[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 9791
1. Lacroix A, Bourdeau I, Lampron A, Mazzuco TL, Tremblay J, Hamet P: Aberrant G-protein coupled receptor expression in relation to adrenocortical overfunction. Clin Endocrinol (Oxf); 2010 Jul;73(1):1-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aberrant adrenal expression and function of one or several G-protein coupled receptors can lead to cell proliferation and abnormal regulation of steroidogenesis in unilateral adenomas, carcinomas or in ACTH-independent macronodular adrenal hyperplasia (AIMAH).
  • The identification of aberrant receptors can offer specific pharmacological approach to prevent disease progression and control abnormal steroidogenesis; alternatively, unilateral or bilateral adrenalectomy remains the treatment of choice.
  • [MeSH-minor] Adrenal Gland Neoplasms / physiopathology. Adrenal Glands / metabolism. Adrenalectomy. Adrenocorticotropic Hormone / physiology. Angiotensins / physiology. Animals. Catecholamines / physiology. Chorionic Gonadotropin / physiology. Gastric Inhibitory Polypeptide / physiology. Humans. Hydrocortisone / metabolism. Hyperaldosteronism / physiopathology. Hyperplasia / metabolism. Luteinizing Hormone / physiology. Serotonin / physiology

  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19719763.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensins; 0 / Catecholamines; 0 / Chorionic Gonadotropin; 0 / Receptors, G-Protein-Coupled; 333DO1RDJY / Serotonin; 59392-49-3 / Gastric Inhibitory Polypeptide; 9002-60-2 / Adrenocorticotropic Hormone; 9002-67-9 / Luteinizing Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


2. Carling T, Udelsman R: Follicular neoplasms of the thyroid: what to recommend. Thyroid; 2005 Jun;15(6):583-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Follicular neoplasms of the thyroid are usually diagnosed following fine-needle aspiration (FNA) biopsy of a dominant thyroid nodule.
  • An FNA diagnosis of a follicular neoplasm represents a heterogeneous group of lesions including benign follicular hyperplasia, follicular adenomas, follicular carcinomas, and the follicular variant of papillary carcinoma.

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16029125.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 33
  •  go-up   go-down


3. Vender JR, Laird MD, Dhandapani KM: Inhibition of NFkappaB reduces cellular viability in GH3 pituitary adenoma cells. Neurosurgery; 2008 May;62(5):1122-7; discussion 1027-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of NFkappaB reduces cellular viability in GH3 pituitary adenoma cells.
  • OBJECTIVE: Adenomas of the pituitary gland are among the most common types of tumors of the adult brain.
  • Although adenomas are histologically benign, they may be associated with significant morbidity and mortality, mostly because of their invasive growth pattern and hormone hypersecretion.
  • We investigated the possible role of the NFkappaB transcription factor in pituitary tumor cell growth.
  • METHODS: The effect of NFkappaB pathway inhibition on cellular viability was studied in the GH3 pituitary adenoma cell line, a well-characterized rat cell line that secretes growth hormone and prolactin.
  • Cells were treated with mechanistically diverse pharmacological NFkappaB pathway inhibitors or with molecular inhibitors that were overexpressed in tumor cells before the assessment of cellular viability.
  • Treatment with wedelolactone, an IkappaB kinase inhibitor, or overexpression of an IkappaB super-repressor reduced cell viability, further implicating NFkappaB in pituitary tumor cell growth.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Coumarins / pharmacology. Enzyme Inhibitors / pharmacology. Proto-Oncogene Proteins c-akt. Rats

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18580810.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coumarins; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 524-12-9 / wedelolactone; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


Advertisement
4. Song SY, Kim YH, Yu MK, Kim JH, Lee JM, Son HJ, Rhee PL, Kim JJ, Paik SW, Rhee JC: Comparison of malignant potential between serrated adenomas and traditional adenomas. J Gastroenterol Hepatol; 2007 Nov;22(11):1786-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of malignant potential between serrated adenomas and traditional adenomas.
  • BACKGROUND: Serrated adenoma is a discrete colorectal epithelial neoplastic lesion that can evolve into colorectal cancer.
  • The purpose of the present paper was to compare the malignant potential and clinicopathological features between serrated and traditional adenomas.
  • METHODS: A total of 124 serrated adenomas from 116 patients were assessed, and 419 traditional adenomas from 200 were randomly selected.
  • The combination of nuclear dysplasia and serration of > or =20% of crypts was regarded as serrated adenoma.
  • The clinicopathological features of serrated and traditional adenomas were compared, and multivariate analysis performed to confirm whether the malignant potential of serrated adenoma was similar to that of traditional adenoma.
  • RESULTS: The differences in age, sex, total number of adenomas, and synchronous lesions including adenoma with high-grade dysplasia and carcinoma between subjects with and without serrated adenoma were not significant.
  • Serrated adenomas were more frequently located in the rectum and sigmoid colon (P < 0.001), and the average size of serrated adenomas was greater than that of traditional adenomas (P < 0.05).
  • The incidence of malignant lesions including high-grade dysplasia and carcinoma in serrated adenomas was found to be lower than in traditional adenomas (3.2% vs 9.3%, P < 0.05).
  • In the multivariate analysis, adenoma type and polyp size constituted the risk factors for the incidence of high-grade dysplasia and carcinoma.
  • CONCLUSIONS: Serrated adenoma is a premalignant lesion, but it has a lower potential for the development of malignancy than traditional adenomas.
  • [MeSH-major] Adenoma / pathology. Cell Transformation, Neoplastic / pathology. Colon, Sigmoid / pathology. Colorectal Neoplasms / pathology. Intestinal Mucosa / pathology. Intestinal Polyps / pathology. Precancerous Conditions / pathology. Rectum / pathology

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Gastroenterol Hepatol. 2007 Nov;22(11):1701-3 [17914936.001]
  • (PMID = 17914951.001).
  • [ISSN] 0815-9319
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Australia
  •  go-up   go-down


5. Leonetti JP, Marzo SJ, Petruzzelli GJ, Herr B: Recurrent pleomorphic adenoma of the parotid gland. Otolaryngol Head Neck Surg; 2005 Sep;133(3):319-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent pleomorphic adenoma of the parotid gland.
  • OBJECTIVES: To assess the long-term results in the management of 42 patients with recurrent pleomorphic adenoma of the parotid gland.
  • STUDY DESIGN: A retrospective analysis of 42 patients who underwent parotidectomy for recurrent pleomorphic adenoma was performed to study presenting clinicoradiographic features, surgical technique, facial nerve management, and the long-term risk of recurrence.
  • Twenty-nine of the remaining 40 patients had no recurrent disease.
  • Seven patients developed local parotid bed or cutaneous recurrent disease, 2 patients died of unrelated causes, and 2 patients were lost to follow-up.
  • CONCLUSIONS: All 7 patients with recurrent disease underwent subtotal parotidectomy with "negative" surgical margins.
  • Total parotidectomy or subtotal petrosectomy with facial nerve resection in selected cases may reduce the risk of multiple episodes of pleomorphic adenoma recurrence.
  • Two of 42 patients were found to have carcinoma ex-pleomorphic adenoma, both of these patients underwent prior radiotherapy, and both died of metastatic disease.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Parotid Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Facial Nerve / surgery. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Recurrence, Local. Otorhinolaryngologic Surgical Procedures / methods. Petrous Bone / surgery. Postoperative Complications / epidemiology. Retrospective Studies. Sural Nerve / transplantation. Survival Rate. Transplantation, Autologous

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16143173.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


6. Vinci A, Bacci B, Benazzi C, Caldin M, Sarli G: Progesterone receptor expression and proliferative activity in uterine tumours of pet rabbits. J Comp Pathol; 2010 May;142(4):323-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The present immunohistochemical study examined the expression of cytokeratin 19 (CK19), the progesterone receptor (PR), the proliferation-associated antigen Ki-67 and telomerase in normal rabbit uterine tissue and examples of endometrial hyperplasia, adenoma and adenocarcinoma.
  • Tubulopapillary adenomas and adenocarcinomas were the most common histological subtypes in this series.
  • Cytoplasmic expression of CK19 was recorded in two of three samples of normal endometrium and in one of three samples of endometrial hyperplasia, in all adenomas and five of six adenocarcinomas.
  • PR was expressed within the nucleus of normal endometrial cells and in one of three samples of endometrial hyperplasia, each of four adenomas and in four of six adenocarcinomas.
  • This finding suggests that PR expression is not directly involved in neoplastic transformation of the endometrium and that such expression is not a prognostic indicator.
  • Nuclear labelling of telomerase activity was found in one of three normal uteri, all samples of endometrial hyperplasia, two of four adenomas, but none of the adenocarcinomas.
  • The proliferation index as determined by Ki-67 expression was 9.7+/-2.75% (mean+/- standard-deviation (SD)) for normal endometrium, 11.29+/-2.5% for hyperplastic endometrium, 19.40+/-3.01% for benign tumours and 19.41+/-7.9% for malignant tumours.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenoma / metabolism. Adenoma / pathology. Animals. Cell Nucleus / metabolism. Cell Nucleus / pathology. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Endometrium / metabolism. Endometrium / pathology. Female. Ki-67 Antigen / metabolism. Mitotic Index. Progesterone / metabolism. Prognosis. Rabbits. Telomerase / metabolism. Uterine Neoplasms / metabolism. Uterine Neoplasms / pathology

  • Hazardous Substances Data Bank. PROGESTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20096851.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; EC 2.7.7.49 / Telomerase
  •  go-up   go-down


7. Roelfsema F, Kok S, Kok P, Pereira AM, Biermasz NR, Smit JW, Frolich M, Keenan DM, Veldhuis JD, Romijn JA: Pituitary-hormone secretion by thyrotropinomas. Pituitary; 2009;12(3):200-10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We conclude that TSH secretion by thyrotropinomas shares many characteristics of other pituitary hormone-secreting adenomas.
  • [MeSH-major] Adenoma / physiopathology. Pituitary Hormones / blood. Pituitary Hormones / secretion. Pituitary Neoplasms / blood

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Endocrinol. 1994 Oct;131(4):331-40 [7921220.001]
  • [Cites] J Clin Invest. 1994 Sep;94(3):1277-88 [8083369.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Dec;79(6):1706-15 [7989479.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Aug;80(8):2518-22 [7543115.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14100-5 [8943067.001]
  • [Cites] Endocr Rev. 1996 Dec;17(6):610-38 [8969971.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Nov;47(5):599-612 [9425400.001]
  • [Cites] Thyroid. 1998 Jan;8(1):9-14 [9492147.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):476-86 [10022404.001]
  • [Cites] Eur J Endocrinol. 1999 Mar;140(3):192-200 [10216513.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2005 Feb;288(2):R440-6 [15486096.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Feb;62(2):176-81 [15670193.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1570-7 [15598691.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Jul;289(1):E160-5 [15727954.001]
  • [Cites] Tissue Cell. 2005 Aug;37(4):269-80 [15921714.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Nov;90(11):6185-91 [16091498.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16880-5 [16272219.001]
  • [Cites] Eur J Endocrinol. 2007 Jul;157(1):39-46 [17609400.001]
  • [Cites] J Neuroendocrinol. 2008 Jan;20(1):1-70 [18081553.001]
  • [Cites] J Neurosurg. 2008 Jul;109(1):17-22 [18590428.001]
  • [Cites] J Neuroendocrinol. 2008 Jun;20(6):687-91 [18601690.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2003 Sep;285(3):R664-73 [12738612.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2290-300 [15126555.001]
  • [Cites] Am J Physiol. 1999 Nov;277(5 Pt 1):E948-57 [10567024.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1487-91 [10770186.001]
  • [Cites] Methods Enzymol. 2000;321:149-82 [10909056.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):700-12 [11158034.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R721-9 [11171650.001]
  • [Cites] Am J Physiol Regul Integr Comp Physiol. 2001 Jun;280(6):R1755-71 [11353681.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2849-53 [11397898.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):3304-10 [11443205.001]
  • [Cites] Mol Endocrinol. 2001 Sep;15(9):1529-38 [11518802.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5572-6 [11701737.001]
  • [Cites] Rev Endocr Metab Disord. 2000 Jan;1(1-2):97-108 [11704998.001]
  • [Cites] J Neurooncol. 2001 Sep;54(2):179-86 [11761434.001]
  • [Cites] Ultrastruct Pathol. 2002 Jul-Aug;26(4):219-28 [12227947.001]
  • [Cites] Eur J Endocrinol. 2003 Apr;148(4):433-42 [12656664.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Jun;60(6):765-72 [15163342.001]
  • [Cites] Acta Neuropathol. 2004 Aug;108(2):147-53 [15185102.001]
  • [Cites] J Clin Endocrinol Metab. 1987 Aug;65(2):315-20 [3597710.001]
  • [Cites] Acta Neuropathol. 1988;76(5):458-64 [2847475.001]
  • [Cites] J Clin Endocrinol Metab. 1989 Jun;68(6):1211-5 [2723029.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Jun;70(6):1631-6 [2347898.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1616-23 [2172282.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):415-21 [1704010.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Feb;72(2):477-83 [1704011.001]
  • [Cites] J Clin Endocrinol Metab. 1991 Dec;73(6):1281-8 [1955510.001]
  • [Cites] Clin Endocrinol (Oxf). 1992 Dec;37(6):504-10 [1286520.001]
  • [Cites] Ann Intern Med. 1993 Aug 1;119(3):236-40 [8323093.001]
  • [Cites] Eur J Endocrinol. 1994 Feb;130(2):113-20 [8130883.001]
  • [Cites] Eur J Endocrinol. 1994 Oct;131(4):355-8 [7921223.001]
  • (PMID = 19051037.001).
  • [ISSN] 1573-7403
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000585
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pituitary Hormones; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
  • [Other-IDs] NLM/ PMC2712623
  •  go-up   go-down


8. Jevdjovic T, Bernays RL, Eppler E: Insulin-like growth factor-I mRNA and peptide in the human anterior pituitary. J Neuroendocrinol; 2007 May;19(5):335-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Because insulin-like growth factor (IGF)-I appears to be involved in tumour pathogenesis, progression, and persistence, and only few data exist on the cellular synthesis sites of IGF-I, the present study aims to create a basis for further research on pituitary adenomas by investigating the presence of IGF-I in the human pituitary using reverse transcriptase-polymerase chain reaction, in situ hybridisation, immunohistochemistry and immunocytochemistry.
  • [MeSH-major] Adrenocorticotropic Hormone / metabolism. Growth Hormone / metabolism. Insulin-Like Growth Factor I / metabolism. Pituitary Gland, Anterior / metabolism. RNA, Messenger / metabolism

  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17425608.001).
  • [ISSN] 0953-8194
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 67763-96-6 / Insulin-Like Growth Factor I; 9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone
  •  go-up   go-down


9. Williams MD, Chakravarti N, Kies MS, Maruya S, Myers JN, Haviland JC, Weber RS, Lotan R, El-Naggar AK: Implications of methylation patterns of cancer genes in salivary gland tumors. Clin Cancer Res; 2006 Dec 15;12(24):7353-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Implications of methylation patterns of cancer genes in salivary gland tumors.
  • PURPOSE: We investigated the methylation status and protein expression of four tumor suppressor genes to determine their role in salivary gland tumorigenesis.
  • EXPERIMENTAL DESIGN: We performed methylation-specific PCR and protein analyses of 29 normal salivary glands, 23 benign, and 79 malignant salivary gland neoplasms to determine the pattern and potential diagnostic and/or biological role of the RASSF1, RARbeta2, DAPK, and MGMT tumor suppressor gene methylation in these tumors.
  • Methylation occurred in 9 of 23 (39.1%) benign tumors; 3 (25.0%) pleomorphic adenomas and 6 (66.7%) Warthin's tumors at the MGMT, DAPK, or RASSF1 genes.
  • CONCLUSIONS: (a) Benign and malignant salivary tumors differed in the frequency and pattern of gene methylation;.
  • [MeSH-major] Carcinoma / metabolism. DNA Methylation. Salivary Gland Neoplasms / genetics. Salivary Gland Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Apoptosis Regulatory Proteins / metabolism. Calcium-Calmodulin-Dependent Protein Kinases / metabolism. Carcinoma, Acinar Cell / metabolism. Carcinoma, Adenoid Cystic / metabolism. Carcinoma, Mucoepidermoid / metabolism. Child. DNA Modification Methylases. DNA Repair Enzymes. Death-Associated Protein Kinases. Female. Gene Expression Regulation, Neoplastic. Genes, Neoplasm. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism. Receptors, Retinoic Acid / metabolism. Tumor Suppressor Protein p14ARF / metabolism. Tumor Suppressor Proteins / metabolism

  • Genetic Alliance. consumer health - Salivary Gland Cancer.
  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17189407.001).
  • [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] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / RASSF1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor beta; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 6.5.1.- / DNA Repair Enzymes
  •  go-up   go-down


10. Raappana A, Koivukangas J, Ebeling T, Pirilä T: Incidence of pituitary adenomas in Northern Finland in 1992-2007. J Clin Endocrinol Metab; 2010 Sep;95(9):4268-75
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of pituitary adenomas in Northern Finland in 1992-2007.
  • CONTEXT: Data on the incidence of pituitary adenomas (PAs) are scant and outdated.
  • The incidence rates of the Oulu University Hospital regional district were used as a reference to assess the applicability of our case finding over the rest of NFi.
  • [MeSH-major] Adenoma / epidemiology. Pituitary Neoplasms / epidemiology

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20534753.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


11. Erridge SC, Conkey DS, Stockton D, Strachan MW, Statham PF, Whittle IR, Grant R, Kerr GR, Gregor A: Radiotherapy for pituitary adenomas: long-term efficacy and toxicity. Radiother Oncol; 2009 Dec;93(3):597-601
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiotherapy for pituitary adenomas: long-term efficacy and toxicity.
  • BACKGROUND: Radiotherapy for pituitary adenomas is an effective treatment but remains controversial due to toxicity concerns.
  • [MeSH-major] Adenoma / radiotherapy. Pituitary Neoplasms / radiotherapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasms, Second Primary. Radiation Injuries. Survival Rate. Young Adult

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19900729.001).
  • [ISSN] 1879-0887
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  •  go-up   go-down


12. Sereg M, Szappanos A, Toke J, Karlinger K, Feldman K, Kaszper E, Varga I, Gláz E, Rácz K, Tóth M: Atherosclerotic risk factors and complications in patients with non-functioning adrenal adenomas treated with or without adrenalectomy: a long-term follow-up study. Eur J Endocrinol; 2009 Apr;160(4):647-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atherosclerotic risk factors and complications in patients with non-functioning adrenal adenomas treated with or without adrenalectomy: a long-term follow-up study.
  • OBJECTIVE: Despite the increased prevalences of hypertension, type 2 diabetes mellitus (T2DM), hyperlipidemy, and obesity in patients with non-functioning adrenal adenomas (NFAAs), there is a paucity of data on long-term atherosclerotic morbidity as well as the long-term cardiovascular effects of adrenalectomy in these patients.

  • MedlinePlus Health Information. consumer health - Atherosclerosis.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19174533.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


13. Mendoza V, Sosa E, Espinosa-de-Los-Monteros AL, Salcedo M, Guinto G, Cheng S, Sandoval C, Mercado M: GSPalpha mutations in Mexican patients with acromegaly: potential impact on long term prognosis. Growth Horm IGF Res; 2005 Feb;15(1):28-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The frequency of activating mutations of the GSPalpha gene as the etiology of GH-secreting pituitary adenomas has been the subject of important ethnogenetic variability.
  • We also sought to establish whether or not the presence of these mutations correlates in any way with the clinical or biochemical characteristics of the disease.
  • STUDY DESIGN AND METHODS: Fifty eight GH-secreting pituitary adenomas were examined for the presence of point mutations in either codon 201 or 227 of the GSPalpha gene, using PCR and direct sequencing of DNA extracted from either fresh or paraffin-embedded tissues.
  • [MeSH-major] Acromegaly / genetics. Adenoma / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. GTP-Binding Protein alpha Subunits, Gs / physiology. Mutation. Pituitary Neoplasms / genetics

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15701569.001).
  • [ISSN] 1096-6374
  • [Journal-full-title] Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
  • [ISO-abbreviation] Growth Horm. IGF Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Codon; 0 / DNA Primers; 9002-72-6 / Growth Hormone; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  •  go-up   go-down


14. Gaisa NT, Klöppel G, Brehmer B, Neulen J, Stephan P, Knüchel R, Donner A: [Virilizing adrenal ganglioneuroma : A rare differential diagnosis in testosterone secreting adrenal tumours]. Pathologe; 2009 Sep;30(5):407-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Testosterone secreting tumours of the adrenal glands are usually adrenal carcinomas or adenomas.
  • Clinically it is characterized by symptoms of virilization, histologically by the occurrence of a population of eosinophilic cells.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / secretion. Ganglioneuroma / pathology. Ganglioneuroma / secretion. Testosterone / secretion. Virilism / pathology
  • [MeSH-minor] Adrenal Cortex / pathology. Adrenal Gland Diseases / pathology. Adrenal Gland Diseases / surgery. Adrenalectomy. Aged. Biomarkers, Tumor / analysis. Calbindin 2. Choristoma / pathology. Choristoma / surgery. Diagnosis, Differential. Female. Humans. Inhibins / analysis. Laparoscopy. Leydig Cells. Male. S100 Calcium Binding Protein G / analysis. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Acta Chir Belg. 1993 Jul-Aug;93(4):181-4 [8237234.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2002 Jun;10(2):159-62 [12051635.001]
  • [Cites] Cancer. 1961 Mar-Apr;14:421-5 [13749451.001]
  • [Cites] Am J Surg Pathol. 1983 Oct;7(7):699-705 [6685441.001]
  • [Cites] Pathologe. 2003 Jul;24(4):280-6 [14513275.001]
  • [Cites] Mod Pathol. 1998 Aug;11(8):774-9 [9720507.001]
  • [Cites] Ann Diagn Pathol. 2008 Feb;12(1):29-32 [18164412.001]
  • [Cites] JAMA. 1978 May 26;239(21):2273-4 [650810.001]
  • (PMID = 19396442.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / S100 Calcium Binding Protein G; 3XMK78S47O / Testosterone; 57285-09-3 / Inhibins
  •  go-up   go-down


15. Dachman AH, Obuchowski NA, Hoffmeister JW, Hinshaw JL, Frew MI, Winter TC, Van Uitert RL, Periaswamy S, Summers RM, Hillman BJ: Effect of computer-aided detection for CT colonography in a multireader, multicase trial. Radiology; 2010 Sep;256(3):827-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nineteen blinded readers interpreted each case at two different times, with and without the assistance of a commercial CAD system.
  • Average reader sensitivity also improved with CAD by more than 0.08 for small adenomas.
  • CAD improves reader sensitivity when measured per segment, per patient, and per polyp for small polyps and adenomas and also reduces specificity by a small amount.

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) RSNA, 2010.
  • [Cites] Acad Radiol. 2000 Jul;7(7):516-25 [10902960.001]
  • [Cites] Radiology. 2008 Oct;249(1):167-77 [18796675.001]
  • [Cites] N Engl J Med. 2003 Dec 4;349(23):2191-200 [14657426.001]
  • [Cites] J Comput Assist Tomogr. 2004 May-Jun;28(3):318-26 [15100534.001]
  • [Cites] Ann Intern Med. 2004 Sep 7;141(5):352-9 [15353426.001]
  • [Cites] Biometrics. 1988 Sep;44(3):837-45 [3203132.001]
  • [Cites] Biometrics. 1997 Jun;53(2):567-78 [9192452.001]
  • [Cites] Stat Med. 1998 Jul 15;17(13):1495-507 [9695194.001]
  • [Cites] Ann Intern Med. 2005 Apr 19;142(8):635-50 [15838071.001]
  • [Cites] Br J Radiol. 2005;78 Spec No 1:S57-62 [15917447.001]
  • [Cites] Radiology. 2005 Jul;236(1):3-9 [15987959.001]
  • [Cites] Radiology. 2005 Oct;237(1):26-7 [16183923.001]
  • [Cites] Endoscopy. 2005 Oct;37(10):937-44 [16189765.001]
  • [Cites] Radiology. 2006 Jun;239(3):768-76 [16714460.001]
  • [Cites] Gastroenterology. 2006 Dec;131(6):1690-9 [17087934.001]
  • [Cites] Stat Med. 2007 Feb 10;26(3):596-619 [16538699.001]
  • [Cites] Radiology. 2007 Jul;244(1):165-73 [17581901.001]
  • [Cites] Eur Radiol. 2007 Oct;17(10):2598-607 [17351780.001]
  • [Cites] Eur Radiol. 2007 Oct;17(10):2608-15 [17429646.001]
  • [Cites] AJR Am J Roentgenol. 2007 Oct;189(4):W172-6 [17885028.001]
  • [Cites] Radiology. 2007 Oct;245(1):140-9 [17885187.001]
  • [Cites] Radiology. 2008 Jan;246(1):148-56 [18096536.001]
  • [Cites] Radiology. 2008 Feb;246(2):463-71 [18094263.001]
  • [Cites] N Engl J Med. 2008 Sep 18;359(12):1207-17 [18799557.001]
  • [Cites] Radiology. 2009 Feb;250(2):488-97 [19188317.001]
  • [Cites] AJR Am J Roentgenol. 2009 Jun;192(6):1682-9 [19457835.001]
  • [Cites] AJR Am J Roentgenol. 2009 Jul;193(1):70-8 [19542397.001]
  • [Cites] AJR Am J Roentgenol. 2006 Mar;186(3):696-702 [16498097.001]
  • [Cites] Radiology. 2002 Nov;225(2):391-9 [12409571.001]
  • [Cites] Br J Radiol. 2008 Mar;81(963):180-6 [18180260.001]
  • [Cites] Radiology. 2008 Apr;247(1):133-40 [18292478.001]
  • [Cites] Clin Radiol. 2008 May;63(5):549-56 [18374719.001]
  • [Cites] CA Cancer J Clin. 2008 May-Jun;58(3):130-60 [18322143.001]
  • [Cites] Eur Radiol. 2008 Aug;18(8):1666-73 [18389248.001]
  • [Cites] Radiology. 2008 Sep;248(3):860-8 [18710980.001]
  • [Cites] Radiology. 2006 Jun;239(3):759-67 [16543593.001]
  • (PMID = 20663975.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2923726
  •  go-up   go-down


16. Romanchishen AF, Matveeva ZS: [Clinical symptoms of hyperparathyroidism and sizes of the parathyroid gland tumors]. Vestn Khir Im I I Grek; 2006;165(2):37-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical symptoms of hyperparathyroidism and sizes of the parathyroid gland tumors].
  • Three groups of patients with different degrees of primary hyperparathyroidism were compared: 36 patients with asymptomatic tumors (incidentalomas) of the parathyroid glands, 20 patients with parathyreoadenomas of medium size and mild signs of hyperparathyroidism and 26 patients with large adenomas and severe manifestations of the disease.
  • [MeSH-minor] Adolescent. Adult. Aged. Disease Progression. Female. Follow-Up Studies. Humans. Male. Middle Aged. Retrospective Studies. Severity of Illness Index

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16752637.001).
  • [ISSN] 0042-4625
  • [Journal-full-title] Vestnik khirurgii imeni I. I. Grekova
  • [ISO-abbreviation] Vestn. Khir. Im. I. I. Grek.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  •  go-up   go-down


17. Sakamoto T, Uozaki H, Kondo K, Imauchi Y, Yamasoba T, Sugasawa M, Kaga K: Cyclooxygenase-2 regulates the degree of apoptosis by modulating bcl-2 protein in pleomorphic adenoma and mucoepidermoid carcinoma of the parotid gland. Acta Otolaryngol; 2005 Feb;125(2):191-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclooxygenase-2 regulates the degree of apoptosis by modulating bcl-2 protein in pleomorphic adenoma and mucoepidermoid carcinoma of the parotid gland.
  • The purpose of this study was to verify that COX-2 regulates the degree of apoptosis by modulating bcl-2 protein in benign and malignant parotid gland tumors.
  • : We examined archival formalin-fixed, paraffin-embedded tissue sections of 10 pleomorphic adenomas (PMAs) and 10 mucoepidermoid carcinomas (MECs) by immunostaining with anti-COX-2, anti-bcl-2 and anti-single-stranded DNA (ssDNA) antibodies.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Apoptosis / physiology. Carcinoma, Mucoepidermoid / metabolism. Parotid Neoplasms / metabolism. Prostaglandin-Endoperoxide Synthases / physiology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Up-Regulation

  • Genetic Alliance. consumer health - Mucoepidermoid carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15880952.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antibodies; 0 / DNA, Single-Stranded; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  •  go-up   go-down


18. Vilar L, Czepielewsk MA, Naves LA, Rollin GA, Casulari LA, Coelho CE: Substantial shrinkage of adenomas cosecreting growth hormone and prolactin with use of cabergoline therapy. Endocr Pract; 2007 Jul-Aug;13(4):396-402
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Substantial shrinkage of adenomas cosecreting growth hormone and prolactin with use of cabergoline therapy.
  • By 6 months after the patients began to take cabergoline, tumor shrinkage of 94% (in case 1) and of 70% (in case 2) was demonstrated by magnetic resonance imaging.
  • CONCLUSION: Our findings demonstrate that cabergoline should be considered for medical treatment of adenomas cosecreting growth hormone and prolactin, even in the presence of large tumors with appreciable suprasellar extension, because substantial tumor shrinkage is possible with this therapy.
  • [MeSH-major] Adenoma / drug therapy. Antineoplastic Agents / administration & dosage. Ergolines / administration & dosage. Growth Hormone-Secreting Pituitary Adenoma / drug therapy. Pituitary Neoplasms / drug therapy. Prolactinoma / drug therapy

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17669717.001).
  • [ISSN] 1934-2403
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ergolines; LL60K9J05T / cabergoline
  •  go-up   go-down


19. Bergeron S, Lemieux E, Durand V, Cagnol S, Carrier JC, Lussier JG, Boucher MJ, Rivard N: The serine protease inhibitor serpinE2 is a novel target of ERK signaling involved in human colorectal tumorigenesis. Mol Cancer; 2010 Oct 13;9:271
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In a previous report, we had shown that expression of a constitutive active mutant of MEK1 (caMEK) in normal rat intestinal epithelial cells (IECs) induced morphological transformation associated with epithelial to mesenchymal transition, growth in soft agar, invasion and metastases in nude mice.
  • 3- RNAi directed against serpinE2 in caMEK-transformed rat IECs or in human CRC cell lines HCT116 and LoVo markedly decreased foci formation, anchorage-independent growth in soft agarose, cell migration and tumor formation in nude mice.
  • 5- Finally, Q-PCR analyses demonstrated that mRNA levels of serpinE2 were markedly increased in human adenomas in comparison to healthy adjacent tissues and in colorectal tumors, regardless of tumor stage and grade.

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Exp Immunol. 2000 May;120(2):317-23 [10792382.001]
  • [Cites] Carcinogenesis. 2010 Jul;31(7):1165-74 [20047953.001]
  • [Cites] J Biol Chem. 2001 Sep 7;276(36):33293-6 [11435447.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6451-5 [12438234.001]
  • [Cites] Mol Reprod Dev. 2003 Feb;64(2):152-65 [12506347.001]
  • [Cites] Virology. 2003 Apr 25;309(1):114-24 [12726732.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):263-4 [12796781.001]
  • [Cites] Cancer Metastasis Rev. 2003 Dec;22(4):395-403 [12884914.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4945-51 [12941819.001]
  • [Cites] Prostate. 2004 Apr 1;59(1):1-12 [14991861.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 May;286(5):G736-46 [14701721.001]
  • [Cites] APMIS. 2004 Apr-May;112(4-5):233-8 [15233637.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Sep 17;322(2):609-13 [15325273.001]
  • [Cites] Cell. 1980 Aug;21(1):37-45 [6157479.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Apr;78(4):2340-4 [7017731.001]
  • [Cites] J Biol Chem. 1985 Jun 10;260(11):7029-34 [3997857.001]
  • [Cites] Int J Cancer. 1988 Feb 15;41(2):287-96 [3338874.001]
  • [Cites] J Cell Physiol. 1988 Feb;134(2):179-88 [3279057.001]
  • [Cites] Biochem Biophys Res Commun. 1989 May 30;161(1):300-4 [2786418.001]
  • [Cites] Eur J Biochem. 1990 Sep 24;192(3):797-803 [1698627.001]
  • [Cites] EMBO J. 1993 May;12(5):1871-8 [8491179.001]
  • [Cites] Int J Cancer. 1995 Feb 8;60(4):501-6 [7829264.001]
  • [Cites] J Biol Chem. 1995 Sep 15;270(37):22044-9 [7665626.001]
  • [Cites] Curr Opin Cell Biol. 1996 Apr;8(2):205-15 [8791420.001]
  • [Cites] Gastroenterology. 1997 Nov;113(5):1589-98 [9352861.001]
  • [Cites] Dig Dis Sci. 1998 Jul;43(7):1454-64 [9690379.001]
  • [Cites] Nat Med. 1998 Aug;4(8):923-8 [9701244.001]
  • [Cites] Jpn J Cancer Res. 1998 Sep;89(9):903-9 [9818025.001]
  • [Cites] Oncogene. 1999 Jan 21;18(3):813-22 [9989833.001]
  • [Cites] Gut. 1999 Jun;44(6):834-8 [10323886.001]
  • [Cites] Mol Cell Biochem. 1999 May;195(1-2):99-111 [10395074.001]
  • [Cites] Int J Cancer. 1999 Sep 24;83(1):30-3 [10449603.001]
  • [Cites] Exp Biol Med (Maywood). 2004 Dec;229(11):1090-6 [15564434.001]
  • [Cites] Lancet Oncol. 2005 May;6(5):322-7 [15863380.001]
  • [Cites] Gastroenterology. 2005 Aug;129(2):577-90 [16083714.001]
  • [Cites] Mol Cancer. 2006;5:2 [16403224.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 May;290(5):G1067-74 [16399877.001]
  • [Cites] J Biol Chem. 2006 Apr 21;281(16):10663-8 [16507572.001]
  • [Cites] J Cell Biochem. 2006 Oct 15;99(3):936-51 [16741952.001]
  • [Cites] Oncogene. 2007 Mar 22;26(13):1954-8 [17001349.001]
  • [Cites] Oncogene. 2007 May 14;26(22):3291-310 [17496923.001]
  • [Cites] Curr Top Med Chem. 2007;7(14):1364-78 [17692026.001]
  • [Cites] Oral Oncol. 2008 Mar;44(3):309-13 [17468036.001]
  • [Cites] Int J Cancer. 2008 Jun 1;122(11):2462-70 [18271008.001]
  • [Cites] Physiol Rev. 2008 Apr;88(2):489-513 [18391171.001]
  • [Cites] J Clin Oncol. 2008 May 1;26(13):2139-46 [18390968.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2008 May;294(5):L932-41 [18310226.001]
  • [Cites] Cancer Cell. 2008 Oct 7;14(4):324-34 [18835034.001]
  • [Cites] BMC Cancer. 2008;8:337 [19014680.001]
  • [Cites] Recent Pat Anticancer Drug Discov. 2009 Jan;4(1):28-35 [19149686.001]
  • [Cites] Tumour Biol. 2008;29(6):343-50 [19023234.001]
  • [Cites] Neoplasia. 2009 Apr;11(4):355-64 [19308290.001]
  • [Cites] Nucl Med Biol. 2009 Apr;36(3):313-21 [19324277.001]
  • [Cites] J Cell Physiol. 2009 Sep;220(3):655-63 [19472211.001]
  • [Cites] Cancer Res. 2009 Jul 15;69(14):5690-8 [19584287.001]
  • [Cites] BMC Cancer. 2009;9:201 [19555470.001]
  • [Cites] Int J Cancer. 2009 Oct 1;125(7):1575-86 [19462441.001]
  • [Cites] Biochem Biophys Res Commun. 2010 Jan 22;391(4):1641-6 [20035713.001]
  • [Cites] Gastroenterology. 2001 Feb;120(2):423-38 [11159883.001]
  • (PMID = 20942929.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / MT-14405
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Nitriles; 0 / Serpin E2; 0 / U 0126; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC2967542
  •  go-up   go-down


20. Alesina PF, Hommeltenberg S, Meier B, Petersenn S, Lahner H, Schmid KW, Mann K, Walz MK: Posterior retroperitoneoscopic adrenalectomy for clinical and subclinical Cushing's syndrome. World J Surg; 2010 Jun;34(6):1391-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Partial adrenalectomy represents a new option in the treatment of cortisol-producing adenomas.

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] World J Surg. 2011 Jan;35(1):237; author reply 238 [20563723.001]
  • [Cites] J Laparoendosc Adv Surg Tech A. 2009 Apr;19(2):181-9 [19216698.001]
  • [Cites] World J Surg. 1996 Sep;20(7):769-74 [8678949.001]
  • [Cites] World J Surg. 2006 Sep;30(9):1665-71 [16927063.001]
  • [Cites] Ann Surg Oncol. 2008 Sep;15(9):2506-8 [18618188.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1440-8 [10770179.001]
  • [Cites] World J Surg. 2001 Jun;25(6):728-34 [11376407.001]
  • [Cites] Surg Endosc. 2008 Mar;22(3):622-6 [18163169.001]
  • [Cites] Zentralbl Chir. 1995;120(1):53-8 [7887040.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602 [14671138.001]
  • [Cites] World J Surg. 2008 May;32(5):856-62 [18074172.001]
  • [Cites] Surgery. 2006 Dec;140(6):943-8; discussion 948-50 [17188142.001]
  • [Cites] Surg Endosc. 2002 Jan;16(1):108-11 [11961617.001]
  • [Cites] Ann Surg. 1997 Sep;226(3):238-46; discussion 246-7 [9339930.001]
  • [Cites] Arch Surg. 2006 Aug;141(8):771-4; discussion 774-6 [16924084.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Sep;75(3):826-32 [1517373.001]
  • [Cites] World J Surg. 2008 May;32(5):882-9 [18214589.001]
  • [Cites] Langenbecks Arch Surg. 2009 May;394(3):447-50 [18784938.001]
  • [Cites] World J Surg. 2008 May;32(5):847-53 [18343972.001]
  • [Cites] Ann Surg. 1996 Dec;224(6):727-34; discussion 734-6 [8968227.001]
  • [Cites] World J Surg. 2006 May;30(5):899-908 [16617419.001]
  • [Cites] J Endocrinol Invest. 2005 Apr;28(4):327-32 [15966505.001]
  • [Cites] Dig Surg. 2004;21(5-6):363-70 [15467378.001]
  • [Cites] N Engl J Med. 1992 Oct 1;327(14):1033 [1387700.001]
  • [Cites] J Clin Endocrinol Metab. 2008 May;93(5):1526-40 [18334580.001]
  • [Cites] Ann Surg. 1985 May;201(5):586-94 [2986563.001]
  • [Cites] World J Surg. 2007 Jul;31(7):1425-32 [17534556.001]
  • [Cites] Ann Surg. 2009 Mar;249(3):388-91 [19247023.001]
  • [Cites] Surg Endosc. 2008 Feb;22(2):522-6 [17705067.001]
  • [Cites] Ann Surg. 1951 Sep;134(3):464-75 [14869034.001]
  • [Cites] Surgery. 2008 Dec;144(6):1008-14; discussion 1014-5 [19041011.001]
  • [Cites] Surgery. 2008 Dec;144(6):1054-60; discussion 1060-1 [19041018.001]
  • [Cites] Ann Chir. 2002 Sep;127(7):512-9 [12404845.001]
  • [Cites] Surgery. 1990 Dec;108(6):1079-84 [2247833.001]
  • (PMID = 20143066.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


21. Krzizok T, Schwerdtfeger G: [Bitemporal hemianopia in road traffic]. Klin Monbl Augenheilkd; 2006 Sep;223(9):775-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Patients suffering from pituitary adenomas and diseases of the chiasma typically show a bitemporal hemianopia.
  • The intact half fields fit geometrically to one virtual normal field, that seems to correspond in the centre of a normal field.
  • PATIENTS: The case of a patient with typical bitemporal hemianopia illustrates the sensorial peculiarities: the functioning temporal retinal halves do not correspond.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16986090.001).
  • [ISSN] 0023-2165
  • [Journal-full-title] Klinische Monatsblätter für Augenheilkunde
  • [ISO-abbreviation] Klin Monbl Augenheilkd
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


22. García Sánchez Mdel V, González R, Iglesias Flores E, Gómez Camacho F, Casais Juanena L, Cerezo Ruiz A, Montero Pérez-Barquero M, Muntané J, de Dios Vega JF: [Diagnostic value of fecal calprotectin in predicting an abnormal colonoscopy]. Med Clin (Barc); 2006 Jun 10;127(2):41-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aims of this study were to analyze the usefulness of FCP to predict an abnormal colonoscopy and to correlate the levels of FCP with the degree of activity in inflammatory bowel disease (IBD).
  • People were divided in: normal colonoscopy: 117 people, and 28 colon adenomas, 20 colorectal cancer (CRC) and 25 IBD.

  • MedlinePlus Health Information. consumer health - Bowel Movement.
  • MedlinePlus Health Information. consumer health - Colonic Diseases.
  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16801001.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] spa
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Leukocyte L1 Antigen Complex
  •  go-up   go-down


23. Melmed S, Sternberg R, Cook D, Klibanski A, Chanson P, Bonert V, Vance ML, Rhew D, Kleinberg D, Barkan A: A critical analysis of pituitary tumor shrinkage during primary medical therapy in acromegaly. J Clin Endocrinol Metab; 2005 Jul;90(7):4405-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A critical analysis of pituitary tumor shrinkage during primary medical therapy in acromegaly.
  • CONTEXT: Somatostatin analogs have been successfully used to treat patients with GH-secreting pituitary adenomas because they are safe, effective, and usually well tolerated.
  • EVIDENCE ACQUISITION: We therefore undertook a systematic literature overview to characterize the results of studies involving primary therapy with somatostatin analogs and their effects on pituitary tumor size.
  • Because most studies in which pituitary tumor shrinkage has been assessed involve uncontrolled, open-label, prospective trials or retrospective case series, the lack of a control arm does not permit pooling of data in a metaanalytic fashion to determine tumor size reduction.
  • Therefore, this systematic review was designed to document and stratify data by study design, summarize therapeutic regimens and patient characteristics, assess the percentage of patients showing changes in tumor size, and calculate the weighted average effect on size reduction.
  • Fourteen studies (n = 424) provided a definition of significant tumor shrinkage, and the results showed that 36.6% (weighted mean percentage) of patients receiving primary SRL therapy for acromegaly experienced a significant reduction in tumor size.
  • The weighted mean percent reduction in tumor size was 19.4% for those studies in which all patients received SRLs and change in tumor size was reported for all patients.
  • CONCLUSIONS: Clinical implications are discussed for patients in whom tumor size control with SRLs is an important objective, typically those who have failed surgery or are being treated with primary medical therapy with large tumors.

  • Genetic Alliance. consumer health - Acromegaly.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15827109.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agonists; 51110-01-1 / Somatostatin; 67763-96-6 / Insulin-Like Growth Factor I
  •  go-up   go-down


24. Telang N, Katdare M: Combinatorial prevention of carcinogenic risk in a model for familial colon cancer. Oncol Rep; 2007 Apr;17(4):909-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Germ line mutations in the tumor suppressor adenomatous polyposis coli (APC) gene, predispose for the clinical familial adenomatous polyposis (FAP) syndrome, a high risk precursor for early onset colon cancer.
  • Similar mutations in the murine homolog of the APC gene, however, produce adenomas predominantly in the small intestine, rather than in the colon.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17342335.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 122394; United States / NCI NIH HHS / CA / CA 29502-20; United States / NCI NIH HHS / CA / CA 29502-S1; United States / NCI NIH HHS / CN / CN 75029-63
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


25. Otani T, Iwasaki M, Ikeda S, Kozu T, Saito H, Mutoh M, Wakabayashi K, Tsugane S: Serum triglycerides and colorectal adenoma in a case-control study among cancer screening examinees (Japan). Cancer Causes Control; 2006 Dec;17(10):1245-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum triglycerides and colorectal adenoma in a case-control study among cancer screening examinees (Japan).
  • OBJECTIVE: Most epidemiologic studies have shown serum triglycerides to be associated with colorectal adenoma.
  • We cross-sectionally investigated the association of serum triglycerides with the risk of adenoma by smoking status.
  • METHODS: We identified 782 newly diagnosed adenoma cases from the examinees of a colorectal cancer screening program.
  • We determined 738 controls without present illness or past history of adenoma from among the examinees.
  • We calculated odds ratios (OR) and 95% confidence intervals (CI) of colorectal adenoma for serum triglycerides.
  • RESULTS: High serum triglycerides were associated with colorectal adenoma (OR 1.5; 95% CI 1.1-2.0 for the highest versus the lowest quartile, P (trend, )0.030).
  • A stronger association was observed between three or more adenoma cases and study controls (OR 2.3; 95% CI 1.3-4.2, P (trend,) < 0.0010).
  • CONCLUSIONS: Our results suggested that a higher serum triglyceride level may be related to a larger number of adenomas.
  • Adenoma development involving an elevated serum triglyceride level may be modified by smoking.
  • [MeSH-major] Adenoma / blood. Adenoma / diagnosis. Colorectal Neoplasms / blood. Colorectal Neoplasms / diagnosis. Mass Screening. Triglycerides / blood

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17111255.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Triglycerides
  •  go-up   go-down


26. Beggs AD, Hain SF: Localization of parathyroid adenomas using 11C-methionine positron emission tomography. Nucl Med Commun; 2005 Feb;26(2):133-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localization of parathyroid adenomas using 11C-methionine positron emission tomography.
  • BACKGROUND AND AIM: In symptomatic hyperparathyroidism, pre-surgical localization of the suspected site of adenoma is desirable.
  • The aim of this study was to determine whether 11C-methionine positron emission tomography (PET) could accurately localize parathyroid adenomas in patients in whom conventional imaging had failed.
  • PATIENTS AND METHODS: Fifty-one patients presenting with hyperparathyroidism, and in whom other imaging techniques had failed to definitely identify the site of adenoma, were reviewed retrospectively after 11C-methionine PET scanning.
  • RESULTS: 11C-Methionine PET scanning was found to have a sensitivity of 83%, a specificity of 100% and an accuracy of 88% in successfully locating parathyroid adenomas.
  • Most false negatives were due to adenomas in the lower mediastinum that was outside the area of scanning.
  • CONCLUSIONS: 11C-Methionine PET is a reliable and highly accurate technique for localizing parathyroid adenomas in patients in whom conventional imaging techniques have failed.
  • [MeSH-major] Adenoma / radionuclide imaging. Hyperthyroidism / radionuclide imaging. Methionine. Parathyroid Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods

  • MedlinePlus Health Information. consumer health - Hyperthyroidism.
  • Hazardous Substances Data Bank. (L)-Methionine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15657506.001).
  • [ISSN] 0143-3636
  • [Journal-full-title] Nuclear medicine communications
  • [ISO-abbreviation] Nucl Med Commun
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 58576-49-1 / carbon-11 methionine; AE28F7PNPL / Methionine
  •  go-up   go-down


27. Wilschut JA, Habbema JD, Ramsey SD, Boer R, Looman CW, van Ballegooijen M: Increased risk of adenomas in individuals with a family history of colorectal cancer: results of a meta-analysis. Cancer Causes Control; 2010 Dec;21(12):2287-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased risk of adenomas in individuals with a family history of colorectal cancer: results of a meta-analysis.
  • OBJECTIVE: It is unclear to what extent the increased risk of colorectal cancer in individuals with a family history of colorectal cancer and no known genetic disorders is associated with a higher adenoma prevalence.
  • Our aim is to estimate the relative difference in adenoma prevalence and its age-pattern in individuals with a family history of colorectal cancer compared to those without.
  • METHODS: We performed a literature search to identify colonoscopy studies reporting the adenoma prevalence by age.
  • Using multilevel logistic regression, we examined how the adenoma prevalence by age differed between individuals with and without a family history of colorectal cancer.
  • We excluded members of families with a known genetic disorder.
  • The adenoma prevalence was significantly higher in individuals with a family history than in those without (OR 1.7, 95% CI 1.4-3.5).
  • The adenoma prevalence increased with age (OR per year of age 1.06, 95% CI 1.05-1.07).
  • CONCLUSION: Individuals with a family history of colorectal cancer have a considerably higher prevalence of adenomas compared to individuals without a family history.
  • [MeSH-major] Adenoma / etiology. Colorectal Neoplasms / etiology. Family Health
  • [MeSH-minor] Adult. Algorithms. Disease Susceptibility / epidemiology. Female. Humans. Male. Medical History Taking. Middle Aged. Prevalence. Risk Factors

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20981482.001).
  • [ISSN] 1573-7225
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 R01 CA114794
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  •  go-up   go-down


28. Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL: Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol; 2007 May 15;165(10):1178-86
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women.
  • The authors examined intakes of calcium and vitamin D, and interaction with retinol, in relation to risk of adenoma of the distal colon or rectum among 48,115 US women who were free of colorectal cancer or polyps, completed a food frequency questionnaire in 1980, and underwent endoscopy by 2002.
  • They documented 2,747 cases of adenoma (1,064 large, 1,531 small, 2,085 distal colon, and 779 rectal).
  • Total calcium intake was weakly associated with distal colorectal adenoma risk (multivariable relative risk (RR) for extreme quintiles = 0.88, 95% confidence interval (CI): 0.74, 1.04; p(trend) = 0.06), particularly for large adenoma (RR = 0.73, 95% CI: 0.56, 0.96; p(trend) = 0.02).
  • Total vitamin D intake was weakly associated with reduced risk of distal colorectal adenoma (RR = 0.79, 95% CI: 0.63, 0.99; p(trend) = 0.07), but more strongly with distal colon adenoma risk (RR = 0.67, 95% CI: 0.52, 0.87; p(trend) = 0.004).
  • The combinations of high vitamin D and low retinol intake (RR = 0.55, 95% CI: 0.28, 1.10) further decreased risk of distal colorectal adenoma when compared with the opposite extreme.

  • MedlinePlus Health Information. consumer health - Calcium.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Vitamin A.
  • MedlinePlus Health Information. consumer health - Vitamin D.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VITAMIN A .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17379616.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK040561; None / None / / P30 DK040561-12; United States / NCI NIH HHS / CA / CA 87969; United States / NIDDK NIH HHS / DK / P30 DK040561-12; United States / NCI NIH HHS / CA / CA 55075
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium, Dietary; 11103-57-4 / Vitamin A; 1406-16-2 / Vitamin D
  •  go-up   go-down


29. Gong Z, Xie D, Deng Z, Bostick RM, Muga SJ, Hurley TG, Hebert JR: The PPAR{gamma} Pro12Ala polymorphism and risk for incident sporadic colorectal adenomas. Carcinogenesis; 2005 Mar;26(3):579-85
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The PPAR{gamma} Pro12Ala polymorphism and risk for incident sporadic colorectal adenomas.
  • We investigated the hypothesis that the PPARgamma Pro12Ala polymorphism is associated with colorectal adenoma risk in a recently concluded case-control study of incident sporadic colorectal adenomas (163 cases and 212 controls).
  • The multivariate-adjusted odds ratio (OR) for incident sporadic colorectal adenoma was 0.65 (95% CI 0.39-1.09) for those with the Pro12Ala or Ala12Ala genotype compared with those with the Pro12Pro genotype.
  • Smoking was a very strong risk factor (OR 2.34, 95%CI 1.37-4.02) for colorectal adenoma among those with the wild-type (Pro12Ala) genotype, but not those with the Ala12 variant (OR 0.86, 95%CI 0.35-2.09).
  • Larger studies are needed to validate these results, which suggest that the PPARgamma Pro12Ala polymorphism may interact with other factors to protect against colorectal adenoma.
  • [MeSH-major] Adenoma / genetics. Alanine / genetics. Colorectal Neoplasms / genetics. PPAR gamma / genetics. Polymorphism, Genetic. Proline / genetics

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. (L)-PROLINE .
  • Hazardous Substances Data Bank. (L)-ALANINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15564289.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA-51932; United States / NCRR NIH HHS / RR / RR017698
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / PPAR gamma; 9DLQ4CIU6V / Proline; OF5P57N2ZX / Alanine
  •  go-up   go-down


30. Chen X, Halberg RB, Burch RP, Dove WF: Intestinal adenomagenesis involves core molecular signatures of the epithelial-mesenchymal transition. J Mol Histol; 2008 Jun;39(3):283-94
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Microarray data demonstrated elevation of vimentin, a mesenchymal marker, in intestinal adenomas from Apc Min/+ (Min) mice.
  • Elevated vimentin RNA expression and protein production were detected within neoplastic cells in murine intestinal adenomas.
  • Similarly, vimentin protein was detected in both adenomas and invasive adenocarcinomas of the human colon, but not in the normal colonic epithelium or in hyperplastic polyps.
  • Canonical E-cadherin suppressors, such as Snail, were not elevated in the same tumor.
  • Elevated vimentin expression in the adenoma was not correlated with persistent Ras signaling, but was strongly correlated with reduced proliferation indices, active Wnt signaling, and TGF-beta signaling, as demonstrated by its dependence on Smad3.
  • These unexpected observations are interpreted as reflecting the involvement of a core of the EMT system during the tissue remodeling of early tumorigenesis.

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1992 May 1;256(5057):668-70 [1350108.001]
  • [Cites] Science. 1990 Jan 19;247(4940):322-4 [2296722.001]
  • [Cites] Science. 1994 May 6;264(5160):835-9 [7513443.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8969-73 [8090754.001]
  • [Cites] Lancet. 1996 May 18;347(9012):1377-81 [8637346.001]
  • [Cites] Cancer Surv. 1996;27:101-25 [8909797.001]
  • [Cites] Development. 2004 Dec;131(23):5817-24 [15525667.001]
  • [Cites] Curr Opin Oncol. 2005 Jan;17(1):49-54 [15608513.001]
  • [Cites] J Clin Invest. 2005 Feb;115(2):339-47 [15668738.001]
  • [Cites] Oncogene. 2005 Mar 17;24(12):2032-41 [15688013.001]
  • [Cites] Cells Tissues Organs. 2005;179(1-2):56-65 [15942193.001]
  • [Cites] Nature. 2005 Jun 23;435(7045):1126-30 [15973414.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):5996-6000; discussion 6000-1 [16024596.001]
  • [Cites] J Natl Cancer Inst. 2005 Aug 3;97(15):1124-32 [16077070.001]
  • [Cites] Cancer Biol Ther. 2005 Apr;4(4):365-70 [15846061.001]
  • [Cites] Oncogene. 2005 Aug 29;24(37):5764-74 [16123809.001]
  • [Cites] Cell Cycle. 2005 Dec;4(12):1719-21 [16294041.001]
  • [Cites] Oncogene. 2006 Aug 24;25(37):5134-44 [16568079.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8319-26 [16951136.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4036-41 [17360473.001]
  • [Cites] Genetics. 2007 Jun;176(2):1237-44 [17435219.001]
  • [Cites] Science. 2007 Nov 16;318(5853):1108-13 [17932254.001]
  • [Cites] FASEB J. 2007 Dec;21(14):3853-65 [17622569.001]
  • [Cites] Genome Biol. 2007;8(7):R131 [17615082.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1402-7 [9037065.001]
  • [Cites] Nature. 1997 Dec 4;390(6659):465-71 [9393997.001]
  • [Cites] Science. 1998 Apr 24;280(5363):596-9 [9554852.001]
  • [Cites] Cell. 1998 Sep 18;94(6):703-14 [9753318.001]
  • [Cites] J Cell Biol. 2000 Jan 10;148(1):173-88 [10629227.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):76-83 [10655586.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):3031-8 [10850453.001]
  • [Cites] Am J Gastroenterol. 2000 Nov;95(11):3053-63 [11095318.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(2):575-94 [11134344.001]
  • [Cites] Cancer Res. 2001 Apr 15;61(8):3508-17 [11309315.001]
  • [Cites] Mol Cell. 2001 Jun;7(6):1267-78 [11430829.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10356-61 [11526241.001]
  • [Cites] CA Cancer J Clin. 2001 Jan-Feb;51(1):38-75; quiz 77-80 [11577479.001]
  • [Cites] Bioessays. 2001 Oct;23(10):912-23 [11598958.001]
  • [Cites] J Cell Biol. 2002 Jan 21;156(2):299-313 [11790801.001]
  • [Cites] Biochim Biophys Acta. 2002 Jun 21;1602(2):97-113 [12020798.001]
  • [Cites] N Engl J Med. 2002 Dec 19;347(25):1999-2009 [12490681.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2658-64 [12750294.001]
  • [Cites] Ann N Y Acad Sci. 2003 May;995:1-10 [12814934.001]
  • [Cites] Cancer Sci. 2003 Jul;94(7):593-7 [12841867.001]
  • [Cites] J Cell Sci. 2003 Aug 15;116(Pt 16):3269-76 [12857786.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9530-5 [12886021.001]
  • [Cites] J Clin Invest. 2003 Aug;112(4):503-16 [12925691.001]
  • [Cites] Mutat Res. 2004 Jan;566(1):9-20 [14706509.001]
  • [Cites] Cancer Sci. 2004 Jun;95(6):475-80 [15182426.001]
  • [Cites] Cell. 2004 Jun 25;117(7):927-39 [15210113.001]
  • [Cites] Expert Rev Anticancer Ther. 2004 Aug;4(4):649-61 [15270668.001]
  • [Cites] Cell. 2004 Aug 6;118(3):277-9 [15294153.001]
  • [Cites] J Cell Biol. 1982 Oct;95(1):333-9 [7142291.001]
  • [Cites] Ann N Y Acad Sci. 1985;455:144-57 [3909879.001]
  • [Cites] Chest. 1992 Jun;101(6):1663-73 [1534744.001]
  • (PMID = 18327651.001).
  • [ISSN] 1567-2379
  • [Journal-full-title] Journal of molecular histology
  • [ISO-abbreviation] J. Mol. Histol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA084227-05; United States / NCI NIH HHS / CA / U01 CA084227; United States / NCI NIH HHS / CA / R37 CA063677; United States / NCI NIH HHS / CA / R37 CA063677-14; United States / NCI NIH HHS / CA / R37-CA63677; United States / NCI NIH HHS / CA / U01-CA-84227; United States / NCI NIH HHS / CA / U01 CA084227-05; United States / NCI NIH HHS / CA / CA063677-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cadherins; 0 / Fibronectins; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 0 / Vimentin; 0 / Wnt Proteins; 0 / snail family transcription factors; EC 3.6.5.2 / ras Proteins; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS59539; NLM/ PMC2544376
  •  go-up   go-down


31. Baek YH, Chang E, Kim YJ, Kim BK, Sohn JH, Park DI: Stool methylation-specific polymerase chain reaction assay for the detection of colorectal neoplasia in Korean patients. Dis Colon Rectum; 2009 Aug;52(8):1452-9; discussion 1459-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stool methylation-specific polymerase chain reaction assay for the detection of colorectal neoplasia in Korean patients.
  • PURPOSE: To investigate the feasibility of detecting hypermethylation in stool samples as a noninvasive screening tool for colorectal cancer and precancerous lesions, we evaluated the hypermethylation of three genes in the stool samples of patients with colorectal cancer, patients with colorectal adenomas, and healthy control subjects.
  • METHODS: Stool samples were obtained from 37 endoscopically diagnosed healthy controls, 52 patients with adenomas, and 60 patients with colorectal cancer.
  • %, and 15.4% of colorectal adenomas, respectively.
  • The sensitivities of the combined study, using three markers for the detection of colorectal cancer and colorectal adenomas, were 75.0% and 59.6%.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Colorectal Neoplasms / diagnosis. DNA, Neoplasm / genetics. Feces / chemistry. Nuclear Proteins / metabolism. O(6)-Methylguanine-DNA Methyltransferase / metabolism. Polymerase Chain Reaction / methods. Vimentin / metabolism
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. DNA Methylation. DNA Repair Enzymes. Diagnosis, Differential. Epigenesis, Genetic. Female. Humans. Korea / epidemiology. Male. Middle Aged. Prevalence. Promoter Regions, Genetic. Retrospective Studies. Risk Factors

  • MedlinePlus Health Information. consumer health - Bowel Movement.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19617759.001).
  • [ISSN] 1530-0358
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0 / Vimentin; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 6.5.1.- / DNA Repair Enzymes
  •  go-up   go-down


32. Carmack SW, Genta RM, Schuler CM, Saboorian MH: The current spectrum of gastric polyps: a 1-year national study of over 120,000 patients. Am J Gastroenterol; 2009 Jun;104(6):1524-32
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The prevalence of gastric polyps in the EGD population was 6.35%; 77% were fundic gland polyps, 17% hyperplastic polyps/polypoid foveolar hyperplasia, 0.69% adenomas, and 0.1% inflammatory fibroid polyps.
  • None of the benign gastric polyps had a significant positive association with concurrent H. pylori infection; intestinal metaplasia was detected in the background of 52.2% of carcinoids, 29.6% of adenomas, 20.1% of xanthomas, and 13% of adenocarcinomas and hyperplastic polyps.
  • Adenomas were rarely associated with synchronous adenocarcinomas.
  • CONCLUSIONS: The relative prevalence of fundic gland polyps in this population was much higher than that reported earlier, most likely because of the widespread use of proton pump inhibitors. H. pylori- and atrophy-associated polyps, including adenomas, were less common than in earlier series.

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19491866.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


33. Tanaka K, Toyoda H, Kadowaki S, Kosaka R, Shiraishi T, Imoto I, Shiku H, Adachi Y: Features of early gastric cancer and gastric adenoma by enhanced-magnification endoscopy. J Gastroenterol; 2006 Apr;41(4):332-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Features of early gastric cancer and gastric adenoma by enhanced-magnification endoscopy.
  • BACKGROUND: Changes to the mucosal surface of early gastric carcinomas and gastric adenomas as viewed by enhanced-magnification endoscopy with acetic acid have not been investigated thoroughly.
  • METHODS: Forty-seven consecutive patients with early gastric carcinomas or gastric adenomas underwent enhanced-magnification endoscopy following 1.5% acetic acid instillation.
  • Although all elevated adenomas showed type II or type III surface patterns, both depressed adenomas showed type IV.
  • [MeSH-major] Adenoma / pathology. Carcinoma / pathology. Endoscopy, Gastrointestinal / methods. Image Enhancement. Stomach Neoplasms / pathology
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Follow-Up Studies. Humans. Neoplasm Staging. Prospective Studies. Video Recording

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Gastroenterol. 2006 Apr;41(4):397-8 [16741625.001]
  • [Cites] Endoscopy. 2004 Feb;36(2):165-9 [14765314.001]
  • [Cites] Gastrointest Endosc. 2004 Jan;59(1):15-21 [14722541.001]
  • [Cites] Am J Surg Pathol. 1995;19 Suppl 1:S37-43 [7762738.001]
  • [Cites] Gastrointest Endosc. 2001 May;53(6):559-65 [11323579.001]
  • [Cites] Gastrointest Endosc. 2003 Apr;57(4):498-504 [12665759.001]
  • [Cites] Gastrointest Endosc. 2002 Aug;56(2):279-84 [12145613.001]
  • [Cites] Endoscopy. 2003 May;35(5):437-45 [12701018.001]
  • [Cites] Endoscopy. 2002 Oct;34(10):772-7 [12244497.001]
  • [Cites] Endoscopy. 1978 Nov;10(4):269-74 [738222.001]
  • [Cites] Endoscopy. 2004 Dec;36(12):1080-4 [15578298.001]
  • [Cites] Aliment Pharmacol Ther. 2002 Mar;16 Suppl 1:3-15 [11849122.001]
  • (PMID = 16741612.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


34. Gualco G, Reissenweber N, Cliché I, Bacchi CE: Flat elevated lesions of the colon and rectum: a spectrum of neoplastic and nonneoplastic entities. Ann Diagn Pathol; 2006 Dec;10(6):333-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim of this prospective study is to establish the frequency and the type (neoplastic and nonneoplastic) lesions defined endoscopically as flat elevated lesion (FEL) in the colon and rectum, as well as to compare flat adenomas (FAs) to polypoid lesions of the same size with morphometric and immunohistochemical analysis.
  • Using histopathologic criteria, they were divided in neoplastic (adenomas and carcinomas) and nonneoplastic ones.
  • The ISA also reached significant differences between both groups of adenomas.
  • Following the endoscopic criteria of FELs, nonneoplastic lesions predominated over the adenomatous lesions, demonstrating that FELs and FAs are not homologous terms.
  • The frequency of high-grade dysplasia was significantly more elevated in the adenomatous FELs than in polypoid adenomas.
  • The ISA, SI, p53 expression, and Ki-67 label index were helpful in differentiating adenomatous FELs from polypoid lesions.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Colonic Neoplasms / pathology. Endoscopy, Gastrointestinal / methods. Rectal Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Cell Proliferation. Colitis / pathology. Colonic Diseases / metabolism. Colonic Diseases / pathology. Colonic Polyps / pathology. Female. Humans. Ki-67 Antigen / analysis. Ki-67 Antigen / metabolism. Male. Prospective Studies. Tumor Suppressor Protein p53 / analysis. Tumor Suppressor Protein p53 / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17126250.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


35. Wang Y, Li Y, Zhang WY, Xia QJ, Li HG, Wang R, Yang L, Sun XF, Zhou ZG: mRNA expression of minichromosome maintenance 2 in colonic adenoma and adenocarcinoma. Eur J Cancer Prev; 2009 Feb;18(1):40-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] mRNA expression of minichromosome maintenance 2 in colonic adenoma and adenocarcinoma.
  • As proliferation is essential for progression from normal cells to tumor, certain markers specific to proliferating cells may permit detection of premalignant lesions.
  • Here, we aimed to evaluate the possible value of a proliferation marker, minichromosome maintenance 2 (MCM2), in the early diagnosis of colorectal cancer, by analyzing the difference in MCM2 expression among normal mucosa, adenoma, and adenocarcinoma, and investigating the relationship of MCM2 expression in adenomas with clinicopathologic variables.
  • Using immunohistochemistry and real-time reverse transcription-PCR, we observed that the expression of MCM2 protein was present on basal third to half of colonic crypts in normal mucosa, whereas throughout the epithelium in adenomas and adenocarcinomas, the expression of MCM2 mRNA in adenocarcinomas was significantly higher than in adenomas (P=0.001), whereas the difference between adenoma and normal mucosa was not significant (P=0.184); we also found that the expression of MCM2 mRNA tended to be increased in the adenomas with high-grade dysplasia, or in older patients, respectively, compared with those with low-grade dysplasia, and younger patients.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Cell Cycle Proteins / genetics. Colonic Neoplasms / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Case-Control Studies. Early Detection of Cancer. Feasibility Studies. Feces / chemistry. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Minichromosome Maintenance Complex Component 2. RNA, Messenger / analysis. RNA, Messenger / isolation & purification. RNA, Messenger / metabolism. Sensitivity and Specificity. Software. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19077563.001).
  • [ISSN] 1473-5709
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; EC 3.6.4.12 / MCM2 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 2
  •  go-up   go-down


36. Krysiak R, Okopień B, Marek B, Szkróbka W: [Prolactinoma]. Przegl Lek; 2009;66(4):198-205
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Gruczolak przysadki wydzielajacy prolaktyne.
  • Prolactin-secreting tumours (prolactinomas) are benign neoplasms constituting about 40 percent of all pituitary tumours.
  • Differential diagnosis of the disease should include the intake of various drugs, hypothyroidism, renal failure, liver cirrhosis, compression of the pituitary stalk by other pathologies, idiopathic hyperprolactinemia and other types of pituitary adenomas.
  • [MeSH-minor] Adult. Age Distribution. Causality. Dopamine Agonists / therapeutic use. Female. Humans. Iatrogenic Disease / epidemiology. Male. Pregnancy. Pregnancy Complications, Neoplastic / diagnosis. Pregnancy Complications, Neoplastic / epidemiology. Pregnancy Complications, Neoplastic / therapy. Prevalence. Sex Distribution. Young Adult

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19708510.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Dopamine Agonists
  • [Number-of-references] 53
  •  go-up   go-down


37. Bricaire L, Brue T: [New medical treatments in Cushing disease]. Ann Endocrinol (Paris); 2007 Jun;68 Suppl 1:18-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [New medical treatments in Cushing disease].
  • The standard treatment of Cushing disease is surgery.
  • Some studies have shown that SSTR5 is predominantly expressed in corticotroph pituitary adenomas and that SOM230 has more efficacy than octreotid in the treatment of Cushing disease.
  • It has been suggested that the thiazolinidinediones, PPAR-gamma agonists, might also be useful in the treatment of this disease, but studies are still limited and give conflicting results.
  • In a recent study conducted on dogs, Castillo et al have shown that the retinoïds give encouraging results and might open a new pathway in the treatment of Cushing disease.
  • Labeur and his team have contributed a study on the use of gamma-interferon on murine pituitary cells and on human and murine corticotroph pituitary adenoma cells, and they have evidenced a 20 to 60% decrease in the production of ACTH in 5 cases out of 7 in the tumoral cells treated--versus the non-treated ones.
  • Thus they have suggested that the dopaminergic agonists--such as cabergoline-could be used in corticotroph pituitary adenomas derivated from the intermediary zone.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Ann Endocrinol (Paris). 2008 Nov;69(5):459-60
  • (PMID = 17961656.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Receptors, Dopamine; 0 / Retinoids; 0 / Thiazolidinediones; 51110-01-1 / Somatostatin; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


38. Ikematsu H, Matsuda T, Emura F, Saito Y, Uraoka T, Fu KI, Kaneko K, Ochiai A, Fujimori T, Sano Y: Efficacy of capillary pattern type IIIA/IIIB by magnifying narrow band imaging for estimating depth of invasion of early colorectal neoplasms. BMC Gastroenterol; 2010;10:33
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Capillary patterns (CP) observed by magnifying Narrow Band Imaging (NBI) are useful for differentiating non-adenomatous from adenomatous colorectal polyps.
  • RESULTS: There were 15 adenomas, 66 intramucosal cancers (pM) and 49 submucosal cancers (pSM): 16 pSM superficial (pSM1) and 33 pSM deep cancers (pSM2-3).
  • Among lesions diagnosed as CP IIIA 86 out of 91 (94.5%) were adenomas, pM-ca, or pSM1; among lesions diagnosed as CP IIIB 28 out of 39 (72%) were pSM2-3.
  • [MeSH-major] Capillaries / pathology. Colonoscopy / methods. Colorectal Neoplasms / blood supply. Early Detection of Cancer / methods. Neoplasm Invasiveness / pathology. Neoplasm Staging / methods

  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gut. 2000 Aug;47(2):251-5 [10896917.001]
  • [Cites] Gastrointest Endosc. 2009 Feb;69(2):278-83 [18951131.001]
  • [Cites] J Biomed Opt. 2004 May-Jun;9(3):568-77 [15189095.001]
  • [Cites] J Gastroenterol. 2004 Jun;39(6):534-43 [15235870.001]
  • [Cites] Gastrointest Endosc. 2004 Oct;60(4):520-6 [15472672.001]
  • [Cites] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153.001]
  • [Cites] Gut. 1984 May;25(5):437-44 [6714785.001]
  • [Cites] Gastroenterology. 1985 Aug;89(2):328-36 [4007423.001]
  • [Cites] Nature. 1989 May 4;339(6219):58-61 [2469964.001]
  • [Cites] Clin Cancer Res. 1999 Jan;5(1):135-42 [9918211.001]
  • [Cites] Endoscopy. 2004 Dec;36(12):1094-8 [15578301.001]
  • [Cites] J Gastroenterol Hepatol. 2007 Nov;22(11):1722-7 [17565585.001]
  • [Cites] Aliment Pharmacol Ther. 2008 Jun;27(12):1269-74 [18284647.001]
  • [Cites] Dig Dis Sci. 2008 Jul;53(7):1886-92 [18080834.001]
  • [Cites] World J Gastroenterol. 2008 Aug 21;14(31):4867-72 [18756593.001]
  • [Cites] Am J Gastroenterol. 2008 Nov;103(11):2700-6 [18853968.001]
  • [Cites] Gastrointest Endosc. 2003 Dec;58(6 Suppl):S3-43 [14652541.001]
  • (PMID = 20346170.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2868042
  •  go-up   go-down


39. Klopfleisch R, Gruber AD: Increased expression of BRCA2 and RAD51 in lymph node metastases of canine mammary adenocarcinomas. Vet Pathol; 2009 May;46(3):416-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The BRCA/RAD51 complex of tumor suppressor genes plays a major role in the DNA damage response.
  • In this explorative study, BRCA1, BRCA2, and RAD51 mRNA expression was quantified in highly defined laser microdissected tissue samples of simple adenomas, adenocarcinomas of the mammary gland, and their lymph node metastases by real-time quantitative reverse transcription polymerase chain reaction.
  • In adenomas, mRNA expression was reduced for BRCA1 (6/10 dogs, 60%), BRCA2 (4/10 dogs, 40%), and RAD51 (4/10, 40%).
  • In adenocarcinomas BRCA1 expression varied with increased expression in 3 of 10 (30%) dogs and no differences in 7 of 10 (70%) dogs when compared with normal mammary gland.
  • Further experimental studies are needed to clarify whether these changes in gene expression are a direct carcinogenetic stimulus or a protective response due to genetic instability during tumor progression.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19176491.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BRCA1 Protein; 0 / BRCA2 Protein; EC 2.7.7.- / Rad51 Recombinase
  •  go-up   go-down


40. Heald A, Parr C, Gibson C, O'driscoll K, Fowler H: A cross-sectional study to investigate long-term cognitive function in people with treated pituitary Cushing's disease. Exp Clin Endocrinol Diabetes; 2006 Oct;114(9):490-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A cross-sectional study to investigate long-term cognitive function in people with treated pituitary Cushing's disease.
  • INTRODUCTION: It has been proposed that exposure to high levels of endogenous steroids in untreated pituitary Cushing's disease damages hippocampal structures leading to impairment in learning and memory processes.
  • We hypothesised that patients with treated pituitary Cushing's disease would perform significantly worse on tests of cognitive ability than those with nonfunctioning pituitary adenomas.
  • DESIGN: Sixteen adults with pituitary Cushing's disease (PCD) and 16 adults with non-functioning pituitary adenomas (NFA) undertook the following comprehensive neuropsychological assessments: National Adult Reading Test (NART: premorbid abilities), California Verbal Learning Test (CVLT 2 UK: learning and recall), Stroop (executive functioning), Trail-Making Test (TMT: executive functioning and attention), Adult Memory and Information Processing Battery (AMIPB: Information Processing Speed and Story Recall subtests).
  • The results suggest a discrepancy between patients' subjective perception of functional cognitive impairments and objective findings on psychometric testing and point to the influence of affective symptoms on cognitive performance, particularly in Cushing's disease.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17115346.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


41. Johnson KT, Harmsen WS, Limburg PJ, Carston MJ, Johnson CD: Visceral fat analysis at CT colonography. Acad Radiol; 2006 Aug;13(8):963-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RATIONALE AND OBJECTIVES: Obesity is associated with increased risks for colorectal neoplasia.
  • MATERIALS AND METHODS: Case (n = 25) and control (n = 25) subjects with proven large (>1 cm) colorectal adenomas or normal colons respectively were randomly selected from among an established CT colonography research study cohort.
  • CONCLUSION: In this pilot study, visceral fat measures at CT colonography were not significantly associated with the presence of large colorectal adenomas.

  • MedlinePlus Health Information. consumer health - Colonic Polyps.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16843848.001).
  • [ISSN] 1076-6332
  • [Journal-full-title] Academic radiology
  • [ISO-abbreviation] Acad Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


42. Shono T, Mizoguchi M, Yoshimoto K, Amano T, Natori Y, Sasaki T: Clinical course of abducens nerve palsy associated with skull base tumours. Acta Neurochir (Wien); 2009 Jul;151(7):733-8; discussion 738
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The conditions included two pituitary adenomas, two trigeminal schwannomas and five meningiomas.
  • In the four patients with pituitary adenomas and trigeminal schwannomas, all nerves were anatomically preserved and showed complete recovery of function within 6 months after surgery.
  • CONCLUSIONS: The abducens nerve palsies in pituitary adenomas and trigeminal schwannomas showed a better clinical course compared to those in skull base meningiomas.
  • [MeSH-minor] Adenoma / complications. Adenoma / pathology. Adenoma / surgery. Adult. Aged. Cranial Fossa, Posterior / pathology. Cranial Fossa, Posterior / surgery. Cranial Nerve Neoplasms / complications. Cranial Nerve Neoplasms / pathology. Cranial Nerve Neoplasms / surgery. Female. Fibrin Tissue Adhesive / therapeutic use. Humans. Male. Meningeal Neoplasms / complications. Meningeal Neoplasms / pathology. Meningeal Neoplasms / surgery. Meningioma / complications. Meningioma / pathology. Meningioma / surgery. Middle Aged. Neurilemmoma / complications. Neurilemmoma / pathology. Neurilemmoma / surgery. Neurosurgical Procedures / adverse effects. Neurosurgical Procedures / methods. Pituitary Neoplasms / complications. Pituitary Neoplasms / pathology. Pituitary Neoplasms / surgery. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Prognosis. Reconstructive Surgical Procedures / methods. Recovery of Function / physiology. Retrospective Studies. Treatment Outcome. Trigeminal Nerve Diseases / complications. Trigeminal Nerve Diseases / pathology. Trigeminal Nerve Diseases / surgery

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19387538.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Fibrin Tissue Adhesive
  •  go-up   go-down


43. Winczyk K, Kunert-Radek J, Gruszka A, Radek M, Ławnicka H, Pawlikowski M: Effects of rosiglitazone--peroxisome proliferators-activated receptor gamma (PPARgamma) agonist on cell viability of human pituitary adenomas in vitro. Neuro Endocrinol Lett; 2009 Mar;30(1):107-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of rosiglitazone--peroxisome proliferators-activated receptor gamma (PPARgamma) agonist on cell viability of human pituitary adenomas in vitro.
  • It was shown that tumoral tissue, including the pituitary adenomas, posses PPARgamma receptors.
  • The aim of the present study was to examine the anti-tumour effect of RGZ on human pituitary adenomas in vitro.
  • MATERIALS AND METHODS: Cells of eight pituitary adenomas removed neurosurgically were used to our experiment.
  • RESULTS: On the basis of the pre-operative diagnosis the 6 clinically non-functioning adenomas (CNFPA), one case of acromegaly and one case of Cushing's disease were recognized.
  • THE MAIN FINDING: The obtained results indicate that RZG exerts a suppressive effect on the cell viability in non-functioning pituitary adenomas.
  • CONCLUSION: Our data suggest that rosiglitazone may be useful in the treatment of non-functioning pituitary adenomas, but its efficacy in Cushing's disease and acromegaly requires further study.
  • [MeSH-major] Adenoma / pathology. PPAR gamma / agonists. Pituitary Neoplasms / pathology. Thiazolidinediones / pharmacology
  • [MeSH-minor] Acromegaly / etiology. Acromegaly / pathology. Adrenocorticotropic Hormone / secretion. Adult. Aged. Cell Proliferation / drug effects. Cell Survival / drug effects. Drug Evaluation, Preclinical. Female. Human Growth Hormone / secretion. Humans. Hypoglycemic Agents / pharmacology. Male. Middle Aged. Pituitary ACTH Hypersecretion / etiology. Pituitary ACTH Hypersecretion / pathology. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • Hazardous Substances Data Bank. ROSIGLITAZONE .
  • Hazardous Substances Data Bank. Corticotropin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19300395.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone
  •  go-up   go-down


44. van Nederveen FH, de Krijger RR: Precursor lesions of the adrenal gland. Pathobiology; 2007;74(5):285-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precursor lesions of the adrenal gland.
  • RESULTS: In the adrenal cortex hyperplasia and adenomas are frequently observed tumours or tumour-like conditions.
  • Based on well-validated histopathological scoring systems, benign and malignant adrenocortical tumours can be separated, although a small subset of tumours remains hard to classify.
  • They can be divided into benign and malignant PCC, but the distinction can only be made when metastases are present.
  • In contrast to cortical tumours, the frequent 1p and 3q loss as an early event in tumourigenesis of benign PCC is verified in multiple studies.
  • CONCLUSION: Taken together, there appears to be a relationship between cortical and medullary hyperplasia on the one hand and cortical adenomas and PCC on the other.
  • However, whether there is a transition from benign to malignant tumours, both cortical and medullary, remains to be determined.
  • [MeSH-major] Adenoma / pathology. Adrenal Gland Neoplasms / pathology. Carcinoma / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adrenal Cortex / pathology. Adrenal Cortex / physiology. Adrenal Medulla / pathology. Adrenal Medulla / physiology. Disease Progression. Humans. Hyperplasia / pathology

  • MedlinePlus Health Information. consumer health - Adrenal Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17890895.001).
  • [ISSN] 1423-0291
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 44
  •  go-up   go-down


45. Newman RJ, Nichols DB, Cummings DM: Outpatient colonoscopy by rural family physicians. Ann Fam Med; 2005 Mar-Apr;3(2):122-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: The adenoma detection rate was 27.2% for men and 21.4% for women older than age 50 years.
  • Six adenocarcinomas and 5 large (>2 cm) villous adenomas were detected, and the patients were referred for definitive surgical resection.

  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gastroenterology. 1997 Jan;112(1):24-8 [8978338.001]
  • [Cites] J Fam Pract. 1996 Dec;43(6):561-6 [8969704.001]
  • [Cites] J Fam Pract. 1997 May;44(5):473-80 [9152265.001]
  • [Cites] Fam Med. 1997 Sep;29(8):575-9 [9310757.001]
  • [Cites] Tenn Med. 1998 Jan;91(1):21-6 [9439182.001]
  • [Cites] J Am Board Fam Pract. 1998 Nov-Dec;11(6):492-6 [9876008.001]
  • [Cites] Gastrointest Endosc. 2001 Nov;54(5):662-7 [11677497.001]
  • [Cites] Am J Gastroenterol. 2002 Jun;97(6):1296-308 [12094842.001]
  • [Cites] Rev Gastroenterol Disord. 2001;1(2):73-86 [12120177.001]
  • [Cites] Gastrointest Endosc. 2003 Mar;57(3):352-7 [12612515.001]
  • [Cites] JAMA. 2003 Mar 12;289(10):1288-96 [12633191.001]
  • [Cites] JAMA. 2003 Mar 12;289(10):1297-302 [12633192.001]
  • [Cites] N Engl J Med. 2003 Dec 4;349(23):2191-200 [14657426.001]
  • [Cites] Fam Med. 2004 Jun;36(6):407-11 [15181552.001]
  • [Cites] Fam Pract Res J. 1992 Sep;12(3):313-20 [1414436.001]
  • [Cites] Fam Pract Res J. 1993 Mar;13(1):43-52 [8484340.001]
  • [Cites] Arch Fam Med. 1997 Jan-Feb;6(1):52-8 [9003171.001]
  • (PMID = 15798037.001).
  • [ISSN] 1544-1717
  • [Journal-full-title] Annals of family medicine
  • [ISO-abbreviation] Ann Fam Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1466847
  •  go-up   go-down


46. Hosoyama T, Nishijo K, Garcia MM, Schaffer BS, Ohshima-Hosoyama S, Prajapati SI, Davis MD, Grant WF, Scheithauer BW, Marks DL, Rubin BP, Keller C: A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas. Genes Cancer; 2010 Apr 1;1(4):388-402
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas.
  • Pituitary adenomas are classified into functioning and nonfunctioning (silent) tumors on the basis of hormone secretion.
  • However, the mechanism of tumorigenesis and the cell of origin for pituitary adenoma subtypes remain to be elucidated.
  • Employing a tamoxifen-inducible mouse model, we demonstrate that a novel postnatal Pax7(+) progenitor cell population in the pituitary gland gives rise to silent corticotroph macro-adenomas when the retinoblastoma tumor suppressor is conditionally deleted.
  • Taken together, our results strongly suggest that human silent corticotroph adenomas may in fact arise from a Pax7 lineage of the intermediate lobe, a region of the human pituitary bearing closer scientific interest as a reservoir of pituitary progenitor cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20811506.001).
  • [ISSN] 1947-6019
  • [Journal-full-title] Genes & cancer
  • [ISO-abbreviation] Genes Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA133229-03; United States / NCRR NIH HHS / RR / P41 RR012553; United States / NCI NIH HHS / CA / R01 CA133229
  • [Publication-type] JOURNAL ARTICLE
  • [Publication-country] United States
  •  go-up   go-down


47. Blanc V, Henderson JO, Newberry RD, Xie Y, Cho SJ, Newberry EP, Kennedy S, Rubin DC, Wang HL, Luo J, Davidson NO: Deletion of the AU-rich RNA binding protein Apobec-1 reduces intestinal tumor burden in Apc(min) mice. Cancer Res; 2007 Sep 15;67(18):8565-73
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deletion of the AU-rich RNA binding protein Apobec-1 reduces intestinal tumor burden in Apc(min) mice.
  • Cox-2 overexpression accompanies intestinal adenoma formation in both humans and mice.
  • Evidence from both genetic deletion studies as well as from pharmacologic inhibition has implicated Cox-2 in the development of intestinal adenomas in experimental animals and in adenomas and colorectal cancer in humans.
  • Here, we show that small intestinal adenoma formation is dramatically reduced in compound Apc(min/+) apobec-1(-/-) mice when compared with the parental Apc(min/+) strain.
  • This reduced tumor burden was found in association with increased small intestinal apoptosis and reduced proliferation in small intestinal crypt-villus units from compound Apc(min/+) apobec-1(-/-) mice.
  • Intestinal adenomas from compound Apc(min/+) apobec-1(-/-) mice showed a <2-fold increase in Cox-2 mRNA abundance and reduced prostaglandin E(2) content compared with adenomas from the parental Apc(min/+) strain.
  • In addition, there was reduced expression in adenomas from compound Apc(min/+) apobec-1(-/-) mice of other mRNAs (including epidermal growth factor receptor, peroxisome proliferator-activated receptor delta, prostaglandin receptor EP4, and c-myc), each containing the apobec-1 consensus binding site within their 3'-UTR.
  • These findings suggest that deletion of apobec-1, by modulating expression of AU-rich RNA targets, provides an important mechanism for attenuating a dominant genetic restriction point in intestinal adenoma formation.
  • [MeSH-major] Adenoma / enzymology. Cytidine Deaminase / deficiency. Intestinal Neoplasms / enzymology

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17875695.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-52574; United States / NIDDK NIH HHS / DK / DK-56260; United States / NIDDK NIH HHS / DK / DK-61261; United States / NIDDK NIH HHS / DK / DK-64798; United States / NHLBI NIH HHS / HL / HL-38180; United States / NIDDK NIH HHS / DK / T32 DK-07130
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.5.4.5 / Cytidine Deaminase; EC 3.5.4.5 / apolipoprotein B mRNA editing enzyme
  •  go-up   go-down


48. Young WF Jr, Thompson GB: Laparoscopic adrenalectomy for patients who have Cushing's syndrome. Endocrinol Metab Clin North Am; 2005 Jun;34(2):489-99, xi
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The laparoscopic approach is the procedure of choice for the surgical management of cortisol-producing adenomas and for patients who have corticotropin (ACTH)-dependent Cushing's syndrome for whom surgery failed to remove the source of ACTH.

  • Genetic Alliance. consumer health - Cushing's Syndrome.
  • MedlinePlus Health Information. consumer health - Cushing's Syndrome.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15850855.001).
  • [ISSN] 0889-8529
  • [Journal-full-title] Endocrinology and metabolism clinics of North America
  • [ISO-abbreviation] Endocrinol. Metab. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 48
  •  go-up   go-down


49. Carr NJ, Mahajan H, Tan KL, Hawkins NJ, Ward RL: Serrated and non-serrated polyps of the colorectum: their prevalence in an unselected case series and correlation of BRAF mutation analysis with the diagnosis of sessile serrated adenoma. J Clin Pathol; 2009 Jun;62(6):516-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serrated and non-serrated polyps of the colorectum: their prevalence in an unselected case series and correlation of BRAF mutation analysis with the diagnosis of sessile serrated adenoma.
  • A diagnosis of sessile serrated adenoma was made even if the characteristic features were present only focally.
  • If there was more than one polyp of a particular type in any patient, one lesion was chosen at random so that the results represent the number of patients with each type of polyp rather than the total number of polyps.
  • Non-serrated ("conventional") adenomas were found in 964 patients (65%), hyperplastic polyps in 437 (30%), sessile serrated adenomas in 57 (3.9%), traditional serrated adenomas in 11 (0.7%) and mixed hyperplastic adenomatous polyps in 10 (0.7%).
  • BRAF V600E mutation analysis was performed in 148 selected cases; mutations were found in 44/49 (90%) of lesions diagnosed as sessile serrated adenoma, in 10/34 (29%) of hyperplastic polyps of microvesicular type, in 4/11 (36%) of traditional serrated adenomas, in 10/10 (100%) of mixed hyperplastic adenomatous polyps, and in 2/42 (5%) of "conventional" adenomas.
  • CONCLUSIONS: Sessile serrated adenomas are encountered commonly in routine endoscopy practice.
  • [MeSH-minor] Adenoma / epidemiology. Adenoma / genetics. Adenoma / pathology. Age Distribution. Aged. Chi-Square Distribution. Colonic Polyps / genetics. Colonic Polyps / pathology. Colorectal Neoplasms / epidemiology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. New South Wales / epidemiology. Prevalence

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19126563.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf
  •  go-up   go-down


50. Tzelepi VN, Tsamandas AC, Vlotinou HD, Vagianos CE, Scopa CD: Tight junctions in thyroid carcinogenesis: diverse expression of claudin-1, claudin-4, claudin-7 and occludin in thyroid neoplasms. Mod Pathol; 2008 Jan;21(1):22-30
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ninety-one thyroid neoplasms (15 follicular adenomas, 15 follicular carcinomas, 26 papillary carcinomas, 16 papillary microcarcinomas, 8 medullary carcinomas, 3 poorly differentiated carcinomas, 8 undifferentiated carcinomas) were immunostained with antibodies against occludin and claudin-1, -4 and -7.
  • Thirteen out of 15 follicular adenomas, 10/15 follicular carcinomas, 24/26 papillary carcinomas, 15/16 papillary microcarcinomas, 1/8 medullary carcinomas, 2/3 poorly differentiated carcinomas and 2/8 undifferentiated carcinomas exhibited claudin-1 expression, whereas claudin-4 was expressed in 13/15, 12/15, 23/26, 13/16, 7/8, 2/3 and 2/8 of the tumors, respectively, and claudin-7 expression was found in 67, 33, 73, 69, 25, 0 and 13% of the cases, respectively.
  • Occludin was expressed in 100% follicular adenomas, 80% follicular carcinomas, 96% papillary carcinomas, 50% papillary microcarcinomas, 50% medullary carcinomas, 33% poorly differentiated carcinomas and 88% undifferentiated carcinomas.
  • A correlation between loss of claudin-1 expression and worse disease-free survival was noted on univariate analysis.
  • A differential expression of tight junction proteins in the different histologic types of thyroid gland is noted.
  • [MeSH-major] Biomarkers, Tumor / analysis. Membrane Proteins / analysis. Thyroid Neoplasms / chemistry. Tight Junctions / chemistry
  • [MeSH-minor] Adenoma / chemistry. Adult. Aged. Aged, 80 and over. Carcinoma, Medullary / chemistry. Carcinoma, Papillary / chemistry. Cell Differentiation. Claudin-1. Claudin-4. Claudins. Disease-Free Survival. Down-Regulation. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Occludin. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17962811.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLDN1 protein, human; 0 / CLDN4 protein, human; 0 / CLDN7 protein, human; 0 / Claudin-1; 0 / Claudin-4; 0 / Claudins; 0 / Membrane Proteins; 0 / OCLN protein, human; 0 / Occludin
  •  go-up   go-down


51. Liao CH, Lai MK, Li HY, Chen SC, Chueh SC: Laparoscopic adrenalectomy using needlescopic instruments for adrenal tumors less than 5cm in 112 cases. Eur Urol; 2008 Sep;54(3):640-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Transperitoneal laparoscopic adrenalectomy with needlescopic instruments for 112 patients with presumptively benign adrenal tumors < 5cm were enrolled from July 2000 to February 2005.
  • Only one patient required a blood transfusion and application of a hand-assisted device.
  • Larger tumors, previous abdominal surgery, and pheochromocytoma group were independent risk factors of a longer operative time.
  • Except for one leiomyosarcoma, all other tumors were benign adrenal pathologies (57 aldosterone-producing adenomas, 23 Cushing's adenomas, 12 pheochromocytomas, and 20 incidentalomas).

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Eur Urol. 2008 Sep;54(3):493-5; author reply 495-7 [18281144.001]
  • [CommentIn] Nat Clin Pract Urol. 2009 Jan;6(1):10-1 [19048004.001]
  • (PMID = 18164803.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


52. Beckers A, Daly AF: The clinical, pathological, and genetic features of familial isolated pituitary adenomas. Eur J Endocrinol; 2007 Oct;157(4):371-82
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical, pathological, and genetic features of familial isolated pituitary adenomas.
  • Pituitary adenomas occur in a familial setting in multiple endocrine neoplasia type 1 (MEN1) and Carney's complex (CNC), which occur due to mutations in the genes MEN1 and PRKAR1A respectively.
  • Pituitary adenomas of all types--not limited to IFS--can occur in a familial setting in the absence of MEN1 and CNC; this phenotype is termed familial isolated pituitary adenomas (FIPA).
  • In FIPA, both homogeneous and heterogeneous pituitary adenoma phenotypes can occur within families; virtually all FIPA kindreds contain at least one prolactinoma or somatotropinoma.
  • FIPA differs from MEN1 in terms of a lower proportion of prolactinomas and more frequent somatotropinomas in the FIPA cohort.
  • Patients with FIPA are significantly younger at diagnosis and have significantly larger pituitary adenomas than matched sporadic pituitary adenoma counterparts.
  • In families with AIP mutations, pituitary adenomas have a penetrance of over 50%.
  • AIP mutations are extremely rare in patients with sporadic pituitary adenomas.
  • This review deals with pituitary adenomas that occur in a familial setting, describes in detail the clinical, pathological, and genetic features of FIPA, and addresses aspects of the clinical approach to FIPA families with and without AIP mutations.


53. Li SR, Wang HH, Hu JC, Li N, Liu YL, Wu ZT, Zheng Y, Wang HH, Wu K, Ye H: [Comparison of three FOBT protocols for colorectal cancer screening in Chinese--a multicenter study]. Zhonghua Yi Xue Za Zhi; 2005 Mar 16;85(10):697-700
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: 323 eligible patients including 49 colorectal cancers, 60 colon adenomas, 60 chronic colitis, 15 hemorrhoids and 139 normal colon were observed.
  • 41.6% approximately 48.3% of adenomas was found by the 3 protocols, and 87.5% of adenomas over 2 cm in diameter were detected by any one of FOBT.
  • The majority of adenomas in that advanced lesion existed might be detected by FOBT.
  • [MeSH-minor] Adenoma / prevention & control. Colonoscopy. Cost-Benefit Analysis. Female. Humans. Male


54. De Jesus-Monge WE, Gonzalez-Keelan C, Cruz-Correa M: Serrated adenomas. Curr Gastroenterol Rep; 2009 Oct;11(5):420-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serrated adenomas.
  • Serrated adenomas are categorized as sessile serrated adenomas (SSAs) and traditional serrated adenomas (TSAs).
  • Serrated adenomas may progress to colorectal adenocarcinoma through diverse molecular alterations.
  • Colonoscopy is the only test for the early detection of serrated adenomas that allows inspection of the entire colon and same-session biopsy sampling or polypectomy, if necessary.
  • [MeSH-major] Adenoma / pathology. Biopsy. Colonic Polyps / pathology. Colorectal Neoplasms / pathology


55. Müller-Brüsselbach S, Ebrahimsade S, Jäkel J, Eckhardt J, Rapp UR, Peters JM, Moll R, Müller R: Growth of transgenic RAF-induced lung adenomas is increased in mice with a disrupted PPARbeta/delta gene. Int J Oncol; 2007 Sep;31(3):607-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth of transgenic RAF-induced lung adenomas is increased in mice with a disrupted PPARbeta/delta gene.
  • Both the PPARbeta (also referred to as PPARdelta) and PPARgamma subtype have been reported to either attenuate or potentiate tumorigenesis in a number of different models of intestinal and skin carcinogenesis.
  • In the present study, we have addressed the role of PPARbeta and PPARgamma in lung tumorigenesis in a transgenic mouse model of RAF-induced lung adenoma using two different strategies: i) crossing with PPARbeta null mice, and ii) chronic treatment with the PPARgamma agonist rosiglitazone.
  • Histological examination revealed a significant enhancement of tumor growth in mice lacking one or both alleles of Pparb, but no significant effect in response to rosiglitazone.
  • These observations indicate i) that RAF-induced lung tumorigenesis is attenuated in mice with a disrupted Pparb gene, and ii) that chronic PPARgamma activation does not affect lung adenoma growth.
  • [MeSH-major] Adenoma / genetics. Gene Expression Regulation, Neoplastic. Lung Neoplasms / genetics. PPAR delta / genetics. PPAR-beta / genetics. Proto-Oncogene Proteins c-raf / genetics


56. Hong HH, Ton TV, Kim Y, Wakamatsu N, Clayton NP, Chan PC, Sills RC, Lahousse SA: Genetic alterations in K-ras and p53 cancer genes in lung neoplasms from B6C3F1 mice exposed to cumene. Toxicol Pathol; 2008 Jul;36(5):720-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The incidences of alveolar/bronchiolar adenomas and carcinomas in cumene-treated B6C3F1 mice were significantly greater than those of the control animals.
  • We evaluated these lung neoplasms for point mutations in the K-ras and p53 genes that are often mutated in humans.
  • Cumene-induced lung carcinomas showed loss of heterozygosity (LOH) on chromosome 4 near the p16 gene (13%) and on chromosome 6 near the K-ras gene (12%).
  • [MeSH-major] Benzene Derivatives / toxicity. Genes, p53 / genetics. Genes, ras. Lung Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Isopropylbenzene .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Toxicol Pathol. 2000 Jul-Aug;28(4):529-34 [10930038.001]
  • [Cites] Toxicol Pathol. 2008 Jul;36(5):743-52 [18648096.001]
  • [Cites] Cell Signal. 2000 Jul;12(7):425-34 [10989276.001]
  • [Cites] Curr Biol. 2001 Apr 17;11(8):614-9 [11369207.001]
  • [Cites] Nat Genet. 2001 Sep;29(1):25-33 [11528387.001]
  • [Cites] Carcinogenesis. 2002 Oct;23(10):1737-43 [12376484.001]
  • [Cites] Oncogene. 2002 Oct 21;21(48):7421-34 [12379883.001]
  • [Cites] Toxicol Appl Pharmacol. 2003 Sep 15;191(3):227-34 [13678655.001]
  • [Cites] Carcinogenesis. 2004 Apr;25(4):605-12 [14688030.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2307-16 [15059877.001]
  • [Cites] Toxicol Sci. 2004 May;79(1):82-9 [14976336.001]
  • [Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]
  • [Cites] Scand J Work Environ Health. 1987 Apr;13(2):81-93 [3299685.001]
  • [Cites] N Engl J Med. 1987 Oct 8;317(15):929-35 [3041218.001]
  • [Cites] Science. 1987 Sep 11;237(4820):1309-16 [3629242.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4690-4 [2052552.001]
  • [Cites] Free Radic Biol Med. 1991;10(3-4):211-6 [1650737.001]
  • [Cites] Carcinogenesis. 1993 May;14(5):803-10 [8504472.001]
  • [Cites] Lab Invest. 1993 Sep;69(3):261-74 [8377469.001]
  • [Cites] Science. 1993 Dec 24;262(5142):1980-1 [8266092.001]
  • [Cites] Cancer Res. 1994 Sep 15;54(18):4855-78 [8069852.001]
  • [Cites] Carcinogenesis. 1995 Jul;16(7):1623-8 [7614698.001]
  • [Cites] Toxicology. 1995 Aug 25;101(3):125-56 [7676462.001]
  • [Cites] Genes Chromosomes Cancer. 1995 Nov;14(3):164-70 [8589032.001]
  • [Cites] Carcinogenesis. 1996 Jun;17(6):1187-98 [8681432.001]
  • [Cites] Cancer Res. 1996 Aug 1;56(15):3415-20 [8758904.001]
  • [Cites] Toxicol Appl Pharmacol. 1996 Nov;141(1):205-13 [8917693.001]
  • [Cites] Environ Health Perspect. 1996 Dec;104 Suppl 6:1165-71 [9118888.001]
  • [Cites] Environ Health Perspect. 1996 Dec;104 Suppl 6:1211-8 [9118895.001]
  • [Cites] Carcinogenesis. 1999 Apr;20(4):657-62 [10223196.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3634-40 [10446974.001]
  • [Cites] Semin Cancer Biol. 2005 Apr;15(2):103-12 [15652455.001]
  • [Cites] Mutat Res. 2005 Apr 1;571(1-2):33-42 [15748636.001]
  • [Cites] Genes Dev. 2005 Mar 15;19(6):643-64 [15769940.001]
  • [Cites] Toxicol Pathol. 2005;33(2):292-9 [15902973.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5076-83 [15958551.001]
  • [Cites] Environ Mol Mutagen. 2007 Apr-May;48(3-4):299-306 [16395694.001]
  • [Cites] Carcinogenesis. 2000 Sep;21(9):1691-700 [10964101.001]
  • (PMID = 18648094.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES021219-11; 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 / Benzene Derivatives; 0 / Codon; 0 / Tumor Suppressor Protein p53; 8Q54S3XE7K / cumene
  • [Other-IDs] NLM/ NIHMS87816; NLM/ PMC2803761
  •  go-up   go-down


57. Kristoffersen US, Hesse B, Rasmussen AK, Kjaer A: Radioiodine therapy in hyperthyroid disease: poorer outcome in patients with high 24 hours radioiodine uptake. Clin Physiol Funct Imaging; 2006 May;26(3):167-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radioiodine therapy in hyperthyroid disease: poorer outcome in patients with high 24 hours radioiodine uptake.
  • METHODS: Retrospective analysis of 72 patients who underwent radioiodine treatment for toxic goiter at our outpatient clinic [29 diffuse goiters (DG), 30 toxic multinodular goiters (TMG) and 13 toxic adenomas (TA)].
  • CONCLUSION: In patients with hyperthyroid disease treated with radioiodine the outcome is poorer for patients with high 24 h RIU compared with low 24 h RIU measured prior to treatment when the radioiodine dose is calculated on the basis of 24 h RIU.

  • MedlinePlus Health Information. consumer health - Hyperthyroidism.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LEVOTHYROXINE .
  • Hazardous Substances Data Bank. LIOTHYRONINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16640512.001).
  • [ISSN] 1475-0961
  • [Journal-full-title] Clinical physiology and functional imaging
  • [ISO-abbreviation] Clin Physiol Funct Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 06LU7C9H1V / Triiodothyronine; 9002-71-5 / Thyrotropin; Q51BO43MG4 / Thyroxine
  •  go-up   go-down


58. Ma W, Xia X, Stafford LJ, Yu C, Wang F, LeSage G, Liu M: Expression of GCIP in transgenic mice decreases susceptibility to chemical hepatocarcinogenesis. Oncogene; 2006 Jul 13;25(30):4207-16
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the diethylnitrosamine (DEN)-induced mouse hepatocarcinogenesis, we demonstrated that overexpression of GCIP in mouse liver suppressed DEN-induced hepatocarcinogenesis at an early stage of tumor development.
  • The number of hepatic adenomas at 24 weeks was significantly lower or not detected in GCIP transgenic male mice compared to the control mice under the same treatment.
  • Furthermore, we demonstrate that GCIP functions as a transcriptional suppressor, regulates the expression of cyclin D1, and inhibits anchorage-independent cell growth and colony formation in HepG2 cells, suggesting a significant role of GCIP in tumor initiation and development.
  • [MeSH-major] Genetic Predisposition to Disease. Liver Neoplasms, Experimental / chemically induced. Liver Neoplasms, Experimental / genetics. Transcription Factors / biosynthesis. Transcription Factors / genetics
  • [MeSH-minor] Animals. Carbon Tetrachloride / toxicity. Carcinogens / toxicity. Cell Line, Tumor. Female. Humans. Male. Mice. Mice, Transgenic

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CARBON TETRACHLORIDE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16501603.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA106479; United States / NHLBI NIH HHS / HL / 5R01HL064792
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCNDBP1 protein, human; 0 / Carcinogens; 0 / Transcription Factors; CL2T97X0V0 / Carbon Tetrachloride
  •  go-up   go-down


59. Di Cristofaro J, Vasko V, Savchenko V, Cherenko S, Larin A, Ringel MD, Saji M, Marcy M, Henry JF, Carayon P, De Micco C: ret/PTC1 and ret/PTC3 in thyroid tumors from Chernobyl liquidators: comparison with sporadic tumors from Ukrainian and French patients. Endocr Relat Cancer; 2005 Mar;12(1):173-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In adenomas the prevalence of rearrangement was significantly higher in all Ukrainians than in French patients (P = 0.004).
  • This finding suggests that irradiation had the same effect regardless of age.

  • MedlinePlus Health Information. consumer health - Radiation Emergencies.
  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15788648.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NCOA4 protein, human; 0 / Nuclear Receptor Coactivators; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / ret-PTC fusion oncoproteins, human
  •  go-up   go-down


60. Tian C, Ye F, Wang L, Deng Y, Dong Y, Wang X, Xu T, Lei T, Wang X: Nitric oxide inhibits ghrelin-induced cell proliferation and ERK1/2 activation in GH3 cells. Endocrine; 2010 Dec;38(3):412-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ghrelin stimulates growth hormone release and cell proliferation, which strongly supports a significant role for this peptide in the control of growth hormone-releasing adenomas function and growth.
  • Nitric oxide can influence the stimulatory effects of ghrelin on growth hormone secretion in growth hormone-releasing adenomas.
  • However, the effect of nitric oxide (NO) on ghrelin-induced cell proliferation and the mechanism of this effect in the adenoma were not clarified.
  • A NO donor, S-nitroso-N-acetylpenicillamine (SNAP), blunted basal, and ghrelin-induced cell proliferation.

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurosci Lett. 2008 Jul 4;439(1):94-9 [18511197.001]
  • [Cites] Neurochem Res. 2007 Apr-May;32(4-5):681-94 [17043768.001]
  • [Cites] Neuroendocrinology. 2004;80(2):83-91 [15475661.001]
  • [Cites] Endocr J. 1999 Dec;46(6):779-85 [10724353.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jan 3;92(1):170-4 [7529411.001]
  • [Cites] Neuropeptides. 1996 Dec;30(6):528-32 [9004249.001]
  • [Cites] Nitric Oxide. 2009 Sep;21(2):92-103 [19602444.001]
  • [Cites] Pharmacol Rev. 2005 Dec;57(4):541-6 [16382107.001]
  • [Cites] Nature. 1999 Dec 9;402(6762):656-60 [10604470.001]
  • [Cites] J Neuroendocrinol. 2008 Mar;20(3):406-12 [18208548.001]
  • [Cites] Eur J Endocrinol. 2004 Aug;151(2):233-40 [15296479.001]
  • [Cites] J Neurochem. 2003 Mar;84(6):1367-77 [12614337.001]
  • [Cites] Nature. 1990 Oct 25;347(6295):768-70 [1700301.001]
  • [Cites] Tissue Cell. 2009 Apr;41(2):133-40 [19019400.001]
  • [Cites] Sci STKE. 2000 Jul 11;2000(40):re1 [11752597.001]
  • [Cites] Neuroendocrinology. 1997 Dec;66(6):426-31 [9430448.001]
  • [Cites] Mol Vis. 2008 May 28;14:983-91 [18523663.001]
  • [Cites] Endocrine. 2009 Feb;35(1):112-7 [18953675.001]
  • [Cites] Neuroendocrinology. 1996 Aug;64(2):146-52 [8857609.001]
  • [Cites] Mol Endocrinol. 2004 Sep;18(9):2291-301 [15178745.001]
  • [Cites] Neuroendocrinology. 2001 Oct;74(4):213-9 [11598377.001]
  • [Cites] Science. 1996 Aug 16;273(5277):974-7 [8688086.001]
  • [Cites] Zhonghua Wai Ke Za Zhi. 2004 Nov 22;42(22):1349-52 [15634400.001]
  • [Cites] Mol Endocrinol. 2001 Jun;15(6):1010-22 [11376118.001]
  • [Cites] Inflamm Res. 2000 Oct;49(10):541-7 [11089907.001]
  • [Cites] Endocrine. 2005 Nov;28(2):209-16 [16388095.001]
  • [Cites] Am J Physiol Cell Physiol. 2006 Jan;290(1):C233-43 [16207796.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5667-74 [11724768.001]
  • [Cites] Endocr Rev. 2004 Jun;25(3):426-57 [15180951.001]
  • [Cites] Free Radic Biol Med. 2008 Jul 1;45(1):18-31 [18439435.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):1300-8 [11889202.001]
  • (PMID = 20972719.001).
  • [ISSN] 1559-0100
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Protein Kinase Inhibitors; 31C4KY9ESH / Nitric Oxide; EC 2.7.11.24 / Mapk1 protein, rat; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  •  go-up   go-down


61. Hwang SL, Chang JH, Cheng TS, Sy WD, Lieu AS, Lin CL, Lee KS, Howng SL, Hong YR: Expression of Rac3 in human brain tumors. J Clin Neurosci; 2005 Jun;12(5):571-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Rac3 may play an important role in tumor growth but little is known about its expression and mutation in human tumor tissues.
  • Overexpression of the Rac3 gene occurred in 19% (5/26) of brain tumors; 3 of 9 (33%) meningiomas, 1 of 11 (9%) astrocytomas and 1 of 6 (17%) pituitary adenomas.
  • Mutation of the Rac3 gene occurred in 63% (12/19) of brain tumours; 4 of 7 (57.1%) meningiomas, 4 of 5 (80%) pituitary adenomas and 4 of 7 (57.1%) astrocytomas.
  • Except in one astrocytoma, the other four tumors with Rac3 overexpression (3 meningiomas and one pituitary adenoma) did not have Rac3 mutations.
  • Overexpression may be associated with aggressive tumor behavior.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Neoplastic / genetics. Mutation / genetics. rac GTP-Binding Proteins / genetics
  • [MeSH-minor] Astrocytoma / diagnosis. Astrocytoma / genetics. Astrocytoma / metabolism. Chromosomes, Human, Pair 17 / genetics. DNA Mutational Analysis. GTP Phosphohydrolases / metabolism. Genetic Testing. Humans. Meningioma / diagnosis. Meningioma / genetics. Meningioma / metabolism. Neoplasm Invasiveness / genetics. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / genetics. Pituitary Neoplasms / metabolism. Predictive Value of Tests. RNA, Messenger / analysis. RNA, Messenger / genetics. Signal Transduction / genetics

  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15993075.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RAC3 protein, human; 0 / RNA, Messenger; EC 3.6.1.- / GTP Phosphohydrolases; EC 3.6.5.2 / rac GTP-Binding Proteins
  •  go-up   go-down


62. Xu T, Ye F, Wang B, Tian C, Wang S, Shu K, Guo D, Lei T: Elevation of growth hormone secretagogue receptor type 1a mRNA expression in human growth hormone-secreting pituitary adenoma harboring G protein alpha subunit mutation. Neuro Endocrinol Lett; 2010;31(1):147-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevation of growth hormone secretagogue receptor type 1a mRNA expression in human growth hormone-secreting pituitary adenoma harboring G protein alpha subunit mutation.
  • OBJECTIVE: The purpose of this study was to investigate the relationship between the ghrelin or GHSR-1a mRNA levels and clinical characteristics and to confirm the effect of gsp mutations on ghrelin/GHSR-1a system in human GH-secreting pituitary adenomas.
  • The gsp mutations in 43 cases of human GH-secreting pituitary adenomas were detected using PCR-DNA direct sequencing analysis.
  • RESULTS: The expression of GHSR-1a correlated positvely with tumor size (R=0.411, p=0.006) and invasiveness (p<0.05).
  • In contrast, ghrelin mRNA levels correlated positively only with tumor size (R=0.331, p=0.030) but not with tumor invasiveness (p>0.05).
  • The expression level of GHSR-1a mRNA was significantly higher in gsp positive adenomas than in negative adenomas (p<0.05).
  • Whereas, there was no significant difference in the expression of ghrelin mRNA between gsp mutation-positive and -negative adenomas (p>0.05).
  • Additionally there was a significant positve correlation between the ghrelin and GHSR-1a mRNA expression levels in gsp-positive (R=0.553, p=0.040) or -negative adenomas (R=0.489, p=0.007).
  • CONCLUSIONS: GHSR-1a correlated positively with tumor size and invasiveness, while ghrelin correlated positively only with tumor size.
  • Gsp mutations may upregulate the expression of GHSR-1a mRNA and have no effect on ghrelin mRNA levels in human GH-secreting pituitary adenomas.
  • [MeSH-major] Adenoma / genetics. GTP-Binding Protein alpha Subunits / genetics. Growth Hormone-Secreting Pituitary Adenoma / genetics. Mutation. Receptors, Ghrelin / genetics
  • [MeSH-minor] Acromegaly / etiology. Acromegaly / genetics. Adult. Female. Ghrelin / genetics. Ghrelin / metabolism. Humans. Male. Middle Aged. RNA, Messenger / metabolism. Retrospective Studies. Tumor Burden. Up-Regulation. Young Adult

  • Genetic Alliance. consumer health - Pituitary adenoma, growth hormone-secreting.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20150876.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / GTP-Binding Protein alpha Subunits; 0 / Ghrelin; 0 / RNA, Messenger; 0 / Receptors, Ghrelin
  •  go-up   go-down


63. Ok KS, Kim YS, Kim HH, Ryu SH, Lee JH, Moon JS, Kang YK: [The difference of clinicopathologic features according to leptin expression in colorectal adenoma]. Korean J Gastroenterol; 2010 Jul;56(1):20-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The difference of clinicopathologic features according to leptin expression in colorectal adenoma].
  • BACKGROUND/AIMS: Colorectal adenoma and cancer are known to be associated with obesity.
  • However, the association between adenoma and leptin remains controversial.
  • We evaluated the leptin expression in human colorectal adenoma and its correlation to clinicopathologic factors.
  • METHODS: Leptin expression was assessed by immunohistochemistry in 91 samples of colorectal adenoma larger than 5 mm, which were removed by endoscopic polypectomy.
  • In leptin positive group, the correlation of leptin expression with adenoma size and histological showed positive tendency without statistical significance.
  • CONCLUSIONS: Leptin expression of colorectal adenoma was associated with BMI.
  • The question of whether leptin contributes to colorectal adenoma development is unresolved and will require additional studies.
  • [MeSH-major] Adenoma / pathology. Colorectal Neoplasms / pathology. Leptin / metabolism

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20664314.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Leptin
  •  go-up   go-down


64. Shaukat A, Oancea C, Bond JH, Church TR, Allen JI: Variation in detection of adenomas and polyps by colonoscopy and change over time with a performance improvement program. Clin Gastroenterol Hepatol; 2009 Dec;7(12):1335-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variation in detection of adenomas and polyps by colonoscopy and change over time with a performance improvement program.
  • BACKGROUND & AIMS: There has been no prospective, community-based study to track changes in adenoma detection by individual physicians over time and to determine the effectiveness of targeted educational interventions.
  • During a period of 3 years, 5 specific interventions were implemented; each was designed to improve adenoma detection rates.
  • Controlling for patient-related and procedure-related factors, rates of adenoma detection and 3-year trends for individual physicians were plotted, and intraclass correlation coefficients were calculated.
  • Generalized estimating equations were used to identify factors associated with detection of adenomas and polyps.
  • RESULTS: At least 1 polyp and 1 adenoma were found in 36% and 22% of examinations, respectively.
  • Adenoma detection rates by endoscopists ranged from 10%-39%.
  • Factors associated with adenoma detection included age of the patient (odds ratio [OR], 1.02; 95% confidence interval [CI], 1.02-1.02), male sex (OR, 1.53; 95% CI, 1.34-1.74), and adequate preparation quality (OR, 2.26; 95% CI, 1.64-3.12).
  • CONCLUSIONS: The detection of adenomas by individual physicians during a 3-year period varied and did not appear to change between individual endoscopists, despite planned, systematic interventions.
  • This indicates that other targeted interventions might be required to improve adenoma detection rates among experienced, community gastroenterologists.
  • [MeSH-major] Adenoma / diagnosis. Colonic Neoplasms / diagnosis. Colonoscopy / methods. Colonoscopy / standards. Health Services Research. Polyps / diagnosis

  • MedlinePlus Health Information. consumer health - Colonoscopy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19665583.001).
  • [ISSN] 1542-7714
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


65. Yang YX, Habel LA, Capra AM, Achacoso NS, Quesenberry CP Jr, Ferrara A, Levin TR, Lewis JD: Serial glycosylated hemoglobin levels and risk of colorectal neoplasia among patients with type 2 diabetes mellitus. Cancer Epidemiol Biomarkers Prev; 2010 Dec;19(12):3027-36
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serial glycosylated hemoglobin levels and risk of colorectal neoplasia among patients with type 2 diabetes mellitus.
  • BACKGROUND: Hyperglycemia may increase the risk of colorectal neoplasia by serving as an energy source for neoplastic growth.
  • We sought to determine whether glycemic control measured by serial hemoglobin A1c (HbA1c) was associated with the risk of colorectal adenoma.
  • Cases had at least 1 colorectal adenoma identified at either colonoscopy (analysis 1) or sigmoidoscopy (analysis 2).
  • Controls had no colorectal neoplasia identified at the corresponding endoscopic examination.
  • RESULTS: Case-control analysis 1 included 4,248 patients, of whom 1,296 (31%) had at least 1 adenoma.
  • The adjusted mean HbA1c levels among those without any adenomas was 8.20% versus 8.26% among those with at least 1 adenoma, a difference of 0.06% (95% CI = -0.02 to 0.14, P = 0.16).
  • Case-control analysis 2 included 9,813 patients, of whom 951 (10%) had at least 1 distal adenoma.
  • The adjusted mean HbA1c levels among those without any distal adenomas was 8.32% versus 8.37% among those with at least 1 distal adenoma, a difference of 0.05% (95% CI = -00.04 to 0.14, P = 0.25).
  • The results were similar for advanced adenomas.
  • CONCLUSIONS: Glycemic control was not associated with the risk of colorectal adenoma among diabetic persons.

  • Genetic Alliance. consumer health - Diabetes.
  • Genetic Alliance. consumer health - Diabetes, Type 2.
  • Genetic Alliance. consumer health - Diabetes mellitus type 2.
  • MedlinePlus Health Information. consumer health - A1C.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Diabetes Type 2.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • [Cites] Gastrointest Endosc. 2000 Jun;51(6):647-51 [10840294.001]
  • [Cites] Diabetologia. 2010 Sep;53(9):1823-6 [20523967.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):412-8 [12750235.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jun;13(6):915-9 [15184246.001]
  • [Cites] Gastroenterology. 2004 Oct;127(4):1044-50 [15480982.001]
  • [Cites] Cancer Res. 1991 Jul 15;51(14):3721-5 [2065328.001]
  • [Cites] Mutat Res. 1993 Nov;290(1):111-8 [7694090.001]
  • [Cites] Am J Gastroenterol. 1995 Mar;90(3):353-65 [7872270.001]
  • [Cites] Cancer Causes Control. 1995 Mar;6(2):164-79 [7749056.001]
  • [Cites] Diabetes Care. 1997 Sep;20(9):1396-402 [9283786.001]
  • [Cites] Int J Epidemiol. 1998 Oct;27(5):794-8 [9839735.001]
  • [Cites] J Natl Cancer Inst. 1999 Jul 7;91(13):1147-54 [10393723.001]
  • [Cites] Cancer Causes Control. 1999 Oct;10(5):379-86 [10530607.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):850-5 [15824155.001]
  • [Cites] J Natl Cancer Inst. 2005 Nov 16;97(22):1679-87 [16288121.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Dec;14(12):3010-2 [16365028.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3108-15 [18990751.001]
  • [Cites] Gastroenterology. 2008 Dec;135(6):1914-23, 1923.e1 [18930061.001]
  • [Cites] Diabetologia. 2009 Sep;52(9):1766-77 [19572116.001]
  • [Cites] JAMA. 2010 Feb 3;303(5):446-7 [20124540.001]
  • [Cites] Lancet. 2010 Feb 6;375(9713):481-9 [20110121.001]
  • [Cites] Cancer Lett. 2001 Jun 26;167(2):135-43 [11369133.001]
  • (PMID = 20937982.001).
  • [ISSN] 1538-7755
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA102599-03; United States / NCI NIH HHS / CA / R01 CA102599; United States / NCI NIH HHS / CA / CA102599; United States / NCI NIH HHS / CA / R01 CA102599-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobin A, Glycosylated
  • [Other-IDs] NLM/ NIHMS244408; NLM/ PMC3005371
  •  go-up   go-down


66. Biller BM, Colao A, Petersenn S, Bonert VS, Boscaro M: Prolactinomas, Cushing's disease and acromegaly: debating the role of medical therapy for secretory pituitary adenomas. BMC Endocr Disord; 2010;10:10
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolactinomas, Cushing's disease and acromegaly: debating the role of medical therapy for secretory pituitary adenomas.
  • Pituitary adenomas are associated with a variety of clinical manifestations resulting from excessive hormone secretion and tumor mass effects, and require a multidisciplinary management approach.
  • This article discusses the treatment modalities for the management of patients with a prolactinoma, Cushing's disease and acromegaly, and summarizes the options for medical therapy in these patients.First-line treatment of prolactinomas is pharmacotherapy with dopamine agonists; recent reports of cardiac valve abnormalities associated with this class of medication in Parkinson's disease has prompted study in hyperprolactinemic populations.
  • Patients with resistance to dopamine agonists may require other treatment.First-line treatment of Cushing's disease is pituitary surgery by a surgeon with experience in this condition.
  • Current medical options for Cushing's disease block adrenal cortisol production, but do not treat the underlying disease.
  • The multi-receptor targeted somatostatin analogue pasireotide (SOM230) shows promise as a pituitary-directed medical therapy in Cushing's disease; further studies will determine its efficacy and safety.
  • Radiation therapy, with medical adrenal blockade while awaiting the effects of radiation, and bilateral adrenalectomy remain standard treatment options for patients not cured with pituitary surgery.In patients with acromegaly, surgery remains the first-line treatment option when the tumor is likely to be completely resected, or for debulking, especially when the tumor is compressing neurovisual structures.
  • Pegvisomant is indicated in patients who have not responded to surgery and other medical therapy, although there are regional differences in when it is prescribed.In conclusion, the treatment of patients with pituitary adenomas requires a multidisciplinary approach.
  • Current medical therapies for Cushing's disease primarily focus on adrenal blockade of cortisol production, although pasireotide and cabergoline show promise as pituitary-directed medical therapy for Cushing's disease; further long-term evaluation of efficacy and safety is important.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4081-6 [15886256.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):135-41 [15994755.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Aug;63(2):168-75 [16060910.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Aug;63(2):176-84 [16060911.001]
  • [Cites] Eur J Endocrinol. 2005 Sep;153(3):R7-R10 [16131595.001]
  • [Cites] Horm Res. 2005;64(3):140-3 [16192738.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Nov;63(5):549-59 [16268808.001]
  • [Cites] Eur J Endocrinol. 2005 Dec;153(6):737-40 [16322377.001]
  • [Cites] Horm Metab Res. 2005 Dec;37(12):722-8 [16372224.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1239-45 [16403824.001]
  • [Cites] Endocr J. 2005 Dec;52(6):775-9 [16410672.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Feb;64(2):219-24 [16430724.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Apr;91(4):1397-403 [16449332.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Mar;64(3):342-51 [16487447.001]
  • [Cites] J Endocrinol Invest. 2005;28(11 Suppl International):21-7 [16625841.001]
  • [Cites] Endocr Rev. 2006 Aug;27(5):485-534 [16705142.001]
  • [Cites] Endocrinology. 2006 Sep;147(9):4438-44 [16740975.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Oct;91(10):3746-53 [16868050.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Sep;65(3):389-95 [16918962.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Nov;91(11):4482-8 [16940446.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Oct;2(10):552-61 [17024154.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jan;92(1):172-9 [17062771.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2558-73 [17167139.001]
  • [Cites] N Engl J Med. 2007 Jan 4;356(1):29-38 [17202453.001]
  • [Cites] N Engl J Med. 2007 Jan 4;356(1):39-46 [17202454.001]
  • [Cites] Eur J Endocrinol. 2007 Jan;156(1):91-8 [17218730.001]
  • [Cites] Clin Endocrinol (Oxf). 2007 Jun;66(6):859-68 [17465997.001]
  • [Cites] N Engl J Med. 2007 Jun 14;356(24):2457-71 [17517853.001]
  • [Cites] Endocrinology. 2007 Dec;148(12):6107-14 [17656461.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):2861-5 [17682084.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Dec;92(12):4598-601 [17895318.001]
  • [Cites] Mol Cell Endocrinol. 2008 May 14;286(1-2):69-74 [17977644.001]
  • [Cites] Eur J Endocrinol. 2007 Nov;157(5):579-87 [17984237.001]
  • [Cites] Neurosurg Focus. 2007;23(6):E14 [18081479.001]
  • [Cites] Eur J Endocrinol. 2008 Jan;158(1):91-9 [18166822.001]
  • [Cites] Endocr Pract. 2007 Nov-Dec;13(7):726-34 [18194929.001]
  • [Cites] Eur J Endocrinol. 2008 Jul;159(1):1-5 [18456868.001]
  • [Cites] Int J Clin Pract. 2008 Dec;62(12):1864-9 [18462372.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3348-56 [18559921.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3436-42 [18593770.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Sep;93(9):3515-8 [18611977.001]
  • [Cites] Eur J Endocrinol. 2008 Oct;159(4):R11-4 [18625690.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):3853-9 [18647806.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Oct;93(10):3777-84 [18682513.001]
  • [Cites] Neurosurgery. 2008 Jun;62(6):1262-9; discussion 1269-70 [18824992.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):223-30 [18957500.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jan;94(1):115-22 [18957506.001]
  • [Cites] Endocr Pract. 2008 Sep;14(6):672-7 [18996784.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 Jan;70(1):104-8 [19128367.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Apr;94(4):1118-24 [19141584.001]
  • [Cites] Clin Endocrinol (Oxf). 2009 May;70(5):757-68 [19178516.001]
  • [Cites] J Endocrinol Invest. 2008 Dec;31(12):1119-23 [19246980.001]
  • [Cites] Eur J Endocrinol. 2009 Jun;160(6):1003-10 [19289534.001]
  • [Cites] Clin Endocrinol (Oxf). 2010 Jan;72(1):53-8 [19508591.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1281-7 [12379847.001]
  • [Cites] Endocr Rev. 2003 Feb;24(1):28-47 [12588807.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jul;93(7):2454-62 [18413427.001]
  • [Cites] Eur J Endocrinol. 2008 May;158(5):595-603 [18426817.001]
  • [Cites] N Engl J Med. 1979 Mar 1;300(9):459-64 [215912.001]
  • [Cites] Clin Endocrinol (Oxf). 1991 Aug;35(2):169-78 [1657460.001]
  • [Cites] J Endocrinol Invest. 1990 Mar;13(3):257-61 [1973178.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Mar;32(3):275-81 [2160871.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Apr;60(4):698-705 [3882737.001]
  • [Cites] JAMA. 1982 Mar 5;247(9):1320 [6121067.001]
  • [Cites] Ann Intern Med. 1980 May;92(5):613-9 [6247946.001]
  • [Cites] Clin Endocrinol (Oxf). 1981 Nov;15(5):479-84 [6276051.001]
  • [Cites] Endocr Rev. 1993 Aug;14(4):443-58 [7693447.001]
  • [Cites] Clin Endocrinol (Oxf). 1994 Jul;41(1):95-102 [8050136.001]
  • [Cites] Am J Med. 1993 Sep;95(3):305-8 [8396322.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jul;81(7):2647-52 [8675592.001]
  • [Cites] Drug Saf. 1996 Apr;14(4):228-38 [8713691.001]
  • [Cites] J Endocrinol. 1997 Oct;155 Suppl 1:S23-9; discussion S31-2 [9389992.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Feb;83(2):374-8 [9467544.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2730-4 [9709939.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3034-40 [9745397.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Oct;83(10):3542-4 [9768661.001]
  • [Cites] Lancet. 1998 Oct 31;352(9138):1455-61 [9808008.001]
  • [Cites] Ann Med. 1998 Oct;30(5):452-9 [9814831.001]
  • [Cites] Eur J Endocrinol. 1998 Nov;139(5):516-21 [9849816.001]
  • [Cites] J Endocrinol Invest. 1999 Apr;22(4):306-9 [10342366.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] Mol Cell Endocrinol. 1999 Nov 25;157(1-2):75-85 [10619399.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):8-13 [10634356.001]
  • [Cites] N Engl J Med. 2000 Apr 20;342(16):1171-7 [10770982.001]
  • [Cites] Acta Med Austriaca. 2000;27(1):27-31 [10812460.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Jun;85(6):2247-52 [10852458.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2779-86 [11397887.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):2929-34 [11443145.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3568-73 [11502780.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4104-8 [11549633.001]
  • [Cites] Endocr Relat Cancer. 2001 Dec;8(4):287-305 [11733226.001]
  • [Cites] Lancet. 2001 Nov 24;358(9295):1754-9 [11734231.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jan;87(1):99-104 [11788630.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Jan;56(1):65-71 [11849248.001]
  • [Cites] Eur J Endocrinol. 2002 May;146(5):707-16 [11980628.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Eur J Endocrinol. 2003 Mar;148(3):325-31 [12611613.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3105-12 [12843150.001]
  • [Cites] Ann Intern Med. 1960 Mar;52:560-9 [14426442.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2023-33 [14627787.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Dec;88(12):5593-602 [14671138.001]
  • [Cites] Pituitary. 2003;6(1):19-27 [14674720.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):638-45 [14764775.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):667-74 [14764779.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Mar;60(3):375-81 [15009004.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Apr;89(4):1577-85 [15070915.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2452-62 [15126577.001]
  • [Cites] Clin Endocrinol (Oxf). 2004 Aug;61(2):209-15 [15272916.001]
  • [Cites] Cancer. 2004 Aug 1;101(3):613-9 [15274075.001]
  • [Cites] J Clin Invest. 2004 Aug;114(3):349-56 [15286801.001]
  • [Cites] Eur J Endocrinol. 2004 Aug;151(2):173-8 [15296471.001]
  • [Cites] Endocr Pract. 2004 May-Jun;10(3):213-25 [15382339.001]
  • [Cites] Neuroendocrinology. 2004;80 Suppl 1:47-50 [15477717.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1588-93 [15585549.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1340-6 [15585550.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63 [15613435.001]
  • [Cites] Eur J Endocrinol. 2005 Mar;152(3):379-87 [15757854.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E278-87 [15769796.001]
  • [Cites] Eur J Endocrinol. 2005 Apr;152(4):645-54 [15817922.001]
  • [Cites] Lancet. 2005 May 7-13;365(9471):1644-6 [15885297.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Aug;90(8):4465-73 [15886238.001]
  • (PMID = 20478050.001).
  • [ISSN] 1472-6823
  • [Journal-full-title] BMC endocrine disorders
  • [ISO-abbreviation] BMC Endocr Disord
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2887860
  •  go-up   go-down


67. van der Weyden L, Arends MJ, Dovey OM, Harrison HL, Lefebvre G, Conte N, Gergely FV, Bradley A, Adams DJ: Loss of Rassf1a cooperates with Apc(Min) to accelerate intestinal tumourigenesis. Oncogene; 2008 Jul 24;27(32):4503-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study we set out to test the hypothesis that loss of Rassf1a can cooperate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate intestinal tumourigenesis using the Apc-Min (Apc(Min/+)) mouse model, as mutational or deletional inactivation of APC is a frequent early event in the genesis of intestinal cancer.
  • Further, loss of RASSF1A has also been reported to occur in premalignant adenomas of the bowel.
  • By interbreeding isoform specific Rassf1a knockout mice with Apc(+/Min) mice, we showed that loss of Rassf1a results in a significant increase in adenomas of the small intestine and accelerated intestinal tumourigenesis leading to the earlier death of adenocarcinoma-bearing mice and decreased overall survival.
  • Comparative genomic hybridization of adenomas from Rassf1a(-/-); Apc(+/Min) mice revealed no evidence of aneuploidy or gross chromosomal instability (no difference to adenomas from Rassf1a(+/+); Apc(+/Min) mice).
  • Immunohistochemical analysis of adenomas revealed increased nuclear beta-catenin accumulation in adenomas from Rassf1a(-/-); Apc(+/Min) mice, compared to those from Rassf1a(+/+); Apc(+/Min) mice, but no differences in proliferation marker (Ki67) staining patterns.
  • Collectively these data demonstrate cooperation between inactivation of Rassf1a and Apc resulting in accelerated intestinal tumourigenesis, with adenomas showing increased nuclear accumulation of beta-catenin, supporting a mechanistic link via loss of the known interaction of Rassf1 with beta-TrCP that usually mediates degradation of beta-catenin.
  • [MeSH-major] Genes, APC. Intestinal Neoplasms / etiology. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Adenoma / etiology. Adenoma / genetics. Aneuploidy. Animals. Cell Nucleus / metabolism. Chromosomal Instability. Humans. Ki-67 Antigen / analysis. Mice. Mice, Inbred C57BL. Signal Transduction. beta Catenin / metabolism

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1991 Aug 9;253(5020):665-9 [1651563.001]
  • [Cites] Biochim Biophys Acta. 2007 Sep;1776(1):58-85 [17692468.001]
  • [Cites] Cancer Res. 1994 Nov 15;54(22):5947-52 [7954427.001]
  • [Cites] Bioinformatics. 2004 Dec 12;20(18):3413-22 [15381628.001]
  • [Cites] Nature. 2001 Mar 29;410(6828):536-7 [11279479.001]
  • [Cites] J Biol Chem. 2001 Oct 19;276(42):39094-102 [11483600.001]
  • [Cites] Oncogene. 2002 May 23;21(23):3792-5 [12032847.001]
  • [Cites] Genome Res. 2004 Jan;14(1):188-96 [14707179.001]
  • [Cites] Nat Cell Biol. 2004 Feb;6(2):129-37 [14743218.001]
  • [Cites] Nat Genet. 2004 Apr;36(4):320-2 [15054482.001]
  • [Cites] Lab Invest. 2004 Jul;84(7):884-93 [15122305.001]
  • [Cites] J Immunol. 1984 Oct;133(4):1710-5 [6206131.001]
  • [Cites] Science. 1990 Jan 19;247(4940):322-4 [2296722.001]
  • [Cites] Cancer Res. 2005 Jan 1;65(1):92-8 [15665283.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):843-50 [15829953.001]
  • [Cites] Nat Genet. 2005 May;37(5):532-6 [15852006.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(18):8356-67 [16135822.001]
  • [Cites] Oncogene. 2005 Nov 17;24(51):7630-4 [16007118.001]
  • [Cites] Nat Genet. 2006 Aug;38(8):853 [16874317.001]
  • [Cites] Trends Genet. 2006 Dec;22(12):678-89 [17045694.001]
  • [Cites] Am J Pathol. 2007 Jan;170(1):377-87 [17200209.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1054-61 [17283138.001]
  • [Cites] Curr Biol. 2007 Apr 17;17(8):700-5 [17379520.001]
  • [Cites] PLoS Genet. 2007 Jan 5;3(1):e3 [17206864.001]
  • [Cites] Science. 1992 May 1;256(5057):668-70 [1350108.001]
  • (PMID = 18391979.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 079643; United Kingdom / Cancer Research UK / / A8449; United Kingdom / Cancer Research UK / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 0 / RASSF1 protein, mouse; 0 / Tumor Suppressor Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ EMS52273; NLM/ PMC3706934
  •  go-up   go-down


68. Tömböl Z, Szabó PM, Molnár V, Wiener Z, Tölgyesi G, Horányi J, Riesz P, Reismann P, Patócs A, Likó I, Gaillard RC, Falus A, Rácz K, Igaz P: Integrative molecular bioinformatics study of human adrenocortical tumors: microRNA, tissue-specific target prediction, and pathway analysis. Endocr Relat Cancer; 2009 Sep;16(3):895-906
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Thirty-six tissue samples including normal adrenocortical tissues, benign adenomas, and adrenocortical carcinomas (ACC) were studied by simultaneous miR and mRNA profiling.
  • Expression of miR-210 was significantly lower in cortisol-secreting adenomas than in ACCs.
  • By calculating the difference between dCT(miR-511) and dCT(miR-503) (delta cycle threshold), ACCs could be distinguished from benign adenomas with high sensitivity and specificity.
  • [MeSH-major] Adenoma / genetics. Adrenal Cortex Neoplasms / genetics. Adrenocortical Carcinoma / genetics. Computational Biology / methods. Gene Expression Profiling / methods. MicroRNAs / genetics. Signal Transduction / genetics
  • [MeSH-minor] Adult. Algorithms. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Drug Delivery Systems / methods. Female. Forecasting / methods. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Models, Biological. Organ Specificity / genetics

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19546168.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
  •  go-up   go-down


69. Schommartz B, Cupisti K, Antke C, Schmidt D, Knoefel WT, Müller HW: [Localisation of parathyroid glands using planar (99m)Tc-sestamibi scintigraphy. Comparison between subtraction- and dual-phase technique]. Nuklearmedizin; 2006;45(3):115-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: In the context of presurgical localisation of parathyroid adenomas in primary hyper-parathyreoidism (pHPT) using (99m)Tc-sestamibi scintigraphy, subtraction- and dualphase technique are compared with each other and with the surgical findings.
  • For visualisation of parathyroid adenomas, an image of the thyroid ((99m)Tc-pertechnetat) was subtracted from a perfusion image ((99m)Tc-sestamibi) and 2 h p. i. another image was acquired for identification of retention of activity.
  • From 129 resected parathyroid adenomas 118 were localised correctly (sensitivity 91%, positive predictive value 94%).

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16710507.001).
  • [ISSN] 0029-5566
  • [Journal-full-title] Nuklearmedizin. Nuclear medicine
  • [ISO-abbreviation] Nuklearmedizin
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 971Z4W1S09 / Technetium Tc 99m Sestamibi
  •  go-up   go-down


70. Abdulamir AS, Hafidh RR, Mahdi LK, Al-jeboori T, Abubaker F: Investigation into the controversial association of Streptococcus gallolyticus with colorectal cancer and adenoma. BMC Cancer; 2009;9:403
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Investigation into the controversial association of Streptococcus gallolyticus with colorectal cancer and adenoma.
  • BACKGROUND: The seroprevalence of IgG antibodies of Streptococcus gallolyticus subspecies gallolyticus, CIP 105428, was evaluated to investigate the controversial association of S. gallolyticus with colorectal carcinoma and adenoma in attempt to investigate the nature of such association if any, by exploring the mRNA expression of NF-kappaB and IL-8.
  • METHODS: ELISA was used to measure IgG antibodies of S. gallolyticus and B. fragilis in sera of 50 colorectal cancer, 14 colorectal adenoma patients, 30 age- and sex- matched apparently healthy volunteers (HV) and 30 age- and sex- matched colonoscopically-proven tumor-free control subjects.
  • NF-kappaB and IL-8 mRNA expression was evaluated in tumorous and non-tumorous tissue sections of carcinoma and adenoma patients in comparison with that of control subjects by using in situ hybridization assay.
  • RESULTS: Colorectal cancer and adenoma patients were associated with higher levels of serum S. gallolyticus IgG antibodies in comparison with HV and control subjects (P < 0.05) while no similar association was found with serum IgG antibodies of B. fragilis (P > 0.05).
  • ELISA cutoff value for the seropositivity of S. gallolyticus IgG was calculated from tumor-free control group.
  • The expression of NF-kappaB mRNA was higher in tumorous than non-tumorous tissue sections of adenoma and carcinoma, higher in carcinoma/adenoma sections than in control subjects, higher in tumorous sections of carcinoma than in adenoma patients, and higher in S. gallolyticus IgG seropositive than in seronegative groups in both tumorous and non-tumorous sections (P < 0.05).
  • IL-8 mRNA expression in tumorous sections of adenoma and carcinoma was higher than in non-tumorous sections, higher in carcinoma/adenoma than in control subjects, and higher in S. gallolyticus IgG seropositive than in seronegative groups in tumorous rather than non-tumorous sections (P < 0.05).
  • CONCLUSION: S. gallolyticus most likely plays an essential role in the oncogenic progression of normal colorectal mucosa to adenoma and to CRC.
  • [MeSH-major] Adenocarcinoma / microbiology. Adenoma / microbiology. Colorectal Neoplasms / microbiology. Streptococcal Infections / epidemiology

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Streptococcal Infections.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Chem. 1999 Jan;45(1):7-17 [9895331.001]
  • [Cites] Mutat Res. 1994 Mar 1;305(2):253-64 [7510036.001]
  • [Cites] Oncogene. 1999 Apr 22;18(16):2567-77 [10353600.001]
  • [Cites] Breast Cancer Res Treat. 2005 Nov;94(1):71-80 [16142438.001]
  • [Cites] Scand J Gastroenterol. 2009;44(2):153-61 [18985541.001]
  • [Cites] Carcinogenesis. 2000 Apr;21(4):753-6 [10753212.001]
  • [Cites] Vet Microbiol. 2000 May 11;73(4):319-25 [10781730.001]
  • [Cites] Trends Genet. 1993 Dec;9(12):427-33 [8122310.001]
  • [Cites] Infect Immun. 1995 Mar;63(3):840-6 [7532627.001]
  • [Cites] J Clin Invest. 1997 Dec 15;100(12):2952-60 [9399940.001]
  • [Cites] Nutrition. 1997 Nov-Dec;13(11-12):959-64 [9433711.001]
  • [Cites] J Clin Microbiol. 1998 Dec;36(12):3520-3 [9817865.001]
  • [Cites] Int J Hematol. 2000 Dec;72(4):391-8 [11197203.001]
  • [Cites] J Histochem Cytochem. 2001 Jul;49(7):927-8 [11410620.001]
  • [Cites] J Infect Dis. 2001 Jul 15;184(2):227-30 [11424022.001]
  • [Cites] Ann Periodontol. 2001 Dec;6(1):20-9 [11887466.001]
  • [Cites] Crit Care. 2002 Jun;6(3):205-11 [12133179.001]
  • [Cites] Am J Pathol. 2002 Dec;161(6):1961-71 [12466110.001]
  • [Cites] Int J Syst Evol Microbiol. 2003 May;53(Pt 3):631-45 [12807180.001]
  • [Cites] World J Gastroenterol. 2004 Jan 15;10(2):177-81 [14716817.001]
  • [Cites] Carcinogenesis. 2004 Aug;25(8):1477-84 [14742316.001]
  • [Cites] J Clin Microbiol. 1984 Sep;20(3):519-24 [6386867.001]
  • [Cites] Infect Immun. 1985 Jul;49(1):197-201 [4008048.001]
  • [Cites] Lancet. 1987 Mar 28;1(8535):748 [2882164.001]
  • [Cites] Rev Infect Dis. 1988 Mar-Apr;10(2):347-64 [3287564.001]
  • [Cites] J Clin Microbiol. 1989 Feb;27(2):305-8 [2915024.001]
  • [Cites] Ann Surg. 1990 Jun;211(6):786-91; discussion 791-2 [2357141.001]
  • [Cites] Infection. 1991 Nov-Dec;19(6):435-9 [1816114.001]
  • [Cites] J Clin Pathol. 1993 Dec;46(12):1116-9 [8282836.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1372-7 [10096573.001]
  • (PMID = 19925668.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Immunoglobulin G; 0 / Interleukin-8; 0 / NF-kappa B; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2785837
  •  go-up   go-down


71. Chacko A, Dutta AK: Endoscopic resection of ampullary adenomas: novel technique to reduce post procedure pancreatitis. J Gastroenterol Hepatol; 2010 Aug;25(8):1338-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endoscopic resection of ampullary adenomas: novel technique to reduce post procedure pancreatitis.
  • [MeSH-major] Adenoma / surgery. Ampulla of Vater / surgery. Common Bile Duct Neoplasms / surgery. Pancreatitis / prevention & control. Sphincterotomy, Endoscopic. Stents

  • Genetic Alliance. consumer health - Pancreatitis.
  • MedlinePlus Health Information. consumer health - Pancreatitis.
  • Hazardous Substances Data Bank. TEFLON .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] J Gastroenterol Hepatol. 2010 Aug;25(8):1381-5 [20659227.001]
  • (PMID = 20659220.001).
  • [ISSN] 1440-1746
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] Australia
  • [Chemical-registry-number] 9002-84-0 / Polytetrafluoroethylene
  •  go-up   go-down


72. Hirose M, Kono S, Tabata S, Ogawa S, Yamaguchi K, Mineshita M, Hagiwara T, Yin G, Lee KY, Tsuji A, Ikeda N: Genetic polymorphisms of methylenetetrahydrofolate reductase and aldehyde dehydrogenase 2, alcohol use and risk of colorectal adenomas: Self-Defense Forces Health Study. Cancer Sci; 2005 Aug;96(8):513-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms of methylenetetrahydrofolate reductase and aldehyde dehydrogenase 2, alcohol use and risk of colorectal adenomas: Self-Defense Forces Health Study.
  • This study investigated the relationship of functional MTHFR C677T and ALDH2 polymorphisms to colorectal adenomas with reference to alcohol consumption in a case-control study of male officials in the Self-Defense Forces (SDF) who received a preretirement health examination at two SDF hospitals.
  • The study subjects were 452 cases of colorectal adenoma and 1050 controls with no polyp who underwent total colonoscopy.
  • Neither MTHFR C677T nor ALDH2 showed a measurable association with colorectal adenoma.
  • While high alcohol consumption was associated with a moderately increased risk of colorectal adenoma, neither of the two polymorphisms showed a significant effect on the association between alcohol and colorectal adenoma.
  • Individuals with the variant alleles ALDH2*2 and MTHFR 677T had a decreased risk of colorectal adenomas, showing adjusted odds ratios of 0.70 (95% confidence interval 0.49-1.00) for all adenomas and 0.57 (0.34-0.95) for large adenomas (> or = 5 mm), as compared to individuals with ALDH2*1/1 and MTHFR 677CC genotypes combined.
  • The findings may be interpreted as suggesting that folate inhibits the growth of colorectal adenomas, but further confirmation is needed.
  • [MeSH-major] Adenoma / genetics. Alcohol Drinking. Aldehyde Dehydrogenase / genetics. Colorectal Neoplasms / genetics. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Single Nucleotide

  • MedlinePlus Health Information. consumer health - Alcohol.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16108833.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
  •  go-up   go-down


73. Futagami S, Hiratsuka T, Shindo T, Horie A, Hamamoto T, Suzuki K, Kusunoki M, Miyake K, Gudis K, Crowe SE, Tsukui T, Sakamoto C: Expression of apurinic/apyrimidinic endonuclease-1 (APE-1) in H. pylori-associated gastritis, gastric adenoma, and gastric cancer. Helicobacter; 2008 Jun;13(3):209-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of apurinic/apyrimidinic endonuclease-1 (APE-1) in H. pylori-associated gastritis, gastric adenoma, and gastric cancer.
  • To investigate the role of APE-1 in the development of gastric cancer, we examined APE-1 expression and localization in cultured cells and gastric biopsies from patients with H. pylori-infected gastritis or gastric adenoma, and from surgically resected gastric cancer.
  • Localization of APE-1 and IkappaBalpha phosphorylation in gastric adenoma and gastric cancer tissues were evaluated by single- and double-label immunohistochemistry.
  • APE-1 expression was mainly localized in epithelial cells within gastric adenoma and in mesenchymal cells of gastric cancer tissues.
  • APE-1 expression in gastric cancer tissues was significantly reduced compared to that in H. pylori-infected gastric adenoma, while 8-OHdG index and IkappaBalpha phosphorylation levels did not differ between these two neoplastic tissue types.
  • Co-localization of APE-1 and IkappaBalpha phosphorylation was observed not in gastric cancer cells but in gastric adenoma cells.
  • CONCLUSION: H. pylori infection is associated with increased APE-1 expression in human cell lines and in gastric tissues from subjects with gastritis and gastric adenomas.
  • The observed distinct expression patterns of APE-1 and 8-OHdG in gastric adenoma and gastric cancer tissues may provide insight into the progression of these conditions and warrants further investigation.
  • [MeSH-minor] Adenoma / enzymology. Adenoma / genetics. Adenoma / microbiology. Adult. Aged. Cells, Cultured. Female. Gastric Mucosa / metabolism. Gastric Mucosa / microbiology. Humans. Male. Middle Aged. RNA, Messenger / metabolism

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18466396.001).
  • [ISSN] 1523-5378
  • [Journal-full-title] Helicobacter
  • [ISO-abbreviation] Helicobacter
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK061769
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase
  •  go-up   go-down


74. Sporn MB, Hong WK: Concomitant DFMO and sulindac chemoprevention of colorectal adenomas: a major clinical advance. Nat Clin Pract Oncol; 2008 Nov;5(11):628-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Concomitant DFMO and sulindac chemoprevention of colorectal adenomas: a major clinical advance.
  • In a randomized, placebo-controlled, double-blind clinical trial by Meyskens et al. the combination of difluoromethylornithine and sulindac has been shown to be strikingly effective for prevention of sporadic colorectal adenomas.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] PMID: 18841250. Difluoromethylornithine plus sulindac for the prevention of sporadic colorectal adenomas: a randomized placebo-controlled, double-blind trial.; Cancer Prev Res Phila Pa. 2008;1:9-11
  • (PMID = 18725921.001).
  • [ISSN] 1743-4262
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] England
  •  go-up   go-down


75. Gupta AK, Schoen RE: Aberrant crypt foci: are they intermediate endpoints of colon carcinogenesis in humans? Curr Opin Gastroenterol; 2009 Jan;25(1):59-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE OF REVIEW: There is a wealth of literature, both from epidemiological and molecular studies, which support the role of aberrant crypt foci (ACF) as a putative precursor to colorectal adenomas and a potential biomarker for colorectal carcinoma.
  • The prevalence of ACF has not correlated with colorectal adenomas, and the technique for ACF detection using high-magnification chromoendoscopy has demonstrated considerable variability across endoscopists and over time.
  • Dysplastic ACF, once postulated as the ACF destined for adenomatous transformation, have been rarely identified in US individuals, in contrast to European and Japanese investigations.
  • [MeSH-major] Adenoma / pathology. Colorectal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Colon / pathology. Disease Progression. Global Health. Humans. Intestinal Mucosa / pathology. Prevalence. Rectum / pathology. Risk Factors

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19114775.001).
  • [ISSN] 1531-7056
  • [Journal-full-title] Current opinion in gastroenterology
  • [ISO-abbreviation] Curr. Opin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 53
  •  go-up   go-down


76. Yamada T, Obo Y, Furukawa M, Hotta M, Yamasaki A, Honoki K, Fukushima N, Tsujiuchi T: Mutations of lysophosphatidic acid receptor-1 gene during progression of lung tumors in rats. Biochem Biophys Res Commun; 2009 Jan 16;378(3):424-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • No LPA1 mutations were detected in 15 hyperplasias, but 2 out of 12 adenomas (16.7%) and 7 out of 17 adenocarcinomas (41.2%).
  • These results suggest that mutations of LPA1 gene may be involved in the acquisition of growth advantage from adenomas to adenocarcinomas in lung carcinogenesis induced in rats by BHP.
  • [MeSH-major] Adenocarcinoma / genetics. Adenoma / genetics. Cell Transformation, Neoplastic / genetics. Lung Neoplasms / genetics. Receptors, Lysophosphatidic Acid / genetics
  • [MeSH-minor] Animals. Carcinogens / toxicity. DNA Mutational Analysis. Disease Models, Animal. Male. Mutation. Nitrosamines / toxicity. Polymorphism, Single-Stranded Conformational. Rats. Rats, Wistar

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19026987.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosamines; 0 / Receptors, Lysophosphatidic Acid; 53609-64-6 / diisopropanolnitrosamine
  •  go-up   go-down


77. Cafferty FH, Sasieni PD, Duffy SW: A deterministic model for estimating the reduction in colorectal cancer incidence due to endoscopic surveillance. Stat Methods Med Res; 2009 Apr;18(2):163-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There is evidence that the removal of adenomas, by endoscopy, from the large bowel can prevent the occurrence of colorectal cancer (CRC).
  • Studies of cohorts of adenoma patients typically rely on comparisons with groups of historical controls.
  • We present a model for disease progression which enables estimation of this quantity without direct comparison to a reference group.
  • Rates of adenoma recurrence and progression to carcinoma are estimated based on study data and relevant literature.
  • The majority of the effect was due to the initial removal of adenomas rather than the follow-up surveillance.
  • [MeSH-minor] Adenoma / surgery. Aged. Biometry. Colonoscopy / statistics & numerical data. Female. Great Britain / epidemiology. Humans. Intestinal Polyps / surgery. Male. Middle Aged. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18765505.001).
  • [ISSN] 0962-2802
  • [Journal-full-title] Statistical methods in medical research
  • [ISO-abbreviation] Stat Methods Med Res
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 10406
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


78. Boozari B, Kubicka S: [Differentiated therapy of liver tumors]. Internist (Berl); 2010 Jan;51(1):53-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In contrast to FNH growth of adenoma is dependent on sexual hormones.
  • Solitary HNFalpha-inactivated and inflammatory adenomas larger than 5 cm should be removed because of risk of tumor rupture or bleeding, while beta-catenin mutated adenomas should be surgically removed at any stage because of risk of malignant transformation.
  • The prognosis of patients with HCC is dependent on the tumor stage, but also on the liver function.

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Liver Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hepatology. 2009 Feb;49(2):453-9 [19065676.001]
  • [Cites] Hepatology. 2009 Aug;50(2):481-9 [19585623.001]
  • [Cites] Onkologie. 2008 Oct;31(10):550-5 [18854656.001]
  • [Cites] Internist (Berl). 2007 Jan;48(1):46-9 [17177032.001]
  • [Cites] Internist (Berl). 2007 Jan;48(1):30-9 [17195060.001]
  • [Cites] Gastroenterology. 2000 Mar;118(3):560-4 [10702207.001]
  • [Cites] Internist (Berl). 2007 Jan;48(1):40-5 [17160664.001]
  • [Cites] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514.001]
  • [Cites] J Hepatol. 2001 Sep;35(3):421-30 [11592607.001]
  • [Cites] BMC Gastroenterol. 2009 May 11;9:31 [19432967.001]
  • [Cites] Hepatol Res. 2009 Jun;39(6):553-62 [19527484.001]
  • [Cites] J Am Coll Surg. 2009 Feb;208(2):218-28 [19228533.001]
  • [Cites] Lancet Oncol. 2009 Jan;10(1):25-34 [19095497.001]
  • [Cites] Chirurg. 2008 Aug;79(8):722-8 [18563376.001]
  • [Cites] Hepatology. 2008 Sep;48(3):808-18 [18688875.001]
  • [Cites] Hepatology. 2003 Feb;37(2):429-42 [12540794.001]
  • [Cites] Hepatology. 2005 Nov;42(5):1208-36 [16250051.001]
  • [Cites] Hepatology. 2006 Mar;43(3):515-24 [16496320.001]
  • [Cites] Z Gastroenterol. 2009 Jan;47(1):37-54 [19156591.001]
  • [Cites] Am J Gastroenterol. 2009 Feb;104(2):514-24 [19174803.001]
  • (PMID = 20062959.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


79. Tagliati F, Gentilin E, Buratto M, Molè D, degli Uberti EC, Zatelli MC: Magmas, a gene newly identified as overexpressed in human and mouse ACTH-secreting pituitary adenomas, protects pituitary cells from apoptotic stimuli. Endocrinology; 2010 Oct;151(10):4635-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Magmas, a gene newly identified as overexpressed in human and mouse ACTH-secreting pituitary adenomas, protects pituitary cells from apoptotic stimuli.
  • Pituitary tumors are mostly benign, being locally invasive in 5-35% of cases.
  • We here report the identification of a cDNA, corresponding to Magmas gene (mitochondria-associated protein involved in granulocyte-macrophage colony-stimulating factor signal transduction), which is highly expressed in two different ACTH-secreting mouse pituitary adenoma cell lines as compared with normal pituitary as well as in two thirds of 64 examined pituitary adenomas as compared with human normal pituitary.
  • Tim 16, the mitochondrial protein encoded by Magmas, was indeed expressed in a mouse ACTH-secreting pituitary adenoma cell line, AtT-20 D16v-F2 cells, in a subcellular compartment likely corresponding to mitochondria.
  • Our data demonstrate that Magmas is overexpressed in mouse and human ACTH-secreting pituitary adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / genetics. Adenoma / genetics. Apoptosis / genetics. Mitochondrial Proteins / physiology
  • [MeSH-minor] Animals. Cell Proliferation. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Cells, Cultured. Cytoprotection / drug effects. Cytoprotection / genetics. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Pituitary Gland / metabolism. RNA, Small Interfering / pharmacology. Up-Regulation / drug effects


80. Hatiboglu MA, Iplikcioglu AC, Ozcan D: Abscess formation within invasive pituitary adenoma. J Clin Neurosci; 2006 Aug;13(7):774-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Abscess formation within invasive pituitary adenoma.
  • Pituitary abscess secondary to an adenoma is rare.
  • This is the first report of a patient who presented with bilateral total ophthalmoplegia.
  • Magnetic resonance imaging was suggestive of a pituitary abscess with adenoma.
  • Pituitary abscess with adenoma is a serious condition that has a high mortality rate.
  • [MeSH-major] Abscess. Pituitary Gland / pathology. Pituitary Neoplasms

  • MedlinePlus Health Information. consumer health - Abscess.
  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16931019.001).
  • [ISSN] 0967-5868
  • [Journal-full-title] Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
  • [ISO-abbreviation] J Clin Neurosci
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
  •  go-up   go-down


81. Faggiano A, Tavares LB, Tauchmanova L, Milone F, Mansueto G, Ramundo V, De Caro ML, Lombardi G, De Rosa G, Colao A: Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism (PHP) in multiple endocrine neoplasia type 1 (MEN1) patients. Clin Endocrinol (Oxf); 2008 Nov;69(5):756-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of treatment with depot somatostatin analogue octreotide on primary hyperparathyroidism (PHP) in multiple endocrine neoplasia type 1 (MEN1) patients.
  • BACKGROUND: In patients with multiple endocrine neoplasia type 1 (MEN1), expression of somatostatin receptor (SST) in parathyroid adenomas and effectiveness of therapy with somatostatin analogues on primary hyperparathyroidism (PHP) have been scarcely investigated.
  • SST subtype 2A immunohistochemistry was performed on parathyroid tumour samples from three patients undergone parathyroidectomy after OCT-LAR therapy.
  • SST subtype 2A immunostaining was found in all parathyroid adenomas investigated, while SST scintigraphy showed a positive parathyroid tumour uptake in three of eight patients (37.5%).
  • [MeSH-major] Duodenal Neoplasms / drug therapy. Hyperparathyroidism, Primary / complications. Multiple Endocrine Neoplasia Type 1 / drug therapy. Neuroendocrine Tumors / drug therapy. Octreotide / administration & dosage. Pancreatic Neoplasms / drug therapy


82. Algaba F: Renal adenomas: pathological differential diagnosis with malignant tumors. Adv Urol; 2008;:974848
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Renal adenomas: pathological differential diagnosis with malignant tumors.
  • The renal adenomas can be confused by imaging diagnosis with malignant renal tumors, but there are also real biological dilemmas to determine their behavior.
  • The consensus decisions are the following. (1) The adenoma of clear cells is not accepted, instead it is considered that all the clear-cell tumors are carcinomas, with greater or lesser aggressiveness. (2) Among the papillary neoplasms the WHO 2004 renal cell tumors classification are considered as papillary adenomas tumors with a maximum diameter of 5 mm and may represent a continuum biological process to papillary renal cell carcinoma.
  • The papillary adenomas associated with End-kidney and/or acquired cystic disease may have a different pathogenesis. (3) To consider a tumor as an oncocytoma the size is not important, only the cytological features, microscopic, ultrastructural, and immunohistochemically can help, but some chromosomal observations introduce some questions about its relation with the chromophobe renal cell carcinoma. (4) Finally, the metanephric adenoma, a tumor with some morphological similarity with the nephroblastoma must be considered in the renal adenomas diagnosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Endourol. 2007 Aug;21(8):819-23 [17867935.001]
  • [Cites] Am J Surg Pathol. 2007 Apr;31(4):489-500 [17414095.001]
  • [Cites] Hum Pathol. 2007 Feb;38(2):239-46 [17056094.001]
  • [Cites] Urology. 2006 Oct;68(4):737-40 [17070344.001]
  • [Cites] Mod Pathol. 2006 Feb;19(2):218-24 [16424894.001]
  • [Cites] Am J Clin Pathol. 2006 Feb;125(2):217-22 [16393684.001]
  • [Cites] BJU Int. 2005 Dec;96(9):1275-9 [16287444.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Jul 1;152(1):23-8 [15193438.001]
  • [Cites] Hum Pathol. 2001 Jan;32(1):101-4 [11172302.001]
  • (PMID = 18846240.001).
  • [ISSN] 1687-6369
  • [Journal-full-title] Advances in urology
  • [ISO-abbreviation] Adv Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2563151
  •  go-up   go-down


83. Takeuchi H, Greep NC, Hoon DS, Giuliano AE, Hansen NM, Umetani N, Singer FR: Hypermethylation of adenosine triphosphate-binding cassette transporter genes in primary hyperparathyroidism and its effect on sestamibi imaging. J Clin Endocrinol Metab; 2007 May;92(5):1785-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONTEXT: Retention of technetium-(99m)-sestamibi ((99m)Tc-sestamibi) by parathyroid adenomas appears to be due to the loss of at least one membrane transporter, multidrug resistance 1 (MDR1), and possibly another, multidrug resistance-associated protein 1 (MRP1).
  • PATIENTS: Forty-eight patients with primary hyperparathyroidism and five patients without parathyroid disease undergoing thyroid surgery provided 27 adenomatous, 10 hyperplastic, and 16 normal parathyroid glands.
  • RESULTS: The MDR1 gene was methylated in none of 12 normal glands, 19 of 27 adenomas, and three of 10 hyperplastic glands.
  • CONCLUSION: In parathyroid tissue, hypermethylation of the MDR1 gene decreases its expression and is associated with increased detection of parathyroid adenomas by (99m)Tc-sestamibi parathyroid scans.
  • [MeSH-minor] ATP-Binding Cassette, Sub-Family B, Member 1 / genetics. Adenoma / diagnostic imaging. Adenoma / pathology. Gene Silencing / physiology. Humans. Immunohistochemistry. Methylation. Multidrug Resistance-Associated Proteins / genetics. Parathyroid Glands / diagnostic imaging. Parathyroid Glands / pathology. Parathyroid Neoplasms / diagnostic imaging. Parathyroid Neoplasms / pathology. Promoter Regions, Genetic / genetics. RNA / biosynthesis. RNA / isolation & purification. Radionuclide Imaging. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Hyperparathyroidism, primary.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17299072.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Multidrug Resistance-Associated Proteins; 0 / Radiopharmaceuticals; 63231-63-0 / RNA; 971Z4W1S09 / Technetium Tc 99m Sestamibi; Y49M64GZ4Q / multidrug resistance-associated protein 1
  •  go-up   go-down


84. Saeger W, Lüdecke B, Lüdecke DK: Clinical tumor growth and comparison with proliferation markers in non-functioning (inactive) pituitary adenomas. Exp Clin Endocrinol Diabetes; 2008 Feb;116(2):80-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical tumor growth and comparison with proliferation markers in non-functioning (inactive) pituitary adenomas.
  • BACKGROUND: As the development of clinically silent pituitary adenomas is not yet fully understood, the radiologically measured growth of inactive pituitary adenomas should be compared with adenoma classification and immunostainings for proliferation markers.
  • MATERIAL AND METHODS: In 32 patients with non-functioning adenomas (NFA) from 45 operations with retrospectively available preoperative series of magnetic resonance imaging (MRI) we measured the largest growing diameter (LGD) in mm/ year.
  • The adenomas were immunostained for Ki-67 (MiB-1), PCNA, p53 protein, IGF- and PTH-related protein.
  • RESULTS: MiB-1 positive nuclei were found in 42% of adenomas, PCNA positive nuclei in 58% and p53 positive nuclei in 16%.
  • IGF 1 was immuno-stained in 84% of adenomas.
  • The mean LI for MiB-1 was 0.12 in adenomas growing less than 1.5 mm and 0.34 in adenomas growing more than 1.5 mm per year.
  • For non-invasive adenomas, the MiB-1 LI was 0.03, for invasive adenomas it was 0.126 and for strongly invasive adenomas 0.212.
  • The MiB-1 LI was lower in null cell adenomas than in FSH/LH adenomas.
  • PCNA LI in adenomas growing less than 1.5 mm per year was 0.51 in contrast to LI of 1.12 for those growing more than 1.5 mm.
  • In non-invasive adenomas the PCNA LI was 0.796, in invasive adenomas 0.655 and in diffuse strongly invasive ones 1.011.
  • Null cell adenomas had a lower PCNA LI than FSH/LH cell adenomas.
  • P53 was immunostained in invasive adenomas only.
  • We recommend the use of PCNA if correlations to progression of tumor growth are wanted.
  • [MeSH-major] Adenoma / pathology. Biomarkers, Tumor / analysis. Cell Proliferation. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Insulin-Like Growth Factor I / analysis. Insulin-Like Growth Factor I / metabolism. Ki-67 Antigen / analysis. Ki-67 Antigen / metabolism. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm, Residual. Parathyroid Hormone-Related Protein / analysis. Parathyroid Hormone-Related Protein / metabolism. Proliferating Cell Nuclear Antigen / analysis. Proliferating Cell Nuclear Antigen / metabolism. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18072009.001).
  • [ISSN] 0947-7349
  • [Journal-full-title] Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • [ISO-abbreviation] Exp. Clin. Endocrinol. Diabetes
  • [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 / Ki-67 Antigen; 0 / Parathyroid Hormone-Related Protein; 0 / Proliferating Cell Nuclear Antigen; 67763-96-6 / Insulin-Like Growth Factor I
  •  go-up   go-down


85. Sevriukov FA, Puchkin AB, Krupin VN, Chebykin AV, Sorokin DA, Karpukhin IV, Malinina OIu, Zorin DG: [Transurethral electrosurgery of a new generation (TURis) in the treatment of the lower urinary tract and prostate diseases]. Urologiia; 2007 May-Jun;(3):28-32, 35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Transurethral electrosurgery of a new generation (TURis) in the treatment of the lower urinary tract and prostate diseases].
  • Surgical interventions were made in 175 patients aged 23-87 years (mean age 64.8 years) with different diseases of the lower urinary tract (adenoma, prostatic cancer, cancer of the urinary bladder, etc.) with application of a new generation of endoscopic technique--transurethral resection in saline (TURis system) with a generator UES-40 SurgMaster (Olympus).
  • The size of the prostate in prostatic adenoma ranged from 4.8 to 121 cm3 (mean 62.5 cm3), residual urine--92.3 ml (42.6 to 310.2 ml).
  • Mean amount of the resected tissue in sclerosis of urinary bladder cervix was 7 g (5-11 g), in prostatic adenoma--41 g (10-85 g), prostatic cancer--27 g (17-49 g).
  • Informative value of histological material rose significantly in view of a minimal zone of coagulatory changes in the samples.
  • Standard time limitation for transurethral resection (60-90 min) becomes insignificant in using isotonic irrigation allowing urologists to resect safely larger adenomas than it was possible earlier.

  • MedlinePlus Health Information. consumer health - Prostate Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17724828.001).
  • [ISSN] 1728-2985
  • [Journal-full-title] Urologii︠a︡ (Moscow, Russia : 1999)
  • [ISO-abbreviation] Urologiia
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  •  go-up   go-down


86. Mecklin JP, Järvinen HJ: Surveillance in Lynch syndrome. Fam Cancer; 2005;4(3):267-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Therefore, screening for colorectal adenomas and carcinomas by regular colonoscopies is the main topic of the present review.
  • However, it should be remembered, that primary prevention - whether through the use of chemoprevention or the promotion of a healthy life-style may form a significant part of such surveillance in the future.
  • Observational studies indicate that the adenoma carcinoma sequence is the main pathway in the development of colorectal cancer in Lynch syndrome.
  • A colonoscopy every 1-3 years starting at age 20 to 25 years and the removal of observed adenomas is recommended for individuals known to have Lynch syndrome associated mutations.

  • Genetic Alliance. consumer health - Lynch syndrome.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3629-37 [14512394.001]
  • [Cites] Anticancer Res. 1994 Jul-Aug;14(4B):1675-8 [7979205.001]
  • [Cites] Gastroenterology. 1996 Apr;110(4):1020-7 [8612988.001]
  • [Cites] Am J Med Genet A. 2003 Aug 30;121A(2):159-62 [12910497.001]
  • [Cites] Int J Cancer. 2000 Jan 20;89(1):44-50 [10719730.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]
  • [Cites] JAMA. 1997 Mar 19;277(11):915-9 [9062331.001]
  • [Cites] J Gastrointest Surg. 1998 Jan-Feb;2(1):67-71 [9841970.001]
  • [Cites] Gut. 2002 Jun;50(6):857-60 [12010890.001]
  • [Cites] Gastroenterology. 2004 Jul;127(1):17-25 [15236168.001]
  • [Cites] Ann Intern Med. 1998 Nov 15;129(10):787-96 [9841584.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]
  • [Cites] Cancer. 2002 Mar 15;94(6):1708-12 [11920532.001]
  • [Cites] Cancer Detect Prev. 2001;25(6):503-10 [12132870.001]
  • [Cites] Dis Colon Rectum. 2002 Feb;45(2):273-9 [11852345.001]
  • [Cites] Int J Cancer. 1996 Feb 8;65(4):422-5 [8621220.001]
  • [Cites] Langenbecks Arch Surg. 2003 Mar;388(1):9-16 [12690475.001]
  • [Cites] Dis Colon Rectum. 2003 Aug;46(8):1001-12 [12907889.001]
  • [Cites] Lancet. 1995 May 6;345(8958):1183-4 [7723574.001]
  • [Cites] Dis Colon Rectum. 1991 May;34(5):424-5 [2022152.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):919-32 [12621137.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1014-9 [11861375.001]
  • [Cites] N Engl J Med. 1995 Mar 30;332(13):839-47 [7661930.001]
  • [Cites] Am J Med Genet A. 2004 Mar 15;125A(3):318-9 [14994245.001]
  • [Cites] J Med Genet. 2001 May;38(5):318-22 [11333868.001]
  • [Cites] Dis Colon Rectum. 1998 Oct;41(10):1250-3; discussion 1253-5 [9788388.001]
  • [Cites] Gastroenterology. 2003 Aug;125(2):328-36 [12891533.001]
  • [Cites] Cancer. 1991 Sep 1;68(5):1109-12 [1913482.001]
  • [Cites] Gastroenterology. 2000 May;118(5):829-34 [10784581.001]
  • [Cites] Int J Cancer. 1995 Dec 20;64(6):430-3 [8550246.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):142-4 [10508506.001]
  • [Cites] Ann Intern Med. 2001 Oct 16;135(8 Pt 1):577-88 [11601929.001]
  • [Cites] JAMA. 1999 May 5;281(17):1618-22 [10235155.001]
  • [Cites] Br J Cancer. 2004 Feb 23;90(4):882-7 [14970868.001]
  • [Cites] Cancer. 1998 May 1;82(9):1632-7 [9576281.001]
  • [Cites] Gut. 2003 Dec;52(12):1752-5 [14633956.001]
  • [Cites] Am J Hum Genet. 1997 Aug;61(2):329-35 [9311737.001]
  • [Cites] Int J Cancer. 1999 Apr 12;81(2):214-8 [10188721.001]
  • [Cites] Int J Cancer. 2002 Nov 10;102(2):198-200 [12385019.001]
  • [Cites] J Clin Oncol. 2000 Nov 1;18(21 Suppl):81S-92S [11060333.001]
  • (PMID = 16136388.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 40
  •  go-up   go-down


87. Risio M: The natural history of adenomas. Best Pract Res Clin Gastroenterol; 2010 Jun;24(3):271-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The natural history of adenomas.
  • It is well known that adenomas represent the morphologically categorised precursor of the vast majority of colorectal cancers.
  • Only few adenomas actually develop invasive cancer (progressive adenomas), although every adenoma has the capacity of malignant evolution.
  • Most adenomas stabilise their progression or even regress.
  • Easily identifiable but widely ranged pathological features (size, architectural growth, type, grade and gross organisation of dysplasia) are predictive of their natural history in terms of potential of cancerisation and duration of the adenoma-carcinoma sequence.
  • [MeSH-major] Adenoma / pathology. Carcinoma / pathology. Cell Transformation, Neoplastic / pathology. Colorectal Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Disease Progression. Humans. Neoplasm Invasiveness. Phenotype

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • [ReprintIn] Best Pract Res Clin Gastroenterol. 2010 Aug;24(4):397-406 [20833344.001]
  • (PMID = 20510828.001).
  • [ISSN] 1532-1916
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 59
  •  go-up   go-down


88. Kettle AG, O'Doherty MJ: Parathyroid imaging: how good is it and how should it be done? Semin Nucl Med; 2006 Jul;36(3):206-11
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This has been suggested from the literature to be primarily the result of a parathyroid adenoma (80-85% of cases), hyperplasia involving more than 1 gland, usually with all 4 glands being involved (10-15% of cases), or the result, albeit rarely, of parathyroid carcinoma (0.5-1% of cases).
  • Surgical removal of the hypersecreting gland is the primary treatment; this procedure is best performed by a skilled surgeon who would normally find the abnormality in 95% of cases.
  • Imaging, however, should be used to identify the site of abnormality, potentially reducing inpatient stay and improving the patient experience.
  • A recent systematic review reported the percentage sensitivity (95% confidence intervals) for sestamibi in the identification of solitary adenomas as 88.44 (87.48-89.40), multigland hyperplasia 44.46 (41.13-47.8), double adenomas 29.95 (-2.19 to 62.09), and carcinoma 33 (33).
  • The subtraction technique using (99m)Tc-sestamibi and (123)I is the optimal technique enabling the site to be related to the thyroid tissue when the parathyroid gland is in the neck in a normal position.
  • With ectopic glands, the combined use of single-photon emission computed tomography may then provide anatomical information to enable localization of the functional abnormality.
  • [MeSH-minor] Adenoma / radionuclide imaging. Adult. Aged. Choristoma / radionuclide imaging. Diagnostic Imaging / methods. Female. Humans. Hyperparathyroidism / radionuclide imaging. Male. Middle Aged. Postoperative Complications / prevention & control. Preoperative Care. Radiopharmaceuticals / pharmacokinetics. Sensitivity and Specificity. Subtraction Technique

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16762611.001).
  • [ISSN] 0001-2998
  • [Journal-full-title] Seminars in nuclear medicine
  • [ISO-abbreviation] Semin Nucl Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals
  • [Number-of-references] 41
  •  go-up   go-down


89. Lips EH, de Graaf EJ, Tollenaar RA, van Eijk R, Oosting J, Szuhai K, Karsten T, Nanya Y, Ogawa S, van de Velde CJ, Eilers PH, van Wezel T, Morreau H: Single nucleotide polymorphism array analysis of chromosomal instability patterns discriminates rectal adenomas from carcinomas. J Pathol; 2007 Jul;212(3):269-77
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Single nucleotide polymorphism array analysis of chromosomal instability patterns discriminates rectal adenomas from carcinomas.
  • Total mesorectal excision (TME) is the standard treatment for rectal cancer, while transanal endoscopic microsurgery (TEM) is a recently introduced surgical approach for the treatment of rectal adenomas.
  • Specifically, the chromosomal events: gain of 8q22-24, 13q and 20q, and loss of 17p and 18q12-22, were far more abundant in carcinoma than in adenoma.
  • In adenoma fractions from cases with a carcinoma (infiltrating at least in the submucosa), twice the amount of such 'malignant aberrations' was observed, compared to pure adenomas.
  • Furthermore, combined aberrations such as gain of 13q and loss of 18q were only found in adenomatous fractions of carcinomas and not in benign lesions.
  • Based on these five genomic events associated with carcinoma, a clear distinction between adenoma and carcinoma tissue could be made.
  • [MeSH-major] Adenoma / pathology. Carcinoma / pathology. Chromosomal Instability. Oligonucleotide Array Sequence Analysis. Polymorphism, Single Nucleotide. Rectal Neoplasms / genetics. Rectal Neoplasms / pathology
  • [MeSH-minor] Analysis of Variance. Diagnosis, Differential. Genome. Humans. Logistic Models. Loss of Heterozygosity. Neoplasm Staging

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17471469.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


90. Mizokami Y, Egashira N, Takekoshi S, Itoh J, Itoh Y, Osamura RY, Matsumae M: Expression of MSX1 in human normal pituitaries and pituitary adenomas. Endocr Pathol; 2008;19(1):54-61
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of MSX1 in human normal pituitaries and pituitary adenomas.
  • Transcription factors play specific roles in the development and differentiation of normal pituitary tissues and pituitary adenoma.
  • In addition, 50 pituitary adenomas were examined using immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) to clarify the role of MSX1 in the development and functional differentiation of pituitary adenoma cells.
  • It is interesting to note that, in the pituitary adenoma, MSX1 was expressed in the nucleus of GH- and TSH-producing adenomas.
  • RT-PCR using RNA extracted and purified from formalin-fixed paraffin-embedded pituitary adenoma specimens revealed MSX1 mRNA expressed in GH- and TSH-producing adenomas.
  • These results suggest that MSX1 plays a specific role in human pituitary adenoma.
  • [MeSH-major] Adenoma / genetics. MSX1 Transcription Factor / genetics. Pituitary Gland / physiology. Pituitary Neoplasms / genetics
  • [MeSH-minor] Animals. Autopsy. Blotting, Western. Cell Differentiation. DNA Primers. Humans. Immunohistochemistry. Mice. Microscopy, Immunoelectron. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):2133-9 [10473097.001]
  • [Cites] Pathol Int. 1996 Oct;46(10 ):726-37 [8916141.001]
  • [Cites] Exp Cell Res. 1999 Apr 10;248(1):1-9 [10094807.001]
  • [Cites] Clin Cancer Res. 2001 Apr;7(4):892-5 [11309338.001]
  • [Cites] J Histochem Cytochem. 2003 Aug;51(8):989-94 [12871980.001]
  • [Cites] Acta Neurochir (Wien). 1996;138(10):1186-92 [8955438.001]
  • [Cites] J Electron Microsc Tech. 1988 Apr;8(4):401-32 [3058887.001]
  • [Cites] Genes Dev. 1989 Jan;3(1):26-37 [2565278.001]
  • [Cites] Int J Cancer. 1992 Jul 30;51(6):892-7 [1379214.001]
  • [Cites] Science. 1998 Nov 6;282(5391):1136-8 [9804553.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2004 Apr;9(2):195-205 [15300013.001]
  • [Cites] Br Med Bull. 2006 May 09;75-76:81-97 [16684928.001]
  • [Cites] J Cell Biol. 1999 Jun 14;145(6):1119-31 [10366586.001]
  • [Cites] Trends Genet. 1995 Oct;11(10):405-11 [7482767.001]
  • [Cites] Expert Rev Anticancer Ther. 2006 Sep;6 Suppl 9:S3-14 [17004855.001]
  • [Cites] J Neuroendocrinol. 2006 Jan;18(1):50-6 [16451220.001]
  • [Cites] Eur J Surg Oncol. 2007 Mar;33(2):129-32 [17045774.001]
  • [Cites] Gene. 2003 Nov 13;319:1-19 [14597167.001]
  • [Cites] Annu Rev Genet. 1995;29:577-605 [8825487.001]
  • [Cites] J Histochem Cytochem. 1995 Jan;43(1):11-9 [7822759.001]
  • [Cites] Mol Cell Endocrinol. 1998 Nov 25;146(1-2):77-86 [10022765.001]
  • [Cites] J Clin Pathol. 1998 Jul;51(7):506-11 [9797726.001]
  • [Cites] Blood. 1991 Dec 1;78(11):2996-3003 [1683261.001]
  • [Cites] Mol Endocrinol. 1997 Nov;11(12):1782-94 [9369446.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Jul 15;194(1):187-93 [7687426.001]
  • [Cites] Development. 2003 Dec;130(26):6441-52 [14627721.001]
  • [Cites] Development. 2001 Jun;128(12):2373-84 [11493556.001]
  • [Cites] Nat Rev Cancer. 2002 Nov;2(11):836-49 [12415254.001]
  • [Cites] Bioessays. 1999 Oct;21(10):824-32 [10497332.001]
  • [Cites] Mod Pathol. 1996 May;9(5):526-33 [8733768.001]
  • [Cites] Mol Endocrinol. 2006 Nov;20(11):2796-805 [16840539.001]
  • [Cites] EMBO J. 1989 Jan;8(1):91-100 [2565810.001]
  • [Cites] Gene. 2000 Apr 18;247(1-2):17-31 [10773441.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1987;411(4):323-30 [2442884.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Mar;281(5):1234-40 [11243867.001]
  • [Cites] Endocrine. 2005 Oct;28(1):43-7 [16311409.001]
  • [Cites] Science. 2002 Mar 22;295(5563):2231-5 [11910101.001]
  • [Cites] Genes Dev. 1997 Jun 1;11(11):1370-80 [9192866.001]
  • [Cites] Science. 1998 Apr 24;280(5363):547-53 [9554838.001]
  • [Cites] Mod Pathol. 2000 Oct;13(10):1097-108 [11048804.001]
  • [Cites] Exp Biol Med (Maywood). 2003 Oct;228(9):1004-17 [14530508.001]
  • [Cites] Mol Cell Biol. 1991 Jan;11(1):554-7 [1670897.001]
  • (PMID = 18379900.001).
  • [ISSN] 1559-0097
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / MSX1 Transcription Factor; 0 / MSX1 protein, human; 0 / Msx1 protein, mouse; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  •  go-up   go-down


91. Cho YG, Song JH, Kim CJ, Nam SW, Yoo NJ, Lee JY, Park WS: Genetic and epigenetic analysis of the KLF4 gene in gastric cancer. APMIS; 2007 Jul;115(7):802-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, the molecular basis of the KLF4 inactivation in gastric cancer was investigated by analyzing the somatic mutation, the allelic loss with two microsatellite markers, D9S53 and D9S105, and hypermethylation of the KLF4 gene in 47 gastric adenomas and 81 gastric adenocarcinomas.
  • Mutational analysis revealed one mutation of the KLF4 gene in a diffuse-type advanced gastric adenocarcinoma, but not in the gastric adenoma.
  • An allelic loss was found in 7 (22.6%) of the 31 informative gastric adenoma cases and 15 (31.3%) of the 48 informative cancer cases at one or both markers.

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17614846.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / GKLF protein; 0 / Kruppel-Like Transcription Factors
  •  go-up   go-down


92. Kim H, Kang HJ, You KT, Kim SH, Lee KY, Kim TI, Kim C, Song SY, Kim HJ, Lee C, Kim H: Suppression of human selenium-binding protein 1 is a late event in colorectal carcinogenesis and is associated with poor survival. Proteomics; 2006 Jun;6(11):3466-76
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Suppression of SELENBP1 was further analyzed in another eight-paired adenomas and carcinomas from the same patients using Western blot analysis and immunohistochemistry, and revealed that one adenoma and seven carcinomas exhibited markedly reduced SELENBP1 expression.
  • [MeSH-major] Adenoma / metabolism. Carcinoma / metabolism. Colorectal Neoplasms / metabolism. Intestinal Mucosa / metabolism. Proteome / metabolism. Selenium-Binding Proteins / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Colon / metabolism. Colon / pathology. Down-Regulation. Electrophoresis, Gel, Two-Dimensional. Humans. Prognosis. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Tissue Array Analysis

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16645984.001).
  • [ISSN] 1615-9853
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proteome; 0 / SELENBP1 protein, human; 0 / Selenium-Binding Proteins
  •  go-up   go-down


93. Jaquet P, Gunz G, Saveanu A, Barlier A, Dufour H, Taylor J, Dong J, Kim S, Moreau JP, Culler MD: BIM-23A760, a chimeric molecule directed towards somatostatin and dopamine receptors, vs universal somatostatin receptors ligands in GH-secreting pituitary adenomas partial responders to octreotide. J Endocrinol Invest; 2005;28(11 Suppl International):21-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BIM-23A760, a chimeric molecule directed towards somatostatin and dopamine receptors, vs universal somatostatin receptors ligands in GH-secreting pituitary adenomas partial responders to octreotide.
  • We report the comparative efficacy of a somatostatin receptor 1 and 5 subtypes (SSTR2 and SSTR5), and dopamine D2 (DAD2) compound, BIM-23A760, in suppressing GH secretion, in cell culture from human GH-secreting tumors, from patients partially responsive to long-term treatments with octreotide or lanreotide.
  • The higher efficacy of BIM-23A760 is, at least partially, linked to its high affinity for the SSTR2 receptor subtype (IC50: 3 pmol/l).

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16625841.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BIM 23197; 0 / Oligopeptides; 0 / Piperazines; 0 / RNA, Messenger; 0 / Receptors, Dopamine; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
  •  go-up   go-down


94. Kim DW, Jung SA, Park SA, Kim CG: Multifocal Colonic Lesions Detected by (18)F-FDG PET/CT: Correlation with Histopathology and Gross Specimen. Nucl Med Mol Imaging; 2010 Sep;44(3):226-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The histopathologic examination of the postoperative gross specimen revealed a tubular adenoma, a tubulovillous adenoma and an adenocarinoma.
  • The maximal standardized uptake value (SUVmax) of a tubulovillous adenoma was much higher than that of adenocarcinoma.
  • This patient could be considered as a representative case highlighting that SUVmax is not a reliable indicator for discriminating colon cancer from colonic adenomas.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 24899955.001).
  • [ISSN] 1869-3474
  • [Journal-full-title] Nuclear medicine and molecular imaging
  • [ISO-abbreviation] Nucl Med Mol Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC4042939
  • [Keywords] NOTNLM ; 18F-FDG PET/CT / Colon cancer / Colonic adenoma
  •  go-up   go-down


95. Loitsch SM, Shastri Y, Stein J: Stool test for colorectal cancer screening--it's time to move! Clin Lab; 2008;54(11-12):473-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The analysis of fecal DNA represents an emerging new field for early detection of colorectal neoplasia.
  • Small trials of multitarget assays demonstrated a sensitivity for CRC of 62 to 91% and a sensitivity for adenomas of 26 to 73%.
  • [MeSH-major] Biomarkers, Tumor / analysis. Colorectal Neoplasms / diagnosis. Feces / chemistry. Mass Screening / methods


96. Evans CO, Moreno CS, Zhan X, McCabe MT, Vertino PM, Desiderio DM, Oyesiku NM: Molecular pathogenesis of human prolactinomas identified by gene expression profiling, RT-qPCR, and proteomic analyses. Pituitary; 2008;11(3):231-45
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The molecular pathogenesis of prolactinomas has resisted elucidation; with the exception of a RAS mutation in a single aggressive prolactinoma, no mutational changes have been identified.
  • Using high-throughput analysis from a large bank of human pituitary adenomas, we examined these tumors according to their molecular profiles rather than traditional immunohistochemistry.
  • [MeSH-major] Adenoma / diagnosis. Gene Expression Profiling. Molecular Diagnostic Techniques. Oligonucleotide Array Sequence Analysis. Pituitary Neoplasms / diagnosis. Prolactinoma / diagnosis. Proteomics. Reverse Transcriptase Polymerase Chain Reaction
  • [MeSH-minor] Adult. Cluster Analysis. DNA, Neoplasm / analysis. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Proteins / analysis. RNA, Neoplasm / analysis. Reproducibility of Results

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 1997 Jun;82(6):1675-81 [9177361.001]
  • [Cites] J Carcinog. 2006 Jan 20;5:4 [16426442.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6236-42 [11103776.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
  • [Cites] Br J Haematol. 2002 Dec;119(4):1070-4 [12472590.001]
  • [Cites] J Immunol. 2003 Aug 1;171(3):1376-84 [12874228.001]
  • [Cites] Electrophoresis. 2003 Jun;24(11):1818-33 [12783459.001]
  • [Cites] Endocr Rev. 1998 Dec;19(6):798-827 [9861546.001]
  • [Cites] Cancer Sci. 2007 May;98(5):621-8 [17355265.001]
  • [Cites] J Clin Endocrinol Metab. 1990 Dec;71(6):1427-33 [1977759.001]
  • [Cites] Pituitary. 2005;8(1):17-23 [16411064.001]
  • [Cites] Mol Endocrinol. 1992 Nov;6(11):1825-33 [1480172.001]
  • [Cites] Endocr Rev. 1996 Dec;17(6):639-69 [8969972.001]
  • [Cites] N Engl J Med. 2007 Jan 4;356(1):29-38 [17202453.001]
  • [Cites] Clin Endocrinol (Oxf). 2006 Oct;65(4):524-9 [16984247.001]
  • [Cites] J Endocrinol Invest. 2000 May;23(5):304-9 [10882148.001]
  • [Cites] Int J Cancer. 2007 Sep 15;121(6):1245-52 [17514647.001]
  • [Cites] World J Surg. 2007 Jan;31(1):65-71 [17180554.001]
  • [Cites] Br J Cancer. 1999 Apr;80(1-2):44-50 [10389976.001]
  • [Cites] Mol Endocrinol. 1994 May;8(5):635-42 [8058071.001]
  • [Cites] Treat Endocrinol. 2003;2(1):23-32 [15871552.001]
  • [Cites] Oncol Rep. 2006 Jun;15(6):1569-74 [16685397.001]
  • [Cites] Eur J Endocrinol. 1999 Apr;140(4):358-61 [10097256.001]
  • [Cites] Endocrine. 2006 Jun;29(3):435-44 [16943582.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Jul;77(1):50-5 [8100831.001]
  • [Cites] Int J Cancer. 2006 Jan 15;118(2):263-73 [16052521.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2002 Jul;7(3):291-312 [12751893.001]
  • [Cites] Gene. 2000 May 16;249(1-2):1-16 [10831834.001]
  • [Cites] Mol Endocrinol. 1994 Mar;8(3):356-73 [8015553.001]
  • [Cites] Brain Pathol. 2001 Jul;11(3):328-41 [11414475.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):143-51 [15994756.001]
  • [Cites] Neurochem Int. 1997 Apr-May;30(4-5):499-506 [9106266.001]
  • [Cites] Nat Neurosci. 2005 Sep;8(9):1169-78 [16116448.001]
  • [Cites] J Natl Cancer Inst. 1995 Feb 15;87(4):299-303 [7707421.001]
  • [Cites] Endocr Rev. 2001 Feb;22(1):2-35 [11159814.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10214-22 [16288009.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4515-8 [9788592.001]
  • [Cites] Clin Chem. 2003 Oct;49(10):1740-51 [14500615.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):3097-107 [11443173.001]
  • [Cites] Proteomics. 2003 May;3(5):699-713 [12748949.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Sep;83(9):3210-2 [9745428.001]
  • [Cites] Curr Opin Obstet Gynecol. 2004 Aug;16(4):331-7 [15232488.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jun;90(6):3715-23 [15769981.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4218-24 [12874029.001]
  • [Cites] Electrophoresis. 2003 Jun;24(11):1834-46 [12783460.001]
  • [Cites] Growth Factors. 2004 Mar;22(1):1-11 [15179939.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R80-7 [17613552.001]
  • [Cites] Biostatistics. 2003 Apr;4(2):249-64 [12925520.001]
  • (PMID = 18183490.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2R01-CA077337; United States / NCI NIH HHS / CA / K22-CA96560; United States / NINDS NIH HHS / NS / NS 42843; United States / NCI NIH HHS / CA / R01-CA106826; United States / NCRR NIH HHS / RR / RR-10522; United States / NCRR NIH HHS / RR / RR-14593
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm
  •  go-up   go-down


97. Jeong G, Lee JH, Yu MK, Moon W, Rhee PL, Paik SW, Rhee JC, Kim JJ: Non-surgical management of microperforation induced by EMR of the stomach. Dig Liver Dis; 2006 Aug;38(8):605-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PATIENT AND METHOD: From January 2002 to June 2004, 109 early gastric cancers and 300 adenomas were treated with endoscopic mucosal resection.
  • [MeSH-minor] Abdominal Pain / etiology. Abdominal Pain / therapy. Adenoma / surgery. Aged. Aged, 80 and over. Analgesics / therapeutic use. Anti-Bacterial Agents / therapeutic use. Drainage. Fasting. Female. Follow-Up Studies. Gastrointestinal Hemorrhage / etiology. Gastrointestinal Hemorrhage / therapy. Hospitalization. Humans. Intubation, Gastrointestinal. Male. Middle Aged. Retrospective Studies. Stomach Neoplasms / surgery. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Nat Clin Pract Gastroenterol Hepatol. 2007 Mar;4(3):134-5 [17290237.001]
  • (PMID = 16824812.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Analgesics; 0 / Anti-Bacterial Agents
  •  go-up   go-down


98. de Fraipont F, El Atifi M, Cherradi N, Le Moigne G, Defaye G, Houlgatte R, Bertherat J, Bertagna X, Plouin PF, Baudin E, Berger F, Gicquel C, Chabre O, Feige JJ: Gene expression profiling of human adrenocortical tumors using complementary deoxyribonucleic Acid microarrays identifies several candidate genes as markers of malignancy. J Clin Endocrinol Metab; 2005 Mar;90(3):1819-29
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim of this study was to identify predictor sets of genes whose over- or underexpression in human sporadic adrenocortical tumors would help to identify malignant vs. benign tumors and to predict postsurgical metastatic recurrence.
  • For this, we analyzed the expression of 230 candidate genes using cDNA microarrays in a series of 57 well-characterized human sporadic adrenocortical tumors (33 adenomas and 24 carcinomas).
  • Among these genes, there are probably new markers of tumor evolution that will deserve additional validation on a larger scale.
  • Taken together, these results show that the parallel analysis of the expression levels of a selected group of genes on microgram quantities of tumor RNA (a quantity that can be obtained from fine needle aspirations) appears as a complementary method to histopathology for the diagnosis and prognosis of evolution of adrenocortical carcinomas.
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / genetics. Disease-Free Survival. Female. Gene Expression Regulation, Neoplastic. Genetic Markers. Humans. Male. Middle Aged. RNA, Messenger / analysis. Steroids / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Endocrinol Metab. 2005 Mar;90(3):1900-2 [15758065.001]
  • (PMID = 15613424.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / RNA, Messenger; 0 / Steroids
  •  go-up   go-down


99. Zatelli MC, Piccin D, Ambrosio MR, Bondanelli M, degli Uberti EC: Antiproliferative effects of somatostatin analogs in pituitary adenomas. Pituitary; 2006;9(1):27-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiproliferative effects of somatostatin analogs in pituitary adenomas.
  • The antisecretory effects of somatostatin (SRIF) and its analogs are widely recognised and provide the basis for treatment of hormonal hypersecretion in pituitary adenomas, especially in the settings of acromegaly.
  • This review focuses on the mechanisms transducing the antiproliferative effects of SRIF and its analogs on pituitary adenomas, and on the clinical consequences on tumor volume of pharmacological treatment of pituitary adenomas with these drugs.
  • [MeSH-major] Adenoma / drug therapy. Pituitary Neoplasms / drug therapy. Somatostatin / analogs & derivatives. Somatostatin / therapeutic use

  • MedlinePlus Health Information. consumer health - Pituitary Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Invest. 1997 Nov 1;100(9):2386-92 [9410919.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Mar;90(3):1856-63 [15613435.001]
  • [Cites] Eur J Endocrinol. 2005 Apr;152(4):645-54 [15817922.001]
  • [Cites] Science. 1978 Oct 27;202(4366):390-402 [212832.001]
  • [Cites] Neuroendocrinology. 2004 Mar;79(3):142-8 [15103227.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jul;86(7):2976-81 [11443154.001]
  • [Cites] J Endocrinol Invest. 1998 Sep;21(8):512-9 [9801992.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):4405-10 [15827109.001]
  • [Cites] Clin Endocrinol (Oxf). 1985 May;22(5):679-86 [4028461.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E278-87 [15769796.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Sep;79(3):724-9 [7521350.001]
  • [Cites] J Clin Endocrinol Metab. 1989 May;68(5):917-24 [2565913.001]
  • [Cites] N Engl J Med. 1996 Jan 25;334(4):246-54 [8532003.001]
  • [Cites] Eur J Endocrinol. 2005 Aug;153(2):187-93 [16061822.001]
  • [Cites] Dig Liver Dis. 2004 Feb;36 Suppl 1:S17-25 [15077907.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Jun 7;259(2):379-84 [10362518.001]
  • [Cites] Endocrinology. 2005 Jul;146(7):2952-62 [15817666.001]
  • [Cites] Eur J Endocrinol. 1994 Jan;130(1):80-91 [8124483.001]
  • [Cites] Endocrinology. 1983 Jan;112(1):220-5 [6128222.001]
  • [Cites] Metabolism. 1996 Aug;45(8 Suppl 1):49-50 [8769380.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):398-403 [8106629.001]
  • [Cites] J Clin Neurosci. 2003 Jul;10 (4):444-8 [12852883.001]
  • [Cites] J Endocrinol Invest. 1993 Jul-Aug;16(7):541-3 [8227984.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jun;88(6):2797-802 [12788890.001]
  • [Cites] Endocrinology. 1992 Aug;131(2):571-7 [1322274.001]
  • [Cites] J Surg Res. 1993 Oct;55(4):446-50 [7692142.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Jul;79(1):113-8 [8027215.001]
  • [Cites] J Endocrinol Invest. 1999 Jun;22(6):409-18 [10435849.001]
  • [Cites] Ann N Y Acad Sci. 1994 Sep 15;733:138-46 [7978861.001]
  • [Cites] Clin Cancer Res. 1997 Feb;3(2):265-72 [9815682.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jul;87(7):3013-8 [12107192.001]
  • [Cites] Eur J Endocrinol. 1995 Oct;133(4):430-9 [7581966.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Aug;86(8):3809-14 [11502816.001]
  • [Cites] J Neuroendocrinol. 1996 Aug;8(8):605-10 [8866248.001]
  • [Cites] J Endocrinol Invest. 2001 Jun;24(6):430-7 [11434667.001]
  • [Cites] Endocrine. 2001 Apr;14(3):329-36 [11444429.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Oct;61(4):666-71 [2863281.001]
  • [Cites] N Engl J Med. 1983 Dec 22;309(25):1556-63 [6140639.001]
  • [Cites] Neuro Endocrinol Lett. 2001 Oct;22(5):343-8 [11600876.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):956-62 [9041201.001]
  • [Cites] Clin Endocrinol (Oxf). 1986 Nov;25(5):561-72 [3621623.001]
  • [Cites] Horm Res. 2000;53 Suppl 3:76-87 [10971110.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Apr;83(4):1368-75 [9543168.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Dec;80(12):3601-7 [8530606.001]
  • [Cites] Endocrinology. 2005 Jun;146(6):2692-8 [15746253.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Oct;89(10):5181-8 [15472224.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Nov;86(11):5194-200 [11701676.001]
  • [Cites] Mol Cell Endocrinol. 2003 Aug 29;206(1-2):49-62 [12943989.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Feb;85(2):781-92 [10690891.001]
  • [Cites] Cancer Res. 1990 Oct 1;50(19):6238-42 [2169342.001]
  • [Cites] Endocr Rev. 1991 Nov;12(4):450-82 [1684746.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Jan;54(1):23-30 [11167922.001]
  • [Cites] Eur J Clin Invest. 1997 Apr;27(4):277-84 [9134375.001]
  • [Cites] N Engl J Med. 1983 Dec 15;309(24):1495-501 [6139753.001]
  • [Cites] Mayo Clin Proc. 1997 Oct;72(10):893-900 [9379690.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7862-9 [10713101.001]
  • [Cites] J Clin Endocrinol Metab. 1985 Jul;61(1):98-103 [2860120.001]
  • [Cites] Nat Rev Drug Discov. 2003 Dec;2(12):999-1017 [14654798.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jul;59(1):115-28 [12807513.001]
  • [Cites] Neuroendocrinology. 1994 Sep;60(3):314-22 [7969790.001]
  • [Cites] J Biol Chem. 1996 Mar 15;271(11):6129-36 [8626400.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14530-5 [12391292.001]
  • [Cites] Growth Horm IGF Res. 2003 Aug;13 Suppl A:S144-51 [12914744.001]
  • [Cites] Eur J Endocrinol. 2001 Aug;145(2):137-45 [11454508.001]
  • [Cites] FEBS Lett. 1994 Jul 11;348(2):192-6 [8034040.001]
  • [Cites] Life Sci. 2006 Jan 11;78(7):689-93 [16115652.001]
  • [Cites] Ann Intern Med. 1992 Nov 1;117(9):711-8 [1416572.001]
  • [Cites] Science. 2000 Apr 7;288(5463):154-7 [10753124.001]
  • [Cites] Front Neuroendocrinol. 1999 Jul;20(3):157-98 [10433861.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Apr;80(4):1386-92 [7714115.001]
  • [Cites] Clin Endocrinol (Oxf). 2005 Jul;63(1):39-44 [15963059.001]
  • [Cites] J Clin Endocrinol Metab. 1998 Aug;83(8):2997-3000 [9709982.001]
  • [Cites] Life Sci. 1995;56(5):333-42 [7530798.001]
  • [Cites] Eur J Endocrinol. 1999 Oct;141(4):396-408 [10526255.001]
  • [Cites] Science. 1973 Jan 5;179(4068):77-9 [4682131.001]
  • [Cites] Arch Intern Med. 1989 Jun;149(6):1443-5 [2730266.001]
  • [Cites] J Clin Invest. 1997 Feb 15;99(4):789-98 [9045884.001]
  • [Cites] Rev Physiol Biochem Pharmacol. 1998;133:55-108 [9600011.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Feb;89(2):638-45 [14764775.001]
  • (PMID = 16703406.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 51110-01-1 / Somatostatin
  • [Number-of-references] 81
  •  go-up   go-down


100. Power C, Kavanagh D, Hill AD, O'Higgins N, McDermott E: Unusual presentation of a giant parathyroid adenoma: report of a case. Surg Today; 2005;35(3):235-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual presentation of a giant parathyroid adenoma: report of a case.
  • Parathyroid adenomas account for most cases of primary hyperparathyroidism (1 degrees HPT).
  • Certain symptoms and biochemical abnormalities alert the surgeon to their presence, since these benign tumors are rarely evident on physical examination.
  • Parathyroid adenomas rarely attain huge proportions.
  • We report a case of a parathyroid adenoma measuring 8 x 5 x 3.5 cm and weighing 110 g; to our knowledge the greatest mass reported in the literature.
  • Interestingly, despite its huge size it did not cause many of the hypercalcemic symptoms usually associated with larger adenomas, but rather it manifested with symptoms of local pressure, another unusual property of this atypical tumor.
  • [MeSH-major] Adenoma / pathology. Adenoma / surgery. Parathyroid Neoplasms / pathology. Parathyroid Neoplasms / surgery
  • [MeSH-minor] Aged. Aged, 80 and over. Biopsy, Needle. Female. Follow-Up Studies. Humans. Hyperparathyroidism / diagnosis. Hyperparathyroidism / etiology. Immunohistochemistry. Ireland. Neoplasm Staging. Parathyroidectomy / methods. Risk Assessment. Severity of Illness Index. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15772795.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down






Advertisement