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1. Vieni S, Cabibi D, Cipolla C, Fricano S, Graceffa G, Latteri MA: Secretory breast carcinoma with metastatic sentinel lymph node. World J Surg Oncol; 2006;4:88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secretory breast carcinoma with metastatic sentinel lymph node.
  • BACKGROUND: Secretory mammary carcinoma is a rare breast neoplasia originally described in children but sometimes also found in adults.
  • It presents a more favourable outcome than more common histological types of breast carcinoma; published literature in fact reports only a few cases with axillary lymph node metastases and only four cases with distant metastases.
  • CLINICAL PRESENTATION: In this paper we report a rare case of secretory breast carcinoma with axillary lymph node metastases in a 33-year-old woman.
  • To our knowledge, this is the first case of secretory carcinoma involving biopsy of the sentinel lymph node and investigation of the e-cadherin expression.
  • We found positivity for e-cadherin, which would support the hypothesis that this type of tumour is a variant of the infiltrating ductal carcinoma.
  • CONCLUSION: After a careful analysis of reported data, we have come to the conclusion that the treatment of choice for patients with secretory breast carcinoma should be conservative surgery with sentinel lymph node biopsy, followed by accurate follow-up.
  • Although several cases of secretory carcinoma have been treated with adjuvant chemotherapy, there are still no reliable data regarding the real value of such a choice.

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  • (PMID = 17150092.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1764883
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2. Arce C, Cortes-Padilla D, Huntsman DG, Miller MA, Dueñnas-Gonzalez A, Alvarado A, Pérez V, Gallardo-Rincón D, Lara-Medina F: Secretory carcinoma of the breast containing the ETV6-NTRK3 fusion gene in a male: case report and review of the literature. World J Surg Oncol; 2005;3:35

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  • [Title] Secretory carcinoma of the breast containing the ETV6-NTRK3 fusion gene in a male: case report and review of the literature.
  • SUMMARY: Secretory carcinoma (SC) of the breast is a rare and indolent tumor.
  • CASE PRESENTATION: A 52-year-old male was diagnosed with secretory breast carcinoma and underwent a modified radical mastectomy.
  • At 18 months the tumor recurred at the chest wall and the patient developed lung metastases.
  • He was treated concurrently with radiation and chemotherapy without response.
  • There are insufficient data to support the use of adjuvant radiation or chemotherapy.
  • Its association with the ETV6-NTRK3 fusion gene gives some clues for the better understanding of this neoplasm and eventually, the development of specific therapies.

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  • (PMID = 15963235.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1184104
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3. Meyer AN, McAndrew CW, Donoghue DJ: Nordihydroguaiaretic acid inhibits an activated fibroblast growth factor receptor 3 mutant and blocks downstream signaling in multiple myeloma cells. Cancer Res; 2008 Sep 15;68(18):7362-70
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  • Activating mutations within fibroblast growth factor receptor 3 (FGFR3), a receptor tyrosine kinase, are responsible for human skeletal dysplasias including achondroplasia and the neonatal lethal syndromes, Thanatophoric Dysplasia (TD) type I and II.
  • Several of these same FGFR3 mutations have also been identified somatically in human cancers, including multiple myeloma, bladder carcinoma, and cervical cancer.
  • Based on reports that strongly activated mutants of FGFR3 such as the TDII (K650E) mutant signal preferentially from within the secretory pathway, the inhibitory properties of nordihydroguaiartic acid (NDGA), which blocks protein transport through the Golgi, were investigated.
  • In addition, signaling molecules downstream of FGFR3 activation such as signal transducers and activators of transcription (STAT)1, STAT3, and mitogen-activated protein kinase (MAPK) were inhibited by NDGA treatment.

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  • (PMID = 18794123.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA090900-05; United States / NCI NIH HHS / CA / R01 CA090900; United States / NCI NIH HHS / CA / R01 CA090900-05; United States / NCI NIH HHS / CA / R01-CA90900
  • [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 / Lipoxygenase Inhibitors; 103107-01-3 / Fibroblast Growth Factor 2; 132880-11-6 / zileuton; 7BO8G1BYQU / Masoprocol; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 3; X6Q56QN5QC / Hydroxyurea
  • [Other-IDs] NLM/ NIHMS70602; NLM/ PMC2745924
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4. Rosenzweig SA, Atreya HS: Defining the pathway to insulin-like growth factor system targeting in cancer. Biochem Pharmacol; 2010 Oct 15;80(8):1115-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dysregulation of the IGF system is well recognized as a key contributor to the progression of multiple cancers, with IGF-1R activation increasing the tumorigenic potential of breast, prostate, lung, colon and head and neck squamous cell carcinoma (HNSCC).
  • Despite this relationship, targeting the IGF-1R has only recently undergone development as a molecular cancer therapeutic.
  • This is accentuated by the list of over 30 drugs, including monoclonal antibodies (mAbs) and tyrosine kinase inhibitors (TKIs) that are under evaluation as single agents or in combination therapies.
  • The IGF-binding proteins (IGFBPs) represent the third component of the IGF system consisting of a class of six soluble secretory proteins.

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  • (PMID = 20599789.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA138313; United States / NCI NIH HHS / CA / R01 CA134845; United States / NCI NIH HHS / CA / R01 CA-134845
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Somatomedins; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Number-of-references] 110
  • [Other-IDs] NLM/ NIHMS216911; NLM/ PMC2934757
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5. Weiglmeier PR, Rösch P, Berkner H: Cure and curse: E. coli heat-stable enterotoxin and its receptor guanylyl cyclase C. Toxins (Basel); 2010 09;2(9):2213-29
The Lens. Cited by Patents in .

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  • Additionally, GC-C is a specific marker for colorectal carcinoma and STa is suggested to have an inhibitory effect on intestinal carcinogenesis.
  • To understand the conformational events involved in ligand binding to GC-C and to devise therapeutic strategies to treat both diarrheal diseases and colorectal cancer, it is paramount to obtain structural information on the receptor ligand system.
  • Here we summarize the currently available structural data and report on physiological consequences of STa binding to GC-C in intestinal epithelia and colorectal carcinoma cells.
  • [MeSH-major] Bacterial Toxins. Colorectal Neoplasms / drug therapy. Diarrhea / microbiology. Enterotoxigenic Escherichia coli / physiology. Enterotoxins. Escherichia coli Infections / microbiology. Receptors, Guanylate Cyclase-Coupled / metabolism

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  • (PMID = 22069681.001).
  • [ISSN] 2072-6651
  • [Journal-full-title] Toxins
  • [ISO-abbreviation] Toxins (Basel)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Enterotoxins; 0 / Escherichia coli Proteins; 0 / Ligands; 0 / heat stable toxin (E coli); EC 4.6.1.2 / Receptors, Guanylate Cyclase-Coupled
  • [Other-IDs] NLM/ PMC3153297
  • [Keywords] NOTNLM ; colorectal cancer (major topic) / guanylyl cyclase C (major topic) / heat-stable enterotoxin (major topic) / secretory diarrhea (major topic)
  • [General-notes] NLM/ Original DateCompleted: 20111110
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6. Wu CJ, Peng YJ, Yu MH, Chen CH: Secretory endometrial adenocarcinoma in a tamoxifen user with breast cancer after menopause. Taiwan J Obstet Gynecol; 2007 Mar;46(1):88-90
Hazardous Substances Data Bank. TAMOXIFEN .

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  • [Title] Secretory endometrial adenocarcinoma in a tamoxifen user with breast cancer after menopause.
  • [MeSH-major] Antineoplastic Agents, Hormonal / adverse effects. Breast Neoplasms / drug therapy. Carcinoma, Endometrioid / chemically induced. Endometrial Neoplasms / chemically induced. Neoplasms, Second Primary / chemically induced. Postmenopause. Tamoxifen / adverse effects
  • [MeSH-minor] Aged. Dose-Response Relationship, Drug. Female. Humans

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  • [CommentIn] Taiwan J Obstet Gynecol. 2007 Jun;46(2):93-5 [17638615.001]
  • (PMID = 17389201.001).
  • [ISSN] 1875-6263
  • [Journal-full-title] Taiwanese journal of obstetrics & gynecology
  • [ISO-abbreviation] Taiwan J Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen
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7. Costa NM, Rodrigues H, Pereira H, Pardal F, Matos E: Secretory breast carcinoma--case report and review of the medical literature. Breast; 2004 Aug;13(4):353-5
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  • [Title] Secretory breast carcinoma--case report and review of the medical literature.
  • Secretory breast carcinoma (SBC) is a rare type of invasive breast cancer.
  • We present the case of an 18-year-old woman with a SBC treated by mastectomy (Madden) and axillary node dissection (stage pT3N1M0) followed by chemotherapy (FEC regimen) and radiotherapy.
  • The authors review the literature and summarize relevant findings concerning definition, pathology, clinical picture, treatment, and follow-up.
  • [MeSH-major] Breast Neoplasms / secretion. Breast Neoplasms / surgery. Carcinoma / secretion. Carcinoma / surgery. Mastectomy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Axilla. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Epirubicin / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Lymph Node Excision. Radiotherapy, Adjuvant. Treatment Outcome

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  • (PMID = 15325674.001).
  • [ISSN] 0960-9776
  • [Journal-full-title] Breast (Edinburgh, Scotland)
  • [ISO-abbreviation] Breast
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; FEC protocol
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8. Ozguroglu M, Tascilar K, Ilvan S, Soybir G, Celik V: Secretory carcinoma of the breast. Case report and review of the literature. Oncology; 2005;68(2-3):263-8
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  • [Title] Secretory carcinoma of the breast. Case report and review of the literature.
  • We report an elderly case of an indolent breast tumor in a 66-year-old woman.
  • The patient presented with a locally advanced mass in the right breast that was present for 13 years, accompanied by bleeding and ulceration since the last 5 years.
  • She was found to have secretory carcinoma with a tumor size of 8 x 4 x 4 cm in diameter.
  • The secretory material stained positive with lactalbumin, as well as showed positivity with PAS.
  • The patient received six cycles of adjuvant chemotherapy followed by chest wall irradiation.
  • She is disease free with a follow-up period of 24 months.
  • Preoperative chemotherapy should be primarily replaced by curative surgery in such indolent cancers, despite locally advanced disease.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma / pathology
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Female. Hemorrhage / etiology. Humans. Lymphatic Metastasis. Radiotherapy, Adjuvant. Ulcer / etiology

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16015043.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 54
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9. Herz H, Cooke B, Goldstein D: Metastatic secretory breast cancer. Non-responsiveness to chemotherapy: case report and review of the literature. Ann Oncol; 2000 Oct;11(10):1343-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Metastatic secretory breast cancer. Non-responsiveness to chemotherapy: case report and review of the literature.
  • Secretory carcinoma of the breast is a rare and indolent tumour originally described in children but occurring equally in the adult population.
  • The principal management problems following primary surgical treatment are local recurrence and axillary lymph node metastases.
  • We present the case of a 27-year-old woman with pulmonary metastases from a secretory breast cancer treated by mastectomy and axillary lymph node dissection 12 years previously.
  • There was no response to chemotherapy; however, the patient remained alive and active two years from presentation with metastatic disease and one year from cessation of all cytotoxic chemotherapy.
  • To our knowledge, this is only the fourth reported case of distant metastases from secretory breast cancer and the second reported case in which current active chemotherapy has been used.
  • In the absence of any proven effective chemotherapy we believe that symptom control becomes the focus of management and offers patients with metastatic secretory breast cancer the greatest chance of a functional and good quality existence.


10. Jensen SB, Mouridsen HT, Reibel J, Brünner N, Nauntofte B: Adjuvant chemotherapy in breast cancer patients induces temporary salivary gland hypofunction. Oral Oncol; 2008 Feb;44(2):162-73
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

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  • [Title] Adjuvant chemotherapy in breast cancer patients induces temporary salivary gland hypofunction.
  • It is an open question if chemotherapy (CT) per se imposes adverse effects on salivary gland function.
  • The aim of the present study was to investigate effects of CT on salivary function in breast cancer patients during and after adjuvant CT.
  • Forty-five breast cancer patients, eligible for adjuvant CT with CEF or CMF (cyclophosphamide, epirubicin or methotrexate, 5-fluorouracil) were followed before, during, six months and one year after CT.
  • Findings were compared to those in a control group of 31 breast cancer patients not receiving CT.
  • Xerostomia scores rose during CT and stayed elevated one year after treatment.
  • UWS and SWS total protein output and UWS secretory IgA output decreased in response to CT.
  • These adverse drug reactions are temporary, as salivary findings generally returned to baseline values within one year following treatment.
  • [MeSH-major] Breast Neoplasms / drug therapy. Carcinoma, Ductal, Breast / drug therapy. Salivary Glands / drug effects. Xerostomia / chemically induced
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Chemotherapy, Adjuvant / adverse effects. Chi-Square Distribution. Electrolytes / analysis. Female. Humans. Hydrogen-Ion Concentration. Immunoglobulin A, Secretory / analysis. Middle Aged. Saliva / chemistry. Salivary Proteins and Peptides / analysis. Salivation / drug effects. Secretory Rate


11. Constantinidou A, Jones RL, Reis-Filho JS: Beyond triple-negative breast cancer: the need to define new subtypes. Expert Rev Anticancer Ther; 2010 Aug;10(8):1197-213
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  • [Title] Beyond triple-negative breast cancer: the need to define new subtypes.
  • Advances in the systemic treatment of early breast cancer have led to significant improvements in survival for patients with hormone receptor- and/or HER2-positive disease.
  • These tumors, however, encompass a wide range of subtypes with varying prognosis, including a number of special types with a good prognosis (e.g., adenoid cystic carcinomas and secretory carcinoma).
  • The similarities between sporadic triple-negative cancers and tumors arising in BRCA1 mutation carriers and the fact that the majority of BRCA1 tumors display a triple-negative phenotype have led to studies demonstrating a potential loss of BRCA1 function in triple-negative cancers and offered potential therapeutic avenues for patients with these cancers.
  • However, it should be noted that triple-negative breast cancers comprise a heterogeneous group of tumors.
  • Understanding the molecular underpinning of distinct subgroups of these cancers is crucial for the identification of novel therapeutic targets and individualization of treatment for patients with triple-negative disease.
  • [MeSH-major] Breast Neoplasms / classification. Breast Neoplasms / metabolism. Receptor, ErbB-2 / classification. Receptor, ErbB-2 / deficiency. Receptors, Estrogen / classification. Receptors, Estrogen / deficiency. Receptors, Progesterone / classification. Receptors, Progesterone / deficiency
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Drug Delivery Systems / trends. Female. Gene Expression Profiling / trends. Humans


12. Rivera-Hueto F, Hevia-Vázquez A, Utrilla-Alcolea JC, Galera-Davidson H: Long-term prognosis of teenagers with breast cancer. Int J Surg Pathol; 2002 Oct;10(4):273-9
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  • [Title] Long-term prognosis of teenagers with breast cancer.
  • We report 4 new cases of breast carcinoma in teenage girls diagnosed by use of histochemical and immunohistochemical methods.
  • These cases of breast carcinoma in women under 20 years of age were found in the files of our department in the last 24 years (1976-2000).
  • The patients had operable breast carcinomas corresponding to various histologic types (1 invasive ductal carcinoma associated with fibroadenoma, 2 secretory carcinomas, and 1 invasive lobular-type carcinoma).
  • Only 1 patient received adjuvant chemotherapy (case 4).
  • The correlations with prognosis-related risk factors (stage, age, previous benign lesions, family history, histologic types, hormonal receptors, and pregnancy) were examined.
  • [MeSH-major] Adenocarcinoma / pathology. Breast Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Child. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Mastectomy. Pregnancy. Pregnancy Complications, Neoplastic. Spain / epidemiology. Treatment Outcome

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  • (PMID = 12490977.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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13. Szántó J, András C, Tsakiris J, Gomba S, Szentirmay Z, Bánlaki S, Szilágyi I, Kiss C, Antall P, Horváth A, Lengyel L, Castiglione-Gertsch M: Secretory breast cancer in a 7.5-year old boy. Breast; 2004 Oct;13(5):439-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secretory breast cancer in a 7.5-year old boy.
  • Breast cancer is extremely rare in children, and consequently no consensus has been reached on the optimal treatment modalities.
  • The medical history and treatment plan for a 7.5-year old male breast cancer patient is described.
  • As no malignant cells were detected in the sentinel node, and no BRCA1-2 mutations were detected, no further radio- or chemotherapy was performed.
  • Further treatment will be given if this becomes necessary with the development of metastases.
  • [MeSH-major] Breast Neoplasms, Male / pathology. Carcinoma / pathology

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  • (PMID = 15454204.001).
  • [ISSN] 0960-9776
  • [Journal-full-title] Breast (Edinburgh, Scotland)
  • [ISO-abbreviation] Breast
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Scotland
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14. Putz T, Ramoner R, Gander H, Rahm A, Bartsch G, Thurnher M: Antitumor action and immune activation through cooperation of bee venom secretory phospholipase A2 and phosphatidylinositol-(3,4)-bisphosphate. Cancer Immunol Immunother; 2006 Nov;55(11):1374-83
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  • [Title] Antitumor action and immune activation through cooperation of bee venom secretory phospholipase A2 and phosphatidylinositol-(3,4)-bisphosphate.
  • We evaluated tumor cell growth modulation by bee venom secretory phospholipase A2 (bv-sPLA2) and phosphatidylinositol-(3,4)-bisphosphate as well as potential cooperative effects.
  • In addition, the immunomodulatory impact of tumor cell treatment was examined by monitoring changes in phenotype and function of monocyte-derived dendritic cells (moDCs) cocultured with pretreated tumor cells.
  • Bv-sPLA2 or phosphatidylinositol-(3,4)-bisphosphate alone displayed moderate effects on the proliferation of A498 renal cell carcinoma cells, T-47D breast cancer cells, DU145 prostate cancer cells and BEAS-2B transformed lung cells.
  • Such tumor lysates which represent complex mixtures of tumor antigens and simultaneously display potent adjuvant properties meet all requirements of a tumor vaccine.
  • [MeSH-major] Neoplasms / drug therapy. Phosphatidylinositol Phosphates / chemistry. Phospholipases A / metabolism

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  • (PMID = 16485125.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bee Venoms; 0 / Cancer Vaccines; 0 / Phosphatidylinositol Phosphates; 0 / phosphatidylinositol 3,4-diphosphate; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Group II Phospholipases A2; EC 3.1.1.4 / Phospholipases A2
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15. Sasano H, Suzuki T, Takeyama J, Utsunomiya H, Ito K, Ariga N, Moriya T: 17-beta-hydroxysteroid dehydrogenase in human breast and endometrial carcinoma. A new development in intracrinology. Oncology; 2000;59 Suppl 1:5-12
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  • [Title] 17-beta-hydroxysteroid dehydrogenase in human breast and endometrial carcinoma. A new development in intracrinology.
  • Intratumoral metabolism and synthesis of estrogens are considered to play very important roles in the pathogenesis and development of various sex steroid-dependent neoplasms including breast and endometrial carcinoma.
  • 17 beta-Hydroxysteroid dehydrogenase (17 beta-HSD) isozymes catalyze the interconversion of estradiol (E(2)) and estrone (E(1)), and thereby serve to modulate the tissue levels of bioactive E(2).
  • 17 beta-HSD type 1 primarily catalyzes the reduction of E(1) to E(2), whereas 17 beta-HSD type 2 primarily catalyzes the oxidation of E(2) to E(1).
  • In the human breast and its disorders, 17 beta-HSD type 1 is expressed in proliferative diseases without atypia, atypical ductal hyperplasia, ductal carcinoma in situ and invasive ductal carcinoma.
  • 17 beta-HSD type 2 is not detected in any of the lesions.
  • In addition, 17 beta-HSD type 1 coexpression is significantly correlated with estrogen receptor status in invasive ductal carcinoma cases.
  • These results indicate that breast carcinoma can effectively convert E(1), produced as a result of in situ aromatization, to E(2), a biologically potent estrogen, and exerts estrogenic actions on tumor cells through the estrogen receptor.
  • On the other hand, in the human endometrium, 17 beta-HSD type 2 is expressed, but not 17 beta-HSD type 1.
  • 17 beta-HSD type 2 is expressed in the secretory phase but not in any proliferative phase in the endometrial mucosa.
  • The enzyme is expressed in 75% of endometrial hyperplasias and 37% of carcinoma cases.
  • In endometrial carcinoma cases, a significant inverse correlation has been detected between 17 beta-HSD type 2 immunoreactivity and age (p < 0.02).
  • These results indicate that oxidation of E(2) to E(1) is dominant in endometrial carcinoma, 17 beta-HSD types 1 and 2 play an important role in the regulation of in situ estrogen production in breast and endometrial carcinoma.
  • [MeSH-major] Breast Neoplasms / drug therapy. Endometrial Neoplasms / drug therapy. Estradiol Dehydrogenases / therapeutic use

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  • [Copyright] Copyright 2000 S. Karger AG, Basel
  • (PMID = 11096350.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] EC 1.1.1.62 / Estradiol Dehydrogenases
  • [Number-of-references] 42
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16. Miettinen M: From morphological to molecular diagnosis of soft tissue tumors. Adv Exp Med Biol; 2006;587:99-113
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  • [Title] From morphological to molecular diagnosis of soft tissue tumors.
  • Cytogenetic discoveries of balanced translocations in soft tissue tumors have opened the way to molecular genetic definition of these translocations as gene fusions from the late 1980s.
  • Many sarcomas are known to have such fusions, and the demonstration of the fusion transcripts in tumor tissue is of great value in specific diagnosis of synovial sarcoma (SYT-SSX), Ewing sarcoma (EWS-Fli1), clear cell sarcoma (EWS-ATF1), myxoid liposarcoma (FUS-CHOP), and other sarcomas.
  • Demonstration of SYT-SSX and EWS-ATF1 fusion assists in the diagnosis of synovial and clear cell sarcomas in unusual locations, such as the gastrointestinal tract, where these tumors occur with low frequency.
  • In two exceptional instances, the same translocation and gene fusion occurs in two unrelated diseases: ETV6-NTRK fusion in infantile fibrosarcoma and secretory carcinoma of the breast, and ALK-TPM3 fusion in inflammatory myofibroblastic tumor and large cell anaplastic lymphoma.
  • Activating mutations in two related receptor tyrosine kinases (RTKs), KIT, and platelet-derived growth factor receptor alpha (PDGFRA) is central to the pathogenesis of gastrointestinal stromal tumors (GISTs), and countering the mutational activation by specific tyrosine kinase inhibitors, such as Imatinib mesylate, is now standard treatment for metastatic GISTs.
  • Mutation type influences therapy responsiveness, but fortunately very few GISTs carry primarily Imatinib-resistant mutations.
  • Secondary drug resistance acquired during Imatinib treatment based on new, Imatinib-resistant mutations is a major problem limiting treatment success.
  • Schwannoma types may differ in their pathogenesis: gastrointestinal schwannomas lack NF2 changes suggesting a different pathogenesis.
  • [MeSH-major] Genetic Testing. Soft Tissue Neoplasms / genetics. Soft Tissue Neoplasms / pathology

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  • (PMID = 17163160.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 70
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17. Wheeler DT, Bristow RE, Kurman RJ: Histologic alterations in endometrial hyperplasia and well-differentiated carcinoma treated with progestins. Am J Surg Pathol; 2007 Jul;31(7):988-98
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  • [Title] Histologic alterations in endometrial hyperplasia and well-differentiated carcinoma treated with progestins.
  • The treatment of complex atypical hyperplasia (CAH) and well-differentiated endometrioid carcinoma (WDC) by progestin therapy has been shown to be a safe alternative to hysterectomy.
  • Accurate assessment for regressive changes induced by the progestins is critical to successful treatment.
  • However, there are few studies detailing the histopathologic changes associated with progestin therapy.
  • The pretreatment and posttreatment endometrial samples were evaluated for response to treatment and for the histologic features of gland-to-stroma ratio, architectural abnormalities [back-to-back glands and confluency (cribriform and/or papillary patterns)], glandular cellularity, mitotic activity, cytologic atypia, and cytoplasmic changes.
  • Histologic changes seen in progestin-treated endometria included a decreased gland-to-stroma ratio, decreased glandular cellularity, decreased to absent mitotic activity, loss of cytologic atypia, and a variety of cytoplasmic changes including mucinous, secretory, squamous, and eosinophilic metaplasia.
  • Architectural changes tended to resolve later in the course of treatment.
  • Three instances of disease progression occurred, presumably only after discontinuing progestin treatment.
  • Only persistent architectural abnormalities and/or cytologic atypia in the 7 to 9-month biopsies were predictive of treatment failure, with a trend for cytologic atypia to be the most powerful predictor.
  • These findings indicate that progestin therapy should be continued for no less than 6 months to accurately assess treatment response.
  • [MeSH-major] Carcinoma, Endometrioid / pathology. Endometrial Hyperplasia / pathology. Endometrial Neoplasms / pathology. Progestins / therapeutic use
  • [MeSH-minor] Adult. Cell Nucleus / drug effects. Disease Progression. Endometrium / drug effects. Endometrium / pathology. Female. Humans. Middle Aged. Retrospective Studies

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  • (PMID = 17592264.001).
  • [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 / Progestins
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18. Polyzos PT, Arvanitis LD, Charchanti A, Galani V, Havaki S, Kallioras VA, Nakou M, Faros EG, Marinos E, Sgantzos MN, Kittas C: Decidualized and pre-decidualized normal endometrial stromal cells produce more O-linked N-acetylglucosamine containing epitope H than non-decidualized normal endometrial stromal cells. Histol Histopathol; 2006 11;21(11):1193-8
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  • In addition, in extracts of cultured MCF-7 breast carcinoma cell line cells it stains cytokeratin 8 and five polypeptides originating from Triton X-100-soluble (Mr x10(-3) of 232, 67 and 37) and from the Triton X-100-insoluble (Mr x10(-3) of 51 and 50) fractions, respectively.
  • In our previous studies we used the mAbH to investigate by immunostaining the expression of the epitope H in normal human brains, human brains with a variety of lesions, astrocytic tumors, infiltrating ductal breast carcinomas, fibroadenomas, and mitochondria-rich normal, metaplastic and neoplastic cells.
  • In order to gain further insight into the expression patterns of the epitope H in human tissues we used the mAbH to investigate the immunohistochemical expression of the epitope H in normal human endometrium, including 30 cases of proliferative endometrium, 30 cases of early secretory endometrium, 30 cases of mid secretory endometrium, 30 cases of late secretory endometrium and 30 cases of decidual tissues.
  • 1) The decidual stromal cells presented in all cases high cytoplasmic expression of the epitope H;.
  • 2) The pre-decidual stromal cells presented in all cases of late secretory endometrium significant cytoplasmic expression of the epitope H ranging from moderate to high expression;.
  • 3) The non pre-decidual stromal cells of the functional endometrial layer presented in all cases insignificant cytoplasmic expression of the epitope H ranging from null to low expression;.

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  • (PMID = 16874662.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / Peptides; 4G7DS2Q64Y / Progesterone; 68238-35-7 / Keratins; 9002-93-1 / Octoxynol; V956696549 / Acetylglucosamine
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