-Leydig cell tumors (5 well differentiated, 4 of intermediate differentiation) with areas containing hollow, sometimes dilated, tubules which resemble endometrioid glands; we refer to these as pseudoendometrioid tubules.
  • The tumors, all of which were unilateral except for one, ranged from 3.5 to 19 cm and were variously described as tan, pale, yellow, or gold.
  • The proportion of the tumor made up of pseudoendometrioid tubules ranged from 10% to >90%.
  • When widespread, their presence sometimes resulted in consideration of a borderline endometrioid adenofibroma or a well-differentiated endometrioid adenocarcinoma.
  • However, all the neoplasms contained typical Sertoli tubules and one or more of the characteristic patterns of Sertoli-Leydig cell tumors as well as Leydig cells, although the latter cells were inconspicuous in some cases.
  • Immunohistochemistry, performed in 4 cases, showed that the pseudoendometrioid tubules, as well as the more typical Sertoli cell elements, were either positive for alpha inhibin (3 of 4 cases) or calretinin (3 of 4 cases) or both, although sometimes focally so.
  • This report illustrates the potential for ovarian Sertoli-Leydig cell tumors to contain tubules with a pseudoendometrioid appearance which mimic a borderline or malignant endometrioid neoplasm.
  • The presence of more typical Sertoli cell elements and Leydig cells, an absence of squamous elements, endometriosis or associated adenofibroma, and the characteristic immunophenotype assist in diagnosis.
  • [MeSH-major] Ovarian Neoplasms / pathology. Sertoli-Leydig Cell Tumor / pathology
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / analysis. Carcinoma, Endometrioid / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Middle Aged

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  • (PMID = 17414107.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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31. Abreu Velez AM, Howard MS: Diagnosis and treatment of cutaneous paraneoplastic disorders. Dermatol Ther; 2010 Nov-Dec;23(6):662-75
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  • [Title] Diagnosis and treatment of cutaneous paraneoplastic disorders.
  • Cutaneous signs of these disorders afford clinicians opportunities for early diagnosis and treatment.
  • We aim to succinctly review the recognition, diagnosis, and treatment of selected cutaneous paraneoplastic diseases.
  • Skin disorders that may be associated with paraneoplastic syndromes include: cutaneous metastases, tripe palms, Sweet's syndrome, glucagonoma, Paget's disease and extramammary Paget's disease, acanthosis nigricans, Birt-Hogg-Dube syndrome, basal cell nevus syndrome, Bazex syndrome (acrokeratosis paraneoplastica), carcinoid syndrome, Cowden's disease(multiple hamartoma syndrome), dermatomyositis, erythema gyratum repens, ichthyosis aquisita, von Recklinghausen's disease, pityriasis rotunda, pyoderma gangrenosum, Quincke's edema (angioedema and paraneoplastic uricaria), paraneoplastic pemphigus, Degos' disease, superior vena cava syndrome, Werner's syndrome, diffuse normolipemic plane xanthomas, and yellow nail syndrome.
  • [MeSH-major] Paraneoplastic Syndromes / diagnosis. Paraneoplastic Syndromes / therapy. Skin Diseases / diagnosis. Skin Diseases / therapy

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054710.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
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32. Yu R, Nissen NN, Dhall D, Heaney AP: Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature. Pancreas; 2008 May;36(4):428-31
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  • [Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.
  • We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.
  • The patient's clinical presentation, diagnosis, treatment, pancreas pathology, and follow-up are reviewed.
  • A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.
  • She was initially diagnosed with glucagonoma, and the tumor was resected.
  • Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.
  • No pancreatic tumors recurred 36 months after surgery.
  • This is the third case of alpha-cell nesidioblastosis reported in the English literature.
  • Nesidioblastosis and hyperplasia of alpha cells should be considered in the differential diagnosis of hyperglucagonemia.
  • Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18437091.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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33. Lu J, Herrera PL, Carreira C, Bonnavion R, Seigne C, Calender A, Bertolino P, Zhang CX: Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development. Gastroenterology; 2010 May;138(5):1954-65
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  • [Title] Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development.
  • BACKGROUND & AIMS: The tumor suppressor menin is recognized as a key regulator of pancreatic islet development, proliferation, and beta-cell function, whereas its role in alpha cells remains poorly understood.
  • The purpose of the current study was to address this issue in relation to islet tumor histogenesis.
  • METHODS: We generated alpha cell-specific Men1 mutant mice with Cre/loxP technology and carried out analyses of pancreatic lesions developed in the mutant mice during aging.
  • RESULTS: We showed that, despite the alpha-cell specificity of the GluCre transgene, both glucagonomas and a large amount of insulinomas developed in mutant mice older than 6 months, accompanied by mixed islet tumors.
  • Interestingly, the cells sharing characteristics of both alpha and beta cells were identified shortly after the appearance of menin-deficient alpha cells but well before the tumor onset.
  • Using a genetic cell lineage tracing analysis, we demonstrated that insulinoma cells were directly derived from transdifferentiating glucagon-expressing cells.
  • CONCLUSIONS: Our work shows cell transdifferentiation as a novel mechanism involved in islet tumor development and provides evidence showing that menin regulates the plasticity of differentiated pancreatic alpha cells in vivo, shedding new light on the mechanisms of islet tumorigenesis.
  • [MeSH-major] Cell Transdifferentiation. Cell Transformation, Neoplastic / metabolism. Glucagon / metabolism. Glucagon-Secreting Cells / metabolism. Glucagonoma / metabolism. Insulinoma / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins / deficiency
  • [MeSH-minor] Age Factors. Aging / metabolism. Aging / pathology. Animals. Biomarkers / metabolism. Cell Fusion. Cell Lineage. Cell Proliferation. Gene Deletion. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genotype. Insulin / metabolism. Insulin-Secreting Cells / metabolism. Insulin-Secreting Cells / pathology. Mice. Mice, Knockout. Phenotype. Transcription Factors / metabolism


34. Arazi L, Cooks T, Schmidt M, Keisari Y, Kelson I: Treatment of solid tumors by interstitial release of recoiling short-lived alpha emitters. Phys Med Biol; 2007 Aug 21;52(16):5025-42
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  • [Title] Treatment of solid tumors by interstitial release of recoiling short-lived alpha emitters.
  • A new method utilizing alpha particles to treat solid tumors is presented.
  • Tumors are treated with interstitial radioactive sources which continually release short-lived alpha emitting atoms from their surface.
  • The atoms disperse inside the tumor, delivering a high dose through their alpha decays.
  • This work aims to demonstrate the feasibility of our method by measuring the activity patterns of the released radionuclides in experimental tumors.
  • Sources carrying (224)Ra activities in the range 10-130 kBq were used in experiments on murine squamous cell carcinoma tumors.
  • These included gamma spectroscopy of the dissected tumors and major organs, Fuji-plate autoradiography of histological tumor sections and tissue damage detection by Hematoxylin-Eosin staining.
  • Both physical and histological measurements confirmed the formation of a 5-7 mm diameter necrotic region receiving a therapeutic alpha-particle dose around the source.
  • The necrotic regions shape closely corresponded to the measured activity patterns. (212)Pb was found to leave the tumor through the blood at a rate which decreased with tumor mass.
  • Our results suggest that the proposed method, termed DART (diffusing alpha-emitters radiation therapy), may potentially be useful for the treatment of human patients.
  • [MeSH-major] Alpha Particles / therapeutic use. Brachytherapy / instrumentation. Brachytherapy / methods. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / radiotherapy. Dose Fractionation
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / radiation effects. Mice

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  • (PMID = 17671351.001).
  • [ISSN] 0031-9155
  • [Journal-full-title] Physics in medicine and biology
  • [ISO-abbreviation] Phys Med Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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35. Knigge U, Hansen CP: [Appendiceal carcinoid tumors and goblet cell carcinoids]. Ugeskr Laeger; 2010 May 31;172(22):1678-81
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  • [Title] [Appendiceal carcinoid tumors and goblet cell carcinoids].
  • Appendiceial carcinoid tumors (CAT) and goblet cell carcinoids (GCCAT) are rare.
  • Non-resectable CAT are treated with interferon-alpha, somatostatin analogs or radionuclides.
  • [MeSH-major] Appendiceal Neoplasms. Carcinoid Tumor. Goblet Cells

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  • (PMID = 20525467.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Denmark
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36. Kinoshita Y, Tajiri T, Souzaki R, Tatsuta K, Higashi M, Izaki T, Takahashi Y, Taguchi T: Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study. J Pediatr Hematol Oncol; 2008 Jun;30(6):447-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study.
  • BACKGROUND AND PURPOSE: The serum alpha-fetoprotein (AFP) level has been used as a tumor marker for hepatoblastoma, and malignant germ cell tumors in pediatric patients.
  • However, there are few reports dealing with various pediatric malignant tumors.
  • MATERIALS AND METHODS: From 2003 to 2006, two cases of hepatoblastoma, and 5 cases of germ cell tumor, all of which were neoinfantile, were treated in our department.
  • RESULTS: In all cases of hepatoblastoma and yolk sac tumor, both the total AFP and the L3 fraction were high, either before treatment or in the presence of malignant tumors.
  • DISCUSSION: Our results indicated that the level of the L3 fraction accurately confirmed the existence, or the malignant potential of hepatic tumor or germ cell tumor.
  • The L3 fraction is useful as a tumor marker during the neoinfantile period.
  • [MeSH-major] Biomarkers, Tumor / blood. Hepatoblastoma / blood. Liver Neoplasms / blood. Neoplasms, Germ Cell and Embryonal / blood. alpha-Fetoproteins / analysis

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  • (PMID = 18525461.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lectins; 0 / Protein Isoforms; 0 / alpha-Fetoproteins
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37. Dimov ND, Zynger DL, Luan C, Kozlowski JM, Yang XJ: Topoisomerase II alpha expression in testicular germ cell tumors. Urology; 2007 May;69(5):955-61
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  • [Title] Topoisomerase II alpha expression in testicular germ cell tumors.
  • OBJECTIVES: Inhibitors of topoisomerase II alpha (TopoIIalpha), an enzyme with a crucial role in DNA maintenance, are included in the chemotherapy protocols for testicular germ cell tumors (GCTs).
  • METHODS: Primary GCT specimens from 109 patients, including 57 seminomas and 52 mixed GCTs (41 embryonal carcinomas, 23 yolk sac tumors, 19 seminomas, 8 choriocarcinomas, 17 teratomas with immature elements, and 16 teratomas with mature elements), were obtained from our archives.
  • The metastatic lesions from 11 of the patients with mixed GCTs included seven teratomas with mature components, five embryonal carcinomas, one yolk sac tumor, one choriocarcinoma, and one teratoma with immature components.
  • RESULTS: Most embryonal carcinoma (100%), yolk sac tumor (95%), seminoma (88%), and choriocarcinoma (62%) components of the GCTs were TopoIIalpha immunoreactive.
  • CONCLUSIONS: The results of our study have shown that TopoIIalpha is expressed in most seminomas, embryonal carcinomas, yolk sac tumors, and choriocarcinomas, suggesting a possible mechanism of sensitivity of these components to TopoIIalpha inhibitors.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Biomarkers, Tumor / analysis. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / antagonists & inhibitors. DNA-Binding Proteins / metabolism. Neoplasms, Germ Cell and Embryonal / enzymology. Testicular Neoplasms / enzymology. Topoisomerase II Inhibitors
  • [MeSH-minor] Adolescent. Adult. Biopsy, Needle. Carcinoma, Embryonal / drug therapy. Carcinoma, Embryonal / enzymology. Carcinoma, Embryonal / pathology. Choriocarcinoma / drug therapy. Choriocarcinoma / enzymology. Choriocarcinoma / pathology. Endodermal Sinus Tumor / drug therapy. Endodermal Sinus Tumor / enzymology. Endodermal Sinus Tumor / pathology. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Sampling Studies. Seminoma / drug therapy. Seminoma / enzymology. Seminoma / pathology. Sensitivity and Specificity. Teratoma / drug therapy. Teratoma / enzymology. Teratoma / pathology. Treatment Outcome

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  • (PMID = 17482942.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Topoisomerase II Inhibitors; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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38. Farinola MA, Gown AM, Judson K, Ronnett BM, Barry TS, Movahedi-Lankarani S, Vang R: Estrogen receptor alpha and progesterone receptor expression in ovarian adult granulosa cell tumors and Sertoli-Leydig cell tumors. Int J Gynecol Pathol; 2007 Oct;26(4):375-82
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  • [Title] Estrogen receptor alpha and progesterone receptor expression in ovarian adult granulosa cell tumors and Sertoli-Leydig cell tumors.
  • The biologic role that estrogen receptor (ER) and progesterone receptor (PR) play in ovarian sex cord-stromal tumors is poorly understood.
  • Furthermore, immunohistochemical data on these hormone receptors in this group of neoplasms are limited and conflicting, with many reports suggesting that expression of ERalpha and/or PR is either infrequent or present at low levels in granulosa and Sertoli cell tumors.
  • Immunohistochemical staining for ERalpha and PR was performed in 69 ovarian sex cord-stromal tumors: 41 adult granulosa cell tumors and 28 Sertoli-Leydig cell tumors.
  • Extent of expression was scored based on the percentage of positive cells: 0, 5% or less; 1+, 6% to 25%; 2+, 26% to 50%; 3+, 51% to 75%; and 4+, 76% to 100%.
  • Estrogen receptor alpha and PR were frequently expressed in adult granulosa cell tumors (66% and 98%, respectively) and Sertoli-Leydig cell tumors (79% and 86%, respectively).
  • Diffuse (3+ or 4+) expression of PR was more common in adult granulosa cell tumors (68% vs. 36%; P = 0.013), whereas diffuse (3+ or 4+) expression of ERalpha was more frequent in Sertoli-Leydig cell tumors (50% vs. 20%; P = 0.010).
  • In cases positive for both markers, adult granulosa cell tumors exhibited a focal (1+ or 2+) ERalpha/diffuse (3+ or 4+) PR coordinate profile more commonly than Sertoli-Leydig cell tumors (52% vs. 18%; P = 0.02), whereas Sertoli-Leydig cell tumors displayed a diffuse (3+ or 4+) ERalpha/focal (1+ or 2+) PR profile more frequently than adult granulosa cell tumors (36% vs. 0%; P = 0.0007).
  • We conclude that expression of hormone receptors (based only on frequency of immunostaining) does not allow for distinction from other tumors in the differential diagnosis that are known to be frequently positive for ERalpha and PR such as endometrioid neoplasms.
  • Most adult granulosa cell tumors and Sertoli-Leydig cell tumors share overlapping patterns of expression of ERalpha and PR with each other, but a subset of cases in each tumor category exhibits unique ERalpha/PR immunoprofiles (eg, focal ERalpha/diffuse PR in adult granulosa cell tumors and diffuse ERalpha/focal PR in Sertoli-Leydig cell tumors).
  • These patterns of expression of ERalpha and PR may aid our understanding of the biologic differences between granulosa and Sertoli cell tumors.
  • [MeSH-major] Estrogen Receptor alpha / biosynthesis. Granulosa Cell Tumor / metabolism. Ovarian Neoplasms / metabolism. Receptors, Progesterone / biosynthesis. Sertoli-Leydig Cell Tumor / metabolism
  • [MeSH-minor] Carcinoma, Endometrioid / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry

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  • (PMID = 17885486.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Receptors, Progesterone
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39. Sato K, Takeuchi H, Kubota T: Pathology of intracranial germ cell tumors. Prog Neurol Surg; 2009;23:59-75
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  • [Title] Pathology of intracranial germ cell tumors.
  • Intra cranial germ cell tumors (GCTs) usually arise in midline structures, including the pineal or suprasellar regions of children and young adults.
  • The classification of GCTs includes germinoma, teratoma, yolk sac tumor, embryonal carcinoma, and choriocarcinoma.
  • However, intracranial GCTs are often of mixed histologic composition (mixed GCTs), and only germinoma and teratoma are likely to be encountered as pure tumor types.
  • Although GCTs are usually identified using conventional histological techniques, immunohistochemical studies are very useful for delineating these entities, using special markers such as human chorionic gonadotropin, alpha-fetoprotein, human placental alkaline phosphatase, cytokeratin, as well as c-kit and OCT4.
  • Ultrastructural examination is also useful in confirming the identity of these tumors.
  • Patients with Klinefelter syndrome or Down syndrome appear to be predisposed to the development of gonadal as well as intracranial germinomas.
  • [MeSH-major] Brain Neoplasms / pathology. Neoplasms, Germ Cell and Embryonal / pathology. Pineal Gland / pathology. Pinealoma / pathology
  • [MeSH-minor] Biomarkers, Tumor. Humans

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  • [Copyright] Copyright (c) 2009 S. Karger AG, Basel.
  • (PMID = 19329861.001).
  • [ISSN] 0079-6492
  • [Journal-full-title] Progress in neurological surgery
  • [ISO-abbreviation] Prog Neurol Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 35
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40. Gan HK, Seruga B, Knox JJ: Sunitinib in solid tumors. Expert Opin Investig Drugs; 2009 Jun;18(6):821-34
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  • [Title] Sunitinib in solid tumors.
  • BACKGROUND: Until recently, few treatments were available for renal cell carcinoma (RCC) and gastrointestinal stromal tumors (GIST).
  • Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET.
  • Other potential roles for this drug in RCC, GIST and other tumor types will be discussed.
  • Sunitinib also shows promise in several other tumor types that lack therapeutic options.
  • What remains less clear is its role in tumors that are not heavily dependent on a central pathogenetic pathway, especially if effective cytotoxic therapies exist.
  • Future clinical trials will clarify whether there is a role for sunitinib in these tumors, possibly in combination with cytotoxic agents.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Renal Cell / drug therapy. Gastrointestinal Stromal Tumors / drug therapy. Indoles / pharmacology. Indoles / therapeutic use. Kidney Neoplasms / drug therapy. Neoplasms / drug therapy. Pyrroles / pharmacology. Pyrroles / therapeutic use

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  • (PMID = 19453268.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 124
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41. Kostopoulou E, Angelidou S, Daponte A, Galani C, Chiotoglou I, Terzis A, Koukoulis G: Fascin can be an auxiliary immunomarker of ovarian granulosa cell tumors: comparison with calretinin and inhibin-alpha. Eur J Gynaecol Oncol; 2008;29(6):638-42
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  • [Title] Fascin can be an auxiliary immunomarker of ovarian granulosa cell tumors: comparison with calretinin and inhibin-alpha.
  • The histopathologic diagnosis of granulosa cell tumor adult type (AGCT) can be supported by the use of established immunomarkers such as inhibin-alpha and calretinin.
  • Previously unreported data is presented on the detection of fascin in AGCT, in nonneoplastic granulosa cells and in other types of sex-cord stromal tumors.
  • In addition, by staining a panel of various tumors, potentially included in the differential diagnosis of AGCT, we assessed the value of fascin as an auxiliary AGCT immunomarker.
  • Intense and strong fascin staining may assist in cases with ambiguous calretinin or inhibin-alpha staining.
  • On the contrary, absence of fascin should question a provisional morphologic diagnosis of AGCT.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carrier Proteins / analysis. Granulosa Cell Tumor / diagnosis. Microfilament Proteins / analysis. Ovarian Neoplasms / diagnosis

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  • (PMID = 19115695.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / Carrier Proteins; 0 / FSCN1 protein, human; 0 / Microfilament Proteins; 0 / S100 Calcium Binding Protein G; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins
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42. Yin RT, Peng ZL, Yang KX, Kang DY: [Survivin expression in ovarian germ cell tumors]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2007 Mar;38(2):243-5
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  • [Title] [Survivin expression in ovarian germ cell tumors].
  • OBJECTIVE: To investigate the relationship between the expression of survivin and the development of ovarian germ cell tumors (OGCT).
  • METHODS: Survivin expressions in normal ovaries (n = 10) and ovarian germ cell tumors (n = 29) were detected with labelled streptavidin biotin method.
  • Survivin protein was found in the cytoplasm and/or the nuclear of cells of 58.6% (17/29) of the ovarian germ cell tumor samples (P < 0.05).
  • There was no significant correlations between surviving protein and the pathologic types, stage, lymphonode metastasis, AFP and volume of ascites of the tumors (P > 0.05).
  • CONCLUSION: High expression of survivin protein may trigger the pathogenesis of the ovarian germ cell tumors.
  • [MeSH-major] Microtubule-Associated Proteins / metabolism. Neoplasms, Germ Cell and Embryonal / genetics. Ovarian Neoplasms / genetics
  • [MeSH-minor] Ascites / complications. Female. Gene Expression Regulation, Neoplastic. Humans. Inhibitor of Apoptosis Proteins. Lymphatic Metastasis / genetics. Middle Aged. Neoplasm Staging. Young Adult. alpha-Fetoproteins / metabolism

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  • (PMID = 17441339.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / alpha-Fetoproteins
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43. Thews O, Lambert C, Kelleher DK, Biesalski HK, Vaupel P, Frank J: Possible protective effects of alpha-tocopherol on enhanced induction of reactive oxygen species by 2-methoxyestradiol in tumors. Adv Exp Med Biol; 2005;566:349-55
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  • [Title] Possible protective effects of alpha-tocopherol on enhanced induction of reactive oxygen species by 2-methoxyestradiol in tumors.
  • Several non-surgical tumor treatment modalities produce their cytotoxic activity by generating reactive oxygen species (ROS).
  • The aim of the present study was to analyze the impact of (i) inhibiting SOD using 2-methoxyestradiol (2-ME), or (ii) application of alpha-tocopherol, on the cellular damage induced by hyperthermia (HT) in experimental tumors.
  • DS-sarcoma cells grew either in culture or as solid tumors subcutaneously implanted in rats.
  • In vitro, DS-cells were incubated with 2-ME, and cell proliferation, ROS formation, lipid peroxidation and apoptosis were measured.
  • In vivo, DS-sarcomas were treated with a ROS-generating hyperthermia combined with 2-ME or alpha-tocopherol application.
  • In vivo, ROS-generating hyperthermia led to local tumor control in 23% of the animals.
  • Application of alpha-tocopherol was found to have no effect on local tumor control, either in combination with ROS-generating hyperthermia or when 2-ME was additionally applied.
  • Inhibition of SOD during ROS-generating hyperthermia results in pronounced cell injury and an improved local tumor control whereas exogenously applied vitamin E seems not to have an impact on oxidative stress.
  • [MeSH-major] Estradiol / analogs & derivatives. Reactive Oxygen Species / metabolism. Sarcoma, Experimental / drug therapy. Sarcoma, Experimental / metabolism. alpha-Tocopherol / pharmacology
  • [MeSH-minor] Animals. Antioxidants / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Enzyme Inhibitors / pharmacology. In Vitro Techniques. Lipid Peroxidation / drug effects. Male. Oxidative Stress / drug effects. Rats. Rats, Sprague-Dawley. Superoxide Dismutase / antagonists & inhibitors

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  • (PMID = 16594172.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Enzyme Inhibitors; 0 / Reactive Oxygen Species; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol; EC 1.15.1.1 / Superoxide Dismutase; H4N855PNZ1 / alpha-Tocopherol
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44. Willoughby V, Sonawala A, Werlang-Perurena A, Donner LR: A comparative immunohistochemical analysis of small round cell tumors of childhood: utility of peripherin and alpha-internexin as markers for neuroblastomas. Appl Immunohistochem Mol Morphol; 2008 Jul;16(4):344-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparative immunohistochemical analysis of small round cell tumors of childhood: utility of peripherin and alpha-internexin as markers for neuroblastomas.
  • Immunohistochemical study of neuroblastomas, Ewing sarcomas, rhabdomyosarcomas, and Wilms tumors demonstrate specific expression of peripherin and alpha-internexin in 20/22 and 6/22 cases of neuroblastomas, respectively.
  • Microtubule-associated protein 1B (MAP 1B) was strongly and diffusely expressed in all 22 cases of neuroblastomas, but was also focally or multifocally expressed in 9/12 rhabdomyosarcomas and also in the blastema and stroma of 8/11 Wilms tumors.
  • All rhabdomyosarcomas strongly and diffusely express nestin, but this marker was also expressed, multifocally, in 15/22 neuroblastomas and also in the blastema and stroma of all 11 Wilms tumors.
  • In contrast, all 7 cases of Ewing sarcoma were negative for peripherin, MAP 1B, alpha-internexin, NeuN, and nestin.
  • Our results confirm that peripherin and alpha-internexin are neuroblastoma markers useful for the differential diagnostic work-up of small round cell tumors of childhood.
  • Strong diffuse immunoreactivity for MAP 1B favors a diagnosis of neuroblastoma, whereas strong diffuse immunoreactivity for nestin favors a diagnosis of rhabdomyosarcoma.

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  • (PMID = 18528283.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Intermediate Filament Proteins; 0 / Membrane Glycoproteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / PRPH protein, human; 0 / Peripherins; 0 / alpha-internexin
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45. Owens DM, Broad S, Yan X, Benitah SA, Watt FM: Suprabasal alpha 5 beta1 integrin expression stimulates formation of epidermal squamous cell carcinomas without disrupting TGFbeta signaling or inducing spindle cell tumors. Mol Carcinog; 2005 Sep;44(1):60-6
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  • [Title] Suprabasal alpha 5 beta1 integrin expression stimulates formation of epidermal squamous cell carcinomas without disrupting TGFbeta signaling or inducing spindle cell tumors.
  • During epidermal chemical carcinogenesis benign papillomas convert to squamous cell carcinomas, some of which undergo epithelial-mesenchymal conversion to highly malignant spindle cell tumors.
  • TGFbeta inhibits early stages of carcinogenesis but promotes the spindle cell phenotype in later stages.
  • One hallmark of spindle cell tumors is upregulation of the alpha 5 beta 1 integrin fibronectin receptor.
  • To examine the significance of altered alpha 5 beta1 integrin expression, we induced tumors in transgenic mice expressing alpha 5 beta1 in the suprabasal epidermal layers.
  • Invalpha 5 beta1 mice developed threefold more papillomas and squamous cell carcinomas than wild-type (Wt) littermates; however, no spindle cell tumors or increased metastases were observed.
  • Suprabasal expression of the alpha 6 beta 4 integrin increases squamous cell carcinoma formation and decreases TGFbeta sensitivity while alpha 3 beta1 may have the opposite effect.
  • In contrast, nuclear phosphoSmad2 labeling in Invalpha 5 beta1 epidermis and tumors was indistinguishable from Wt, and suprabasal alpha 5 beta1 did not block TGFbeta-induced Smad2/3 translocation or growth inhibition in cultured keratinocytes.
  • We conclude that upregulation of alpha 5 beta1 does not predispose the epidermis to undergo conversion to spindle cell tumors and that the mechanism by which alpha 5 beta1 influences susceptibility to carcinogenesis is independent of perturbed TGFbeta signaling.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cell Transformation, Neoplastic / pathology. Gene Expression Regulation, Neoplastic. Integrin alpha5beta1 / metabolism. Signal Transduction. Transforming Growth Factor beta / metabolism

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15924349.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA75638
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Integrin alpha5beta1; 0 / Smad2 Protein; 0 / Smad2 protein, mouse; 0 / Smad3 Protein; 0 / Smad3 protein, mouse; 0 / Trans-Activators; 0 / Transforming Growth Factor beta
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46. Völkl TM, Langer T, Aigner T, Greess H, Beck JD, Rauch AM, Dörr HG: Klinefelter syndrome and mediastinal germ cell tumors. Am J Med Genet A; 2006 Mar 1;140(5):471-81
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  • [Title] Klinefelter syndrome and mediastinal germ cell tumors.
  • Precocious puberty is not a typical manifestation of patients with Klinefelter syndrome (KS).
  • However, there is an increased incidence of mediastinal germ cell tumors (M-GCT) in KS, whereas the discussion of a generally higher tumor risk in this condition is still controversial.
  • A rare subgroup of KS patients consists of prepubertal children with precocious puberty due to human chorionic gonadotropin (hCG)-producing M-GCTs.
  • Laboratory analyses (suppressed gonadotropins, elevated testosterone) and thoracic CT demonstrated a beta-human chorionic gonadotropin (beta-hCG) and alpha(1)-feto protein (alpha-FP) secreting mediastinal tumor.
  • Histological analysis showed a mixed germ cell tumor comprising choriocarcinoma (CH), embryonal carcinoma (EC), mature teratoma (MT), and yolk sac tumor (YS).
  • The histological distribution was also age-dependent with mixed germ cell tumors predominantly in younger patients.
  • There is still no convincing explanation for the association of M-GCTs and KS.
  • [MeSH-major] Klinefelter Syndrome / complications. Mediastinal Neoplasms / complications. Neoplasms, Germ Cell and Embryonal / complications. Puberty, Precocious / complications

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  • (PMID = 16470792.001).
  • [ISSN] 1552-4825
  • [Journal-full-title] American journal of medical genetics. Part A
  • [ISO-abbreviation] Am. J. Med. Genet. A
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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47. Martin LT, Glass M, Dosunmu E, Martin PT: Altered expression of natively glycosylated alpha dystroglycan in pediatric solid tumors. Hum Pathol; 2007 Nov;38(11):1657-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered expression of natively glycosylated alpha dystroglycan in pediatric solid tumors.
  • To date, however, there has been no study of the expression of dystroglycan in pediatric solid tumors.
  • Using a combination of immunostaining on tissue microarrays and immunoblotting of snap-frozen unfixed tissues, we demonstrate a significant reduction in native alpha dystroglycan expression in pediatric alveolar rhabdomyosarcoma (RMS), embryonal RMS, neuroblastoma (NBL), and medulloblastoma, whereas expression of beta dystroglycan, which is cotranslated with alpha dystroglycan, is largely unchanged.
  • Loss of native alpha dystroglycan expression was significantly more pronounced in stage 4 NBL than in pooled samples of stage 1 and stage 2 NBL, suggesting that loss of native alpha dystroglycan expression increases with advancing tumor stage.
  • Neuroblastoma and RMS samples with reduced expression of native alpha dystroglycan also showed reduced laminin binding in laminin overlay experiments.
  • Expression of natively glycosylated alpha dystroglycan was not altered in several other pediatric tumor types when compared with appropriate normal tissue controls.
  • These data provide the first evidence that alpha dystroglycan glycosylation and laminin binding to alpha dystroglycan are altered in certain pediatric solid tumors and suggest that aberrant dystroglycan glycosylation may contribute to tumor cell biology in patients with RMS, medulloblastoma, and NBL.

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  • (PMID = 17640712.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / AR050202-02; United States / NIAMS NIH HHS / AR / R01 AR050202; United States / NIAMS NIH HHS / AR / R01 AR049722-01A2; United States / NIAMS NIH HHS / AR / AR 050202; United States / NIAMS NIH HHS / AR / AR049722-01A2; United States / NIAMS NIH HHS / AR / R01 AR050202-02; United States / NIAMS NIH HHS / AR / R01 AR049722
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Laminin; 146888-27-9 / Dystroglycans
  • [Other-IDs] NLM/ NIHMS190362; NLM/ PMC2850815
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48. Lamba S, Felicioni L, Buttitta F, Bleeker FE, Malatesta S, Corbo V, Scarpa A, Rodolfo M, Knowles M, Frattini M, Marchetti A, Bardelli A: Mutational profile of GNAQQ209 in human tumors. PLoS One; 2009;4(8):e6833
The Lens. Cited by Patents in .

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  • [Title] Mutational profile of GNAQQ209 in human tumors.
  • BACKGROUND: Frequent somatic mutations have recently been identified in the ras-like domain of the heterotrimeric G protein alpha-subunit (GNAQ) in blue naevi 83%, malignant blue naevi (50%) and ocular melanoma of the uvea (46%).
  • METHODOLOGY: To assess if the mutations are present in other tumor types we performed a systematic mutational profile of the GNAQ exon 5 in a panel of 922 neoplasms, including glioblastoma, gastrointestinal stromal tumors (GIST), acute myeloid leukemia (AML), blue naevi, skin melanoma, bladder, breast, colorectal, lung, ovarian, pancreas, and thyroid carcinomas.
  • Changes affecting Q209 were not found in any of the other tumors.
  • Our data indicate that the occurrence of GNAQ mutations display a unique pattern being present in a subset of melanocytic tumors but not in malignancies of glial, epithelial and stromal origin analyzed in this study.

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  • (PMID = 19718445.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.1 / Heterotrimeric GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2730032
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49. Kyritsis AP: Management of primary intracranial germ cell tumors. J Neurooncol; 2010 Jan;96(2):143-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of primary intracranial germ cell tumors.
  • Primary intracranial germ cell tumors are rare and usually localized in the pineal and the suprasellar regions.
  • They are divided into the following histologic types: germinoma, teratoma (mature, immature, malignant), choriocarcinoma, embryonal carcinoma, endodermal sinus tumor (yolk sac tumor), and mixed tumors.
  • The rest of germ cell tumors are managed with various combinations of surgery, chemotherapy, and radiotherapy depending on the tumor type.
  • If the tumors secrete beta-human chorionic gonadotrophin (hCG) or alpha-fetoprotein (FP), these tumor markers can be used to accurately monitor response to treatment.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / classification. Neoplasms, Germ Cell and Embryonal / therapy. Pinealoma / therapy

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  • (PMID = 19588227.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins
  • [Number-of-references] 42
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50. Mauceri HJ, Beckett MA, Liang H, Sutton HG, Pitroda S, Galka E, Efimova E, Darga T, Khodarev NN, King CR, Posner MC, Hellman S, Kufe DW, Weichselbaum RR: Translational strategies exploiting TNF-alpha that sensitize tumors to radiation therapy. Cancer Gene Ther; 2009 Apr;16(4):373-81
Hazardous Substances Data Bank. Etanercept .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translational strategies exploiting TNF-alpha that sensitize tumors to radiation therapy.
  • TNFerade is a radioinducible adenoviral vector expressing tumor necrosis factor-alpha (TNF-alpha) (Ad.Egr-TNF) currently in a phase III trial for inoperable pancreatic cancer.
  • We studied B16-F1 melanoma tumors in TNF receptor wild-type (C57BL/6) and deficient (TNFR1,2-/- and TNFR1-/-) mice.
  • Ad.Egr-TNF+IR inhibited tumor growth compared with IR in C57BL/6 but not in receptor-deficient mice.
  • Tumors resistant to TNF-alpha were also sensitive to Ad.Egr-TNF+IR in C57BL/6 mice.
  • Ad.Egr-TNF+IR produced an increase in tumor-associated endothelial cell apoptosis not observed in receptor-deficient animals.
  • Also, B16-F1 tumors in mice with germline deletions of TNFR1,2, TNFR1 or TNF-alpha, or in mice receiving anti-TNF-alpha exhibited radiosensitivity.
  • These results show that tumor-associated endothelium is the principal target for Ad.Egr-TNF radiosensitization and implicate TNF-alpha signaling in tumor radiosensitivity.
  • [MeSH-major] Genetic Therapy / methods. Melanoma, Experimental / therapy. Radiation-Sensitizing Agents. Tumor Necrosis Factor-alpha / metabolism. X-Ray Therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Endothelial Cells / drug effects. Endothelial Cells / physiology. Etanercept. Humans. Immunoglobulin G / pharmacology. Immunosuppressive Agents / pharmacology. Mice. Neoplasm Transplantation. Receptors, Tumor Necrosis Factor. Receptors, Tumor Necrosis Factor, Type I / deficiency. Receptors, Tumor Necrosis Factor, Type II / deficiency

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  • (PMID = 18974777.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA111423
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; 0 / Radiation-Sensitizing Agents; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
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51. Hiraide A, Hiroishi K, Eguchi J, Ishii S, Doi H, Imawari M: Dendritic cells stimulated with cytidine-phosphate-guanosine oligodeoxynucleotides and interferon-alpha-expressing tumor cells effectively reduce outgrowth of established tumors in vivo. Cancer Sci; 2008 Aug;99(8):1663-9

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  • [Title] Dendritic cells stimulated with cytidine-phosphate-guanosine oligodeoxynucleotides and interferon-alpha-expressing tumor cells effectively reduce outgrowth of established tumors in vivo.
  • Dendritic cells (DC) are potent antigen-presenting cells that elicit immune responses to foreign antigens.
  • We have previously demonstrated the synergistic effects of cytidine-phosphate-guanosine (CpG) oligodeoxynucleotides (ODN) and interferon (IFN)-alpha on DC maturation in vitro.
  • In the present study, the antitumor effects of DC preincubated with IFN-alpha gene-overexpressing murine colorectal cancer MC38 cells (MC38-IFN-alpha) and CpG ODN were evaluated in a poorly immunogenic murine cancer system.
  • When we injected DC preincubated with MC38-IFNalpha and CpG ODN subcutaneously to mice bearing MC38 wild-type tumors, the outgrowth of the established parental tumors was suppressed significantly compared with that following administration of DC with MC38-IFN-alpha (P = 0.008).
  • All mice injected with DC preincubated with MC38-IFN-alpha and CpG ODN rejected a subsequent parental tumor challenge.
  • Immunohistochemical and flow cytometric analyses showed that CD4(+), CD8(+), and NK1.1(+) cells markedly infiltrated the established tumors of mice treated with DC preincubated with MC38-IFN-alpha and CpG ODN.
  • From the results in immune cell-depleted mice, CD4(+) and asialo-GM-1(+) cells seemed to contribute to the antitumor effects induced by the combination DC therapy.
  • Furthermore, non-specific cytolysis was detected when splenocytes of mice inoculated with DC preincubated with MC38-IFNalpha and CpG ODN were used as effector cells.
  • Using an interleukin (IL)-12-neutralizing antibody it was suggested that IL-12 stimulates natural killer cells and contributes in part to the antitumor effects induced by DC incubated with CpG ODN and IFN-alpha.
  • As DC-based immunotherapy with CpG ODN and IFN-alpha-expressing tumor cells induces a potent antitumor immune response, it should be considered for clinical application.
  • [MeSH-major] Dendritic Cells / immunology. Dendritic Cells / metabolism
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / metabolism. Cytosine Nucleotides. Flow Cytometry. Gene Expression. Guanosine. Immunohistochemistry. Interferon-alpha / metabolism. Interleukin-12. Killer Cells, Natural / metabolism. Mice. Oligonucleotides. Up-Regulation

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  • (PMID = 18754881.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytosine Nucleotides; 0 / Interferon-alpha; 0 / Oligonucleotides; 12133JR80S / Guanosine; 187348-17-0 / Interleukin-12
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52. Chuang LS, Ito Y: RUNX3 is multifunctional in carcinogenesis of multiple solid tumors. Oncogene; 2010 May 6;29(18):2605-15
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  • [Title] RUNX3 is multifunctional in carcinogenesis of multiple solid tumors.
  • The study of RUNX3 in tumor pathogenesis is a rapidly expanding area of cancer research.
  • Functional inactivation of RUNX3-through mutation, epigenetic silencing, or cytoplasmic mislocalization-is frequently observed in solid tumors of diverse origins.
  • Conversely, RUNX3 has also been described to have an oncogenic function in a subset of tumors.
  • Although the mechanism of how RUNX3 switches from tumor suppressive to oncogenic activity is unclear, this is of clinical relevance with implications for cancer detection and prognosis.
  • Recent developments have significantly contributed to our understanding of the pleiotropic tumor suppressive properties of RUNX3 that regulate major signaling pathways.
  • This review summarizes the important findings that link RUNX3 to tumor suppression.
  • [MeSH-major] Core Binding Factor Alpha 3 Subunit / physiology. Neoplasms / etiology
  • [MeSH-minor] Animals. Cell Aging. Cytoplasm / metabolism. DNA Methylation. DNA Repair. Gene Deletion. Gene Silencing. Humans. Mutagenesis, Insertional. Protein Transport. Signal Transduction

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  • (PMID = 20348954.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit
  • [Number-of-references] 103
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53. Kobayashi T, Kawakita M, Terachi T, Habuchi T, Ogawa O, Kamoto T: Significance of elevated preoperative alpha-fetoprotein in postchemotherapy residual tumor resection for the disseminated germ cell tumors. J Surg Oncol; 2006 Dec 1;94(7):619-23
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  • [Title] Significance of elevated preoperative alpha-fetoprotein in postchemotherapy residual tumor resection for the disseminated germ cell tumors.
  • BACKGROUND AND OBJECTIVES: The purpose of the study is to determine the significance of elevated serum alpha-fetoprotein (AFP) in the setting prior to residual tumor resection (RTR) following chemotherapy for metastatic germ cell tumor in terms of the prediction of histology of the specimen and postoperative survival.
  • METHODS: We conducted a retrospective review of 68 patients undergoing RTR for metastatic nonseminomatous germ cell tumor or extragonadal germ cell tumor after at least a first-line chemotherapy.
  • Rates of presence of residual malignant cell in RTR specimen were similar between patients with normal AFP (7/28 or 25%) and with mildly elevated (10-30 ng/ml) AFP (3/11 or 27%).
  • [MeSH-major] Biomarkers, Tumor / blood. Chorionic Gonadotropin, beta Subunit, Human / blood. Neoplasms, Germ Cell and Embryonal / surgery. Testicular Neoplasms / surgery. alpha-Fetoproteins / metabolism

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17111392.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins
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54. Juhász C, Chugani DC, Muzik O, Wu D, Sloan AE, Barger G, Watson C, Shah AK, Sood S, Ergun EL, Mangner TJ, Chakraborty PK, Kupsky WJ, Chugani HT: In vivo uptake and metabolism of alpha-[11C]methyl-L-tryptophan in human brain tumors. J Cereb Blood Flow Metab; 2006 Mar;26(3):345-57
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  • [Title] In vivo uptake and metabolism of alpha-[11C]methyl-L-tryptophan in human brain tumors.
  • Abnormal metabolism of tryptophan has been implicated in modulation of tumor cell proliferation and immunoresistance. alpha-[(11)C]Methyl-L-tryptophan (AMT) is a PET tracer to measure cerebral tryptophan metabolism in vivo.
  • In the present study, we have measured tumor tryptophan uptake in 40 patients with primary brain tumors using AMT PET and standard uptake values (SUV).
  • All grade II to IV gliomas and glioneuronal tumors showed increased AMT SUV, including all recurrent/residual tumors.
  • In astrocytic tumors, low grade was associated with high k(3)' and lower VD', while high-grade tumors showed the reverse pattern.
  • The findings show high AMT uptake in primary and residual/recurrent gliomas and glioneuronal tumors.
  • Increased AMT uptake can be due to increased metabolism of tryptophan and/or high volume of distribution, depending on tumor type and grade.
  • High tryptophan metabolic rates in low-grade tumors may indicate activation of the kynurenine pathway, a mechanism regulating tumor cell growth.
  • AMT PET might be a useful molecular imaging method to guide therapeutic approaches aimed at controlling tumor cell proliferation by acting on tryptophan metabolism.

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  • (PMID = 16079785.001).
  • [ISSN] 0271-678X
  • [Journal-full-title] Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • [ISO-abbreviation] J. Cereb. Blood Flow Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan; AU0V1LM3JT / Gadolinium; IY9XDZ35W2 / Glucose
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55. Christodoulou C, Dafni U, Aravantinos G, Koutras A, Samantas E, Karina M, Janinis J, Papakostas P, Skarlos D, Kalofonos HP, Fountzilas G: Effects of epoetin-alpha on quality of life of cancer patients with solid tumors receiving chemotherapy. Anticancer Res; 2009 Feb;29(2):693-702
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  • [Title] Effects of epoetin-alpha on quality of life of cancer patients with solid tumors receiving chemotherapy.
  • BACKGROUND: Erythropoietin corrects and prevents anemia and decreases the need for red blood cell (RBC) transfusions; its impact on quality of life (QOL) of cancer patients receiving chemotherapy is not clear.
  • PATIENTS AND METHODS: 399 patients with solid tumors and Hb level of < or = 12 g/dl receiving chemotherapy were randomized to receive or not 10,000 IU epoetin-alpha thrice weekly.
  • The improvement in Hb levels was significantly higher for the epoetin-alpha group, with a decrease in transfusion requirements compared to the control group.
  • CONCLUSION: Epoetin-alpha does not improve QOL of patients with solid tumors receiving chemotherapy as assessed using FACT-An scale and various subscales, despite improving Hb levels and reducing transfusion requirements.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anemia / drug therapy. Anemia / prevention & control. Blood Transfusion. Epoetin Alfa. Female. Hemoglobins / metabolism. Humans. Male. Middle Aged. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / adverse effects. Quality of Life. Recombinant Proteins. Treatment Outcome. Young Adult

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  • (PMID = 19331224.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Organoplatinum Compounds; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 64FS3BFH5W / Epoetin Alfa
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56. Arendt LM, Schuler LA: Prolactin drives estrogen receptor-alpha-dependent ductal expansion and synergizes with transforming growth factor-alpha to induce mammary tumors in males. Am J Pathol; 2008 Jan;172(1):194-202
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  • [Title] Prolactin drives estrogen receptor-alpha-dependent ductal expansion and synergizes with transforming growth factor-alpha to induce mammary tumors in males.
  • Male NRL-PRL mice did not develop mammary tumors.
  • However, in cooperation with the well-characterized oncogene transforming growth factor-alpha (TGF-alpha), PRL induced mammary tumors in 100% of male bitransgenic mice.
  • Similar to disease in human males, these tumors expressed variable levels of estrogen receptor-alpha (ER-alpha) and androgen receptors.
  • However, carcinogenesis was not responsive to testicular steroids because castration did not alter latency to tumor development or tumor ER-alpha expression.
  • Interestingly, both NRL-TGF-alpha/PRL and NRL-PRL males demonstrated increased ductal development, which occurred during puberty, similar to female mice.
  • Treatment of MCF-7-derived cells with PRL increased phosphorylation of ER-alpha at residues implicated in unliganded ER-alpha activity.
  • Together, these studies suggest that PRL expands the pool of cells susceptible to tumorigenesis, which is then facilitated by PRL and TGF-alpha cross talk.
  • Activation of ER-alpha is one mechanism by which PRL may contribute to breast cancer and points to other therapeutic strategies for male patients.

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  • (PMID = 18156207.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK-62783; United States / NCRR NIH HHS / RR / K01 RR021858; United States / NCRR NIH HHS / RR / K01-RR021858; United States / NIA NIH HHS / AG / T32 AG000265; United States / NIDDK NIH HHS / DK / R01 DK062783; United States / NCI NIH HHS / CA / R01-CA 78312; United States / NIA NIH HHS / AG / T32-AG00265; United States / NCI NIH HHS / CA / R01 CA078312
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Steroids; 0 / Transforming Growth Factor alpha; 9002-62-4 / Prolactin
  • [Other-IDs] NLM/ PMC2189634
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57. Romero-Reyes M, Head C, Cacalano NA, Jewett A: Potent induction of TNF-alpha during interaction of immune effectors with oral tumors as a potential mechanism for the loss of NK cell viability and function. Apoptosis; 2007 Nov;12(11):2063-75
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  • [Title] Potent induction of TNF-alpha during interaction of immune effectors with oral tumors as a potential mechanism for the loss of NK cell viability and function.
  • The inhibitory role of TNF-alpha on survival of naïve and IL-2 treated NK cells has been demonstrated in the past.
  • However, its effect on the function of these cells against tumor cells, in particular against oral tumors has not been established.
  • We investigated the significance of secreted TNF-alpha in death and functional loss of splenocytes and NK cells in ex-vivo cultures with oral tumors.
  • Oral tumors trigger potent secretion of TNF-alpha by human and murine immune effectors.
  • Absence of TNF-alpha increases the cytotoxic activity and secretion of IFN-gamma by IL-2 treated splenocytes and NK cells in co-cultures with MOK L2D1+/p53-/- oral tumor cells.
  • IL-2 treated splenocytes and NK cells from TNF-alpha -/- mice survive and proliferate more when compared to cells from TNF-alpha +/+ mice.
  • Cell death induced by F. nucleatum, an oral bacteria, in TNF-alpha -/- splenocytes are considerably lower than that induced in TNF-alpha +/+ splenocytes where potent release of TNF-alpha is reproducibly observed.
  • Addition of exogenous rTNF-alpha to IL-2 treated splenocytes and NK cells decreased survival and function of splenocytes and NK cells obtained from TNF-alpha -/- mice against oral tumors.
  • These findings suggest that potent induction of TNF-alpha during interaction of immune effectors with oral tumors and/or oral bacteria is an important factor in decreasing the function and survival of cytotoxic immune effectors.
  • Strategies to neutralize TNF-alpha may be beneficial in the treatment of oral cancers.
  • [MeSH-major] Killer Cells, Natural / immunology. Mouth Neoplasms / immunology. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Animals. Apoptosis / immunology. Cell Line, Tumor. Cell Survival / immunology. Humans. Mice. Mice, Knockout. Tumor Cells, Cultured

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  • (PMID = 17713857.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01-12880
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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58. Ishii S, Hiroishi K, Eguchi J, Hiraide A, Imawari M: Dendritic cell therapy with interferon-alpha synergistically suppresses outgrowth of established tumors in a murine colorectal cancer model. Gene Ther; 2006 Jan;13(1):78-87
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  • [Title] Dendritic cell therapy with interferon-alpha synergistically suppresses outgrowth of established tumors in a murine colorectal cancer model.
  • Both dendritic cell (DC)-based immunotherapy and interferon (IFN)-alpha therapy have been proved to have potent long-lasting antitumor effects.
  • In anticipation of synergistic antitumor effects, we performed combination therapy with DCs and IFN-alpha gene-transduced murine colorectal cancer MC38 cells (MC38-IFN-alpha).
  • DCs incubated with MC38-IFN-alpha, but not neomycin-resistance gene-transduced MC38 cells (MC38-Neo), effectively enhanced proliferation of allogeneic splenocytes in vitro.
  • In 12 of 17 mice, DCs in combination with MC38-IFN-alpha prevented the development of a parental tumor, while DCs and MC38-Neo did in only three of 17 mice (P=0.008).
  • In a therapeutic model of an established parental tumor, inoculation of DCs and MC38-IFN-alpha suppressed the growth of the established parental tumors significantly compared with the administration of DCs with MC38-Neo or naive splenocytes with MC38-IFN-alpha (P=0.016 and 0.024, respectively).
  • Analyses of immunohistochemistry and tumor-infiltrating mononuclear cells showed that CD8(+), CD11c(+), and NK1.1(+) cells markedly infiltrated the established tumors of mice treated with DCs and MC38-IFN-alpha.
  • From the results of observation of parental tumor outgrowth in immune cell-depleted mice, CD8(+) cells, and asialo-GM-1(+) cells were thought to contribute to the antitumor effects induced by the combination therapy.
  • Furthermore, MC38-specific cytolysis was detected when splenocytes of mice inoculated with DCs and MC38-IFN-alpha cells were stimulated with MC38-IFN-alpha cells in vitro.
  • Since DC-based immunotherapy in combination with IFN-alpha-expressing tumor cells induces potent antitumor cellular immune responses, it should be considered for clinical application.
  • [MeSH-major] Adoptive Transfer / methods. Colorectal Neoplasms / therapy. Dendritic Cells / immunology. Genetic Therapy / methods. Interferon-gamma / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Genetic Vectors / pharmacology. Lymphocyte Depletion. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Retroviridae / genetics. T-Lymphocytes, Cytotoxic / immunology. Transduction, Genetic / methods

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  • (PMID = 16107857.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
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59. Teng MW, Westwood JA, Darcy PK, Sharkey J, Tsuji M, Franck RW, Porcelli SA, Besra GS, Takeda K, Yagita H, Kershaw MH, Smyth MJ: Combined natural killer T-cell based immunotherapy eradicates established tumors in mice. Cancer Res; 2007 Aug 01;67(15):7495-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined natural killer T-cell based immunotherapy eradicates established tumors in mice.
  • A rational monoclonal antibody (mAb)-based antitumor therapy approach has previously been shown to eradicate various established experimental and carcinogen-induced tumors in a majority of mice.
  • This therapy comprised an agonistic mAb reactive with tumor necrosis factor-related apoptosis-inducing ligand receptor (DR5), expressed by tumor cells, an agonistic anti-CD40 mAb to mature dendritic cells, and an agonistic anti-4-1BB mAb to costimulate CD8(+) T cells.
  • Because agonists of CD40 have been toxic in patients, we were interested in substituting anti-CD40 mAb with other dendritic cell-maturing agents, such as glycolipid ligands recognized by invariant natural killer T (iNKT) cells.
  • Here, we show that CD1d-restricted glycolipid ligands for iNKT cells effectively substitute for anti-CD40 mAb and reject established experimental mouse breast and renal tumors when used in combination with anti-DR5 and anti-4-1BB mAbs (termed "NKTMab" therapy).
  • NKTMab therapy-induced tumor rejection was dependent on CD4(+) and CD8(+) T cells, NKT cells, and the cytokine IFN-gamma.
  • NKTMab therapy containing either alpha-galactosylceramide (alpha-GC) or alpha-C-galactosylceramide (alpha-c-GC) at high concentrations induced similar rates of tumor rejection in mice; however, toxicity was observed at the highest doses of alpha-GC (>250 ng/injection), limiting the use of this glycolipid.
  • By contrast, even very low doses of alpha-c-GC (25 ng/injection) retained considerable antitumor activity when used in combination with anti-DR5/anti-4-1BB, and thus, alpha-c-GC showed a considerably greater therapeutic index.
  • In summary, sequential tumor cell apoptosis and amplification of dendritic cell function by NKT cell agonists represents an exciting and novel approach for cancer treatment.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Carcinoma, Renal Cell / therapy. Galactosylceramides / immunology. Immunotherapy. Killer Cells, Natural / immunology. Mammary Neoplasms, Experimental / therapy. Receptors, TNF-Related Apoptosis-Inducing Ligand / immunology
  • [MeSH-minor] Animals. Apoptosis. CD8-Positive T-Lymphocytes. Cell Line, Tumor. Combined Modality Therapy. Kidney Neoplasms / immunology. Kidney Neoplasms / pathology. Kidney Neoplasms / therapy. Liver / immunology. Lymphocyte Activation. Membrane Glycoproteins / immunology. Mice. Mice, Inbred BALB C. Survival Rate. TNF-Related Apoptosis-Inducing Ligand. Transaminases / blood

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  • (PMID = 17671220.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0400421
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Galactosylceramides; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 2.6.1.- / Transaminases
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60. Thamm DH, Kurzman ID, Clark MA, Ehrhart EJ 3rd, Kraft SL, Gustafson DL, Vail DM: Preclinical investigation of PEGylated tumor necrosis factor alpha in dogs with spontaneous tumors: phase I evaluation. Clin Cancer Res; 2010 Mar 1;16(5):1498-508
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preclinical investigation of PEGylated tumor necrosis factor alpha in dogs with spontaneous tumors: phase I evaluation.
  • PURPOSE: Tumor necrosis factor-alpha (TNF) is a cytokine with potent antitumor activity; however, toxicity and short half-life have limited its utility.
  • EXPERIMENTAL DESIGN: A phase I clinical trial enrolled dogs with measurable tumors in which standard therapy had failed or been declined.
  • Physiologic, hematologic, and biochemical parameters were evaluated and tumor biopsies obtained serially.
  • Biological activity (transient fever and leukopenia, increased tumor inflammation, and necrosis) was observed at all dosages.
  • A significant increase in tumor blood flow was observed with dynamic contrast-enhanced magnetic resonance imaging.
  • Minor/transient antitumor responses were observed in dogs with melanoma, squamous cell carcinoma, and mammary carcinoma, and a partial response was observed in a dog with angiosarcoma.
  • [MeSH-major] Neoplasms / drug therapy. Neoplasms / veterinary. Tumor Necrosis Factor-alpha / administration & dosage

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  • (PMID = 20160058.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 30IQX730WE / Polyethylene Glycols
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61. Bricard G, Cesson V, Devevre E, Bouzourene H, Barbey C, Rufer N, Im JS, Alves PM, Martinet O, Halkic N, Cerottini JC, Romero P, Porcelli SA, Macdonald HR, Speiser DE: Enrichment of human CD4+ V(alpha)24/Vbeta11 invariant NKT cells in intrahepatic malignant tumors. J Immunol; 2009 Apr 15;182(8):5140-51
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  • [Title] Enrichment of human CD4+ V(alpha)24/Vbeta11 invariant NKT cells in intrahepatic malignant tumors.
  • Invariant NKT cells (iNKT cells) recognize glycolipid Ags via an invariant TCR alpha-chain and play a central role in various immune responses.
  • Although human CD4(+) and CD4(-) iNKT cell subsets both produce Th1 cytokines, the CD4(+) subset displays an enhanced ability to secrete Th2 cytokines and shows regulatory activity.
  • We performed an ex vivo analysis of blood, liver, and tumor iNKT cells from patients with hepatocellular carcinoma and metastases from uveal melanoma or colon carcinoma.
  • Frequencies of Valpha24/Vbeta11 iNKT cells were increased in tumors, especially in patients with hepatocellular carcinoma.
  • The proportions of CD4(+), double negative, and CD8alpha(+) iNKT cell subsets in the blood of patients were similar to those of healthy donors.
  • However, we consistently found that the proportion of CD4(+) iNKT cells increased gradually from blood to liver to tumor.
  • Furthermore, CD4(+) iNKT cell clones generated from healthy donors were functionally distinct from their CD4(-) counterparts, exhibiting higher Th2 cytokine production and lower cytolytic activity.
  • Thus, in the tumor microenvironment the iNKT cell repertoire is modified by the enrichment of CD4(+) iNKT cells, a subset able to generate Th2 cytokines that can inhibit the expansion of tumor Ag-specific CD8(+) T cells.
  • Because CD4(+) iNKT cells appear inefficient in tumor defense and may even favor tumor growth and recurrence, novel iNKT-targeted therapies should restore CD4(-) iNKT cells at the tumor site and specifically induce Th1 cytokine production from all iNKT cell subsets.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Liver Neoplasms / immunology. Natural Killer T-Cells / immunology. Receptors, Antigen, T-Cell / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD1d / immunology. Antigens, CD3 / immunology. Cloning, Molecular. Female. HeLa Cells. Health. Humans. Male. Middle Aged

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  • [CommentIn] Immunotherapy. 2009 Sep;1(5):733-6 [20636016.001]
  • (PMID = 19342695.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1d; 0 / Antigens, CD3; 0 / CD1D protein, human; 0 / Receptors, Antigen, T-Cell
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62. Dinc B, Sahin C: Metastatic glucagonoma. Eurasian J Med; 2009 Apr;41(1):70-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic glucagonoma.
  • We report a case of a very rare endocrine tumor of the pancreas.
  • Because the CA 19-9 and glucagon levels were high, and abdominal dynamic CT showed a mass in the pancreas body and metastatic lesions in the liver, the decision was made to operate.
  • The histopathology of the tumor was reported as a neuroendocrine tumor, which was concordant with glucagonoma.

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  • (PMID = 25610069.001).
  • [ISSN] 1308-8734
  • [Journal-full-title] The Eurasian journal of medicine
  • [ISO-abbreviation] Eurasian J Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Other-IDs] NLM/ PMC4261651
  • [Keywords] NOTNLM ; Glucagonoma / Liver / Metastases
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63. Chetaille B, Massard G, Falcoz PE: [Mediastinal germ cell tumors: anatomopathology, classification, teratomas and malignant tumors]. Rev Pneumol Clin; 2010 Feb;66(1):63-70

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  • [Title] [Mediastinal germ cell tumors: anatomopathology, classification, teratomas and malignant tumors].
  • [Transliterated title] Les tumeurs germinales du médiastin: anatomopathologie, classification, tératomes et tumeurs malignes.
  • Mediastinal germ cell tumors are rare tumors.
  • It is classic to divide those tumors into two categories, seminomas and nonseminomatous germ cell tumors: teratomas (mature or immature), embryonal carcinomas, yolk sac tumors, and choriocarcinomas.
  • Each histological sub-type can be associated to another sub-type that realise a so-called mixed germ cell tumor.
  • Diagnosis strategy is currently well codified for malignant mediastinal germ cell tumors.
  • It greatly benefits from tumoral markers (alpha-fetoprotein and beta human chorionic gonadotrophin).
  • The treatment of seminomatous tumors is standardised--chemotherapy/surgery on residual tumor greater than 3 cm/radiotherapy on viable persistent residual tumors--and provides very satisfying results.
  • As for the nonseminomatous germ cell tumors, the situation is dramatically different.
  • [MeSH-major] Mediastinal Neoplasms / pathology. Neoplasms, Germ Cell and Embryonal / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Combined Modality Therapy. Humans. Mediastinum / pathology. Neoplasm Invasiveness. Prognosis. Seminoma / classification. Seminoma / pathology. Seminoma / therapy. Teratoma / classification. Teratoma / pathology. Teratoma / therapy. Tomography, X-Ray Computed

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  • [Copyright] Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20207298.001).
  • [ISSN] 0761-8417
  • [Journal-full-title] Revue de pneumologie clinique
  • [ISO-abbreviation] Rev Pneumol Clin
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 18
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64. Riedinger JM, Eche N, Chevreau C, Fargeot P: [Germ cell testicular tumors: understanding the kinetics of serum alpha-fetoprotein (AFP) during chemotherapy]. Ann Biol Clin (Paris); 2008 Sep-Oct;66(5):523-30
Hazardous Substances Data Bank. CARBOPLATIN .

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  • [Title] [Germ cell testicular tumors: understanding the kinetics of serum alpha-fetoprotein (AFP) during chemotherapy].
  • [Transliterated title] Tumeurs germinales non séminomateuses du testicule : comprendre les cinétiques d'alpha-foetoprotéine (AFP) sous chimiothérapie.
  • The analysis of longitudinal series of tumour markers during chemotherapy in patients with germ cells tumors is not easy.
  • The purpose of this work is to present various characteristic profiles of the evolution of serum alpha-fetoprotein during chemotherapy and review the modalities of the dynamic interpretation of this marker.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor. Cisplatin. Neoplasms, Germ Cell and Embryonal / drug therapy. Testicular Neoplasms / drug therapy. alpha-Fetoproteins / analysis

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  • (PMID = 18957341.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins; 11056-06-7 / Bleomycin; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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65. de Mestier L, Hammel P, Hentic O, Dove P, Lévy P, Ruszniewski P: [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency]. Gastroenterol Clin Biol; 2010 Jan;34(1):106-10
Hazardous Substances Data Bank. FLUOROURACIL .

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  • [Title] [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency].
  • [Transliterated title] Efficacité spectaculaire d'une chimiothérapie par 5-fluoro-uracile et dacarbazine chez un malade atteint de glucagonome métastatique avec insuffisance cardiaque.
  • Malignant glucagonoma is an exceptional pancreatic endocrine tumour, with frequent dermatologic symptoms, diabetes and degradation of the general health status.
  • We report here an observation of a patient who was treated for a glucagonoma with multiple liver metastases, migratory necrolytic erythema, dilated cardiomypathy and diabetes that dramatically improved after a dacarbazin-based chemotherapy, allowing subsequent surgical resection of the primary.
  • The patient was still alive and asymptomatic without progressive disease nearly two years after surgery.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cardiomyopathy, Dilated / complications. Glucagonoma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adult. Dacarbazine / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright 2009. Published by Elsevier Masson SAS.
  • (PMID = 19875259.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; U3P01618RT / Fluorouracil
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66. Riccardi E, Grieco V, Verganti S, Finazzi M: Immunohistochemical diagnosis of canine ovarian epithelial and granulosa cell tumors. J Vet Diagn Invest; 2007 Jul;19(4):431-5
Archivio Istituzionale della Ricerca Unimi. Full text from AIR - Univ. Milan .

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  • [Title] Immunohistochemical diagnosis of canine ovarian epithelial and granulosa cell tumors.
  • In humans and canines, the morphology of granulosa cell tumors is extremely variable and causes diagnostic difficulties.
  • In human pathology, immunohistochemistry has been widely used for the diagnosis of granulosa cell tumors, whereas, limited studies are present in canine species.
  • The aim of this study was to investigate the expression of cytokeratins, vimentin, and inhibin-alpha in canine normal ovaries, epithelial ovarian tumors, and granulosa cell tumors to establish an immunohistochemical panel for the differential diagnosis of ovarian tumors.
  • Formalin-fixed, paraffin-embedded tissue sections from 4 normal ovaries, 8 granulosa cell tumors, and 6 epithelial ovarian tumors (2 adenomas and 4 adenocarcinomas) sections were obtained and stained with hematoxylin and eosin and immunohistochemically for cytokeratin AE1/AE3, cytokeratin 7, vimentin, and inhibin-alpha.
  • Granulosa cells were negative for cytokeratin 7 and displayed variable expression of vimentin, cytokeratin AE1/AE3, and inhibin-alpha toward follicular maturation.
  • Granulosa cell tumors were negative for cytokeratin 7 and positive for inhibin-alpha.
  • Conversely, ovarian epithelial cells tumors were positive for cytokeratin 7 and negative for inhibin-alpha.
  • Both granulosa and epithelial cell tumors displayed variable expression of vimentin.
  • Cytokeratin AE1/AE3 was expressed by all epithelial-derived tumors and 6 of 8 granulosa cell tumors.
  • The results of this study suggest that useful immunohistochemical markers to distinguish epithelial ovarian tumors from granulosa cell tumors are cytokeratin 7 and inhibin-alpha.
  • [MeSH-major] Dog Diseases / diagnosis. Immunohistochemistry / veterinary. Neoplasms, Glandular and Epithelial / veterinary. Ovarian Neoplasms / veterinary

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  • [ErratumIn] J Vet Diagn Invest. 2007 Sep;19(5):586. Greco, Valeria [corrected to Grieco, Valeria]
  • (PMID = 17609358.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Keratin-7; 57285-09-3 / Inhibins
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67. Shilo K, Dracheva T, Mani H, Fukuoka J, Sesterhenn IA, Chu WS, Shih JH, Jen J, Travis WD, Franks TJ: Alpha-methylacyl CoA racemase in pulmonary adenocarcinoma, squamous cell carcinoma, and neuroendocrine tumors: expression and survival analysis. Arch Pathol Lab Med; 2007 Oct;131(10):1555-60
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  • [Title] Alpha-methylacyl CoA racemase in pulmonary adenocarcinoma, squamous cell carcinoma, and neuroendocrine tumors: expression and survival analysis.
  • CONTEXT: Alpha-methylacyl CoA racemase (AMACR) is an oxidative enzyme involved in isomeric transformation of fatty acids entering the beta-oxidation pathway.
  • AMACR serves as a useful marker in establishing a diagnosis of prostatic malignancy; however, limited information is available in regard to its presence in pulmonary neoplasms.
  • DESIGN: Four hundred seventy-seven pulmonary carcinomas, including 150 squamous cell carcinomas, 150 adenocarcinomas, 46 typical carcinoids, 31 atypical carcinoids, 28 large cell neuroendocrine carcinomas, and 72 small cell carcinomas, were studied immunohistochemically using tissue microarray-based samples.
  • RESULTS: Overall, pulmonary tumors were positive for AMACR in a significant percentage (47%) of cases.
  • Among tumor types, 22% of squamous cell carcinoma, 56% of adenocarcinoma, 72% of typical carcinoid, 52% of atypical carcinoid, 70% of large cell neuroendocrine carcinoma, and 51% of small cell lung carcinoma were positive for AMACR.
  • Furthermore, the Kaplan-Meier analysis revealed that the patients with AMACR-positive small cell carcinoma had better survival (19% vs 5% after 5 years, P = .04) than patients with AMACR-negative tumors.
  • Such survival advantage was seen for patients with stage I-II (P = .01) but not stage III-IV small cell carcinomas (P = .58).
  • Additionally, its positive correlation with outcome of stage I-II small cell lung carcinoma warrants further investigation of the AMACR role in the prognosis of this tumor.
  • [MeSH-major] Adenocarcinoma / enzymology. Biomarkers, Tumor / metabolism. Carcinoma, Neuroendocrine / enzymology. Carcinoma, Squamous Cell / enzymology. Lung Neoplasms / enzymology. Racemases and Epimerases / metabolism

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  • (PMID = 17922592.001).
  • [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; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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68. Domino SE, Karnak DM, Hurd EA: Cell surface fucosylation does not affect development of colon tumors in mice with germline Smad3 mutation. Tumour Biol; 2007;28(2):77-83
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • [Title] Cell surface fucosylation does not affect development of colon tumors in mice with germline Smad3 mutation.
  • BACKGROUND/AIMS: Neoplasia-related alterations in cell surface alpha(1,2)fucosylated glycans have been reported in multiple tumors including colon, pancreas, endometrium, cervix, bladder, lung and choriocarcinoma.
  • Spontaneous colorectal tumors from mice with a germline null mutation of transforming growth factor-beta signaling gene Smad3 (Madh3) were tested for alpha(1,2)fucosylated glycan expression.
  • RESULTS: Spontaneous colorectal tumors from Smad3 (-/-) homozygous null mice were found to express alpha(1,2)fucosylated glycans in an abnormal pattern compared to adjacent nonneoplastic colon.
  • Northern blot analysis of alpha(1,2)fucosyltransferase genes Fut1 and Fut2 revealed that Fut2, but not Fut1, steady-state mRNA levels were significantly increased in tumors relative to adjacent normal colonic mucosa.
  • In Smad3 (-/-)/Fut2 (-/-) double knockout mice, UEA-I lectin staining was eliminated from colon and colon tumors; however, the number and size of tumors present by 24 weeks of age did not vary regardless of the Fut2 genotype.
  • CONCLUSIONS: In this model of colorectal cancer, cell surface alpha(1,2)fucosylation does not affect development of colon tumors.

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
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  • (PMID = 17264540.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K01 CA093856; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / K01 CA93856
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Plant Lectins; 0 / Smad3 Protein; 0 / Smad3 protein, mouse; 0 / Ulex europaeus lectins; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.69 / galactoside 2-alpha-L-fucosyltransferase
  • [Other-IDs] NLM/ NIHMS11241; NLM/ PMC1804094
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69. Mulligan JK, Lathers DM, Young MR: Tumors skew endothelial cells to disrupt NK cell, T-cell and macrophage functions. Cancer Immunol Immunother; 2008 Jul;57(7):951-61
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Tumors skew endothelial cells to disrupt NK cell, T-cell and macrophage functions.
  • INTRODUCTION: Patients and mice with solid tumors, such as Lewis lung carcinoma (LLC), have defects in functions of immune effector cells.
  • Endothelial cells, a component of the tumor vasculature, are potential regulators of immune cell functions.
  • Therefore, these studies examined the impact of exposure to LLC tumor on the ability of endothelial cells to modulate immune cell functions.
  • MATERIALS AND METHODS: Endothelial cells were pre-treated with LLC tumor-conditioned medium (Endo(T-sup)) for 24 h.
  • Control endothelial cells that were exposed to medium (Endo(Media)) epithelial cell-conditioned medium or (Endo(Epi-sup)).
  • After the initial 24 h incubation, endothelial cells were washed and fresh media was added.
  • Cells were allowed to incubate for an additional 24 h.
  • NK cell activity, as measured by TNF-alpha and IFN-gamma secretion, was increased following exposure to media conditioned by Endo(Media) and Endo(Epi-sup) Exposure of NK cells to supernatants of Endo(T-sup), also increases TNF-alpha and IFN-gamma secretion, but to a lesser extent than by Endo(Media) and Endo(Epi-sup).
  • Lastly, T-cell responses to stimulation with anti-CD3 in the presence of supernatants from Endo(T-sup) were examined.
  • IFN-gamma production by CD8+ T-cells was reduced after exposure to Endo(T-sup)-conditioned medium, as compared to cells treatments with medium or control conditioned medium.
  • Production of IFN-gamma by CD4+ T-cells exposed to Endo(T-sup) was not altered.
  • CONCLUSIONS: Taken together, these studies demonstrate that tumors skew endothelial cells to disrupt NK cell, T-cell and macrophages functions, and represents a novel mechanism of tumor-induced immune suppression.

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  • (PMID = 18058097.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA085266-06; United States / NCI NIH HHS / CA / R01 CA085266; United States / NCI NIH HHS / CA / R01 CA128837-05; United States / NCI NIH HHS / CA / R01 CA128837; United States / NCI NIH HHS / CA / R01 CA097813; United States / NCI NIH HHS / CA / R01 CA 85266; United States / NCI NIH HHS / CA / R01 CA 97813
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Cytokines
  • [Other-IDs] NLM/ NIHMS370356; NLM/ PMC3333838
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70. Craig R, Cutrera J, Zhu S, Xia X, Lee YH, Li S: Administering plasmid DNA encoding tumor vessel-anchored IFN-alpha for localizing gene product within or into tumors. Mol Ther; 2008 May;16(5):901-6
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  • [Title] Administering plasmid DNA encoding tumor vessel-anchored IFN-alpha for localizing gene product within or into tumors.
  • Tumor-targeted gene delivery has been intensively studied in the field of gene therapy, but no attention has been given to targeting the therapeutic gene products, which are transcribed and translated from the injected genes, into tumors.
  • Targeting immune stimulatory gene products into tumors is the key to triggering tumor-specific CD8(+) T-cell responses and reducing systemic toxicity.
  • To target the gene products generated from the injected genes into tumors, genes encoding the tumor-targeted fusion gene product were generated and administered locally and systemically via electroporation.
  • As anticipated, administration of a therapeutic gene encoding IFN-alpha and the tumor vessel-targeted peptide CDGRC fusion gene product minimizes the leakage of immunostimulatory cytokine from tumors into the blood circulation, increases the infiltration of CD8(+) T cells into tumors, induces a high magnitude of cytotoxic T-cell lysis (CTL) activity, and reduces tumor vessel density.
  • As a result, tumor growth was more significantly inhibited by administering the IFN-alpha-CDGRC gene than by administering the wild-type IFN-alpha gene.
  • The same result was obtained with the systemic administration of the tumor-targeted IFN-alpha gene.
  • This gene product-based tumor-targeted gene therapy approach could complement any other tumor-targeted gene delivery method for improving tumor-targeting efficiency.
  • [MeSH-major] DNA / chemistry. Gene Transfer Techniques. Genetic Therapy / methods. Interferon-alpha / metabolism. Plasmids / metabolism

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  • (PMID = 18388923.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA120895
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 9007-49-2 / DNA; EC 3.4.11.2 / Antigens, CD13
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71. Hsiao HH, Liu YC, Tsai HJ, Tsai KB, Cheng YJ, Chou SH, Chong IW, Yang WC, Liu TC, Lin SF: Poor outcomes in patients with primary malignant mediastinal germ-cell tumors. Kaohsiung J Med Sci; 2005 Dec;21(12):561-5

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  • [Title] Poor outcomes in patients with primary malignant mediastinal germ-cell tumors.
  • Primary mediastinal germ-cell tumors (GCTs) without gonadal involvement are rare and can be divided into benign mature teratoma and malignant seminoma or nonseminoma.
  • Four malignant GCTs (1 seminoma, 1 choriocarcinoma, and 2 yolk-sac tumors) have been treated in our hospital.
  • All patients were men with obvious symptoms before diagnosis.
  • The patient with seminoma was treated with surgery and radiation, while those with nonseminoma tumors were treated with chemotherapy and/or surgery.
  • Two patients died, one with extended pulmonary metastasis and the other with relapsed disease and high levels of tumor markers.
  • These cases highlight the important role of disease staging and tumor-marker levels in malignant GCTs, and suggest that new treatment strategies for malignant GCTs await further investigation.
  • [MeSH-major] Mediastinal Neoplasms / therapy. Neoplasms, Germ Cell and Embryonal / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Male. Retrospective Studies. Survival Rate. Treatment Outcome. alpha-Fetoproteins / analysis

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  • (PMID = 16670048.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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72. Dundr P, Povýsil C, Tvrdík D: Actin expression in neural crest cell-derived tumors including schwannomas, malignant peripheral nerve sheath tumors, neurofibromas and melanocytic tumors. Pathol Int; 2009 Feb;59(2):86-90
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  • [Title] Actin expression in neural crest cell-derived tumors including schwannomas, malignant peripheral nerve sheath tumors, neurofibromas and melanocytic tumors.
  • Tumors that originate from neural crest-derived cells represent a heterogeneous group of neoplasms including benign and malignant tumors with melanocytic and schwannian differentiation.
  • The immunophenotype of these tumors is well known but little is known about the expression of smooth muscle/myofibroblastic markers in these tumors.
  • A total of 590 neural crest-derived tumors (50 benign schwannomas, five malignant peripheral nerve sheath tumors, 80 neurofibromas, 240 nevocytic nevi, 115 primary melanomas, and 100 melanoma metastases) were studied with respect to alpha-smooth muscle actin and muscle-specific actin expression. alpha-Smooth muscle actin and muscle-specific actin-positive tumor cells with a co-expression of S-100 protein were found in one benign schwannoma, one primary cutaneous melanoma, and four melanoma metastases.
  • Other immunohistochemical markers examined including desmin, h-caldesmon and smooth muscle myosin heavy chain were negative in the tumor cells.
  • The present results suggest that neural crest-derived tumors could show expression of alpha-smooth muscle actin on rare occasion.
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Humans. Melanocytes / metabolism. Melanocytes / pathology. Neural Crest / metabolism. Neural Crest / pathology

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  • (PMID = 19154261.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers, Tumor
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73. Yang JX, Wang HB, Shen K, Huang HF, Pan LY, Wu M: [Treatment of malignant ovarian germ cell tumors with relapse or failed in primary therapy]. Zhonghua Fu Chan Ke Za Zhi; 2009 Apr;44(4):273-6
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  • [Title] [Treatment of malignant ovarian germ cell tumors with relapse or failed in primary therapy].
  • OBJECTIVE: To study the clinical characteristic, the optimal treatments and the prognosis for the recurrence and failure of primary treatment in malignant ovarian germ cell tumors (MOGCT).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Germ Cell and Embryonal / therapy. Ovarian Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Chemotherapy, Adjuvant. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / therapy. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Treatment Outcome. Young Adult. alpha-Fetoproteins / analysis

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  • (PMID = 19570465.001).
  • [ISSN] 0529-567X
  • [Journal-full-title] Zhonghua fu chan ke za zhi
  • [ISO-abbreviation] Zhonghua Fu Chan Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha-Fetoproteins
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74. Kumano M, Miyake H, Hara I, Furukawa J, Takenaka A, Fujisawa M: First-line high-dose chemotherapy combined with peripheral blood stem cell transplantation for patients with advanced extragonadal germ cell tumors. Int J Urol; 2007 Apr;14(4):336-8
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  • [Title] First-line high-dose chemotherapy combined with peripheral blood stem cell transplantation for patients with advanced extragonadal germ cell tumors.
  • BACKGROUND: The objective of this study was to evaluate the efficacy and safety of first-line high-dose chemotherapy (HDCT) combined with peripheral blood stem cell transplantation (PBSCT) for patients with advanced extragonadal germ cell tumors (EGGCT).
  • As a rule, HDCT was continuously administered until alpha-fetoprotein (AFP) and beta-human chorionic gonadotropin normalized (beta-HCG).
  • RESULTS: Following 1-6 courses of HDCT (median, 4 courses), beta-HCG and AFP were normalized in all patients, and five and one patient were diagnosed as showing partial remission and stable disease, respectively.
  • Five patients underwent surgical resection of residual tumors after HDCT, yielding necrotic tissue in two, mature teratoma in two, and viable cancer tissue in one, and the surgical margin was negative in all patients.
  • At a median follow-up of 36 months, five patients were alive and disease-free, whereas the remaining one died of disease progression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Mediastinal Neoplasms / therapy. Neoplasms, Germ Cell and Embryonal / therapy. Peripheral Blood Stem Cell Transplantation. Peritoneal Neoplasms / therapy. Retroperitoneal Neoplasms / therapy

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  • (PMID = 17470166.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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75. Sugai M, Umezu H, Yamamoto T, Jiang S, Iwanari H, Tanaka T, Hamakubo T, Kodama T, Naito M: Expression of hepatocyte nuclear factor 4 alpha in primary ovarian mucinous tumors. Pathol Int; 2008 Nov;58(11):681-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of hepatocyte nuclear factor 4 alpha in primary ovarian mucinous tumors.
  • Hepatocyte nuclear factor 4 alpha (HNF4 alpha) is a member of the nuclear receptor superfamily and is expressed in several endodermal tissues.
  • The aim of the present study was to examine the expression of HNF4 alpha on ovarian epithelial tumors with immunocytochemistry and immunohistochemistry using mAbs recognizing P1 and P2 promoter-driven HNF4 alpha.
  • Ovarian mucinous adenoma, mucinous tumors of borderline malignancy, and mucinous adenocarcinoma had positive nuclear staining for HNF4 alpha (41/45, 91%).
  • One-third (34%) of mucinous tumors had P1-positive staining and most had P1/P2-positive staining (93%).
  • MUC2- and MUC5AC-positive staining was observed in 34% and 95% of mucinous tumors, respectively.
  • The histological subtype of these mucinous tumors was not correlated with HNF4 alpha expression.
  • On cytology it was found that cancer cells in the ascites from ovarian mucinous adenocarcinomas were HNF4 alpha positive, but tumor cells in ascites from other types of ovarian carcinomas were negative for HNF4 alpha.
  • Thus, HNF4 alpha is demonstrated to be a useful marker for histological and cytological diagnosis of ovarian mucinous tumors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Cystadenocarcinoma, Mucinous / metabolism. Cystadenoma, Mucinous / metabolism. Hepatocyte Nuclear Factor 4 / metabolism. Ovarian Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Ascitic Fluid / metabolism. Ascitic Fluid / pathology. Cell Nucleus / metabolism. Cell Nucleus / pathology. Female. Humans. Immunohistochemistry. Middle Aged. Mucin 5AC. Mucin-2. Mucins / metabolism

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  • (PMID = 18844932.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HNF4A protein, human; 0 / Hepatocyte Nuclear Factor 4; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucins
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76. Kitamura Y: Gastrointestinal stromal tumors: past, present, and future. J Gastroenterol; 2008;43(7):499-508
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  • [Title] Gastrointestinal stromal tumors: past, present, and future.
  • Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract.
  • The name "GIST" was proposed in 1983, but the cell origin of GIST remained unclear until 1998, when my colleagues and I reported immunohistochemical evidence that GIST originated from interstitial cells of Cajal or their precursors.
  • Although various mutations of Kit and Pdgfr-alpha genes have been found in GISTs, most GISTs are luckily imatinibsensitive.
  • After long-term administration of imatinib, however, new imatinib-resistant clones develop a secondary mutation of the Kit or Pdgfr-alpha gene.
  • [MeSH-major] Gastrointestinal Stromal Tumors
  • [MeSH-minor] Animals. Humans. Mastocytosis / genetics. Mutation. Neoplasms, Germ Cell and Embryonal / genetics. Proto-Oncogene Proteins c-kit / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics

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  • (PMID = 18648736.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 100
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77. Roth LM, Talerman A: Recent advances in the pathology and classification of ovarian germ cell tumors. Int J Gynecol Pathol; 2006 Oct;25(4):305-20
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  • [Title] Recent advances in the pathology and classification of ovarian germ cell tumors.
  • In recent years, our knowledge of ovarian germ cell tumors has increased, and their classification has evolved.
  • The introduction of cisplatin-based chemotherapy and the discovery of tumor markers, including alpha-fetoprotein and human chorionic gonadotropin, have dramatically changed the clinical outlook for most of these patients.
  • In this review, recent advances in the classification and pathology of ovarian germ cell tumors are discussed.
  • Where appropriate, comparisons are made with testicular germ cell tumors.
  • The last section of the article discusses the pathogenesis of germ cell tumors.
  • This review will emphasize the articles written in the last 10 years and those that have significantly advanced our knowledge of germ cell tumors in past decades.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / classification. Neoplasms, Germ Cell and Embryonal / pathology. Ovarian Neoplasms / classification. Ovarian Neoplasms / pathology
  • [MeSH-minor] Carcinoid Tumor / classification. Carcinoid Tumor / pathology. Carcinoma, Embryonal / classification. Carcinoma, Embryonal / pathology. Choriocarcinoma / classification. Choriocarcinoma / pathology. Dysgerminoma / classification. Dysgerminoma / pathology. Endodermal Sinus Tumor / classification. Endodermal Sinus Tumor / pathology. Female. Humans. Teratoma / classification. Teratoma / pathology

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  • (PMID = 16990705.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 102
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78. Seo DW: EUS-Guided Antitumor Therapy for Pancreatic Tumors. Gut Liver; 2010 Sep;4 Suppl 1:S76-81

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  • [Title] EUS-Guided Antitumor Therapy for Pancreatic Tumors.
  • Endoscopic ultrasound (EUS) is a very useful modality for the diagnosis and staging of pancreatic masses.
  • With the advent of EUS-guided fine-needle aspiration technology, this modality has made a tremendous leap from imaging modality to histologic diagnosis and therapeutic intervention.
  • EUS offers high-resolution images of and unparalleled access to the pancreas.
  • After locating the tip of the echoendoscope in the duodenum or stomach, several drugs or local treatment modalities can be delivered directly into the pancreas.
  • EUS-guided ethanol lavage with/without paclitaxel injection has been tested for the treatment of cystic tumors of the pancreas, with complete resolution of cystic tumor being observed in up to 70-80% of patients.
  • Ethanol injection is also performed for the management of solid neuroendocrine tumors of the pancreas.
  • Various type of EUS-guided injection have also been investigated for the treatment of pancreatic cancer.
  • An activated allogenic mixed lymphocyte culture (Cytoimplant) was injected in patients with advanced pancreatic cancer.
  • A replication-deficient adenovirus vector carrying the tumor necrosis factor-alpha gene was also delivered intratumorally by EUS.
  • ONYX-015 is an oncolytic attenuated adenovirus that exhibits replication preferentially in malignant cells, causing cell death, and this has also been injected into pancreatic cancers under EUS guidance.
  • This article reviews the various applications of EUS for the treatment of pancreatic tumors.

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  • (PMID = 21103299.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2989554
  • [Keywords] NOTNLM ; Brachytherapy / Cystic tumor / Cytoimplant / Endoscopic ultrasonography / Immunotherapy / Pancreas cancer / Photodynamic therapy / Radiofrequency ablation
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79. Battaglia M, Ditonno P, Palazzo S, Bettocchi C, Selvaggio O, Garofalo L, Selvaggi FP: Bilateral tumors of the testis in 21-alpha hydroxylase deficiency without adrenal hyperplasia. Urol Oncol; 2005 May-Jun;23(3):178-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral tumors of the testis in 21-alpha hydroxylase deficiency without adrenal hyperplasia.
  • Congenital 21-alpha hydroxylase deficiency is a syndrome characterized by a cortisol synthesis deficiency and, rarely, by testicular masses.
  • We present a case of bilateral nodular hyperplasia of the testis without adrenal hyperplasia in a patient affected by 21-alpha hydroxylase deficiency.
  • This mass mimicked a testicular tumor and made differential diagnosis with a Leydig cell tumor extremely difficult.
  • The final histological diagnosis was that of multiple, well-circumscribed nodules consisting of cord-like and microalveolar-like gonadal stroma, typical of an adrenogenital syndrome, and fibrosis.
  • Differential diagnosis between testicular nodules in patients with congenital adrenal hyperplasia and Leydig cell tumors is a major clinical challenge.
  • In cases of cortisol suppression resistant testicular masses, a serum adrenal hormone profile obtained from the gonadal vein and histology of the testicular nodule (with parenchyma sparing surgery) are recommended to obtain a correct diagnosis.
  • [MeSH-major] Adrenal Hyperplasia, Congenital / complications. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / pathology. Testicular Diseases / diagnosis. Testicular Diseases / pathology. Testicular Neoplasms / diagnosis. Testicular Neoplasms / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Functional Laterality. Humans. Hyperplasia / diagnosis. Male

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  • (PMID = 15907717.001).
  • [ISSN] 1078-1439
  • [Journal-full-title] Urologic oncology
  • [ISO-abbreviation] Urol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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80. Hwang W, Jung K, Jeon Y, Yun S, Kim TW, Choi I: Knockdown of the interleukin-6 receptor alpha chain of dendritic cell vaccines enhances the therapeutic potential against IL-6 producing tumors. Vaccine; 2010 Dec 10;29(1):34-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Knockdown of the interleukin-6 receptor alpha chain of dendritic cell vaccines enhances the therapeutic potential against IL-6 producing tumors.
  • Tumor microenvironment has emerged as one of the major obstacles against the clinical efficacy of dendritic cell (DC) vaccines.
  • Tumor-derived IL-6 may inhibit the differentiation of hematopoietic progenitor cells into DCs and suppress DC maturation, rendering DCs tolerogenic.
  • We hypothesized that silencing the IL-6 receptor alpha chain (IL-6Rα) would restore the functional competence of DC vaccines in mice with an IL-6-producing TC-1 tumor, and eventually give rise to protective immunity.
  • We found that the IL-6Rα knockdown-DC vaccine significantly enhanced the frequency of tumor-specific CD8(+) CTLs-producing effector molecules such as IFN-γ, TNF-α, FasL, perforin, and granzyme B, and generated more CD8(+) memory T cells, leading to the substantially prolonged survival of TC-1 tumor-bearing mice.
  • [MeSH-major] Cancer Vaccines / immunology. Dendritic Cells / immunology. Gene Knockdown Techniques. Interleukin-6 / secretion. Interleukin-6 Receptor alpha Subunit / biosynthesis. Neoplasms / therapy

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20974308.001).
  • [ISSN] 1873-2518
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Interleukin-6; 0 / Interleukin-6 Receptor alpha Subunit
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81. Arazi L, Cooks T, Schmidt M, Keisari Y, Kelson I: The treatment of solid tumors by alpha emitters released from (224)Ra-loaded sources-internal dosimetry analysis. Phys Med Biol; 2010 Feb 21;55(4):1203-18

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The treatment of solid tumors by alpha emitters released from (224)Ra-loaded sources-internal dosimetry analysis.
  • Diffusing alpha-emitters radiation therapy (DART) is a proposed new form of brachytherapy, allowing the treatment of solid tumors by alpha particles.
  • DART utilizes implantable sources carrying small activities of radium-224, which continually release into the tumor radon-220, polonium-216 and lead-212 atoms, while radium-224 itself remains fixed to the source.
  • The released atoms disperse inside the tumor by diffusive and convective processes, creating, through their alpha emissions, a high-dose region measuring several mm in diameter about each source.
  • The efficacy of DART has been demonstrated in preclinical studies on mice-borne squamous cell carcinoma and lung tumors and the method is now being developed toward clinical trials.
  • This work studies DART safety with respect to the dose delivered to distant organs as a result of lead-212 leakage from the tumor through the blood, relying on a biokinetic calculation coupled to internal dose assessments.
  • Assuming a typical source spacing of approximately 5 mm and a typical radium-224 activity density of 0.4-0.8 MBq g(-1) of tumor tissue, it is predicted that tumors weighing up to several hundred grams may be treated without reaching the tolerance dose in any organ.
  • [MeSH-major] Alpha Particles / therapeutic use. Brachytherapy / methods. Radioisotopes / therapeutic use. Radium / therapeutic use
  • [MeSH-minor] Animals. Bone Marrow / radiation effects. Carcinoma, Squamous Cell / radiotherapy. Female. Humans. Kidney / radiation effects. Kinetics. Lead Radioisotopes / adverse effects. Lead Radioisotopes / blood. Lead Radioisotopes / therapeutic use. Lung Neoplasms / radiotherapy. Male. Mice. Models, Biological. Radiometry. Radiotherapy Dosage

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  • (PMID = 20124656.001).
  • [ISSN] 1361-6560
  • [Journal-full-title] Physics in medicine and biology
  • [ISO-abbreviation] Phys Med Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Lead Radioisotopes; 0 / Radioisotopes; W90AYD6R3Q / Radium
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82. Max D, Hesse M, Volkmer I, Staege MS: High expression of the evolutionarily conserved alpha/beta hydrolase domain containing 6 (ABHD6) in Ewing tumors. Cancer Sci; 2009 Dec;100(12):2383-9
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  • [Title] High expression of the evolutionarily conserved alpha/beta hydrolase domain containing 6 (ABHD6) in Ewing tumors.
  • Despite improvements in the treatment of patients with Ewing family tumors (EFT), the prognosis for patients with advanced disease is still unsatisfactory.
  • Lipase I is a member of the large protein superfamilies of alpha/beta hydrolases and serine hydrolases.
  • By DNA microarray data base mining we found exceptional high expression of alpha/beta hydrolase domain containing 6 (ABHD6) in EFT but not in other sarcomas.
  • High expression of ABHD6 in EFT in comparison to normal tissues and other tumors suggests that ABHD6 might be an interesting new diagnostic or therapeutic target for EFT.
  • However, knock down of ABHD6 in EFT cells did not inhibit tumor cell growth.
  • [MeSH-minor] Bone Neoplasms. Carboxylic Ester Hydrolases / genetics. Cell Line, Tumor. Evolution, Molecular. Humans. Lipase / genetics. Prognosis

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  • (PMID = 19793082.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.1 / CES1 protein, human; EC 3.1.1.23 / ABHD6 protein, human; EC 3.1.1.23 / Monoacylglycerol Lipases; EC 3.1.1.3 / Lipase
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83. Moll R, Holzhausen HJ, Mennel HD, Kuhn C, Baumann R, Taege C, Franke WW: The cardiac isoform of alpha-actin in regenerating and atrophic skeletal muscle, myopathies and rhabdomyomatous tumors: an immunohistochemical study using monoclonal antibodies. Virchows Arch; 2006 Aug;449(2):175-91
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  • [Title] The cardiac isoform of alpha-actin in regenerating and atrophic skeletal muscle, myopathies and rhabdomyomatous tumors: an immunohistochemical study using monoclonal antibodies.
  • The two sarcomeric isoforms of actins, cardiac and skeletal muscle alpha-actin, are highly homologous so that their immunohistochemical distinction is extremely difficult.
  • Taking advantage of monoclonal antibodies distinguishing the two conservative amino acid exchanges near the aminoterminus, we have performed an extended immunohistochemical analysis of the cardiac alpha-actin (CAA) isoform in normal, regenerating, diseased and neoplastic human muscle tissues.
  • By contrast, CAA synthesis is markedly induced in regenerating skeletal muscle cells, in Duchenne muscular dystrophy and upon degenerative atrophy.
  • CAA has also been detected in certain vascular and visceral smooth muscle cells.
  • Among tumors, CAA has consistently been seen in rhabdomyosarcomas and rhabdomyomatous cells of nephroblastomas, whereas, smooth muscle tumors have shown only occasional staining.
  • [MeSH-minor] Adult. Biomarkers, Tumor. Cell Differentiation. Fetus / chemistry. Humans. Immunohistochemistry. Myocytes, Smooth Muscle / chemistry

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  • (PMID = 16715231.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Actins; 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor
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84. Mantovani G, Lania AG, Spada A: GNAS imprinting and pituitary tumors. Mol Cell Endocrinol; 2010 Sep 15;326(1-2):15-8
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  • [Title] GNAS imprinting and pituitary tumors.
  • Evidence from in vitro studies and naturally occurring human diseases indicate that several endocrine cells, and particularly somatotrophs, recognize cAMP as a growth factor.
  • Accordingly, mutations of the alpha subunit of the stimulatory G protein gene (GNAS) leading to the constitutive activation of adenylyl cyclase (the so-called gsp oncogene) have been found in a significant proportion of GH-secreting pituitary adenomas.
  • Due to the monoallelic origin of Gsalpha in normal pituitary gsp mutations occur on a maternal allele in order to have a phenotypic effect in both sporadic GH-secreting adenomas and those associated with the McCune-Albright syndrome.
  • Moreover, this imprinted expression pattern appears to be relaxed in the majority of tumors negative for gsp that show biallelic expression of Gsalpha transcript.
  • Interestingly, the clinical phenotype of gsp negative tumors containing high levels of Gsalpha mRNA and protein is similar to that characterizing gsp positive tumors.
  • Therefore, genetic and epigenetic alterations of the GNAS gene, with subsequent dysregulation of the cAMP pathway, appear, to date, the only molecular hallmark of most GH-secreting adenomas.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Pituitary Neoplasms / genetics
  • [MeSH-minor] Animals. Cyclic AMP-Dependent Protein Kinases / metabolism. Fibrous Dysplasia, Polyostotic / genetics. Genomic Imprinting. Growth Hormone-Secreting Pituitary Adenoma / genetics. Humans. Mice. Pituitary Gland / pathology

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20398730.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.1.- / GNAS protein, human; EC 3.6.1.- / Gnas protein, mouse; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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85. Jain SS, Bird RP: Elevated expression of tumor necrosis factor-alpha signaling molecules in colonic tumors of Zucker obese (fa/fa) rats. Int J Cancer; 2010 Nov 1;127(9):2042-50
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  • [Title] Elevated expression of tumor necrosis factor-alpha signaling molecules in colonic tumors of Zucker obese (fa/fa) rats.
  • Zucker obese rats are highly sensitive to colon cancer and possess a plethora of metabolic abnormalities including elevated levels of cytokine tumor necrosis factor-alpha (TNF-alpha).
  • The main objective of this study was to determine if physiologically elevated TNF-alpha affects colonic tumor phenotype with regard to an altered TNF-alpha signaling pathway.
  • After 30 weeks, the animals were terminated and physiological and tumor parameters were assessed.
  • Obese rats had notably higher body and organ weights as well as plasma TNF-alpha, insulin and leptin levels than lean or SD animals.
  • A 100% tumor incidence and significantly higher tumor size, multiplicity and burden were found in obese rats compared to the lean group that had 47.8% tumor incidence.
  • The SD group had the lowest tumor incidence (20.0%).
  • Tumors from obese animals had higher protein levels of TNF-alpha, TNF-alpha-receptor-2 (TNFR2), nuclear transcription factor-kappaB (NF-kappaB) and IkappaB-kinasebeta (IKKbeta) compared to lean animals.
  • In both obese and lean groups, expression levels of these proteins were higher in tumors than in surrounding, normal-appearing colonic mucosae.
  • These findings support an important role for TNF-alpha signaling in tumorigenesis and demonstrate that tumors growing in an obese state had significantly different expression levels of TNFR2 and NF-kappaB, proteins known to play a critical role in growth and survival, than those growing in the lean state.
  • It is concluded that the physiological state of the host intricately affects tumor phenotype.
  • [MeSH-major] Colonic Neoplasms / metabolism. Obesity / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Azoxymethane. Blood Cell Count. Female. NF-kappa B / metabolism. Protein-Serine-Threonine Kinases / metabolism. Rats. Rats, Sprague-Dawley. Rats, Zucker. Receptors, Tumor Necrosis Factor, Type II / metabolism. Signal Transduction

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  • (PMID = 20143392.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.25 / NF-kappa B kinase; MO0N1J0SEN / Azoxymethane
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86. Ritz-Laser B, Mamin A, Brun T, Avril I, Schwitzgebel VM, Philippe J: The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression. Mol Endocrinol; 2005 Mar;19(3):759-70
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  • [Title] The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression.
  • We show here that Gata-4 and/or Gata-6 are not only expressed in the adult exocrine pancreas but also in glucagonoma and insulinoma cell lines, whereas Gata-5 is restricted to the exocrine pancreas.
  • During pancreas development, Gata-4 is expressed already at embryonic d 10.5 and colocalizes with early glucagon+ cells at embryonic d 12.5.
  • Gata-4 was able to transactivate the glucagon gene both in heterologous BHK-21 (nonislet Syrian baby hamster kidney) and in glucagon-producing InR1G9 cells.
  • Using gel-mobility shift assays, we identified a complex formed with nuclear extracts from InR1G9 cells on the G5 control element (-140 to -169) of the glucagon gene promoter as Gata-4.
  • Mutation of the GATA binding site on G5 abrogated the transcriptional activation mediated by Gata-4 and reduced basal glucagon gene promoter activity in glucagon-producing cells by 55%.
  • Furthermore, Gata-4 acted more than additively with Forkhead box A (hepatic nuclear factor-3) to trans-activate the glucagon gene promoter.
  • We conclude that, besides its role in endoderm differentiation, Gata-4 might be implicated in the regulation of glucagon gene expression in the fetal pancreas and that Gata activity itself may be modulated by interactions with different cofactors.
  • [MeSH-major] DNA-Binding Proteins / chemistry. Gene Expression Regulation. Glucagon / metabolism. Islets of Langerhans / metabolism. Transcription Factors / chemistry. Zinc Fingers
  • [MeSH-minor] Animals. Base Sequence. Binding Sites. Cell Differentiation. Cell Line. Cell Nucleus / metabolism. Chloramphenicol O-Acetyltransferase / metabolism. Cricetinae. Dose-Response Relationship, Drug. GATA4 Transcription Factor. GATA6 Transcription Factor. Humans. Mice. Microscopy, Fluorescence. Molecular Sequence Data. Mutation. Pancreas / embryology. Promoter Regions, Genetic. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tissue Distribution. Transcriptional Activation. Transfection


87. Möller E, Mandahl N, Mertens F, Panagopoulos I: Molecular identification of COL6A3-CSF1 fusion transcripts in tenosynovial giant cell tumors. Genes Chromosomes Cancer; 2008 Jan;47(1):21-5
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  • [Title] Molecular identification of COL6A3-CSF1 fusion transcripts in tenosynovial giant cell tumors.
  • Tenosynovial giant cell tumors (TGCTs) are benign lesions of the tendon sheaths that primarily affect the fingers, ankles, or feet.
  • The genes involved in the translocation t(1;2)(p13;q37) were recently identified: the colony-stimulating factor-1 (CSF1 or M-CSF1) at 1p13 and the collagen type VI alpha-3 (COL6A3) at 2q37.
  • [MeSH-major] Collagen Type VI / genetics. Giant Cell Tumors / genetics. Macrophage Colony-Stimulating Factor / genetics. Oncogene Proteins, Fusion / genetics. Synovial Membrane / metabolism

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  • (PMID = 17918257.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type VI; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 81627-83-0 / Macrophage Colony-Stimulating Factor
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88. Yu CH, Hwang DN, Yhee JY, Kim JH, Im KS, Nho WG, Lyoo YS, Sur JH: Comparative immunohistochemical characterization of canine seminomas and Sertoli cell tumors. J Vet Sci; 2009 Mar;10(1):1-7

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  • [Title] Comparative immunohistochemical characterization of canine seminomas and Sertoli cell tumors.
  • Primary testicular tumors are the most common causes of cancer in male dogs.
  • However, tumor markers are not well-known in veterinary medicine.
  • We sought to determine using immunohistochemistry whether the combined human testicular tumor markers (placental alkaline phosphatase, OCT3/4, CD30, alpha-fetoprotein, inhibin-alpha, vimentin, c-KIT, and desmin) are expressed in canine seminomas and Sertoli cell tumors (SCTs).
  • We examined 35 canine testicular tumors, 20 seminomas and 15 SCTs. c-KIT was expressed markedly in canine seminomas.
  • Both inhibin-alpha and vimentin were expressed significantly in canine SCTs.
  • The results of this study demonstrate differences and similarities between tumor marker expression of testicular tumors in dogs and humans.
  • All the main markers in current routine use are discussed as well as potential useful markers for benign and malignant tumors, and tumor progression.
  • [MeSH-major] Dog Diseases / pathology. Immunohistochemistry / veterinary. Seminoma / veterinary. Sertoli Cell Tumor / veterinary
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Dogs. Male

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  • (PMID = 19255517.001).
  • [ISSN] 1229-845X
  • [Journal-full-title] Journal of veterinary science
  • [ISO-abbreviation] J. Vet. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2801099
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89. Akihara Y, Shimoyama Y, Kawasako K, Komine M, Hirayama K, Kagawa Y, Omachi T, Matsuda K, Okamoto M, Kadosawa T, Taniyama H: Immunohistochemical evaluation of canine ovarian tumors. J Vet Med Sci; 2007 Jul;69(7):703-8
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  • [Title] Immunohistochemical evaluation of canine ovarian tumors.
  • Canine ovarian tumors (epithelial tumor, sex-cord stromal tumor, germ cell tumor) classifying into 9 histological types were examined immunohistochemically using placental alkaline phosphatase (PLAP), cytokeratin7 (CK7), desmin, S100, AE1/AE3, inhibin alpha, vimentin, and alfa feto-protein (AFP).
  • The papillary and tubular types observed in epithelial tumors were immunoreactive for desmin and AE1/AE3.
  • The solid type, nest type, cord type, palisade type, cystic type and spindle type, which were observed in sex-cord stromal tumors, showed a positive immunoreaction for S100 but little or no positive immunoreaction for inhibin alpha with an exception of positive result in the palisade type.
  • Most of the sex-cord stromal tumors were AE1/AE3-positive except for the palisade type.
  • In the cobblestone type observed in germ cell tumors, only vimentin and AFP were positive.
  • The present study elucidated the detailed histological and immunohistochemical characteristics of canine ovarian tumors.

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  • (PMID = 17675800.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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90. Duensing S, Duensing A: Targeted therapies of gastrointestinal stromal tumors (GIST)--the next frontiers. Biochem Pharmacol; 2010 Sep 1;80(5):575-83
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  • [Title] Targeted therapies of gastrointestinal stromal tumors (GIST)--the next frontiers.
  • Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal (GI) tract and are caused by activating KIT or PDGFRA mutations.
  • Recent results have shown that although imatinib effectively stimulates apoptotic cell death in sensitive GIST cells, a considerable proportion of cells does not undergo apoptosis, but instead enters a state of quiescence.
  • Quiescence is characterized by a reversible withdrawal from the cell division cycle, during which the cells remain alive and metabolically active.
  • It is conceivable that quiescence not only plays a pivotal role in the emergence of residual disease but also in creating a pool of tumor cells that survive continuous small molecule therapy and may hence represent the "seeds" for the outgrowth of resistant clones.
  • In addition, we will highlight future strategies to design more effective treatment options to overcome these problems with an aim towards cure of this hitherto untreatable tumor entity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gastrointestinal Stromal Tumors / drug therapy. Piperazines / therapeutic use. Proto-Oncogene Proteins c-kit / drug effects. Pyrimidines / therapeutic use. Receptor, Platelet-Derived Growth Factor alpha / drug effects

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20385106.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 150
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91. Höltje M, Richartz A, Zdrazil B, Schwanke A, Dugovic B, Murruzzu C, Reissig HU, Korting HC, Kleuser B, Höltje HD, Schäfer-Korting M: Human polymerase alpha inhibitors for skin tumors. Part 2. Modeling, synthesis and influence on normal and transformed keratinocytes of new thymidine and purine derivatives. J Enzyme Inhib Med Chem; 2010 Apr;25(2):250-65
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  • [Title] Human polymerase alpha inhibitors for skin tumors. Part 2. Modeling, synthesis and influence on normal and transformed keratinocytes of new thymidine and purine derivatives.
  • Recently, the three-dimensional structure of the active site of human DNA polymerase alpha (pol alpha) was proposed based on the application of molecular modeling methods and molecular dynamic simulations.
  • The modeled structure of the enzyme was used for docking selective inhibitors (nucleotide analogs and the non-nucleoside inhibitor aphidicolin) in its active site in order to design new drugs for actinic keratosis and squamous cell carcinoma (SCC).
  • The resulting complexes explained the geometrical and physicochemical interactions of the inhibitors with the amino acid residues involved in binding to the catalytic site, and offered insight into the experimentally derived binding data.
  • The proposed structures were synthesized and tested in vitro for their influence on human keratinocytes and relevant tumor cell lines.
  • Effects were compared to aphidicolin which inhibits pol alpha in a non-competitive manner, as well as to diclofenac and 5-fluorouracil, both approved for therapy of actinic keratosis.
  • Thus, the combination of modeling studies and in vitro tests should allow the derivation of new drug candidates for the therapy of skin tumors, given that the agents are not relevant substrates of nucleotide transporters expressed by skin cancer cells.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. DNA Polymerase I / antagonists & inhibitors. Keratosis, Actinic / drug therapy. Models, Chemical. Models, Molecular. Nucleic Acid Synthesis Inhibitors. Skin Neoplasms / drug therapy
  • [MeSH-minor] Aphidicolin / chemistry. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Keratinocytes. Necrosis. Nucleotide Transport Proteins / genetics. Nucleotide Transport Proteins / metabolism. Protein Binding. Purines / chemistry. Thymidine / chemistry

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  • (PMID = 20222764.001).
  • [ISSN] 1475-6374
  • [Journal-full-title] Journal of enzyme inhibition and medicinal chemistry
  • [ISO-abbreviation] J Enzyme Inhib Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nucleic Acid Synthesis Inhibitors; 0 / Nucleotide Transport Proteins; 0 / Purines; 38966-21-1 / Aphidicolin; EC 2.7.7.- / DNA Polymerase I; VC2W18DGKR / Thymidine; W60KTZ3IZY / purine
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92. da Silva NS, Cappellano AM, Diez B, Cavalheiro S, Gardner S, Wisoff J, Kellie S, Parker R, Garvin J, Finlay J: Primary chemotherapy for intracranial germ cell tumors: results of the third international CNS germ cell tumor study. Pediatr Blood Cancer; 2010 Mar;54(3):377-83
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  • [Title] Primary chemotherapy for intracranial germ cell tumors: results of the third international CNS germ cell tumor study.
  • BACKGROUND: The treatment of central nervous system (CNS) germ cell tumors (GCT) remains controversial.
  • The purpose of this study was to demonstrate efficacy of a chemotherapy only strategy, with less morbidity, when compared to regimens with irradiation.
  • Twenty-five patients aged 4 months to 24.5 years were stratified: Regimen A consisted of 4-6 cycles of carboplatin/etoposide alternating with cyclophosphamide/etoposide for low risk (LR) localized germinoma with normal cerebrospinal fluid (CSF) and serum tumor markers.
  • Regimen B consisted of 4-6 cycles of carboplatin/cyclophosphamide/etoposide for intermediate-risk (IR) germinoma with positive human chorionic gonadotrophin-beta (HCGbeta) and/or CSF HCGbeta <50 mIU/ml and high-risk (HR) biopsy-proven non-germinomatous malignant elements (MMGCT) or elevated serum/CSF alpha-fetoprotein and/or HCGbeta serum/CSF >50 mIU/ml.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Neoplasms, Germ Cell and Embryonal / drug therapy

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 20063410.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin
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93. Zeren T, Inan S, Seda Vatansever H, Ekerbicer N, Sayhan S: Significance of tyrosine kinase activity on malign transformation of ovarian tumors: a comparison between EGF-R and TGF-alpha. Acta Histochem; 2008;110(3):256-63
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  • [Title] Significance of tyrosine kinase activity on malign transformation of ovarian tumors: a comparison between EGF-R and TGF-alpha.
  • Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha) are members of the polypeptide growth factor family.
  • Many types of cancer, including ovarian cancer, display enhanced EGF-R immunoreactivity on their cell surface membranes.
  • Also, an increase in TGF-alpha synthesis and secretion usually occurs in human carcinoma cell lines.
  • In this study, we compared the immunoreactivities of TGF-alpha and EGF-R in ovarian tumors and related immunohistochemical findings to the histological type of the tumors.
  • Formalin-fixed, paraffin wax-embedded tissue sections from 40 patients who had serous-mucinous borderline tumor and serous-mucinous adenocarcinoma of the ovary (n=10 each) were stained with hematoxylin-eosin and labeled for binding of primary antibodies against TGF-alpha and EGF-R using an avidin-biotin-peroxidase method.
  • Increased immunoreactivity of EGF-R and moderate immunoreactivity of TGF-alpha was detected in adenocarcinomas.
  • There was no significant difference in the immunoreactivity of TGF-alpha among the histologic types of ovarian tumors.
  • The results of this study support the hypothesis that EGF-R may be a more useful marker than TGF-alpha in epithelial ovarian tumors.
  • [MeSH-major] Ovarian Neoplasms / pathology. Protein-Tyrosine Kinases / metabolism. Receptor, Epidermal Growth Factor / metabolism. Transforming Growth Factor alpha / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Disease Progression. Epidermal Growth Factor / metabolism. Female. Humans. Immunohistochemistry. Middle Aged. Paraffin Embedding / methods. Receptor Protein-Tyrosine Kinases / metabolism

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  • (PMID = 18054376.001).
  • [ISSN] 0065-1281
  • [Journal-full-title] Acta histochemica
  • [ISO-abbreviation] Acta Histochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor alpha; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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94. Bezerra MG, Latronico AC, Fragoso MC: [Endocrine tumors associated to protein Gsalpha/Gi2alpha mutations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):784-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Endocrine tumors associated to protein Gsalpha/Gi2alpha mutations].
  • Many oncogenic mutations promote tumor growth by inducing autonomous activity of proteins that normally transmit proliferative signal initiated by extracellular factors.
  • G proteins are a family of guanine nucleotide binding proteins, which are structurally homologous and widely distributed in eukaryotic cells.
  • They are composed of three different subunits (alpha, beta e gamma).
  • The alpha subunit, which contains the guanine nucleotide-binding site, is unique to each G protein.
  • The G proteins couple an array of seven transmembrane receptors at the cell surface with a variety of intracellular effectors, which produce second messenger molecules.
  • A subset of endocrine tumors, such as GH- or ACTH-secreting pituitary adenomas, functioning thyroid adenomas, adrenocortical and gonadal tumors were associated with somatic activating mutations in the highly conserved codons of the Gs (Arg201 and Gln227) and Gi (Arg179 and Gln205) proteins.
  • [MeSH-major] Endocrine Gland Neoplasms / genetics. GTP-Binding Protein alpha Subunits, Gi-Go / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mutation / genetics. Oncogenes / genetics

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  • (PMID = 16444361.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 64
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95. Gilbert JA, Adhikari LJ, Lloyd RV, Rubin J, Haluska P, Carboni JM, Gottardis MM, Ames MM: Molecular markers for novel therapies in neuroendocrine (carcinoid) tumors. Endocr Relat Cancer; 2010 Sep;17(3):623-36
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular markers for novel therapies in neuroendocrine (carcinoid) tumors.
  • Neuroendocrine (carcinoid) tumors (NETs) are endocrine neoplasms occurring most frequently in gastrointestinal and bronchopulmonary (BP) systems.
  • The majority of patients present with advanced disease for which few treatment options exist.
  • Activating mutations were assessed in epidermal growth factor receptor (EGFR), stem cell factor receptor (KIT), and platelet-derived growth factor receptor alpha (PDGFRA), as well as non-response mutations in KRAS.
  • Hsp90, TGFBR1, IGF1R, and SSTR5 exhibited highest levels of immunohistochemical staining in the largest percents of tumors.
  • In subsequent in vitro studies, anticancer drug 17-(allylamino)-17-demethoxygeldanamycin (17-AAG) (targeting Hsp90) inhibited proliferation of BP NET lines NCI-H727, NCI-H720, and NCI-H835 with IC(50) values of 70.4, 310, and 788 nM respectively; BMS-754807 (targeting IGF1R/IR) inhibited growth with IC(50) values of 428 nM, 2.8 microM, and 1 microM.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / metabolism. Neuroendocrine Tumors / drug therapy. Neuroendocrine Tumors / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzoquinones / pharmacology. Blotting, Western. Cell Line, Tumor. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Lactams, Macrocyclic / pharmacology. Male. Middle Aged. Polymerase Chain Reaction. Pyrazoles / pharmacology. Retrospective Studies. Tissue Array Analysis. Triazines / pharmacology. Young Adult


96. Lin Q, Lai R, Chirieac LR, Li C, Thomazy VA, Grammatikakis I, Rassidakis GZ, Zhang W, Fujio Y, Kunisada K, Hamilton SR, Amin HM: Constitutive activation of JAK3/STAT3 in colon carcinoma tumors and cell lines: inhibition of JAK3/STAT3 signaling induces apoptosis and cell cycle arrest of colon carcinoma cells. Am J Pathol; 2005 Oct;167(4):969-80
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutive activation of JAK3/STAT3 in colon carcinoma tumors and cell lines: inhibition of JAK3/STAT3 signaling induces apoptosis and cell cycle arrest of colon carcinoma cells.
  • Here, we demonstrate that activated STAT3 (pSTAT3) and activated JAK3 (pJAK3) are expressed constitutively in two colon cancer cell lines, SW480 and HT29.
  • The blockade of JAK3/STAT3 signaling significantly decreased viability of colon cancer cells due to apoptosis and cell-cycle arrest through down-regulation of Bcl-2, Bcl-X(L), Mcl-1, and cyclin D2 and up-regulation of p21(waf1/cip1) and p27(kip1).
  • We also examined histological sections from 22 tumors from patients with stage II or stage IV colon cancer and found STAT3, JAK3, and their activated forms to be frequently expressed.
  • Furthermore, quantitative reverse transcriptase-polymerase chain reaction identified JAK3 mRNA in colon cancer cell lines and primary tumors.
  • [MeSH-major] Apoptosis / physiology. Carcinoma / metabolism. Cell Cycle / physiology. Colonic Neoplasms / metabolism. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Aged. Cell Line, Tumor. Cell Survival / drug effects. Cyclin D2. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclins / metabolism. Enzyme Activation. Enzyme Inhibitors / pharmacology. Female. Gene Expression Regulation, Neoplastic / drug effects. HT29 Cells. Humans. Immunohistochemistry. Janus Kinase 3. Male. Middle Aged. Neoplasm Staging. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Tyrphostins / pharmacology

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  • (PMID = 16192633.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / CDKN1A protein, human; 0 / Cyclin D2; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / JAK3 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Janus Kinase 3
  • [Other-IDs] NLM/ PMC1603671
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97. Pedro RN, Thekke-Adiyat T, Goel R, Shenoi M, Slaton J, Schmechel S, Bischof J, Anderson JK: Use of tumor necrosis factor-alpha-coated gold nanoparticles to enhance radiofrequency ablation in a translational model of renal tumors. Urology; 2010 Aug;76(2):494-8
Hazardous Substances Data Bank. GOLD, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of tumor necrosis factor-alpha-coated gold nanoparticles to enhance radiofrequency ablation in a translational model of renal tumors.
  • OBJECTIVES: Radiofrequency ablation (RFA) has been most effective when the tumors are small, exophytic, and away from vital structures.
  • We enlarged the size of the ablation kill zone by infusing a 30-nm tumor necrosis factor-alpha and polyethylene glycol-coated gold nanoparticle (CYT-6091, CytImmune Sciences, Inc.) before ablation in a rabbit kidney tumor model.
  • MATERIALS AND METHODS: A total of 37 New Zealand White rabbits had VX-2 tumors implanted into their bilateral kidneys; they were then split into 3 treatment groups of 10 rabbits each and a sham group of 7 rabbits as follows:.
  • RESULTS: The RFA + CYT-6091 group had a larger zone of complete cell death than the RFA-only group when measured on microscopic examination (0.30 +/- 0.07 vs 0.23 +/- 0.03 mL, P = .03).
  • CONCLUSIONS: We have demonstrated the efficacy of CYT-6091 in enhancing RFA in a translational kidney tumor model.
  • The potential usage of CYT-6091 to improve RFA of renal cell carcinoma merits further study.
  • [MeSH-major] Catheter Ablation / methods. Disease Models, Animal. Kidney Neoplasms / surgery. Metal Nanoparticles. Tumor Necrosis Factor-alpha / administration & dosage

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [CommentIn] Urology. 2010 Aug;76(2):499 [20696355.001]
  • (PMID = 20451965.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 7440-57-5 / Gold
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98. Gilaberte Y, Vera J, Coscojuela C, Roca MJ, Parrado C, González S: [Expression of galanin in melanocytic tumors]. Actas Dermosifiliogr; 2007 Jan-Feb;98(1):24-34
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of galanin in melanocytic tumors].
  • [Transliterated title] Estudio sobre la expresión de galanina en tumores melanocitarios.
  • Galanin is expressed in different neural, endocrine and neuroendocrine tumors and, on the other hand, several neuropeptides, particularly alpha-MSH, seem to play a role in the pathogenesis of melanoma.
  • OBJECTIVE: To investigate the expression of galanin in cutaneous melanomas and melanocytic nevi and correlate it with alpha-MSH expression and several prognostic factors for melanoma.
  • MATERIAL AND METHODS: We performed an observational and retrospective study of the immunohistochemical expression of galanin and alpha-MSH in samples of cutaneous melanomas diagnosed in the last 5 years in the San Jorge Hospital, Huesca (Spain).
  • Immunostaining with galanin and alpha-MSH was significantly higher in melanomas than in melanocytic nevi (p < 0.001), although spindle cell and blue nevi showed significant expression of alpha-MSH.
  • More than 50 % of nodular melanomas and 90 % of superficial spreading melanomas were positive for galanin and alpha-MSH, and the latter also showed the highest percentage of positive cells for galanin (mean 35.09 +/- 28.16) as well as for alpha-MSH (mean 67.64% +/- 35.38).
  • CONCLUSION: Our study shows the expression of galanin in cutaneous melanoma and its significant correlation with alpha-MSH immunostaining.

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  • (PMID = 17374330.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 88813-36-9 / Galanin
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99. Fan Z, Yu P, Wang Y, Wang Y, Fu ML, Liu W, Sun Y, Fu YX: NK-cell activation by LIGHT triggers tumor-specific CD8+ T-cell immunity to reject established tumors. Blood; 2006 Feb 15;107(4):1342-51
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NK-cell activation by LIGHT triggers tumor-specific CD8+ T-cell immunity to reject established tumors.
  • Natural killer (NK) cells are generally reported as innate effector cells for killing virally infected and transformed cells.
  • It is unclear how NK cells evoke adaptive immunity to eradicate tumors.
  • We now demonstrate that the TNF superfamily member, LIGHT, known as TNFSF14 and a T-cell costimulatory molecule, is a critical ligand for the activation of NK cells.
  • Herpesvirus entry mediator (HVEM) is expressed on NK cells, and its engagement with LIGHT mediates NK-cell activation.
  • The expression of LIGHT inside tumors leads to rapid rejection in a NK-dependent manner.
  • Both NK and CD8+ cells are essential but not sufficient for the rejection of tumors because mice lacking either population fail to reject the tumor.
  • Interestingly, activated NK cells do not kill tumors directly but can facilitate the priming of tumor-specific CD8+ T cells in an IFN-gamma-dependent manner.
  • Conversely, intratumor depletion of either NK cells or IFN-gamma during tumor progression disrupts CD8+ cell-mediated tumor rejection, suggesting that the tumor is the essential site for the crosstalk between NK and CD8+ cells.
  • Furthermore, IFNG-deficient NK cells fail to effectively activate CD8+ T cells, suggesting IFN-gamma plays an important role in NK-mediated activation of cytotoxic T lymphocytes (CTLs).
  • Our findings establish a direct role for LIGHT in NK activation/expansion and a critical helper role of activated NK cells in priming CD8+ T cells and breaking T-cell tolerance at the tumor site.

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  • (PMID = 16223768.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / PHS HHS / / R01-062026; United States / NIDDK NIH HHS / DK / 5T32DK07 074; United States / NCI NIH HHS / CA / P01-CA09296-01; United States / NIDDK NIH HHS / DK / R01-DK58897; United States / NIDDK NIH HHS / DK / P30-DK42086
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / Tnfsf14 protein, mouse; 0 / Tumor Necrosis Factor Ligand Superfamily Member 14; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC1895398
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100. Prat J: Ovarian carcinomas, including secondary tumors: diagnostically challenging areas. Mod Pathol; 2005 Feb;18 Suppl 2:S99-111
MedlinePlus Health Information. consumer health - Ovarian Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ovarian carcinomas, including secondary tumors: diagnostically challenging areas.
  • The differential diagnosis of ovarian carcinomas, including secondary tumors, remains a challenging task.
  • Mucinous carcinomas of the ovary are rare and can be easily confused with metastatic mucinous carcinomas that may present clinically as a primary ovarian tumor.
  • Most of these originate in the gastrointestinal tract and pancreas.
  • International Federation of Gynecology and Obstetrics (FIGO) stage is the single most important prognostic factor, and stage I carcinomas have an excellent prognosis; FIGO stage is largely related to the histologic features of the ovarian tumors.
  • Although immunostains for cytokeratins 7 and 20 can be helpful in the differential diagnosis, they should always be interpreted in the light of all clinical information.
  • Occasionally, endometrioid carcinomas may exhibit a microglandular pattern simulating sex cord-stromal tumors.
  • However, typical endometrioid glands, squamous differentiation, or an adenofibroma component are each present in 75% of these tumors whereas immunostains for calretinin and alpha-inhibin are negative.
  • Most of these tumors have a favorable outcome and they most likely represent independent primary carcinomas arising as a result of a Mullerian field effect.
  • Transitional cell carcinomas are distinguished from undifferentiated carcinomas by the presence of thick, undulating papillae with smooth luminal borders, microspaces, and tumor cells with distinctive 'urothelial' appearance.
  • Krukenberg tumors are metastatic adenocarcinomas traditionally perceived as composed of mucin-filled signet-ring cells associated with a striking proliferation of the ovarian stroma but many variations on this pattern occur.
  • [MeSH-minor] Base Sequence. Colonic Neoplasms / pathology. Cytoskeletal Proteins / genetics. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Intermediate Filament Proteins / analysis. Keratin-20. Keratin-7. Keratins / analysis. Mutation. Prognosis. Trans-Activators / genetics. beta Catenin. ras Proteins / genetics

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  • (PMID = 15492758.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Intermediate Filament Proteins; 0 / KRT20 protein, human; 0 / KRT7 protein, human; 0 / Keratin-20; 0 / Keratin-7; 0 / Trans-Activators; 0 / beta Catenin; 68238-35-7 / Keratins; EC 3.6.5.2 / ras Proteins
  • [Number-of-references] 63
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