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1. Fahim L, Weinreb I, Alexander C, Perez Ordoñez B: Epithelial proliferation in small ducts of salivary cystadenoma resembling atypical ductal hyperplasia of breast. Head Neck Pathol; 2008 Sep;2(3):213-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epithelial proliferation in small ducts of salivary cystadenoma resembling atypical ductal hyperplasia of breast.
  • Cystadenomas may have a considerable intracystic epithelial component, but an epithelial proliferation in small ducts and cysts resembling atypical ductal hyperplasia of breast has not been documented.
  • The ductal cells were surrounded by clear myoepithelial cells.
  • The ductal cells were diffusely positive for keratin 7 and androgen receptors with focal expression of keratin 19 and high-molecular weight keratin.
  • S-100, estrogen and progesterone receptors, and BRST-2 were negative in the ductal cells.
  • Recognition of a prominent intraductal epithelial component in cystadenomas is important to avoid a misdiagnosis of cystadenocarcinoma or low-grade salivary duct carcinoma.
  • Cystadenomas join the list of salivary gland lesions with microscopic similarities to primary lesions of the breast.
  • [MeSH-major] Breast Neoplasms, Male / pathology. Carcinoma, Ductal, Breast / pathology. Cystadenoma / pathology. Salivary Ducts / pathology. Salivary Gland Neoplasms / pathology
  • [MeSH-minor] Aged. Carcinoma in Situ / metabolism. Carcinoma in Situ / pathology. Cell Proliferation. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Hyperplasia. Keratin-19 / metabolism. Keratin-7 / metabolism. Male. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Receptors, Androgen / metabolism

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  • [Cites] Am J Surg Pathol. 1996 Dec;20(12):1440-7 [8944036.001]
  • [Cites] Arch Pathol Lab Med. 2000 Feb;124(2):291-5 [10656742.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Jan;105(1):e28-33 [18155598.001]
  • [Cites] Virchows Arch. 2003 Jun;442(6):548-54 [12712335.001]
  • [Cites] Am J Surg Pathol. 2004 Aug;28(8):1040-4 [15252310.001]
  • [Cites] Cancer. 1971 Mar;27(3):643-50 [5549498.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1988 Sep;66(3):323-33 [2845326.001]
  • [Cites] Am J Surg Pathol. 1996 Feb;20(2):161-70 [8554105.001]
  • [Cites] Cancer. 1996 Sep 1;78(5):958-67 [8780532.001]
  • [Cites] Histopathology. 1997 Aug;31(2):185-8 [9279572.001]
  • [Cites] Arch Pathol Lab Med. 1998 Jul;122(7):644-9 [9674547.001]
  • [Cites] J Oral Pathol Med. 1999 Jul;28(6):282-6 [10426203.001]
  • [Cites] Am J Surg Pathol. 2006 Feb;30(2):154-64 [16434888.001]
  • [Cites] Am J Surg Pathol. 2006 Aug;30(8):1014-21 [16861974.001]
  • [Cites] Am J Surg Pathol. 2007 Jan;31(1):44-57 [17197918.001]
  • [Cites] Virchows Arch. 2000 Oct;437(4):465-8 [11097376.001]
  • (PMID = 20614317.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRT7 protein, human; 0 / Keratin-19; 0 / Keratin-7; 0 / Receptors, Androgen
  • [Other-IDs] NLM/ PMC2807557
  • [Keywords] NOTNLM ; Cystadenocarcinoma / Cystadenoma / Low-grade salivary duct carcinoma / Salivary glands
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2. Tourasse C, Sebag P, Dénier J, Rouyer N, Donné C: [Value of stereotactic breast core biopsy in patients with atypical ductal hyperplasia]. J Radiol; 2008 Jan;89(1 Pt 1):40-6
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  • [Title] [Value of stereotactic breast core biopsy in patients with atypical ductal hyperplasia].
  • [Transliterated title] Valeur des macrobiopsies mammaires sous guidage stéréotaxique en cas de découverte d'une hyperplasie canalaire atypique.
  • RESULTS: The rate of under-diagnosis was 5.9% for ductal carcinoma in-situ (DCIS) and 12.5% for atypical ductal hyperplasia (ADH).
  • Most cases of under-diagnosis involved clusters larger than 20 mm in diameter where the percentage of excision decreased from 98% (clusters<10 mm) to 9%.
  • ADH was never under-diagnosed when 3 or less foci were present.
  • The risk of under-diagnosis for DCIS increased when the number of biopsies containing DCIS was superior to 50% and if the grade was high.
  • CONCLUSION: The presence of ADH on biopsy specimens requires surgical biopsy, but optimal core biopsies with cluster removal and histological analysis by an experienced observer allows identification of low risk patients that could undergo close follow-up.
  • [MeSH-major] Biopsy / methods. Breast Neoplasms / pathology. Calcinosis / pathology. Mammary Glands, Human / pathology. Stereotaxic Techniques
  • [MeSH-minor] Carcinoma in Situ / pathology. Carcinoma in Situ / surgery. Carcinoma, Ductal, Breast / pathology. Carcinoma, Ductal, Breast / surgery. Carcinoma, Lobular / pathology. Carcinoma, Lobular / surgery. Diagnosis, Differential. Female. Humans. Hyperplasia. Mass Screening. Retrospective Studies. Risk Factors

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  • (PMID = 18288025.001).
  • [ISSN] 0221-0363
  • [Journal-full-title] Journal de radiologie
  • [ISO-abbreviation] J Radiol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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3. Menes TS, Kerlikowske K, Jaffer S, Seger D, Miglioretti DL: Rates of atypical ductal hyperplasia have declined with less use of postmenopausal hormone treatment: findings from the Breast Cancer Surveillance Consortium. Cancer Epidemiol Biomarkers Prev; 2009 Nov;18(11):2822-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rates of atypical ductal hyperplasia have declined with less use of postmenopausal hormone treatment: findings from the Breast Cancer Surveillance Consortium.
  • AIM: To examine risk factors and rates of atypical ductal hyperplasia (ADH) with and without associated breast cancer over time and tumor characteristics of breast cancer with and without associated ADH in women previously screened with mammography.
  • METHODS: Data on screening mammograms done between 1996 and 2005 were collected from mammography registries that participate in the Breast Cancer Surveillance Consortium.
  • Associations between age, family history of breast cancer, postmenopausal hormone treatment (HT), and final pathology result (ADH or cancer with or without ADH in the same breast) were examined.
  • Tumor characteristics of cancers with and without associated ADH were compared.
  • RESULTS: A total of 2,453,483 screening mammograms were associated with 1,064 biopsies with ADH, 833 breast cancers with ADH, and 8,161 cancers with no ADH.
  • Rates of ADH decreased from a peak of 5.5/10,000 mammograms in 1999 to 2.4/10,000 in 2005.
  • Rates of cancer with ADH decreased from a peak of 4.3/10,000 mammograms in 2003 to 3.3/10,000 in 2005.
  • ADH and breast cancer were significantly associated with use of postmenopausal HT.
  • Cancer associated with ADH was of lower grade and stage and more estrogen receptor positive than cancer with no ADH.
  • SUMMARY: Postmenopausal HT is associated with an increased risk of ADH with or without cancer.
  • Rates of ADH have decreased over the past decade, which may be partially explained by the significant reduction in use of postmenopausal HT.

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  • [Cites] J Natl Cancer Inst. 2007 Aug 1;99(15):1152-61 [17652280.001]
  • [Cites] Breast Cancer Res. 2007;9(3):R28 [17477859.001]
  • [Cites] Virchows Arch. 2007 Jul;451(1):1-10 [17551752.001]
  • [Cites] Breast Cancer Res. 2007;9(4):108 [17666116.001]
  • [Cites] Breast Cancer Res Treat. 2008 Feb;107(3):427-30 [17453336.001]
  • [Cites] J Natl Cancer Inst. 2008 Apr 16;100(8):563-71 [18398105.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Sep;17(9):2337-43 [18725513.001]
  • [Cites] AJR Am J Roentgenol. 2009 Jan;192(1):229-34 [19098204.001]
  • [Cites] Int J Epidemiol. 2000 Aug;29(4):637-44 [10922339.001]
  • [Cites] Int J Cancer. 2002 Jul 20;100(3):375-8 [12115556.001]
  • [Cites] JAMA. 2003 Jun 25;289(24):3243-53 [12824205.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4314-21 [14645420.001]
  • [Cites] Breast J. 2004 Jan-Feb;10 Suppl 1:S3-4 [14984480.001]
  • [Cites] N Engl J Med. 1985 Jan 17;312(3):146-51 [3965932.001]
  • [Cites] Cancer. 1985 Jun 1;55(11):2698-708 [2986821.001]
  • [Cites] Cancer. 1990 Sep 15;66(6 Suppl):1326-35 [2205361.001]
  • [Cites] Radiology. 1993 Dec;189(3):667-71 [8234688.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Aug 1;42(1):105-15 [9747827.001]
  • [Cites] J Pathol. 1999 Jul;188(3):245-51 [10419590.001]
  • [Cites] J Pathol. 2005 Jan;205(2):248-54 [15641021.001]
  • [Cites] N Engl J Med. 2005 Jul 21;353(3):229-37 [16034008.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):e49-50 [17114650.001]
  • [Cites] Cancer. 2007 Jan 15;109(2):180-7 [17154175.001]
  • [Cites] Am J Surg Pathol. 2007 Mar;31(3):417-26 [17325484.001]
  • [Cites] N Engl J Med. 2007 Apr 19;356(16):1670-4 [17442911.001]
  • [Cites] J Natl Cancer Inst. 2007 Sep 5;99(17):1335-9 [17698950.001]
  • (PMID = 19900937.001).
  • [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 / U01 CA063740; United States / NCI NIH HHS / CA / U01CA70040; United States / NCI NIH HHS / CA / U01CA63740; United States / NCI NIH HHS / CA / U01CA69976; United States / NCI NIH HHS / CA / U01 CA070040; United States / NCI NIH HHS / CA / U01 CA063731-11; United States / NCI NIH HHS / CA / U01CA70013; United States / NCI NIH HHS / CA / U01 CA086082; United States / NCI NIH HHS / CA / U01 CA063731; United States / NCI NIH HHS / CA / U01 CA086076; United States / NCI NIH HHS / CA / U01 CA086082-09; United States / NCI NIH HHS / CA / U01 CA063740-08; United States / NCI NIH HHS / CA / U01CA63736; United States / NCI NIH HHS / CA / U01 CA069976-06; United States / NCI NIH HHS / CA / U01CA86082; United States / NCI NIH HHS / CA / U01 CA069976; United States / NCI NIH HHS / CA / U01CA86076; None / None / / U01 CA086082-09; United States / NCI NIH HHS / CA / U01 CA086076-09; United States / NCI NIH HHS / CA / U01 CA063736; United States / NCI NIH HHS / CA / CA063731-11; None / None / / U01 CA086076-09; United States / NCI NIH HHS / CA / CA063736-07; United States / NCI NIH HHS / CA / U01 CA070013-05; United States / NCI NIH HHS / CA / U01 CA070013; United States / NCI NIH HHS / CA / U01CA63731; United States / NCI NIH HHS / CA / U01 CA070040-05; United States / NCI NIH HHS / CA / CA069976-06; United States / NCI NIH HHS / CA / U01 CA063736-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS150442; NLM/ PMC2920735
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4. Niu Y, Liu T, Tse GM, Sun B, Niu R, Li HM, Wang H, Yang Y, Ye X, Wang Y, Yu Q, Zhang F: Increased expression of centrosomal alpha, gamma-tubulin in atypical ductal hyperplasia and carcinoma of the breast. Cancer Sci; 2009 Apr;100(4):580-7
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  • [Title] Increased expression of centrosomal alpha, gamma-tubulin in atypical ductal hyperplasia and carcinoma of the breast.
  • We sought to determine whether centrosomal dysfunctions occur in the atypical ductal hyperplasia (ADH)-carcinoma sequence of breast cancer.
  • We found that alpha-tubulin or gamma-tubulin mRNA was increasingly expressed from normal breast tissue (NBT) to ADH, ductal carcinoma in situ (DCIS), and infiltrative ductal carcinoma (IDC), respectively, with the highest expressions being found in DCIS.
  • Our results demonstrate that centrosomal aberrations may play key roles in the early stage of breast tumorogenesis.
  • Furthermore, determination of alpha, gamma-tubulins using combined qPCR with ISH may be useful in assisting the diagnosis of premalignant lesions of the breast.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology. Precancerous Conditions / pathology. Tubulin / metabolism

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  • (PMID = 19215229.001).
  • [ISSN] 1349-7006
  • [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] 0 / Tubulin
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5. Doren E, Hulvat M, Norton J, Rajan P, Sarker S, Aranha G, Yao K: Predicting cancer on excision of atypical ductal hyperplasia. Am J Surg; 2008 Mar;195(3):358-61; discussion 361-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predicting cancer on excision of atypical ductal hyperplasia.
  • BACKGROUND: There are no specific histopathologic factors that allow identification of patients with atypical ductal hyperplasia (ADH) who will have cancer on final excision.
  • METHODS: This was a retrospective study of all patients who had ADH on biopsy followed by excision from 1999 to 2006.
  • RESULTS: Fifty-one patients were found to have ADH on core biopsy.
  • Eight (15.7%) patients had invasive carcinoma on surgical excision, 9 (17.5%) had ductal carcinoma-in-situ (DCIS), 21 (41.5%) had ADH, 4 (8%) patients had atypical lobular hyperplasia, and 9 (17.5%) had benign tumors.
  • The grade of atypia on the core biopsy was mild in 13 (25%) patients, moderate in 22 (43%), and marked in 16 (32%).
  • On multivariate analysis of histopathologic factors, the grade of atypia was the only significant variable that predicted a diagnosis of cancer on final surgical excision (P = .001).
  • CONCLUSIONS: The grade of atypia correlated with the presence of cancer on surgical excision.
  • [MeSH-major] Breast / pathology. Breast Neoplasms / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Female. Humans. Hyperplasia. Middle Aged. Predictive Value of Tests. Retrospective Studies

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  • (PMID = 18206849.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Chae BJ, Lee A, Song BJ, Jung SS: Predictive factors for breast cancer in patients diagnosed atypical ductal hyperplasia at core needle biopsy. World J Surg Oncol; 2009;7:77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictive factors for breast cancer in patients diagnosed atypical ductal hyperplasia at core needle biopsy.
  • BACKGROUND: Percutaneous core needle biopsy (CNB) is considered to be the standard technique for histological diagnosis of breast lesions.
  • But, it is less reliable for diagnosing atypical ductal hyperplasia (ADH).
  • The purpose of the present study was to predict, based on clinical and radiological findings, which cases of ADH diagnosed by CNB would be more likely to be associated with a more advanced lesion on subsequent surgical excision.
  • METHODS: Between February 2002 and December 2007, consecutive ultrasound-guided CNBs were performed on suspicious breast lesions at Seoul St. Mary's Hospital.
  • A total of 69 CNBs led to a diagnosis of ADH, and 45 patients underwent follow-up surgical excision.
  • RESULTS: Sixty-nine patients were diagnosed with ADH at CNB.
  • Of these patients, 45 underwent surgical excision and 10 (22.2%) were subsequently diagnosed with a malignancy (ductal carcinoma in situ, n = 8; invasive cancer, n = 2).
  • CONCLUSION: Age (>or= 50) at the time of biopsy is an independent predictive factor for breast cancer at surgical excision in patients with diagnosed ADH at CNB.
  • For patients diagnosed with ADH at CNB, only complete surgical excision is the suitable treatment option, because we could not find any combination of factors that can safely predict the absence of DCIS or invasive cancer in a case of ADH.
  • [MeSH-major] Breast / pathology. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology. Hyperplasia / pathology
  • [MeSH-minor] Adult. Age Distribution. Biopsy, Fine-Needle / methods. Breast Diseases / diagnosis. Breast Diseases / pathology. Diagnosis, Differential. Female. Follow-Up Studies. Forecasting. Humans. Middle Aged. Retrospective Studies. Ultrasonography, Interventional. Ultrasonography, Mammary. Vacuum

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  • [Cites] Arch Surg. 2000 Jun;135(6):700-3 [10843367.001]
  • [Cites] Ann Surg. 1997 Jun;225(6):726-31; discussion 731-3 [9230813.001]
  • [Cites] AJR Am J Roentgenol. 2000 Nov;175(5):1341-6 [11044038.001]
  • [Cites] Am J Surg. 2000 Oct;180(4):313-5 [11113443.001]
  • [Cites] Am J Clin Pathol. 2001 Jul;116(1):92-6 [11447758.001]
  • [Cites] Am J Surg Pathol. 2001 Aug;25(8):1017-21 [11474285.001]
  • [Cites] Breast J. 2001 Nov-Dec;7(6):417-21 [11843854.001]
  • [Cites] Radiology. 2002 Aug;224(2):548-54 [12147855.001]
  • [Cites] Pathology. 2002 Oct;34(5):410-6 [12408338.001]
  • [Cites] Am J Surg. 2002 Dec;184(6):534-7; discussion 537 [12488158.001]
  • [Cites] Am J Clin Pathol. 2003 Feb;119(2):248-53 [12579995.001]
  • [Cites] Mod Pathol. 2003 Feb;16(2):154-60 [12591968.001]
  • [Cites] Adv Anat Pathol. 2003 Sep;10(5):278-90 [12973049.001]
  • [Cites] N Engl J Med. 1985 Jan 17;312(3):146-51 [3965932.001]
  • [Cites] Cancer. 1985 Jun 1;55(11):2698-708 [2986821.001]
  • [Cites] Radiology. 1989 Feb;170(2):411-5 [2536185.001]
  • [Cites] Radiology. 1991 Jun;179(3):759-64 [2027988.001]
  • [Cites] Radiology. 1991 Aug;180(2):403-7 [1648757.001]
  • [Cites] Cancer. 1993 Jun 15;71(12):3798-807 [8508347.001]
  • [Cites] Radiology. 1993 Dec;189(3):667-71 [8234688.001]
  • [Cites] Cancer. 1994 Jan 1;73(1):118-24 [8275415.001]
  • [Cites] Radiology. 1994 Oct;193(1):91-5 [8090927.001]
  • [Cites] Radiology. 1997 Aug;204(2):485-8 [9240540.001]
  • [Cites] J Surg Oncol. 1998 Mar;67(3):168-73 [9530887.001]
  • [Cites] Breast. 2008 Jun;17(3):282-8 [18063369.001]
  • [Cites] Am J Surg. 2008 Sep;196(3):339-45 [18585676.001]
  • [Cites] Breast Cancer Res Treat. 2008 Nov;112(1):189-95 [18060577.001]
  • [Cites] Semin Diagn Pathol. 1994 Aug;11(3):181-92 [7831529.001]
  • [Cites] AJR Am J Roentgenol. 1995 May;164(5):1111-3 [7717215.001]
  • [Cites] Histopathology. 1996 Jun;28(6):537-41 [8803597.001]
  • [Cites] AJR Am J Roentgenol. 2000 Oct;175(4):1047-50 [11000162.001]
  • (PMID = 19852801.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2771003
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7. Jelski W, Orywal K, Szmitkowski M: [Effects of H2-blockers on alcohol dehydrogenase (ADH) activity]. Pol Merkur Lekarski; 2008 Dec;25(150):531-3
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  • [Title] [Effects of H2-blockers on alcohol dehydrogenase (ADH) activity].
  • [Transliterated title] Wpływ H2-blokerów na aktywność dehydrogenazy alkoholowej (ADH).
  • FPM occurs predominantly in the stomach and has been attributed to class IV of alcohol dehydrogenase (ADH) isoenzyme localizated in the gastric mucosa.
  • A number of factors that influence on gastric ADH activity and thereby modulate FPM have been identified.
  • Several H2-receptor antagonists, including cimetidine and ranitidine, inhibit gastric ADH activity and reduce FPM, resulting in higher blood alcohol concentrations after H2-blockers administration.

  • Hazardous Substances Data Bank. CIMETIDINE .
  • Hazardous Substances Data Bank. ETHANOL .
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  • (PMID = 19205389.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 3K9958V90M / Ethanol; 80061L1WGD / Cimetidine; 884KT10YB7 / Ranitidine; EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Number-of-references] 24
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8. Shamloula MM, El-Shorbagy SH, Saied EM: P63 and cytokeratin8/18 expression in breast, atypical ductal hyperplasia, ductal carcinoma in situ and invasive duct carcinoma. J Egypt Natl Canc Inst; 2007 Sep;19(3):202-10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P63 and cytokeratin8/18 expression in breast, atypical ductal hyperplasia, ductal carcinoma in situ and invasive duct carcinoma.
  • Background and Purpose : The pattern and distribution of p63 expression as a myoepithelial/basal stem cell marker can be different between atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) and may denote basal phenotype of breast ductal carcinoma.
  • CK8/18 is a luminal marker and may indicate a luminal phenotype of IDC and its expression in ADH and DCIS may refer to a possible precursor lesion to IDC.
  • This work was designed to study and compare the expression of p63 and cytokeratin 8/18 (CK8/18) in some cases of ADH, DCIS and IDC.
  • Materials and Methods : Histopathological evaluation and immunohistochemical study of anti-p63 and anti- CK8/18 was performed on selected archival cases of 7 ADH, 12 DCIS, 30 IDC of known clinicopathological data and previous estrogen receptor status (ER) for IDC.
  • Results : p63 was expressed in the peripheral rim of the myoepithelial cell layer in ADH and DCIS with occasional gabs in DCIS.
  • Confirmatory ASMA staining decorated the same peripheral rim of cells in ADH and DCIS, but was negative in p63 positive IDC cases.
  • CK8/18 was positive in 100% of ADH, 8/12 (66.7%) of DCIS and 22/30 (73%) of IDC cases.
  • Conclusion : It is concluded from this study that p63 is specific and valuable in differentiating myoepithelial cells and is more specific and valuable than other myoepithelial markers, as ASMA and can differentiate between ADH, DCIS, IDC as it stains peripheral myoepithelial cells in ADH and DCIS with gabs in the latter and does not stain any neoplastic cells.
  • In IDC, it is positive in malignant cells in a minority of cases which may indicate basal/stem cell/myoepithelial cell origin of breast carcinoma.
  • Comparatively, CK8/18 cannot differentiate ADH, DCIS and IDC as there is no difference in its staining pattern among them, which may suggest that they are a continuum or that ADH and DCIS are precursors for the luminal phenotype of IDC.
  • Key Words : p63 -CK8/18 -IDC -ADH -DCIS -Basal/ stem cells.

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  • (PMID = 19190693.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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9. Böcker W, Hungermann D, Weigel S, Roterberg K, Decker T: [Atypical ductal hyperplasia and atypical epithelial proliferation of ductal type]. Pathologe; 2009 Feb;30(1):42-8
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  • [Title] [Atypical ductal hyperplasia and atypical epithelial proliferation of ductal type].
  • The definition of atypical ductal hyperplasia (ADH) encompasses qualitative and quantitative criteria.
  • Qualitative criteria include cytological and architectural features similar to those of low grade ductal carcinoma in situ (DCIS), the quantitative criteria are characterized by metric features (2 mm or 2 ductules) or by the confines of lobules.
  • In this article we discuss the morphology of ADH, the status of ADH in the low grade pathway of breast carcinoma development and its clinical significance.
  • Furthermore, we comment some special forms of atypical epithelial proliferations of the ductal type.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology
  • [MeSH-minor] Biopsy. Carcinoma in Situ / genetics. Carcinoma in Situ / pathology. Cell Division. Epithelial Cells / pathology. Female. Humans. Hyperplasia. Keratins / genetics. Loss of Heterozygosity

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  • [Cites] Oncol Rep. 1999 Nov-Dec;6(6):1277-80 [10523696.001]
  • [Cites] Adv Anat Pathol. 2004 Jan;11(1):1-9 [14676636.001]
  • [Cites] J Natl Cancer Inst. 1998 May 6;90(9):697-703 [9586667.001]
  • [Cites] CA Cancer J Clin. 1997 May-Jun;47(3):171-90 [9152175.001]
  • [Cites] N Engl J Med. 1985 Jan 17;312(3):146-51 [3965932.001]
  • [Cites] Mod Pathol. 2000 Jan;13(1):13-8 [10658905.001]
  • [Cites] Hum Pathol. 1994 Feb;25(2):164-8 [8119716.001]
  • [Cites] Virchows Arch. 1999 Jan;434(1):3-10 [10071228.001]
  • [Cites] Hum Pathol. 1993 Feb;24(2):173-81 [8381766.001]
  • [Cites] Breast Cancer Res Treat. 2006 Jun;97(3):285-91 [16791485.001]
  • [Cites] Ann N Y Acad Sci. 1986;464:262-74 [3524352.001]
  • [Cites] Am J Surg Pathol. 1992 Dec;16(12):1133-43 [1463092.001]
  • [Cites] Cancer. 1996 Jun 15;77(12):2529-37 [8640702.001]
  • [Cites] Hum Pathol. 1992 Oct;23(10):1095-7 [1328030.001]
  • [Cites] Am J Surg Pathol. 1991 Mar;15(3):209-21 [1847606.001]
  • [Cites] Cancer. 1985 Jun 1;55(11):2698-708 [2986821.001]
  • [Cites] Eur J Cancer. 1994;30A(10 ):1414-9 [7833094.001]
  • [Cites] Cancer. 1993 Feb 15;71(4):1258-65 [8435803.001]
  • [Cites] Virchows Arch. 2005 Jul;447(1):1-8 [15926070.001]
  • [Cites] Mod Pathol. 1991 Jan;4(1):1-5 [2020652.001]
  • [Cites] J Clin Pathol. 1995 Jul;48(7):611-5 [7560165.001]
  • [Cites] Cancer. 1990 Feb 1;65(3):518-29 [2297643.001]
  • (PMID = 19156418.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 68238-35-7 / Keratins
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10. Arora S, Menes TS, Moung C, Nagi C, Bleiweiss I, Jaffer S: Atypical ductal hyperplasia at margin of breast biopsy--is re-excision indicated? Ann Surg Oncol; 2008 Mar;15(3):843-7
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  • [Title] Atypical ductal hyperplasia at margin of breast biopsy--is re-excision indicated?
  • BACKGROUND: Atypical duct hyperplasia (ADH) observed during core needle biopsy is associated with a high rate of cancer upon excision.
  • Controversy exists regarding the need to re-excise ADH involving a margin.
  • The purpose of this study was to determine the rate of residual pathology in patients that underwent re-excision for ADH involving the margin.
  • METHODS: In a retrospective review of the pathology database from 1 January 2000 to 1 June 2006, we identified 44 lumpectomy specimens with ADH involving the margin; 24 patients (55%) had a re-excision.
  • Slides were reviewed to verify the diagnosis of ADH near the margin and the presence of residual disease on re-excision associated with the biopsy cavity.
  • RESULTS: Patients had pure ADH (15, 63%), ADH and ductal carcinoma in situ (DCIS) (7, 29%) or ADH with invasive carcinoma (2, 8%).
  • Residual ADH or cancer was found in 14 of 24 patients (58%).
  • Of 15 patients with pure ADH, 6 (40%) had residual pathology: ADH (2), DCIS (2) and invasive carcinoma (2).
  • Of the 9 patients with cancer, 8 (89%) had residual disease in the form of ADH (4) or DCIS (4).
  • CONCLUSIONS: ADH found at the margin of a lumpectomy specimen is associated with a high rate of residual ADH and cancer.
  • Over one quarter of the patients with an initial diagnosis of ADH were reassessed as having DCIS or invasive carcinoma.
  • Re-excision in all patients with ADH involving the margin is recommended.
  • [MeSH-major] Breast / pathology. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology. Neoplasm, Residual / pathology
  • [MeSH-minor] Biopsy, Needle. Female. Humans. Hyperplasia. Reoperation. Retrospective Studies

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  • (PMID = 17987337.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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11. Prasad V, M King J, McLeay W, Raymond W, Cooter RD: Bilateral atypical ductal hyperplasia, an incidental finding in gynaecomastia--case report and literature review. Breast; 2005 Aug;14(4):317-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bilateral atypical ductal hyperplasia, an incidental finding in gynaecomastia--case report and literature review.
  • Male breast cancer is a rare disease.
  • Atypical ductal hyperplasia (ADH) in men is much rarer, and bilateral involvement is exceptional.
  • A 20-year-old male presented with bilateral gynaecomastia who underwent subcutaneous mastectomies and histopathology revealed bilateral ADH.
  • The residual breast tissue revealed ADH similar to the initial specimen.
  • ADH in women increases the risk of breast cancer by four to five times.
  • To our knowledge, this is the first case report of bilateral ADH in a gynaecomastia specimen.
  • [MeSH-major] Breast / pathology. Gynecomastia / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Functional Laterality. Humans. Hyperplasia. Male

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  • (PMID = 15985368.001).
  • [ISSN] 0960-9776
  • [Journal-full-title] Breast (Edinburgh, Scotland)
  • [ISO-abbreviation] Breast
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Scotland
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12. Jang M, Cho N, Moon WK, Park JS, Seong MH, Park IA: Underestimation of atypical ductal hyperplasia at sonographically guided core biopsy of the breast. AJR Am J Roentgenol; 2008 Nov;191(5):1347-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Underestimation of atypical ductal hyperplasia at sonographically guided core biopsy of the breast.
  • OBJECTIVE: The purpose of this study was to determine the rate of underestimation of atypical ductal hyperplasia (ADH) at sonographically guided core biopsy of the breast and to identify the factors involved.
  • Histologic analysis yielded ADH in 60 of the 3,563 lesions (1.7%).
  • The rate of underestimation of ADH was determined by dividing the number of lesions that proved to be carcinoma at surgical excision by 44, the total number of lesions evaluated with excisional biopsy.
  • Clinical, sonographic, and core biopsy features were analyzed to identify factors that affect the rate of underestimation of ADH.
  • RESULTS: The rate of underestimation of ADH was found to be 48% (21 of 44 lesions).
  • Underestimation of ADH was significantly less frequent for lesions evaluated with 11-gauge vacuum-assisted biopsy than for lesions evaluated with 14-gauge automated gun biopsy (22% [four of 18 lesions] vs 65% [17 of 26 lesions], p = 0.012).
  • The other clinical, sonographic, and biopsy features examined did not affect the rate of underestimation of ADH.
  • CONCLUSION: For sonographically guided core biopsy of the breast, the rate of underestimation of ADH was 48%.
  • [MeSH-major] Biopsy, Fine-Needle / statistics & numerical data. Breast Neoplasms / epidemiology. Breast Neoplasms / pathology. Carcinoma, Ductal / epidemiology. Carcinoma, Ductal / pathology. Ultrasonography, Interventional / statistics & numerical data

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  • (PMID = 18941067.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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13. Greene T, Tartter PI, Smith SR, Estabrook A: The significance of surgical margins for patients with atypical ductal hyperplasia. Am J Surg; 2006 Oct;192(4):499-501
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The significance of surgical margins for patients with atypical ductal hyperplasia.
  • BACKGROUND: The significance of surgical margins for patients with atypical ductal hyperplasia is unknown.
  • PATIENTS AND METHODS: We reviewed our experience with atypical ductal hyperplasia and correlated the margin status of the specimens removed with the risk of recurrence as atypical ductal hyperplasia, ductal carcinoma in situ, and invasive carcinoma.
  • Seven hundred forty-seven patients were identified between February 1995 and September 2005 as having biopsy proven atypical ductal hyperplasia (ADH).
  • One hundred fifty-five of these patients were found to have "pure" atypical ductal hyperplasia without associated premalignant or malignant breast disease or a history of ipsilateral disease.
  • RESULTS: Of the 155 patients whose excisional biopsy specimens were "pure" atypical ductal hyperplasia, 44% (68) had negative margins, 5% (7) had positive margins, and 52% (80) were not reported.
  • Seven patients (5%) presented with new findings at the site of their initial excisional biopsy, 1 of whom was found to have an invasive ductal carcinoma and 6 of whom had benign findings.
  • Of the 87 patients with margins positive or unknown for ADH at surgical excision, none went on to develop malignancy.
  • CONCLUSION: Our results suggest that clear surgical margins at surgical excision for atypical ductal hyperplasia did not affect the risk of subsequently developing a malignancy.
  • [MeSH-major] Breast Neoplasms / etiology. Carcinoma, Ductal, Breast / etiology. Carcinoma, Intraductal, Noninfiltrating / etiology. Mammary Glands, Human / pathology. Mammary Glands, Human / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Hyperplasia / surgery. Middle Aged. Recurrence. Retrospective Studies. Risk Factors

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  • (PMID = 16978959.001).
  • [ISSN] 0002-9610
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Ingegnoli A, d'Aloia C, Frattaruolo A, Pallavera L, Martella E, Crisi G, Zompatori M: Flat epithelial atypia and atypical ductal hyperplasia: carcinoma underestimation rate. Breast J; 2010 Jan-Feb;16(1):55-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flat epithelial atypia and atypical ductal hyperplasia: carcinoma underestimation rate.
  • This study was carried out to determine the underestimation rate of carcinoma upon surgical biopsy after a diagnosis of flat epithelial atypia and atypical ductal hyperplasia and 11-gauge vacuum-assisted breast biopsy.
  • A retrospective review was conducted of 476 vacuum-assisted breast biopsy performed from May 2005 to January 2007 and a total of 70 cases of atypia were identified.
  • Fifty cases (71%) were categorized as pure atypical ductal hyperplasia, 18 (26%) as pure flat epithelial atypia and two (3%) as concomitant flat epithelial atypia and atypical ductal hyperplasia.
  • Surgical biopsy was performed in 44 patients with atypical ductal hyperplasia, 15 patients with flat epithelial atypia, and two patients with flat epithelial atypia and atypical ductal hyperplasia.
  • Five cases of atypical ductal hyperplasia were upgraded to ductal carcinoma in situ, three cases of flat epithelial atypia yielded one ductal carcinoma in situ and two cases of invasive ductal carcinoma, and one case of flat epithelial atypia/atypical ductal hyperplasia had invasive ductal carcinoma.
  • The overall rate of malignancy was 16% for atypical ductal hyperplasia (including flat epithelial atypia/atypical ductal hyperplasia patients) and 20% for flat epithelial atypia.
  • The presence of flat epithelial atypia and atypical ductal hyperplasia at biopsy requires careful consideration, and surgical excision should be suggested.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Breast Neoplasms / pathology. Carcinoma in Situ / pathology. Carcinoma, Ductal, Breast / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Age Distribution. Aged. Aged, 80 and over. Cohort Studies. Female. Humans. Hyperplasia / epidemiology. Hyperplasia / pathology. Immunohistochemistry. Incidence. Male. Mammography / methods. Middle Aged. Prognosis. Retrospective Studies. Risk Assessment

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  • (PMID = 19825003.001).
  • [ISSN] 1524-4741
  • [Journal-full-title] The breast journal
  • [ISO-abbreviation] Breast J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Eby PR, Ochsner JE, DeMartini WB, Allison KH, Peacock S, Lehman CD: Is surgical excision necessary for focal atypical ductal hyperplasia found at stereotactic vacuum-assisted breast biopsy? Ann Surg Oncol; 2008 Nov;15(11):3232-8
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  • [Title] Is surgical excision necessary for focal atypical ductal hyperplasia found at stereotactic vacuum-assisted breast biopsy?
  • BACKGROUND: Our goal was to determine the upgrade rate for lesions described as focal atypical ductal hyperplasia (ADH) after 9- or 11-gauge stereotactic vacuum-assisted breast biopsy (VABB) to determine whether surgical excision is indicated in this setting.
  • METHODS: We retrospectively reviewed the results of 991 consecutive 9- or 11-gauge stereotactic core VABB procedures from February 2001 through June 2006 and identified lesions diagnosed as ADH.
  • (1) focal ADH, (2) ADH suspicious for ductal carcinoma-in-situ, or (3) ADH not otherwise specified.
  • The final diagnosis after surgical excisional biopsy was determined from medical records.
  • The frequencies and upgrade rates to carcinoma were calculated and compared for all lesions and for each ADH category.
  • RESULTS: A total of 141 (14.2%) of 991 lesions yielded ADH at stereotactic core VABB, and 123 (87.2%) of 141 underwent surgical excisional biopsy of the stereotactic core VABB site.
  • A total of 56 (45.5%) of 123 were categorized as focal ADH, and 7 (12.5%) of 56 were upgraded to carcinoma.
  • A total of 49 (39.8%) of 123 were categorized as ADH not otherwise specified, and 11 (22.4%) of 49 were upgraded.
  • Eighteen (14.6%) of 123 were categorized as suspicious for ductal carcinoma-in-situ, and 8 (44.4%) of 18 were upgraded.
  • Neither the frequency of ADH (P = .66) nor the upgrade rates (P = .87) were significantly different between 9- and 11-gauge VABB.
  • CONCLUSION: Surgical excisional biopsy is indicated to exclude carcinoma in cases of focal ADH discovered at 9- or 11-gauge VABB.
  • [MeSH-major] Breast Neoplasms / diagnosis. Breast Neoplasms / surgery. Carcinoma, Intraductal, Noninfiltrating / diagnosis. Carcinoma, Intraductal, Noninfiltrating / surgery. Hyperplasia / diagnosis. Hyperplasia / surgery

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  • (PMID = 18696163.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Wiratkapun C, Wibulpholprasert B, Lertsithichai P, Pulpinyo K, Wongwaisayawan S: Breast cancer underestimation rate of atypical ductal hyperplasia diagnosed by core-needle biopsy under imaging guidance. J Med Assoc Thai; 2005 Apr;88(4):460-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Breast cancer underestimation rate of atypical ductal hyperplasia diagnosed by core-needle biopsy under imaging guidance.
  • OBJECTIVE: To evaluate breast cancer underestimation rate of atypical ductal hyperplasia (ADH) diagnosed by core-needle biopsy (CNB) under imaging guidance in Ramathibodi Hospital and to determine the difference between the malignant and benign groups in terms of clinical and imaging characteristics.
  • Thirty-nine patients diagnosed with ADH were enrolled into the present study.
  • RESULTS: Of 39 ADH cases, eight (20.5%) were found to have malignancy on subsequent excisional biopsy.
  • The majority of these were ductal carcinoma in situ (DCIS) (62.5%).
  • Lesion categorized as category 5 according to BI-RADS (Breast imaging reporting and data system) was the only feature which was statistically different between the benign and malignant groups.
  • No statistically significant difference was found between the benign and malignant groups in terms of age, personal and family history of breast cancer, clinical finding, mammographic lesion type, size of lesion, image-guided technique and percentage of lesion removal.
  • CONCLUSION: The underestimation rate of ADH in the present study was comparable to other studies.
  • The finding of Bl-RADS category 5 in patients with ADH diagnosed from CNB is a strong indication for subsequent excisional biopsy.
  • [MeSH-major] Biopsy, Needle. Breast Neoplasms / diagnosis. Carcinoma, Ductal, Breast / diagnosis. Carcinoma, Intraductal, Noninfiltrating / diagnosis

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  • (PMID = 16146248.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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17. Grady I, Gorsuch H, Wilburn-Bailey S: Ultrasound-guided, vacuum-assisted, percutaneous excision of breast lesions: an accurate technique in the diagnosis of atypical ductal hyperplasia. J Am Coll Surg; 2005 Jul;201(1):14-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultrasound-guided, vacuum-assisted, percutaneous excision of breast lesions: an accurate technique in the diagnosis of atypical ductal hyperplasia.
  • BACKGROUND: In October 2002, ultrasound-guided, vacuum-assisted, percutaneous excision was shown to facilitate the complete removal of benign breast lesions up to 3 cm in diameter.
  • This study was performed to ascertain the overall accuracy of ultrasound-guided, vacuum-assisted, percutaneous excision as evidenced by the frequency of atypical ductal hyperplasia (ADH) underestimation.
  • STUDY DESIGN: A retrospective review was conducted of 542 consecutive ultrasound-guided, vacuum-assisted breast biopsies performed between February 2000 and September 2004.
  • Pathology review revealed 52 lesions that demonstrated ADH and no evidence of malignancy.
  • Each patient with this diagnosis was offered surgical excision.
  • RESULTS: Of 542 consecutively diagnosed lesions, 52 displayed ADH with no evidence of malignancy (10%).
  • The rate of ADH underestimation was 6 of 18 (33%) in incisional biopsies and 0 of 29 performed with complete imaged lesion evidence (p=0.002).
  • The rate of ADH underestimation in women who underwent ultrasound-guided, vacuum-assisted, percutaneous excision was zero, a result equivalent to open surgical biopsy.
  • CONCLUSIONS: ADH is a more common finding in sonographic lesions than has been previously reported.
  • [MeSH-major] Biopsy, Needle / methods. Breast / pathology. Ultrasonography, Interventional
  • [MeSH-minor] Breast Neoplasms / pathology. Breast Neoplasms / surgery. Carcinoma in Situ / pathology. Carcinoma, Ductal, Breast / pathology. Carcinoma, Lobular / pathology. Diagnosis, Differential. Female. Humans. Hyperplasia. Retrospective Studies. Vacuum

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  • (PMID = 15978438.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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18. Liberman L, Holland AE, Marjan D, Murray MP, Bartella L, Morris EA, Dershaw DD, Wynn RT: Underestimation of atypical ductal hyperplasia at MRI-guided 9-gauge vacuum-assisted breast biopsy. AJR Am J Roentgenol; 2007 Mar;188(3):684-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Underestimation of atypical ductal hyperplasia at MRI-guided 9-gauge vacuum-assisted breast biopsy.
  • OBJECTIVE: The purposes of this study were to determine the frequency of diagnosis of atypical ductal hyperplasia (ADH) at MRI-guided 9-gauge vacuum-assisted breast biopsy and to assess the rate of underestimation of ADH at subsequent surgical excision.
  • MATERIALS AND METHODS: We conducted a retrospective review of medical records of 237 lesions consecutively detected with MRI and then subjected to MRI-guided 9-gauge vacuum-assisted breast biopsy during a 33-month period.
  • Underestimated ADH was defined as a lesion yielding ADH at vacuum-assisted biopsy and cancer at surgery.
  • RESULTS: Histologic analysis of MRI-guided vacuum-assisted breast biopsy specimens yielded ADH without cancer in 15 (6%) of 237 lesions.
  • Among 15 patients in whom vacuum-assisted breast biopsy yielded ADH, the median age was 52 years (range, 46-68 years).
  • Surgical histologic findings were malignancy in five (38%) of the cases, all ductal carcinoma in situ; high-risk lesion in six (46%) of the cases, including ADH without other high-risk lesions (n = 2), ADH and lobular carcinoma in situ (LCIS) (n = 1), ADH, LCIS, and papilloma (n =1), ADH and papilloma (n = 1), and LCIS (n = 1); and benign in two (15%) of the cases.
  • These data indicated an ADH underestimation rate of 38% (95% CI, 14-68%).
  • CONCLUSION: ADH without cancer was encountered in 6% of MRI-guided 9-gauge vacuum-assisted breast biopsies.
  • ADH at MRI-guided vacuum-assisted breast biopsy is an indication for surgical excision because of the high (38%) frequency of underestimation of these lesions.
  • [MeSH-major] Biopsy, Needle / statistics & numerical data. Breast Neoplasms / epidemiology. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / epidemiology. Carcinoma, Ductal, Breast / pathology. Magnetic Resonance Imaging / statistics & numerical data. Surgery, Computer-Assisted / statistics & numerical data

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  • (PMID = 17312054.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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19. Eby PR, Ochsner JE, DeMartini WB, Allison KH, Peacock S, Lehman CD: Frequency and upgrade rates of atypical ductal hyperplasia diagnosed at stereotactic vacuum-assisted breast biopsy: 9-versus 11-gauge. AJR Am J Roentgenol; 2009 Jan;192(1):229-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequency and upgrade rates of atypical ductal hyperplasia diagnosed at stereotactic vacuum-assisted breast biopsy: 9-versus 11-gauge.
  • OBJECTIVE: Our goals were to determine the frequency and upgrade rate for atypical ductal hyperplasia (ADH) diagnosed with stereotactic 9-gauge vacuum-assisted breast biopsy and to compare the frequencies and upgrade rates of ADH between 9- and 11-gauge vacuum-assisted breast biopsy.
  • MATERIALS AND METHODS: We retrospectively reviewed the pathology results of 991 consecutive 9- or 11-gauge stereotactic vacuum-assisted breast biopsy procedures from February 2001 through June 2006 and identified lesions diagnosed as ADH.
  • The final diagnosis after surgical excision was determined from medical records.
  • The frequencies and upgrade rates to carcinoma were calculated for all ADH lesions and compared between 9- and 11-gauge procedures.
  • RESULTS: One hundred forty-one of 991 (14.2%) lesions yielded a diagnosis of ADH at 9- or 11-gauge stereotactic vacuum-assisted breast biopsy.
  • Upgrade to ductal carcinoma in situ or invasive carcinoma occurred in 26 of 123 (21.1%) patients.
  • The frequency of ADH was 83 of 600 (13.8%) lesions for 9-gauge and 58 of 391 (14.8%) lesions for 11-gauge vacuum-assisted breast biopsy.
  • The 9-gauge upgrade rate was 16 of 74 (21.6%) lesions compared with 10 of 49 (20.4%) lesions for 11-gauge vacuum-assisted breast biopsy.
  • Neither the frequency of ADH (p=0.66) nor the upgrade rates (p=0.87) were significantly different between 9- and 11-gauge vacuum-assisted breast biopsy.
  • CONCLUSION: Compared with an 11-gauge vacuum-assisted breast biopsy device, the use of a larger 9-gauge vacuum-assisted breast biopsy needle does not decrease the upgrade rate of ADH.
  • Our frequency of ADH at vacuum-assisted breast biopsy is higher than any previously reported and may reflect regional differences in the incidence of breast cancer or practice patterns of the pathologist.
  • [MeSH-major] Biopsy, Fine-Needle / instrumentation. Biopsy, Fine-Needle / statistics & numerical data. Breast / pathology. Breast Neoplasms / epidemiology. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / epidemiology. Carcinoma, Ductal, Breast / pathology. Stereotaxic Techniques / statistics & numerical data

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  • [CommentIn] AJR Am J Roentgenol. 2009 Sep;193(3):W253; author reply W254 [19696268.001]
  • (PMID = 19098204.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Hameed O, Ghali VS, Tartter PI, Mizrachi H: Immunohistochemical staining for cyclin D1 and Ki-67 aids in the stratification of atypical ductal hyperplasia diagnosed on breast core biopsy. Am J Clin Pathol; 2005 Dec;124(6):862-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical staining for cyclin D1 and Ki-67 aids in the stratification of atypical ductal hyperplasia diagnosed on breast core biopsy.
  • A diagnosis of atypical ductal hyperplasia (ADH) after breast core biopsy usually is followed by an excisional biopsy to exclude the presence of a more significant lesion.
  • To determine whether the immunohistochemical expression of cyclin D1 (CyD1) and Ki-67 can aid in case stratification for the likelihood of finding ductal carcinoma in situ (DCIS) on subsequent excision, we immunohistochemically stained 21 consecutive ADH cases diagnosed by core biopsy, and proliferation indices (PIs) were calculated for each case.
  • The number of cells with CCND1 amplification was higher in cases with DCIS or ADH on subsequent excision.
  • Immunostaining for CyD1 and Ki-67 might help stratify cases of ADH on core biopsy and identify patients unlikely to have DCIS found on excision.
  • [MeSH-minor] Aged. Breast Neoplasms / diagnosis. Carcinoma, Intraductal, Noninfiltrating / diagnosis. Female. Humans. Hyperplasia / metabolism. Hyperplasia / pathology. Immunohistochemistry. In Situ Hybridization, Fluorescence. Middle Aged

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  • (PMID = 16416735.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 136601-57-5 / Cyclin D1
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21. Larson PS, de las Morenas A, Cerda SR, Bennett SR, Cupples LA, Rosenberg CL: Quantitative analysis of allele imbalance supports atypical ductal hyperplasia lesions as direct breast cancer precursors. J Pathol; 2006 Jul;209(3):307-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative analysis of allele imbalance supports atypical ductal hyperplasia lesions as direct breast cancer precursors.
  • It remains unclear whether hyperplastic breast lesions, especially with atypia, are cancer precursors or markers of increased cancer risk.
  • Therefore, we examined allele imbalance (AI), also known as loss of heterozygosity (LOH), at 20 microsatellite markers on nine chromosome arms, in DNA from 106 samples microdissected from 17 randomly selected cancer-containing breast specimens: 13 simple (DH) and 45 atypical ductal hyperplastic (ADH) lesions, 30 in situ (DCIS) and 18 invasive ductal carcinomas (IDC).
  • ADH had more AIs on 1q (p=0.03) and 16q (p=0.02) and fewer AIs on 17p (p=0.06) and 17q (p<0.0001) than on other arms.
  • The occurrence of any AI in ADH predicted greater AI (p=0.009) and possibly lower grade (p=0.05) in coexisting cancers.
  • We found AIs discordant between ADHs and cancers (always on 1q and 16q), AIs unique to ADH (usually on 11q) and some genetic heterogeneity among coexisting ADHs.
  • We conclude that ADH lesions are genetically advanced, with frequent alterations on 1q and 16q, and are often direct cancer precursors.
  • Their global genetic characteristics predict features of cancers in the same breast.
  • [MeSH-major] Allelic Imbalance. Breast / pathology. Breast Neoplasms / genetics. Precancerous Conditions / genetics
  • [MeSH-minor] Adult. Carcinoma, Ductal, Breast / genetics. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / genetics. Carcinoma, Intraductal, Noninfiltrating / pathology. Disease Progression. Female. Humans. Hyperplasia / genetics. Microdissection. Microsatellite Repeats. Middle Aged. Polymerase Chain Reaction / methods

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  • [Copyright] Copyright (c) 2006 Pathological Society of Great Britain and Ireland.
  • (PMID = 16604511.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA81078
  • [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] England
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22. Youk JH, Kim EK, Kim MJ: Atypical ductal hyperplasia diagnosed at sonographically guided 14-gauge core needle biopsy of breast mass. AJR Am J Roentgenol; 2009 Apr;192(4):1135-41
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  • [Title] Atypical ductal hyperplasia diagnosed at sonographically guided 14-gauge core needle biopsy of breast mass.
  • OBJECTIVE: The purpose of this study was to evaluate the surgical outcome of atypical ductal hyperplasia (ADH) diagnosed at sonographically guided 14-gauge core needle biopsy of breast masses and to determine whether the clinical, procedural, and radiologic features of this lesion can be used to predict upgrade to malignancy.
  • MATERIALS AND METHODS: We retrospectively reviewed the pathologic results of sonographically guided 14-gauge core needle biopsy of solid breast masses.
  • A total of 21 ADH lesions diagnosed with this procedure and surgically excised were included in the study.
  • RESULTS: The results of surgical excision of 21 ADH lesions were malignancy in 13 cases (62% rate of underestimation of ADH).
  • CONCLUSION: ADH diagnosed at sonographically guided 14-gauge core needle biopsy has a high underestimation rate with respect to the results of surgical excision.
  • Surgical excision should be recommended when ADH is diagnosed at sonographically guided 14-gauge core needle biopsy of breast masses.
  • [MeSH-major] Biopsy, Needle / methods. Breast Neoplasms / ultrasonography. Ultrasonography, Interventional. Ultrasonography, Mammary / methods

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  • (PMID = 19304725.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Teng-Swan Ho J, Tan PH, Hee SW, Su-Lin Wong J: Underestimation of malignancy of atypical ductal hyperplasia diagnosed on 11-gauge stereotactically guided Mammotome breast biopsy: an Asian breast screen experience. Breast; 2008 Aug;17(4):401-6
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  • [Title] Underestimation of malignancy of atypical ductal hyperplasia diagnosed on 11-gauge stereotactically guided Mammotome breast biopsy: an Asian breast screen experience.
  • The incidence of malignancy in excision biopsies performed for atypical ductal hyperplasia (ADH) diagnosed on needle biopsies has decreased since the advent of larger tissue sampling and improved accuracy using vacuum-assisted Mammotome biopsy.
  • We undertook a retrospective study to identify predictive factors for understaging of ADH diagnosed on 11-gauge Mammotome biopsy, to determine whether it was possible to avoid surgical excision in women where mammographically visible calcifications had been completely removed.
  • Sixty-one biopsy diagnosed ADH lesions were correlated with surgical excision findings that revealed DCIS in 14 (23%).
  • [MeSH-major] Biopsy, Needle / instrumentation. Breast Neoplasms / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology. Stereotaxic Techniques

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  • (PMID = 18455920.001).
  • [ISSN] 0960-9776
  • [Journal-full-title] Breast (Edinburgh, Scotland)
  • [ISO-abbreviation] Breast
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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24. Kohr JR, Eby PR, Allison KH, DeMartini WB, Gutierrez RL, Peacock S, Lehman CD: Risk of upgrade of atypical ductal hyperplasia after stereotactic breast biopsy: effects of number of foci and complete removal of calcifications. Radiology; 2010 Jun;255(3):723-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk of upgrade of atypical ductal hyperplasia after stereotactic breast biopsy: effects of number of foci and complete removal of calcifications.
  • PURPOSE: To determine if patients with fewer than three foci of atypical ductal hyperplasia (ADH) who have all of their calcifications removed after stereotactic 9- or 11-gauge vacuum-assisted breast biopsy (VABB) have a rate of upgrade to malignancy that is sufficiently low to obviate surgical excision.
  • One pathologist performed a blinded review of the results of procedures performed to assess for calcifications and confirmed ADH in 101 cases with subsequent surgical excision.
  • Each large duct or terminal duct-lobular unit containing ADH was considered a focus and counted.
  • The upgrade rate was significantly higher in cases of three or more foci of ADH (15 [28%] of 53 cases) than in cases of fewer than three foci (five [10%] of 48 cases) (P = .02).
  • Upgrade occurred in two (12%) of 17 cases in which there were fewer than three ADH foci and all calcifications were removed.
  • CONCLUSION: The upgrade rate is significantly higher when ADH involves at least three foci.
  • Surgical excision is recommended even when ADH involves fewer than three foci and all mammographic calcifications have been removed, because the upgrade rate is 12%.
  • [MeSH-major] Biopsy, Fine-Needle / instrumentation. Breast / pathology. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology

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  • [Copyright] Copyright RSNA, 2010
  • [CommentIn] Radiology. 2010 Dec;257(3):893-4; author reply 984 [21084420.001]
  • (PMID = 20173103.001).
  • [ISSN] 1527-1315
  • [Journal-full-title] Radiology
  • [ISO-abbreviation] Radiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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25. Sohn V, Arthurs Z, Herbert G, Keylock J, Perry J, Eckert M, Fellabaum D, Smith D, Brown T: Atypical ductal hyperplasia: improved accuracy with the 11-gauge vacuum-assisted versus the 14-gauge core biopsy needle. Ann Surg Oncol; 2007 Sep;14(9):2497-501
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  • [Title] Atypical ductal hyperplasia: improved accuracy with the 11-gauge vacuum-assisted versus the 14-gauge core biopsy needle.
  • BACKGROUND: Percutaneous stereotactic core needle biopsy (CNB) has become the primary diagnostic modality for evaluating nonpalpable, mammographically detected breast lesions.
  • Atypical ductal hyperplasia (ADH) uncovered by CNB confers a significant risk of harboring an occult malignancy in the excisional biopsy specimen; therefore, we sought to determine the benefits of upsizing biopsy needles from 14- to 11-gauge.
  • METHODS: Patients with isolated ADH diagnosed by CNB were included for analysis in this retrospective review.
  • Seventy eight of 88 patients (89%) diagnosed with ADH on CNB with an 11-gauge vacuum-assisted needle underwent open surgical excision.
  • Of these patients, nine (11%) were upgraded to ductal carcinoma in-situ (DCIS) while five (6%) had invasive cancer (IC), giving a total underestimation rate of 17%.
  • Surgical excision of ADH identified by CNB is required for definitive diagnosis.
  • [MeSH-major] Biopsy, Needle / methods. Breast Neoplasms / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Female. Humans. Hyperplasia. Mammography. Middle Aged. Neoplasm Staging. Retrospective Studies. Vacuum

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  • (PMID = 17564749.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Wagoner MJ, Laronga C, Acs G: Extent and histologic pattern of atypical ductal hyperplasia present on core needle biopsy specimens of the breast can predict ductal carcinoma in situ in subsequent excision. Am J Clin Pathol; 2009 Jan;131(1):112-21
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  • [Title] Extent and histologic pattern of atypical ductal hyperplasia present on core needle biopsy specimens of the breast can predict ductal carcinoma in situ in subsequent excision.
  • Atypical ductal hyperplasia (ADH) diagnosed by core needle biopsy (CNB) is regarded as an indication for surgical excision.
  • We investigated whether histologic subtype and extent of ADH in a series of 123 CNB specimens can predict the presence of carcinoma on surgical excision.
  • We found that ADH present in more than 2 foci in CNB specimens was a strong predictor of ductal carcinoma in situ (DCIS) on excision (>2 foci, 16/41 vs 6/82 for 1 or 2 foci; P < .0001).
  • The micropapillary subtype of ADH also predicted the presence of DCIS (P = .0006).
  • Our study suggests that micropapillary histologic subtype and extent of ADH in CNB specimens can be applied to predict the presence of DCIS on surgical excision.
  • By using the combination of the extent of ADH in CNB specimens (1 or 2 foci), the presence of microcalcifications within the lesion, and the lack of residual mammographic calcifications after CNB, we identified a low-risk group of patients (n = 25), none of whom had carcinoma on surgical excision.
  • Patients with ADH restricted to fewer than 3 foci may not need surgical excision, especially when the mammographic abnormality is completely removed by CNB.
  • [MeSH-major] Breast / pathology. Breast Neoplasms / pathology. Carcinoma, Ductal / pathology. Carcinoma, Intraductal, Noninfiltrating / pathology
  • [MeSH-minor] Biopsy, Needle / methods. Female. Humans. Hyperplasia / pathology. Middle Aged. Retrospective Studies

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  • (PMID = 19095574.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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27. Hoang JK, Hill P, Cawson JN: Can mammographic findings help discriminate between atypical ductal hyperplasia and ductal carcinoma in situ after needle core biopsy? Breast; 2008 Jun;17(3):282-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Can mammographic findings help discriminate between atypical ductal hyperplasia and ductal carcinoma in situ after needle core biopsy?
  • In a screening population of women, the mammographic characteristics for 68 cases of atypical ductal hyperplasia (ADH) diagnosed by needle core biopsy (NCB) were reviewed to seek mammographic findings which differentiate between ductal carcinoma in situ (DCIS) and ADH.
  • The mammographic findings were correlated with the surgical histological results of benign non-atypical, ADH and carcinoma (DCIS or invasive) to identify features which were associated with a higher or lower odds ratio (OR) for malignancy.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma, Intraductal, Noninfiltrating / diagnosis. Mammary Glands, Human / pathology. Mammography. Precancerous Conditions / diagnosis
  • [MeSH-minor] Adult. Aged. Calcinosis / pathology. Diagnosis, Differential. Female. Humans. Hyperplasia. Middle Aged

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  • (PMID = 18063369.001).
  • [ISSN] 0960-9776
  • [Journal-full-title] Breast (Edinburgh, Scotland)
  • [ISO-abbreviation] Breast
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
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28. Ko E, Han W, Lee JW, Cho J, Kim EK, Jung SY, Kang MJ, Moon WK, Park IA, Kim SW, Kim KS, Lee ES, Min KH, Kim SW, Noh DY: Scoring system for predicting malignancy in patients diagnosed with atypical ductal hyperplasia at ultrasound-guided core needle biopsy. Breast Cancer Res Treat; 2008 Nov;112(1):189-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scoring system for predicting malignancy in patients diagnosed with atypical ductal hyperplasia at ultrasound-guided core needle biopsy.
  • BACKGROUND: The aim of this study was to determine factors that predict under-evaluation of malignancy in patients diagnosed with atypical ductal hyperplasia (ADH) at ultrasound-guided core needle biopsy (CNB), and to develop a prediction algorithm for scoring the possibility of a diagnosis upgrade to malignancy based on clinical, radiological and pathological factors.
  • METHODS: The study enrolled patients diagnosed with ADH at ultrasound-guided CNB who subsequently underwent surgical excision of the lesion.
  • RESULTS: A total of 102 patients with ADH at CNB were identified.
  • Focal ADH was a negative predictor.
  • CONCLUSIONS: A scoring system to predict malignancy in patients diagnosed with ADH at CNB was developed based on five factors: age, palpable lesion, microcalcification on mammography, size on imaging and focal ADH.
  • [MeSH-major] Breast / pathology. Breast Neoplasms / pathology. Breast Neoplasms / ultrasonography. Diagnostic Imaging. Hyperplasia / pathology. Hyperplasia / ultrasonography
  • [MeSH-minor] Biopsy, Needle. Carcinoma, Ductal, Breast / pathology. Carcinoma, Ductal, Breast / surgery. Carcinoma, Ductal, Breast / ultrasonography. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Intraductal, Noninfiltrating / surgery. Carcinoma, Intraductal, Noninfiltrating / ultrasonography. Female. Humans. Mammography. Middle Aged. Neoplasm Staging. Prognosis. ROC Curve. Ultrasonography, Mammary

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  • (PMID = 18060577.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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29. Tébar MT, Aguilera L: [Acute intermittent porphyria and inappropriate ADH syndrome]. Rev Esp Anestesiol Reanim; 2010 May;57(5):311-3
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  • [Title] [Acute intermittent porphyria and inappropriate ADH syndrome].
  • [Transliterated title] Porfiria aguda intermitente y síndrome de secreción inadecuada de ADH.
  • The diagnosis was confirmed by laboratory findings of elevated d-aminolevulinic acid and porphobilinogen levels and normal stool porphyrins.
  • [MeSH-major] Inappropriate ADH Syndrome / etiology. Porphyria, Acute Intermittent / complications
  • [MeSH-minor] Abdominal Pain / etiology. Adult. Aminolevulinic Acid / blood. Coproporphyrins / analysis. Delayed Diagnosis. Dietary Carbohydrates / therapeutic use. Feces / chemistry. Female. Hemin / therapeutic use. Humans. Hyponatremia / diet therapy. Hyponatremia / etiology. Paresthesia / etiology. Porphobilinogen / urine. Quadriplegia / etiology. Sodium Chloride, Dietary / therapeutic use. Vomiting / etiology

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  • (PMID = 20527347.001).
  • [ISSN] 0034-9356
  • [Journal-full-title] Revista española de anestesiología y reanimación
  • [ISO-abbreviation] Rev Esp Anestesiol Reanim
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Coproporphyrins; 0 / Dietary Carbohydrates; 0 / Sodium Chloride, Dietary; 743LRP9S7N / Hemin; 74KHC72QXK / Porphobilinogen; 88755TAZ87 / Aminolevulinic Acid
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30. Bedei L, Falcini F, Sanna PA, Casadei Giunchi D, Innocenti MP, Vignutelli P, Saragoni L, Folli S, Amadori D: Atypical ductal hyperplasia of the breast: the controversial management of a borderline lesion: experience of 47 cases diagnosed at vacuum-assisted biopsy. Breast; 2006 Apr;15(2):196-202
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  • [Title] Atypical ductal hyperplasia of the breast: the controversial management of a borderline lesion: experience of 47 cases diagnosed at vacuum-assisted biopsy.
  • The present paper describes our experience of 47 cases of atypical ductal hyperplasia (ADH) diagnosed at vacuum-assisted biopsy.
  • From June 1999 to December 2003, 47 consecutive diagnoses of non-palpable ADH of the breast were made by 11-gauge vacuum-assisted biopsy (Mammotome).
  • Diagnostic underestimation occurred in only two cases, with a surgical diagnosis of ductal carcinoma in situ.
  • Despite the obvious limitations of the present study, it can be concluded that the probability of underestimating ADH diagnosis by Mammotome appears to be related to the radiological features of the lesion (>20 mm) and to the adequacy of specimens.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma in Situ / diagnosis. Carcinoma in Situ / epidemiology. Stereotaxic Techniques

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  • [CommentIn] Breast. 2008 Feb;17(1):6 [18083567.001]
  • (PMID = 16055333.001).
  • [ISSN] 0960-9776
  • [Journal-full-title] Breast (Edinburgh, Scotland)
  • [ISO-abbreviation] Breast
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
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31. Forgeard C, Benchaib M, Guerin N, Thiesse P, Mignotte H, Faure C, Clement-Chassagne C, Treilleux I: Is surgical biopsy mandatory in case of atypical ductal hyperplasia on 11-gauge core needle biopsy? A retrospective study of 300 patients. Am J Surg; 2008 Sep;196(3):339-45
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  • [Title] Is surgical biopsy mandatory in case of atypical ductal hyperplasia on 11-gauge core needle biopsy? A retrospective study of 300 patients.
  • BACKGROUND: Atypical ductal hyperplasia (ADH) is diagnosed in 4% to 10% of directional vacuum-assisted stereotactic biopsies (DVABs) performed for microcalcifications.
  • METHODS AND RESULTS: In this study, we analyzed a retrospective series of 300 patients with ADH on 11-gauge DVAB.
  • Comparing the diagnoses on DVAB and surgical excisions for 116 patients (39%), we identified 3 subsets of patients: no underestimation (size <6 mm and complete removal), low rate of 4% (< or =2 foci ADH in microcalcifications either <6 mm with incomplete removal or > or =6 mm and <21 mm), and high rate of 36% to 38% (>2 foci ADH in microcalcifications either <6 mm with incomplete removal or > or =6 mm and <21 mm, lesion size > or =21 mm).
  • [MeSH-major] Breast / pathology. Breast Diseases / pathology. Calcinosis / pathology
  • [MeSH-minor] Biopsy, Needle. Breast Neoplasms / pathology. Breast Neoplasms / radiography. Female. Humans. Hyperplasia. Mammography. Middle Aged. Retrospective Studies. Stereotaxic Techniques

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  • (PMID = 18585676.001).
  • [ISSN] 1879-1883
  • [Journal-full-title] American journal of surgery
  • [ISO-abbreviation] Am. J. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Travade A, Isnard A, Bouchet F, Bagard C: [Non-palpable breast lesions and core needle biopsy with Mammotome 11G: is surgery required in patients with atypical ductal hyperplasia?]. J Radiol; 2006 Mar;87(3):307-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Non-palpable breast lesions and core needle biopsy with Mammotome 11G: is surgery required in patients with atypical ductal hyperplasia?].
  • Atypical ductal hyperplasia (ADH) of the breast is a difficult histologic diagnosis.
  • The subsequent risk of breast carcinoma is 4 to 5 times more important and the carcinoma can arise in the same breast or in the contralateral breast.
  • Diagnosis can be establish on core needle biopsy with Mammotome 11G.
  • The risk of under-estimation (ductal carcinoma in situ or invasive carcinoma) is about 20%.
  • This study includes 62 cases of ADH found on 633 calcifications biopsied by Mammotome 11G.
  • In 31 cases, surgery was performed and ADH was confirmed in 25 cases (6 cases was under-estimated).
  • [MeSH-major] Biopsy, Needle / instrumentation. Breast / pathology. Breast / surgery. Breast Diseases / pathology. Breast Diseases / surgery. Calcinosis / pathology. Calcinosis / surgery
  • [MeSH-minor] Adult. Aged. Equipment Design. Female. Humans. Hyperplasia. Middle Aged

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  • [CommentIn] J Radiol. 2006 Mar;87(3):263-4 [16550109.001]
  • (PMID = 16550115.001).
  • [ISSN] 0221-0363
  • [Journal-full-title] Journal de radiologie
  • [ISO-abbreviation] J Radiol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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33. Guan H, Sun Y, Zan Q, Xu M, Li Y, Zhou J, He E, Eriksson S, Wen W, Skog S: Thymidine kinase 1 expression in atypical ductal hyperplasia significantly differs from usual ductal hyperplasia and ductal carcinoma in situ: A useful tool in tumor therapy management. Mol Med Rep; 2009 Nov-Dec;2(6):923-9
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  • [Title] Thymidine kinase 1 expression in atypical ductal hyperplasia significantly differs from usual ductal hyperplasia and ductal carcinoma in situ: A useful tool in tumor therapy management.
  • In studies using immunohistochemistry, it was reported to be a more useful proliferation marker than Ki-67 and PCNA in breast, lung and colorectal carcinoma.
  • In this study, we extend the work of prior breast carcinoma studies by investigating the expression of TK1 in 132 patients with usual ductal hyperplasia (UDH), atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC).
  • The expression of TK1 was found to be significantly increased in the breast ductal carcinomas in the following manner: UDH<ADH<DCIS<IDC.
  • TK1 expression was correlated with histological grade in DCIS and IDC patients and with pathological stage in IDC patients.
  • The degree of TK1-positive staining in the tumors of patients with ADH, DCIS and IDC was 80-90%, while the corresponding value for UDH patients was less than 5%.
  • Since the expression of TK1 varied significantly between the breast ductal subgroups, we concluded that TK1 is a reliable proliferation marker for the determination of breast tumor proliferation, particularly of pre-cancerous lesions (ADH).
  • This may enable timely treatment in the early stages of tumor development using minimal access surgery, thus avoiding extensive radical breast surgery and improving survival rates and the quality of life.

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  • (PMID = 21475922.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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34. Hashibe M, McKay JD, Curado MP, Oliveira JC, Koifman S, Koifman R, Zaridze D, Shangina O, Wünsch-Filho V, Eluf-Neto J, Levi JE, Matos E, Lagiou P, Lagiou A, Benhamou S, Bouchardy C, Szeszenia-Dabrowska N, Menezes A, Dall'Agnol MM, Merletti F, Richiardi L, Fernandez L, Lence J, Talamini R, Barzan L, Mates D, Mates IN, Kjaerheim K, Macfarlane GJ, Macfarlane TV, Simonato L, Canova C, Holcátová I, Agudo A, Castellsagué X, Lowry R, Janout V, Kollarova H, Conway DI, McKinney PA, Znaor A, Fabianova E, Bencko V, Lissowska J, Chabrier A, Hung RJ, Gaborieau V, Boffetta P, Brennan P: Multiple ADH genes are associated with upper aerodigestive cancers. Nat Genet; 2008 Jun;40(6):707-9
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  • [Title] Multiple ADH genes are associated with upper aerodigestive cancers.
  • Alcohol is an important risk factor for upper aerodigestive cancers and is principally metabolized by alcohol dehydrogenase (ADH) enzymes.
  • We have investigated six ADH genetic variants in over 3,800 aerodigestive cancer cases and 5,200 controls from three individual studies.
  • Both gene effects were independent of each other, implying that multiple ADH genes may be involved in upper aerodigestive cancer etiology.

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  • (PMID = 18500343.001).
  • [ISSN] 1546-1718
  • [Journal-full-title] Nature genetics
  • [ISO-abbreviation] Nat. Genet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 092039-01A2
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1B protein, human; EC 1.1.1.1 / ADH7 protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase
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35. Zamboli P, De Nicola L, Minutolo R, Iodice C, Avino D, Mascia S, D'Angiò P, Calabria M, Conte G: [Hyponatremia secondary to inappropriate antidiuretic hormone secretion]. G Ital Nefrol; 2008 Sep-Oct;25(5):554-61

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  • [Transliterated title] Iposodiemia da inappropriata secrezione di ADH.
  • The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a disorder of sodium and water balance characterized by hypotonic hyponatremia and impaired water excretion in the absence of renal insufficiency , adrenal insufficiency or any recognized stimulus for the antidiuretic hormone (ADH).
  • An inappropriate increase in ADH release of any cause produces hyponatremia by interfering with urinary dilution, thereby preventing the excretion of ingested water.
  • Despite being the most common cause of hyponatremia in hospitalized patients, SIADH remains a diagnosis of exclusion.
  • [MeSH-major] Hyponatremia / etiology. Inappropriate ADH Syndrome / complications

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  • (PMID = 18985840.001).
  • [ISSN] 0393-5590
  • [Journal-full-title] Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
  • [ISO-abbreviation] G Ital Nefrol
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
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36. Colón-Parrilla WV, Pérez-Chiesa I: Partial characterization and evolution of Adh-Adhr in Drosophila dunni. Biochem Genet; 2007 Apr;45(3-4):225-38
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  • [Title] Partial characterization and evolution of Adh-Adhr in Drosophila dunni.
  • We sequenced 2123 bp of the Adh-Adhr genomic region of Drosophila dunni of the cardini group from two cloned DNA PCR fragments and from two cDNA clones of an Adh transcript.
  • This comprises the Adh coding region and introns, 3' UTR, intergenic sequence, and most of Adhr, which is 260 bp downstream of Adh.
  • Both genes have the typical Drosophila melanogaster Adh structure of three exons and two introns, except for changes in the putative 8 bp sequence involved in downregulation within the 3' UTR of Adh.
  • Two amino acid substitutions could explain the low activity previously reported for this enzyme in D. dunni: Thr --> Lys at position 191 and Val --> Thr at position 189. D. dunni's Adh has the lowest codon bias reported so far for Drosophila species, and based on analysis of the nucleotide substitution rate, it is less conserved than Adhr.

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  • (PMID = 17333331.001).
  • [ISSN] 0006-2928
  • [Journal-full-title] Biochemical genetics
  • [ISO-abbreviation] Biochem. Genet.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / G12 RR 03641-12; United States / NIGMS NIH HHS / GM / GM 61151
  • [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 / Codon; EC 1.1.1.1 / Alcohol Dehydrogenase
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37. Belokon' SV, Khaystova ND, Totskiĭ VN: [Locus Adh and adaptation of cn and vg mutants in the experimental populations of Drosophila melanogaster Meig]. Tsitol Genet; 2007 Mar-Apr;41(2):24-9
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  • [Title] [Locus Adh and adaptation of cn and vg mutants in the experimental populations of Drosophila melanogaster Meig].
  • Complex study of adaptation and allozyme belonging of alcoholdehydrogenase (ADH) in cn and vg mutants has been carried out in the initial pure lines, in their panmixia populations and in condition of substitution of the mutant genotype by saturating crossings.
  • It was shown that the high level of adaptation of cn mutants and the low level of adaptation of vg mutants was combined with the presence of different ADH allozymes.
  • During the saturating crossings the reliable coadaptation of the genes cn and Adh(S) as well as vg and Adh(F) was detected that confirmes the postulated earlier conception of gene adaptation complexes.

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  • (PMID = 17494340.001).
  • [ISSN] 0564-3783
  • [Journal-full-title] T︠S︡itologii︠a︡ i genetika
  • [ISO-abbreviation] Tsitol. Genet.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Drosophila Proteins; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.1 / ADH protein, Drosophila; EC 1.1.1.1 / Alcohol Dehydrogenase
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38. Garabagi F, Duns G, Strommer J: Selective recruitment of Adh genes for distinct enzymatic functions in Petunia hybrida. Plant Mol Biol; 2005 May;58(2):283-94
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  • [Title] Selective recruitment of Adh genes for distinct enzymatic functions in Petunia hybrida.
  • Alcohol dehydrogenase (ADH) activity in plants is generally associated with glycolytic fermentation, which facilitates cell survival during episodes of low-oxygen stress in water-logged roots as well as chronically hypoxic regions surrounding the vascular core.
  • Work with tobacco and potato has implicated ADH activity in additional metabolic roles, including aerobic fermentation, acetaldehyde detoxification and carbon reutilization.
  • Here a combination of approaches has been used to examine tissue-specific patterns of Adh gene expression in order to provide insight into the potential roles of alcohol dehydrogenases, using Petunia hybrida, a solanaceous species with well-characterized genetics.
  • Results of GC-MS analysis suggest the association of ADH with production of aromatic compounds in the nectary.
  • Overall the results demonstrate selective recruitment of Adh gene family members in tissues and organs associated with diverse ADH functions.

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  • [Cites] Genetics. 1993 Apr;133(4):999-1007 [8096485.001]
  • [Cites] Microbiology. 1994 Mar;140 ( Pt 3):601-10 [8012582.001]
  • [Cites] Biochem Genet. 1974 Nov;12(5):407-17 [4461035.001]
  • [Cites] Plant Physiol. 1997 Feb;113(2):397-402 [12223614.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2122-7 [9122158.001]
  • [Cites] Gene. 2000 Mar 21;245(2):299-309 [10717481.001]
  • [Cites] Biochem Genet. 2004 Jun;42(5-6):199-208 [15260144.001]
  • [Cites] Plant Cell. 1990 Apr;2(4):279-289 [12354959.001]
  • [Cites] J Bacteriol. 1996 Jan;178(1):301-5 [8550434.001]
  • [Cites] Planta. 1966 Mar;71(1):98-106 [24553992.001]
  • [Cites] Plant Mol Biol. 1991 Jul;17(1):37-48 [1678286.001]
  • [Cites] Plant Physiol. 1991 Aug;96(4):1294-301 [16668333.001]
  • [Cites] Plant Mol Biol. 1995 Jul;28(4):739-50 [7647304.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Plant Physiol. 1998 Jul;117(3):1047-58 [9662548.001]
  • [Cites] Plant Mol Biol. 1997 Oct;35(3):343-54 [9349258.001]
  • (PMID = 16027979.001).
  • [ISSN] 0167-4412
  • [Journal-full-title] Plant molecular biology
  • [ISO-abbreviation] Plant Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Plant Proteins; 0 / Recombinant Fusion Proteins; 147336-22-9 / Green Fluorescent Proteins; EC 1.1.1.1 / Alcohol Dehydrogenase
  •  go-up   go-down


39. Chase JR, Poolman MG, Fell DA: Contribution of NADH increases to ethanol's inhibition of retinol oxidation by human ADH isoforms. Alcohol Clin Exp Res; 2009 Apr;33(4):571-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Contribution of NADH increases to ethanol's inhibition of retinol oxidation by human ADH isoforms.
  • One molecular mechanism, competitive inhibition by ethanol of the catalytic activity of human alcohol dehydrogenase (EC 1.1.1.1) (ADH) on all-trans-retinol oxidation has been shown for the ADH7 isoform.
  • Ethanol metabolism also causes an increase in the free reduced nicotinamide adenine dinucleotide (NADH) in cells, which might reasonably be expected to decrease the retinol oxidation rate by product inhibition of ADH isoforms.
  • (1) ADH oxidation of ethanol and NAD(+), (2) ADH oxidation of retinol and NAD(+), (3) oxidation of ethanol by a generalized Ethanol(oxidase) that uses NAD(+), (4) NADH(oxidase) which carries out NADH turnover.
  • RESULTS: Using the metabolic modeling package ScrumPy, we have shown that the ethanol-induced increase in NADH contributes from 0% to 90% of the inhibition by ethanol, depending on (ethanol) and ADH isoform.
  • Furthermore, while the majority of flux control of retinaldehyde production is exerted by ADH, Ethanol(oxidase) and the NADH(oxidase) contribute as well.

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  • [Cites] FASEB J. 1996 Jul;10(9):1050-7 [8801166.001]
  • [Cites] FASEB J. 1996 Jul;10(9):993-1001 [8801182.001]
  • [Cites] FEBS Lett. 1998 Apr 24;426(3):362-6 [9600267.001]
  • [Cites] Eur J Biochem. 1998 May 15;254(1):25-31 [9652389.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Aug 10;249(1):191-6 [9705855.001]
  • [Cites] Biochem Pharmacol. 1999 Apr 1;57(7):811-21 [10075087.001]
  • [Cites] Am J Clin Nutr. 1999 Jun;69(6):1071-85 [10357725.001]
  • [Cites] J Biol Chem. 1999 Jun 11;274(24):16796-801 [10358022.001]
  • [Cites] Biochem Pharmacol. 1999 Aug 1;58(3):389-95 [10424757.001]
  • [Cites] Biochim Biophys Acta. 1999 Sep 22;1440(2-3):139-62 [10521699.001]
  • [Cites] Alcohol. 2005 Apr;35(3):251-8 [16054987.001]
  • [Cites] Clin Biochem. 1999 Oct;32(7):585-9 [10614722.001]
  • [Cites] Gut. 2000 Dec;47(6):825-31 [11076882.001]
  • [Cites] Chem Biol Interact. 2001 Jan 30;130-132(1-3):445-56 [11306066.001]
  • [Cites] Alcohol Clin Exp Res. 2001 May;25(5 Suppl ISBRA):207S-217S [11391073.001]
  • [Cites] Alcohol Clin Exp Res. 2006 Jul;30(7):1132-42 [16792560.001]
  • [Cites] Biochem J. 2006 Oct 1;399(1):101-9 [16787387.001]
  • [Cites] Syst Biol (Stevenage). 2006 Sep;153(5):375-8 [16986321.001]
  • [Cites] Cell Mol Life Sci. 2007 Feb;64(4):498-505 [17279314.001]
  • [Cites] Carcinogenesis. 2001 Aug;22(8):1213-9 [11470752.001]
  • [Cites] Eur J Biochem. 2001 Oct;268(19):5045-56 [11589695.001]
  • [Cites] Cell Mol Life Sci. 2002 Mar;59(3):552-9 [11964133.001]
  • [Cites] J Biol Chem. 2002 Jun 21;277(25):22553-7 [11960985.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):25209-16 [11997393.001]
  • [Cites] J Nutr. 2003 Jan;133(1):287S-290S [12514311.001]
  • [Cites] Chem Biol Interact. 2003 Feb 1;143-144:219-27 [12604207.001]
  • [Cites] Med Sci Monit. 2003 Dec;9(12):BR403-6 [14646967.001]
  • [Cites] Am J Epidemiol. 2004 Jan 1;159(1):1-16 [14693654.001]
  • [Cites] Eur J Biochem. 2004 May;271(9):1660-70 [15096205.001]
  • [Cites] Arch Biochem Biophys. 2004 Oct 15;430(2):210-7 [15369820.001]
  • [Cites] Exp Mol Pathol. 1971 Oct;15(2):148-56 [4398759.001]
  • [Cites] Biochem J. 1972 Apr;127(2):387-97 [4342558.001]
  • [Cites] Biochemistry. 1983 Apr 12;22(8):1852-7 [6342668.001]
  • [Cites] Biochemistry. 1983 Apr 12;22(8):1857-63 [6342669.001]
  • [Cites] Biochemistry. 1984 Nov 20;23(24):5847-53 [6395883.001]
  • [Cites] Biochemistry. 1984 Dec 18;23(26):6822-8 [6397229.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Aug;82(15):4979-82 [3161078.001]
  • [Cites] Biochem Biophys Res Commun. 1987 Aug 14;146(3):1127-33 [3619918.001]
  • [Cites] Biochem Pharmacol. 1989 Oct 15;38(20):3573-81 [2818646.001]
  • [Cites] Biochemistry. 1989 Aug 22;28(17):6810-5 [2819035.001]
  • [Cites] J Biol Chem. 1991 Jan 15;266(2):1128-33 [1985938.001]
  • [Cites] Alcohol Clin Exp Res. 1991 Jun;15(3):565-7 [1877745.001]
  • [Cites] Alcohol Clin Exp Res. 1991 Jun;15(3):568-72 [1877746.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Jun;18(3):587-91 [7943659.001]
  • [Cites] J Biol Chem. 1995 Feb 24;270(8):3625-30 [7876099.001]
  • [Cites] Alcohol. 1998 Feb;15(2):147-60 [9476961.001]
  • (PMID = 19183134.001).
  • [ISSN] 1530-0277
  • [Journal-full-title] Alcoholism, clinical and experimental research
  • [ISO-abbreviation] Alcohol. Clin. Exp. Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR016454; United States / NCRR NIH HHS / RR / RR016454-066706; United States / NCRR NIH HHS / RR / P20 RR016454-066706; United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Isoenzymes; 0U46U6E8UK / NAD; 11103-57-4 / Vitamin A; 3K9958V90M / Ethanol; 5688UTC01R / Tretinoin; EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Other-IDs] NLM/ NIHMS207854; NLM/ PMC2884996
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40. van Beek JH, Willemsen G, de Moor MH, Hottenga JJ, Boomsma DI: Associations between ADH gene variants and alcohol phenotypes in Dutch adults. Twin Res Hum Genet; 2010 Feb;13(1):30-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Associations between ADH gene variants and alcohol phenotypes in Dutch adults.
  • Recently, Macgregor et al. (2009) demonstrated significant associations of ADH polymorphisms with reactions to alcohol and alcohol consumption measures in an Australian sample.
  • SNPs in the ADH gene cluster located on chromosome 4q (n = 491) were subdivided in seven gene sets: ADH5, ADH4, ADH6, ADH1A, ADH1B, ADH1C and ADH7.
  • Although these findings do not replicate the earlier findings at the SNP level, the results confirm the role of the ADH gene cluster in alcohol phenotypes.

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  • (PMID = 20158305.001).
  • [ISSN] 1832-4274
  • [Journal-full-title] Twin research and human genetics : the official journal of the International Society for Twin Studies
  • [ISO-abbreviation] Twin Res Hum Genet
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / R01 MH059160
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Twin Study
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / ADH7 protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase
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41. Ma L, Xue Y, Liu Y, Wang Z, Cui X, Li P, Fu S: Polymorphism study of seven SNPs at ADH genes in 15 Chinese populations. Hereditas; 2005 Feb;142(2005):103-11

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphism study of seven SNPs at ADH genes in 15 Chinese populations.
  • It has been shown that the variants of alcohol dehydrogenase (ADH) genes exhibit great diversities among various populations and are associated with susceptibility to alcoholism.
  • To investigate the distribution of SNPs at ADH genes in Chinese populations and the genetic relationship of these groups, we collected 467 individuals from 15 groups distributing widely from north to south in China and genotyped 7 SNPs at ADH genes respectively.
  • (2) haplotypes constructed with ADH SNPs could be used as markers to discern different populations in China, and six-allele haplotype "221211" was the most common one defined in present study;.
  • (3) on the basis of SNPs analysis of ADH genes, the 15 populations were grouped into northern groups and southern groups.

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  • (PMID = 16970620.001).
  • [ISSN] 1601-5223
  • [Journal-full-title] Hereditas
  • [ISO-abbreviation] Hereditas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Sweden
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase
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42. Ren J: Acetaldehyde and alcoholic cardiomyopathy: lessons from the ADH and ALDH2 transgenic models. Novartis Found Symp; 2007;285:69-76; discussion 76-9, 198-9
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  • [Title] Acetaldehyde and alcoholic cardiomyopathy: lessons from the ADH and ALDH2 transgenic models.
  • To explore the role of acetaldehyde in alcoholic cardiomyopathy, we generated transgenic mice with overexpression of the alcohol-metabolizing enzyme alcohol dehydrogenase (ADH) and the acetaldehyde-metabolizing enzyme mitochondrial aldehyde dehydrogenase (ALDH2), driven by myosin heavy chain and chicken beta-actin promoters, respectively.
  • Strikingly, ADH exaggerated whereas ALDH2 attenuated alcohol-induced mechanical and intracellular Ca2+ defects, oxidative stress, lipid peroxidation and protein damage.

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  • (PMID = 17590987.001).
  • [ISSN] 1528-2511
  • [Journal-full-title] Novartis Foundation symposium
  • [ISO-abbreviation] Novartis Found. Symp.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR15640; United States / NIAAA NIH HHS / AA / R01 AA13412; United States / NIAAA NIH HHS / AA / R15 AA13575-01; United States / NCRR NIH HHS / RR / RR-16474
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase; GO1N1ZPR3B / Acetaldehyde; SY7Q814VUP / Calcium
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43. Trcek J, Toyama H, Czuba J, Misiewicz A, Matsushita K: Correlation between acetic acid resistance and characteristics of PQQ-dependent ADH in acetic acid bacteria. Appl Microbiol Biotechnol; 2006 Apr;70(3):366-73
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  • [Title] Correlation between acetic acid resistance and characteristics of PQQ-dependent ADH in acetic acid bacteria.
  • In this study, we compared the growth properties and molecular characteristics of pyrroloquinoline quinone (PQQ)-dependent alcohol dehydrogenase (ADH) among highly acetic acid-resistant strains of acetic acid bacteria.
  • PQQ-dependent ADH activity was twice as high in Ga. europaeus and Ga. intermedius as in A. pasteurinus.
  • These results suggest that high ADH activity in the Ga. europaeus cells and high acetic acid stability of the purified enzyme represent two of the unique features that enable this species to grow and stay metabolically active at extremely high concentrations of acetic acid.

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  • (PMID = 16133326.001).
  • [ISSN] 0175-7598
  • [Journal-full-title] Applied microbiology and biotechnology
  • [ISO-abbreviation] Appl. Microbiol. Biotechnol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AJ888874
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Culture Media; 72909-34-3 / PQQ Cofactor; EC 1.1.1.1 / Alcohol Dehydrogenase; Q40Q9N063P / Acetic Acid
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44. Jelski W, Szmitkowski M: Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in the cancer diseases. Clin Chim Acta; 2008 Sep;395(1-2):1-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in the cancer diseases.
  • Ethanol is metabolized to acetaldehyde by alcohol dehydrogenase (ADH).
  • Moreover the activity of ADH is much higher than the activity of ALDH.
  • In addition significant differences of ADH isoenzymes activities between cancer tissues and healthy organs may be a factor intensifying carcinogenesis by the increased ability to acetaldehyde formation from ethanol and disorders in metabolism of some biologically important substances (e.g. retinoic acid).
  • The changes in activity of particular ADH isoenzymes in the sera of patients with different cancers, seem to be caused by release of these isoenzymes from cancer cells, and may be useful for diagnostics of this cancer.
  • The particular isoenzymes of ADH present in the serum may indicate the cancer localization.

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  • (PMID = 18505683.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Isoenzymes; 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase; GO1N1ZPR3B / Acetaldehyde
  • [Number-of-references] 50
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45. Fukuda T, Yokoyama J, Nakamura T, Song IJ, Ito T, Ochiai T, Kanno A, Kameya T, Maki M: Molecular phylogeny and evolution of alcohol dehydrogenase (Adh) genes in legumes. BMC Plant Biol; 2005;5:6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular phylogeny and evolution of alcohol dehydrogenase (Adh) genes in legumes.
  • The aim of our study is to isolate the alcohol dehydrogenase (Adh) genes in two distantly related legumes, and use these sequences to examine the molecular evolutionary history of this nuclear gene.
  • RESULTS: We isolated the expressed Adh genes from two species of legumes, Sophora flavescens Ait. and Wisteria floribunda DC., by a RT-PCR based approach and found a new Adh locus in addition to homologues of the Adh genes found previously in legumes.
  • To examine the evolution of these genes, we compared the species and gene trees and found gene duplication of the Adh loci in the legumes occurred as an ancient event.
  • CONCLUSION: This is the first report revealing that some legume species have at least two Adh gene loci belonging to separate clades.

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  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10274-9 [8816790.001]
  • [Cites] Mol Biol Evol. 1999 Aug;16(8):1086-97 [10474904.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11735-9 [8876206.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13020-3 [8917537.001]
  • [Cites] Genetics. 1997 Jul;146(3):1131-41 [9215914.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):7791-8 [9223265.001]
  • [Cites] Mol Biol Evol. 1997 Oct;14(10):994-1007 [9335140.001]
  • [Cites] Nucleic Acids Res. 1997 Dec 15;25(24):4876-82 [9396791.001]
  • [Cites] Mol Biol Evol. 1998 May;15(5):552-9 [9580984.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 12;95(10):5637-42 [9576936.001]
  • [Cites] Bioessays. 1998 Oct;20(10):785-8 [10200118.001]
  • [Cites] Science. 1999 Oct 29;286(5441):947-50 [10542147.001]
  • [Cites] Nature. 1999 Nov 25;402(6760):404-7 [10586879.001]
  • [Cites] Plant Mol Biol. 2000 Jan;42(1):115-49 [10688133.001]
  • [Cites] Genetics. 2000 Aug;155(4):1913-26 [10924485.001]
  • [Cites] Science. 2000 Nov 10;290(5494):1151-5 [11073452.001]
  • [Cites] Mol Biol Evol. 2001 Feb;18(2):164-71 [11158375.001]
  • [Cites] Trends Genet. 2001 May;17(5):237-9 [11335019.001]
  • [Cites] J Mol Evol. 2003 Nov;57(5):588-97 [14738317.001]
  • [Cites] Nature. 2004 Jul 1;430(6995):35-44 [15229592.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1408-12 [2937058.001]
  • [Cites] J Biol Chem. 1987 Jun 15;262(17):8367-76 [3036811.001]
  • [Cites] J Mol Biol. 1987 May 5;195(1):115-23 [3309331.001]
  • [Cites] Plant Mol Biol. 1994 Oct;26(2):643-55 [7948919.001]
  • [Cites] Plant Physiol. 1994 Aug;105(4):1075-87 [7972489.001]
  • [Cites] Genetics. 1996 Aug;143(4):1761-70 [8844162.001]
  • (PMID = 15836788.001).
  • [ISSN] 1471-2229
  • [Journal-full-title] BMC plant biology
  • [ISO-abbreviation] BMC Plant Biol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB191334/ AB191335/ AB191336/ AB191337/ AB191338/ AB191339
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Other-IDs] NLM/ PMC1112602
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46. Kowalczyk A, Puchała M, Wesołowska K, Serafin E: Inactivation of alcohol dehydrogenase (ADH) by ferryl derivatives of human hemoglobin. Biochim Biophys Acta; 2007 Jan;1774(1):86-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inactivation of alcohol dehydrogenase (ADH) by ferryl derivatives of human hemoglobin.
  • In this paper, inactivation of alcohol dehydrogenase (ADH) by products of reactions of H2O2 with metHb has been studied.
  • In the first system H2O2 was added to the mixture of metHb and ADH [the (metHb+ADH)+H2O2] system (ADH was present in the system since the moment of addition of H2O2 i. e. since the very beginning of the reaction of metHb with H2O2).
  • In the second system ADH was added to the system 5 min after the initiation of the reaction of H2O2 with metHb [the (metHb+H2O2)5 min+ADH] system.
  • ADH inactivation was observed in both system.
  • Hydrogen peroxide alone did not inactivate ADH at the concentrations employed evidencing that enzyme inactivation was due exclusively to products of reaction of H2O2 with metHb.
  • The rate and extent of ADH inactivation were much higher in the first than in the second system.
  • The dependence of ADH activity on the time of incubation with ferryl derivatives of Hb can be described by a sum of three exponentials in the first system and two exponentials in the second system.

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  • (PMID = 17185051.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 9008-37-1 / Methemoglobin; BBX060AN9V / Hydrogen Peroxide; EC 1.1.1.1 / Alcohol Dehydrogenase
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47. Zhang X, Dong F, Li Q, Borgerding AJ, Klein AL, Ren J: Cardiac overexpression of catalase antagonizes ADH-associated contractile depression and stress signaling after acute ethanol exposure in murine myocytes. J Appl Physiol (1985); 2005 Dec;99(6):2246-54
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardiac overexpression of catalase antagonizes ADH-associated contractile depression and stress signaling after acute ethanol exposure in murine myocytes.
  • Alcohol dehydrogenase (ADH), which oxidizes ethanol into acetaldehyde, exacerbates ethanol-induced cardiac depression, although the mechanism of action remains unclear.
  • ADH-CAT double transgenic mice were generated by crossing CAT and ADH lines.
  • ADH-CAT, ADH, CAT and wild-type FVB myocytes exhibited similar mechanical and intracellular Ca(2+) properties.
  • ADH or ADH-CAT myocytes had higher acetaldehyde-producing ability.
  • Ethanol-induced depression on cell shortening and intracellular Ca(2+) was augmented in ADH group with maximal inhibitions of 66.8 and 69.6%, respectively.
  • Interestingly, myocytes from CAT-ADH mice displayed normal ethanol response with maximal inhibitions of 46.0 and 47.2% for cell shortening and intracellular Ca(2+), respectively.
  • ADH amplified ethanol-induced reactive oxygen species generation, which was nullified by the CAT transgene.
  • The ethanol-induced changes in phosphorylation of ERK and JNK were amplified by ADH.
  • CAT transgene itself did not affect ethanol-induced response in ERK and JNK phosphorylation, but it cancelled ADH-induced effects.
  • These data suggest that antioxidant CAT may effectively antagonize ADH-induced enhanced cardiac depression in response to ethanol.

  • Hazardous Substances Data Bank. ETHANOL .
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  • (PMID = 16109828.001).
  • [ISSN] 8750-7587
  • [Journal-full-title] Journal of applied physiology (Bethesda, Md. : 1985)
  • [ISO-abbreviation] J. Appl. Physiol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR-15640; United States / NIAAA NIH HHS / AA / R15 AA-13575-201; United States / NCRR NIH HHS / RR / RR-16474
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.11.1.6 / Catalase
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48. Ehlers CL: Variations in ADH and ALDH in Southwest California Indians. Alcohol Res Health; 2007;30(1):14-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variations in ADH and ALDH in Southwest California Indians.
  • Researchers have analyzed the frequencies of variants in the alcohol-metabolizing enzymes alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in some Native American populations.

  • MedlinePlus Health Information. consumer health - Alcoholism and Alcohol Abuse.
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  • [Cites] Alcohol Clin Exp Res. 2001 Dec;25(12):1773-7 [11781511.001]
  • [Cites] Alcohol Clin Exp Res. 2007 Feb;31(2):216-20 [17250612.001]
  • [Cites] J Stud Alcohol. 2003 Mar;64(2):176-81 [12713190.001]
  • [Cites] Hum Genet. 2003 Sep;113(4):325-36 [12884000.001]
  • [Cites] Alcohol Clin Exp Res. 2003 Sep;27(9):1389-94 [14506398.001]
  • [Cites] Ann Hum Genet. 2004 Mar;68(Pt 2):93-109 [15008789.001]
  • [Cites] Am J Psychiatry. 2004 Jul;161(7):1204-10 [15229052.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2004 Aug 15;129B(1):110-5 [15274051.001]
  • [Cites] N Engl J Med. 1976 Jan 1;294(1):9-13 [1244489.001]
  • [Cites] Alcohol Clin Exp Res. 1992 Oct;16(5):991-5 [1443441.001]
  • [Cites] Alcohol. 1995 Mar-Apr;12(2):163-7 [7772269.001]
  • [Cites] Alcohol Alcohol. 1997 Sep-Oct;32(5):613-9 [9373704.001]
  • [Cites] Alaska Med. 1999 Jan-Mar;41(1):9-12, 23 [10224678.001]
  • [Cites] Alcohol Clin Exp Res. 2004 Oct;28(10):1481-6 [15597079.001]
  • [Cites] Am J Psychiatry. 2003 Jan;160(1):41-6 [12505800.001]
  • (PMID = 17718395.001).
  • [ISSN] 1535-7414
  • [Journal-full-title] Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism
  • [ISO-abbreviation] Alcohol Res Health
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / R01 AA010201; United States / NIAAA NIH HHS / AA / R37 AA010201; United States / NIAAA NIH HHS / AA / AA10201
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AVP protein, human; 0 / Neurophysins; 0 / Protein Precursors; 11000-17-2 / Vasopressins; EC 1.1.1.1 / ADH1B protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  • [Number-of-references] 16
  • [Other-IDs] NLM/ PMC3860438
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49. Ogueta M, Cibik O, Eltrop R, Schneider A, Scholz H: The influence of Adh function on ethanol preference and tolerance in adult Drosophila melanogaster. Chem Senses; 2010 Nov;35(9):813-22
Hazardous Substances Data Bank. ETHANOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The influence of Adh function on ethanol preference and tolerance in adult Drosophila melanogaster.
  • We also investigated whether Drosophila preference, sensitivity and tolerance to ethanol was related to the activity of alcohol dehydrogenase (Adh), the primary ethanol-metabolizing enzyme in D. melanogaster.
  • Impaired Adh function reduced ethanol preference in both D. melanogaster and a related species, D. sechellia.
  • Adh-impaired flies also displayed reduced aversion to high ethanol concentrations, increased sensitivity to the effects of ethanol on postural control, and negative tolerance/sensitization (i.e., a reduction of the increased resistance to ethanol's effects that normally occurs upon repeated exposure).
  • These data strongly indicate a linkage between ethanol-induced behavior and ethanol metabolism in adult fruit flies: Adh deficiency resulted in reduced preference to low ethanol concentrations and reduced aversion to high ones, despite recovery from ethanol being strongly impaired.

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  • (PMID = 20739429.001).
  • [ISSN] 1464-3553
  • [Journal-full-title] Chemical senses
  • [ISO-abbreviation] Chem. Senses
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alcohols; 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase
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50. Barzegar A, Moosavi-Movahedi AA, Mahnam K, Ashtiani SH: Chaperone-like activity of alpha-cyclodextrin via hydrophobic nanocavity to protect native structure of ADH. Carbohydr Res; 2010 Jan 26;345(2):243-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chaperone-like activity of alpha-cyclodextrin via hydrophobic nanocavity to protect native structure of ADH.
  • The chaperone action of alpha-cyclodextrin (alpha-CyD), based on providing beneficial microenvironment of hydrophobic nanocavity to form molecular complex with alcohol dehydrogenase (ADH) was examined by experimental and computational techniques.
  • The results of UV-vis and dynamic light scattering (DLS) indicated that the chaperone-like activity of alpha-CyD depends on molecular complex formation between alpha-CyD and ADH, which caused to decrease the amount and size of polymerized molecules.
  • Computational calculations of molecular dynamic (MD) simulations and blind docking (BD) demonstrated that alpha-CyD acts as an artificial chaperone because of its high affinity to the region of ADH's two chains interface.
  • Delocalization of ADH subunits, which causes the exposure of Phe110, takes part in the enzyme polymerization and has proven to be beneficial for aggregation inhibition and solubility enhancement within the host alpha-CyD-nanocavity.

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19963209.001).
  • [ISSN] 1873-426X
  • [Journal-full-title] Carbohydrate research
  • [ISO-abbreviation] Carbohydr. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ligands; 0 / Molecular Chaperones; 0 / alpha-Cyclodextrins; EC 1.1.1.1 / Alcohol Dehydrogenase
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51. Ozsoy ED: Distinct electrophoretic polymorphism pattern at alcohol dehydrogenase (Adh) locus of Drosophila melanogaster natural populations from Turkey. Genetika; 2007 Feb;43(2):189-93
FlyBase. FlyBase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct electrophoretic polymorphism pattern at alcohol dehydrogenase (Adh) locus of Drosophila melanogaster natural populations from Turkey.
  • Populations sampled were electrophoresed for a single locus, alcohol dehydrogenase (Adh) to assess population differentiation.
  • Ryear, seems to track this Adh genetic variation pattern.
  • The study also shows that a typical pattern of geographical Adh polymorphism can emerge with a handfull of populations sampled across a relatively small distance.

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  • (PMID = 17385317.001).
  • [ISSN] 0016-6758
  • [Journal-full-title] Genetika
  • [ISO-abbreviation] Genetika
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase
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52. Widmayer MA, Browning JL, Gopinath SP, Robertson CS, Baskin DS: Increased intracranial pressure is associated with elevated cerebrospinal fluid ADH levels in closed-head injury. Neurol Res; 2010 Dec;32(10):1021-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased intracranial pressure is associated with elevated cerebrospinal fluid ADH levels in closed-head injury.
  • Investigators have demonstrated that ischemic injury causes an increase in cerebrospinal fluid (CSF) levels of antidiuretic hormone (ADH); increased CSF ADH levels exacerbate cerebral edema, and inhibition of the ADH system with specific ADH antagonists reduces cerebral edema.
  • The current study was designed to test the hypothesis that elevated levels of ADH are present in the CSF of subjects with head injury.
  • ADH levels were analyzed using radioimmunoassay.
  • RESULTS: Subjects with head injury had higher CSF (3.2 versus 1.2 pg/ml; P<0.02) and plasma (4.1 versus 1.4 pg/ml; P<0.02) levels of ADH than did control subjects.
  • In head-injured subjects, CSF ADH levels positively correlated with severity of ICP.
  • DISCUSSION: The results of this study suggest that ADH plays a role in brain edema associated with closed head injury.

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  • (PMID = 20810023.001).
  • [ISSN] 1743-1328
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA78912
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AVP protein, human; 0 / Neurophysins; 0 / Protein Precursors; 11000-17-2 / Vasopressins
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53. Jelski W, Chrostek L, Laszewicz W, Szmitkowski M: Alcohol dehydrogenase (ADH) isoenzyme activity in the sera of patients with Helicobacter pylori infection. Dig Dis Sci; 2007 Jun;52(6):1513-6
MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol dehydrogenase (ADH) isoenzyme activity in the sera of patients with Helicobacter pylori infection.
  • Human gastric mucosa contains three classes of alcohol dehydrogenase (ADH) isoenzymes: I, III, and IV.
  • Various factors have been found to influence gastric ADH activity.
  • One of them is Helicobacter pylori infection, which is associated with gastric mucosal injury and leads to a decrease in gastric ADH activity.
  • The aim of the study was to assess the effect of H. pylori infection on the serum activity of ADH isoenzymes.
  • The activities of class III and IV ADH isoenzymes were measured by the photometric method with formaldehyde and with m-nitrobenzaldehyde as substrate, respectively.
  • Total activity of ADH was measured by a photometric method with p-nitrosodimethylaniline.
  • The total activities of ADH and class IV isoenzyme were significantly higher in sera of patients with H. pylori infection compared to healthy subjects.
  • The serum activity of other tested isoenzymes of ADH did not differ significantly between infected and noninfected groups.
  • We conclude that H. pylori infection of gastric mucosa is reflected in the serum by a significant increase in class IV and total ADH activity.

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  • [Cites] Alcohol Clin Exp Res. 1993 Dec;17(6):1337-44 [8116851.001]
  • [Cites] Gut. 1993 Oct;34(10):1433-7 [8244116.001]
  • [Cites] FEBS Lett. 1989 Oct 23;257(1):105-9 [2806555.001]
  • [Cites] Alcohol Clin Exp Res. 1990 Dec;14(6):946-50 [1982399.001]
  • [Cites] Anal Biochem. 1989 Apr;178(1):57-62 [2729580.001]
  • [Cites] N Engl J Med. 1990 Jan 11;322(2):95-9 [2248624.001]
  • [Cites] Anal Biochem. 1979 Oct 15;99(1):65-71 [231394.001]
  • [Cites] Life Sci. 1991;49(25):1929-34 [1745108.001]
  • [Cites] Digestion. 2002;66(1):14-8 [12379810.001]
  • [Cites] Alcohol Alcohol. 1994 Nov;29(6):663-71 [7695781.001]
  • [Cites] J Clin Lab Anal. 2003;17(3):93-6 [12696080.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Dec;18(6):1294-9 [7695020.001]
  • [Cites] Clin Sci (Lond). 2006 Mar;110(3):305-14 [16464172.001]
  • [Cites] Digestion. 1998 Jul-Aug;59(4):314-20 [9693201.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Apr;25(4):508-12 [11329489.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Jun;25(6 Suppl):29S-34S [11410738.001]
  • [Cites] Alcohol Alcohol. 1997 Sep-Oct;32(5):543-9 [9373695.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Aug;18(4):795-8 [7978087.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Dec;20(9):1569-76 [8986205.001]
  • [Cites] J Gastroenterol Hepatol. 1991 May-Jun;6(3):209-22 [1912431.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Sep;289(3):G429-33 [15860641.001]
  • [Cites] Dig Dis Sci. 2002 Jul;47(7):1554-7 [12141816.001]
  • [Cites] J Biol Chem. 1991 Jan 15;266(2):1128-33 [1985938.001]
  • (PMID = 17404875.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase
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54. Ohsako T, Matsuoka G: Nucleotide sequence variability of the Adh gene of the coastal plant Calystegia soldanella (Convolvulaceae) in Japan. Genes Genet Syst; 2008 Feb;83(1):89-94

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nucleotide sequence variability of the Adh gene of the coastal plant Calystegia soldanella (Convolvulaceae) in Japan.
  • To clarify the genetic differentiation among local populations, we investigated the nucleotide sequence variability of the Adh gene.
  • In a 1625-bp sequence between exon 2 and the 3' noncoding region of the Adh gene, a total of 44 polymorphic sites were found among 91 individuals from 19 populations.

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  • (PMID = 18379137.001).
  • [ISSN] 1341-7568
  • [Journal-full-title] Genes & genetic systems
  • [ISO-abbreviation] Genes Genet. Syst.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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55. Liu Q, Zhang N, Li L, Liu J: Identification of Elymus (Triticeae, Poaceae) and its related genera genomes by RFLP analysis of PCR-amplified Adh genes. Mol Biol Rep; 2010 Oct;37(7):3249-57

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of Elymus (Triticeae, Poaceae) and its related genera genomes by RFLP analysis of PCR-amplified Adh genes.
  • Here we describe a restriction fragment length polymorphism (RFLP) assay based on digesting alcohol dehydrogenase (Adh) amplicons with two restriction enzyme combinations, EcoRI-HindIII and EcoRI-PstI, which easily can be used to distinguish Elymus and its closely related genera genomes.
  • (1) amplifying nuclear Adh genes with universal primers;.
  • (3) the EcoRI-HindIII combination was effective to distinguish different Adh gene types (Adh1, Adh2, and Adh3);.

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  • [Cites] Theor Appl Genet. 1995 Jun;90(7-8):1035-41 [24173059.001]
  • [Cites] Genome. 1993 Feb;36(1):147-51 [18469977.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):531-6 [11149938.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14400-5 [10588717.001]
  • [Cites] New Phytol. 2006;170(2):411-20 [16608465.001]
  • [Cites] Genome. 2001 Dec;44(6):1136-42 [11768218.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1398-402 [11607153.001]
  • [Cites] Plant Mol Biol. 2007 Aug;64(6):645-55 [17551673.001]
  • [Cites] Theor Appl Genet. 1995 Dec;91(8):1222-36 [24170050.001]
  • [Cites] Mol Phylogenet Evol. 2008 Mar;46(3):897-907 [18262439.001]
  • (PMID = 19885741.001).
  • [ISSN] 1573-4978
  • [Journal-full-title] Molecular biology reports
  • [ISO-abbreviation] Mol. Biol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase
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56. McEwan NR: Codon utilization, DNA landscaping and fractal analysis in bacteriophage phi(adh). Acta Virol; 2005;49(3):169-76
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  • [Title] Codon utilization, DNA landscaping and fractal analysis in bacteriophage phi(adh).
  • The bacteriophage phi(adh) has a low G+C content and encodes its protein products using a restricted number of the codons, which it could theoretically use.

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  • (PMID = 16178514.001).
  • [ISSN] 0001-723X
  • [Journal-full-title] Acta virologica
  • [ISO-abbreviation] Acta Virol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Amino Acids; 0 / DNA, Viral
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57. Guo KK, Ren J: Cardiac overexpression of alcohol dehydrogenase (ADH) alleviates aging-associated cardiomyocyte contractile dysfunction: role of intracellular Ca2+ cycling proteins. Aging Cell; 2006 Jun;5(3):259-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardiac overexpression of alcohol dehydrogenase (ADH) alleviates aging-associated cardiomyocyte contractile dysfunction: role of intracellular Ca2+ cycling proteins.
  • Aging is a complex biological process with contributions from a wide variety of genes including insulin-like growth factor I and alcohol dehydrogenase (ADH), which decline with advanced age.
  • The goal of this study was to examine if ADH enzyme plays any role in cardiac aging.
  • Ventricular myocytes were isolated from young (2-3 months old) or aged (26-28 months old) male FVB wild-type and cardiac-specific ADH (class I, isozyme type 1) transgenic mice.
  • Aged FVB myocytes displayed significantly reduced ADH activity compared with young ones, which was restored by the ADH transgene.
  • Although ADH transgene itself did not alter mechanical properties in young mice, it rescued aging-associated diastolic dysfunction without affecting dampened contractile response to high stimulus frequency.
  • ADH transgene prevented aging-induced reduction in SERCA2a and NCX without affecting up-regulated phospholamban.
  • Our data suggest that aging is associated with a reduced ADH enzymatic activity and diastolic dysfunction, which may be corrected with cardiac overexpression of the ADH enzyme.
  • Alteration in cardiac Ca(2+) cycling proteins including SERCA2a and NCX may play a role in both pathogenesis of cardiac aging and the beneficial effect of ADH enzyme.

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  • (PMID = 16842498.001).
  • [ISSN] 1474-9718
  • [Journal-full-title] Aging cell
  • [ISO-abbreviation] Aging Cell
  • [Language] eng
  • [Grant] United States / NIAAA NIH HHS / AA / 1R15AA/HL13575-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Calcium-Binding Proteins; 0 / Sodium-Calcium Exchanger; 0 / phospholamban; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 3.6.3.8 / Calcium-Transporting ATPases; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium
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58. Ramanathan P, Guo J, Whitehead RN, Brogna S: The intergenic spacer of the Drosophila Adh-Adhr dicistronic mRNA stimulates internal translation initiation. RNA Biol; 2008 Jul-Sep;5(3):149-56
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  • [Title] The intergenic spacer of the Drosophila Adh-Adhr dicistronic mRNA stimulates internal translation initiation.
  • Here we have investigated the translation mechanism of the dicistronic Adh-Adhr mRNA of Drosophila melanogaster.

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  • (PMID = 18758245.001).
  • [ISSN] 1555-8584
  • [Journal-full-title] RNA biology
  • [ISO-abbreviation] RNA Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / DNA, Intergenic; 0 / RNA, Messenger; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.13.12.- / Luciferases
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59. Birley AJ, James MR, Dickson PA, Montgomery GW, Heath AC, Martin NG, Whitfield JB: ADH single nucleotide polymorphism associations with alcohol metabolism in vivo. Hum Mol Genet; 2009 Apr 15;18(8):1533-42
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  • [Title] ADH single nucleotide polymorphism associations with alcohol metabolism in vivo.
  • We have previously found that variation in alcohol metabolism in Europeans is linked to the chromosome 4q region containing the ADH gene family.
  • The combined SNP associations with early- and late-stage metabolism only account for approximately 20% of the total genetic variance linked to the ADH region, and most of the variance for in vivo alcohol metabolism linked to this region is yet to be explained.

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  • [Cites] Prog Nucleic Acid Res Mol Biol. 2000;64:295-341 [10697413.001]
  • [Cites] J Biol Chem. 2006 Jul 21;281(29):19809-21 [16675441.001]
  • [Cites] Br J Clin Pharmacol. 2000 May;49(5):399-408 [10792196.001]
  • [Cites] Am J Hum Genet. 1999 Oct;65(4):1148-60 [10486334.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Sep;25(9):1257-63 [11584143.001]
  • [Cites] J Korean Med Sci. 2001 Dec;16(6):745-50 [11748356.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):97-101 [11731797.001]
  • [Cites] Am J Hum Genet. 2002 Nov;71(5):1247-50; author reply 1250-1 [12452180.001]
  • [Cites] J Stud Alcohol. 2003 Mar;64(2):176-81 [12713190.001]
  • [Cites] Alcohol Clin Exp Res. 2004 Jan;28(1):10-4 [14745297.001]
  • [Cites] Clin Pharmacol Ther. 1971 Mar-Apr;12(2):192-201 [5102974.001]
  • [Cites] Eur J Clin Pharmacol. 1977;11(5):337-44 [560303.001]
  • [Cites] Eur J Clin Pharmacol. 1984;26(5):619-26 [6468479.001]
  • [Cites] Alcohol. 1985 Jan-Feb;2(1):53-6 [3893465.001]
  • [Cites] Alcohol. 1984 Sep-Oct;1(5):385-91 [6537224.001]
  • [Cites] Hepatology. 1986 May-Jun;6(3):502-10 [3519419.001]
  • [Cites] Behav Genet. 1985 Mar;15(2):93-109 [3838073.001]
  • [Cites] Arukoru Kenkyuto Yakubutsu Ison. 1993 Feb;28(1):13-25 [8512495.001]
  • [Cites] Br J Clin Pharmacol. 1994 May;37(5):427-31 [8054248.001]
  • [Cites] Eur J Biochem. 1994 Sep 1;224(2):549-57 [7925371.001]
  • [Cites] Alcohol Alcohol. 1994 Nov;29(6):707-10 [7695788.001]
  • [Cites] Alcohol Clin Exp Res. 1995 Dec;19(6):1494-9 [8749816.001]
  • [Cites] Br J Psychiatry. 1996 Jun;168(6):762-7 [8773821.001]
  • [Cites] Alcohol Alcohol Suppl. 1994;2:29-34 [8974313.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):207-15 [9603606.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):216-21 [9603607.001]
  • [Cites] Alcohol Clin Exp Res. 1998 Oct;22(7):1463-9 [9802529.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1147-57 [10090900.001]
  • [Cites] Pharmacogenetics. 1999 Feb;9(1):25-30 [10208639.001]
  • [Cites] Hum Mutat. 2005 Feb;25(2):150-5 [15643610.001]
  • [Cites] Drug Alcohol Depend. 2006 Sep 15;84(2):195-200 [16600530.001]
  • [Cites] Alcohol Clin Exp Res. 2007 Feb;31(2):216-20 [17250612.001]
  • [Cites] Alcohol Res Health. 2007;30(1):22-7 [17718397.001]
  • [Cites] Nat Genet. 2007 Oct;39(10):1202-7 [17873877.001]
  • [Cites] Hum Mol Genet. 2008 Jan 15;17(2):179-89 [17921519.001]
  • [Cites] Alcohol Clin Exp Res. 2008 May;32(5):785-95 [18331377.001]
  • [Cites] Nat Genet. 2008 Jun;40(6):707-9 [18500343.001]
  • [Cites] PLoS Biol. 2008 May 6;6(5):e107 [18462017.001]
  • [Cites] Hum Mol Genet. 2009 Feb 1;18(3):580-93 [18996923.001]
  • [Cites] Bioinformatics. 2005 Aug 15;21(16):3445-7 [15947021.001]
  • [Cites] Hum Mutat. 2005 Sep;26(3):224-34 [16086315.001]
  • [Cites] Heredity (Edinb). 2005 Sep;95(3):184-97 [16121213.001]
  • [Cites] Behav Genet. 2005 Sep;35(5):509-24 [16184481.001]
  • [Cites] Hum Mol Genet. 2006 May 1;15(9):1539-49 [16571603.001]
  • [Cites] Hum Genet. 2006 Jun;119(5):558-70 [16604350.001]
  • [Cites] Am J Hum Genet. 2006 Jun;78(6):973-87 [16685648.001]
  • [Cites] Hepatology. 2000 Apr;31(4):984-9 [10733556.001]
  • (PMID = 19193628.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / AA007728; United States / NIAAA NIH HHS / AA / AA007535; United States / NIAAA NIH HHS / AA / AA011998; United States / NIAAA NIH HHS / AA / AA013326; United States / PHS HHS / / A014041; United States / NIAAA NIH HHS / AA / AA013321
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1B protein, human; EC 1.1.1.1 / ADH1C protein, human; EC 1.1.1.1 / ADH7 protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Other-IDs] NLM/ PMC2664151
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60. Jelski W, Chrostek L, Zalewski B, Szmitkowski M: Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with gastric cancer. Dig Dis Sci; 2008 Aug;53(8):2101-5
The Lens. Cited by Patents in .

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  • [Title] Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with gastric cancer.
  • BACKGROUND: Investigations have shown that alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are present in some cancer cells and can play role in carcinogenesis.
  • Total ADH activity was measured photometrically and ALDH activity by a fluorimetric method.
  • RESULTS: The activity of the class IV ADH isoenzyme was significantly higher in the sera of patients with gastric cancer.
  • For this reason total ADH activity was also significantly increased.
  • The activities of other tested ADH isoenzymes and ALDH were unchanged.
  • CONCLUSION: Changes in the activity of, especially, class IV ADH in the sera of patients with gastric cancer seems to be caused by release of the isoenzyme from cancer cells.

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  • [Cites] Alcohol Clin Exp Res. 1993 Dec;17(6):1337-44 [8116851.001]
  • [Cites] Histochemistry. 1992 Dec;98(5):311-5 [1283161.001]
  • [Cites] Gastroenterology. 1997 Mar;112(3):766-75 [9041238.001]
  • [Cites] FEBS Lett. 1989 Oct 23;257(1):105-9 [2806555.001]
  • [Cites] Gastroenterology. 1996 Oct;111(4):863-70 [8831581.001]
  • [Cites] Dig Dis Sci. 2007 Feb;52(2):531-5 [17211707.001]
  • [Cites] Alcohol Alcohol Suppl. 1993;1B:59-62 [8003130.001]
  • [Cites] Anal Biochem. 1989 Apr;178(1):57-62 [2729580.001]
  • [Cites] Biochem Int. 1990 Dec;22(5):829-35 [2099148.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):977-81 [15309886.001]
  • [Cites] N Engl J Med. 1990 Jan 11;322(2):95-9 [2248624.001]
  • [Cites] Alcohol Alcohol. 1994 Nov;29(6):663-71 [7695781.001]
  • [Cites] J Clin Lab Anal. 2003;17(3):93-6 [12696080.001]
  • [Cites] Alcohol Clin Exp Res. 1979 Apr;3(2):95-8 [391080.001]
  • [Cites] Chem Biol Interact. 2003 Feb 1;143-144:219-27 [12604207.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Dec;20(9):1569-76 [8986205.001]
  • [Cites] J Protein Chem. 1991 Feb;10(1):69-73 [2054065.001]
  • [Cites] Dig Dis Sci. 2002 Jul;47(7):1554-7 [12141816.001]
  • (PMID = 18231859.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / ADH7 protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.1.1.284 / formaldehyde dehydrogenase (glutathione); EC 1.2.- / Aldehyde Oxidoreductases; EC 1.2.1.3 / Aldehyde Dehydrogenase
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61. Jelski W, Zalewski B, Chrostek L, Szmitkowski M: Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with colorectal cancer. Clin Exp Med; 2007 Dec;7(4):154-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with colorectal cancer.
  • Various isoenzymes of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) exist in human colorectal mucosa.
  • In our last experiments we have shown that ADH and ALDH are present also in colorectal cancer cells.
  • Moreover the activities of total ADH and class I isoenzymes were significantly higher in cancer tissue than healthy mucosa.
  • Therefore, we have measured the activity of total ADH, and classes I-IV of this enzyme and ALDH in the sera of patients suffering from this cancer.
  • Total ADH activity was measured by a photometric method with p-nitrosodimethylaniline (NDMA) as a substrate and ALDH activity by the fluorometric method with 6-methoxy-2-naphtaldehyde as a substrate.
  • The activity of class III ADH was measured by the photometric method with formaldehyde and class IV with m-nitrobenzaldehyde as a substrate.
  • A statistically significant increase of class I ADH isoenzymes was found.
  • Therefore the total ADH activity was also significantly increased.
  • The total ALDH and the activity of other tested ADH isoenzymes were unchanged.
  • We also observed the increasing tendency of ADH I activity in accordance with the advance of disease.
  • The activity of class I ADH isoenzymes was elevated in the serum of patients with colorectal cancer.

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  • [Cites] Gastroenterology. 1997 Mar;112(3):766-75 [9041238.001]
  • [Cites] Dig Dis Sci. 2007 Feb;52(2):531-5 [17211707.001]
  • [Cites] Clin Exp Med. 2006 Jun;6(2):89-93 [16820997.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):977-81 [15309886.001]
  • [Cites] Digestion. 1996;57(2):105-8 [8785998.001]
  • [Cites] Clin Chem. 1984 Feb;30(2):266-70 [6692531.001]
  • [Cites] J Clin Lab Anal. 2003;17(3):93-6 [12696080.001]
  • [Cites] Ann Hum Genet. 1971 Feb;34(3):251-71 [5548434.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Oct;18(5):1256-60 [7847616.001]
  • [Cites] Alcohol Clin Exp Res. 1996 May;20(3):551-5 [8727253.001]
  • [Cites] J Protein Chem. 1991 Feb;10(1):69-73 [2054065.001]
  • [Cites] Dig Dis Sci. 2002 Jul;47(7):1554-7 [12141816.001]
  • (PMID = 18188528.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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62. Konstantopoulou MA, Raptopoulos DG, Stavrakis NG, Mazomenos BE: Microflora species and their volatile compounds affecting development of an alcohol dehydrogenase homozygous strain (Adh-I) of Bactrocera (Dacus) oleae (Diptera: Tephritidae). J Econ Entomol; 2005 Dec;98(6):1943-9
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  • [Title] Microflora species and their volatile compounds affecting development of an alcohol dehydrogenase homozygous strain (Adh-I) of Bactrocera (Dacus) oleae (Diptera: Tephritidae).
  • Microflora species and volatiles emitted from artificial diets were examined from the larvae of three homozygous alcohol dehydrogenase (Adh) strains of the olive fruit fly, Bactrocera (Dacus) oleae (Gmelin), reared under identical conditions.
  • Differences in volatile composition were detected when Adh-I homozygous larvae developed in a diet lacking the preservative p-hydroxybenzoic acid methyl ester (nipagin).
  • Larval development of the Adh-I strain in the preservative-free diet was reduced by 50%, whereas pupal emergence was completely inhibited.
  • The larval development and pupal emergence of Adh-F and Adh-S strains were not affected.
  • Unique microorganisms with characteristic volatile profiles were isolated from the preservative-free diet of the Adh-I strain that were different from those, isolated from Adh-S, Adh-F, laboratory colony, and wild insect populations.
  • Our results indicated that the variations in volatile composition of the artificial diets, and the inhibition of larval development and pupal emergence in Adh-I strain were related to changes in the microflora that developed in the diets of the Adh-I strain.

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  • (PMID = 16539118.001).
  • [ISSN] 0022-0493
  • [Journal-full-title] Journal of economic entomology
  • [ISO-abbreviation] J. Econ. Entomol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Parabens; A2I8C7HI9T / methylparaben; EC 1.1.1.1 / Alcohol Dehydrogenase
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63. Kuo PH, Kalsi G, Prescott CA, Hodgkinson CA, Goldman D, van den Oord EJ, Alexander J, Jiang C, Sullivan PF, Patterson DG, Walsh D, Kendler KS, Riley BP: Association of ADH and ALDH genes with alcohol dependence in the Irish Affected Sib Pair Study of alcohol dependence (IASPSAD) sample. Alcohol Clin Exp Res; 2008 May;32(5):785-95
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  • [Title] Association of ADH and ALDH genes with alcohol dependence in the Irish Affected Sib Pair Study of alcohol dependence (IASPSAD) sample.
  • BACKGROUND: The genes coding for ethanol metabolism enzymes [alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH)] have been widely studied for their influence on the risk to develop alcohol dependence (AD).
  • METHODS: We conducted a case-control association study with 575 independent subjects who met Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, AD diagnosis and 530 controls.
  • A total of 77 single nucleotide polymorphisms (SNPs) in the seven ADH (ADH1-7) and two ALDH genes (ALDH1A1 and ALDH2) were genotyped using the Illumina GoldenGate protocols.
  • Numerous SNPs in ADH genes showed association with AD, including one marker in the coding region of ADH1C (rs1693482 in exon6, Ile271Gln).
  • CONCLUSION: We found evidence for the association of several ADH genes with AD in a sample of Western European origin.
  • The significant interaction effects between markers in ADH and ALDH genes suggest possible epistatic roles between alcohol metabolic enzymes in the risk for AD.

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  • [Cites] Alcohol Clin Exp Res. 2001 Dec;25(12):1773-7 [11781511.001]
  • [Cites] Alcohol Alcohol Suppl. 1994;2:29-34 [8974313.001]
  • [Cites] Am J Hum Genet. 2002 Nov;71(5):1247-50; author reply 1250-1 [12452180.001]
  • [Cites] Alcohol Alcohol. 1997 Mar-Apr;32(2):129-32 [9105506.001]
  • [Cites] Alcohol Clin Exp Res. 1997 Oct;21(7):1272-7 [9347089.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1147-57 [10090900.001]
  • [Cites] Am J Hum Genet. 1999 Sep;65(3):795-807 [10441588.001]
  • [Cites] Ann N Y Acad Sci. 2004 Oct;1025:472-80 [15542751.001]
  • [Cites] Pharmacogenetics. 2004 Nov;14(11):725-32 [15564879.001]
  • [Cites] Alcohol Clin Exp Res. 2004 Oct;28(10):1481-6 [15597079.001]
  • [Cites] Mol Psychiatry. 2005 Mar;10(3):230-1 [15738930.001]
  • [Cites] Alcohol Clin Exp Res. 2005 Mar;29(3):417-29 [15770118.001]
  • [Cites] Am J Psychiatry. 2005 May;162(5):1003-5 [15863807.001]
  • [Cites] Am J Psychiatry. 2005 May;162(5):1005-7 [15863808.001]
  • [Cites] Hum Genomics. 2005 Jun;2(2):138-43 [16004729.001]
  • [Cites] Pharmacogenet Genomics. 2005 Nov;15(11):755-68 [16220108.001]
  • [Cites] Alcohol Clin Exp Res. 2005 Dec;29(12):2091-100 [16385178.001]
  • [Cites] Am J Hum Genet. 2006 Feb;78(2):243-52 [16400608.001]
  • [Cites] Hepatology. 2006 Feb;43(2):352-61 [16440362.001]
  • [Cites] Hum Mol Genet. 2006 May 1;15(9):1539-49 [16571603.001]
  • [Cites] Neuropsychopharmacology. 2006 May;31(5):1085-95 [16237392.001]
  • [Cites] Am J Hum Genet. 2006 Jun;78(6):973-87 [16685648.001]
  • [Cites] Mol Psychiatry. 2006 Jun;11(6):603-11 [16534506.001]
  • [Cites] Behav Genet. 2006 Jul;36(4):473-82 [16710779.001]
  • [Cites] Alcohol Clin Exp Res. 2006 Nov;30(11):1807-16 [17067344.001]
  • [Cites] Am J Hum Genet. 2007 Mar;80(3):531-8 [17273975.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2008 Mar 5;147B(2):179-86 [17918242.001]
  • [Cites] Alcohol Clin Exp Res. 2002 Dec;26(12):1759-63 [12500098.001]
  • [Cites] Am J Psychiatry. 2003 Jan;160(1):41-6 [12505800.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5 [12883005.001]
  • [Cites] Hum Genet. 2003 Sep;113(4):325-36 [12884000.001]
  • [Cites] Alcohol Clin Exp Res. 2003 Sep;27(9):1389-94 [14506398.001]
  • [Cites] Trends Genet. 2003 Oct;19(10):537-42 [14550627.001]
  • [Cites] Arch Gen Psychiatry. 2004 Feb;61(2):184-91 [14757595.001]
  • [Cites] Ann Hum Genet. 2004 Mar;68(Pt 2):93-109 [15008789.001]
  • [Cites] Am J Hum Genet. 2004 Apr;74(4):705-14 [15024690.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2004 Apr 1;126B(1):19-22 [15048643.001]
  • [Cites] Hepatology. 2000 Apr;31(4):984-9 [10733556.001]
  • [Cites] DNA Cell Biol. 2000 Aug;19(8):487-97 [10975466.001]
  • [Cites] Alcohol Clin Exp Res. 2001 May;25(5 Suppl ISBRA):157S-163S [11391066.001]
  • [Cites] Pathol Biol (Paris). 2001 Nov;49(9):676-82 [11762128.001]
  • [Cites] Proc Nutr Soc. 2004 Feb;63(1):49-63 [15099407.001]
  • [Cites] BMC Bioinformatics. 2004 Jul 6;5:89 [15238162.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Sep 1;88(17):7610-4 [1881901.001]
  • [Cites] Hum Genet. 1992 Jan;88(3):344-6 [1733836.001]
  • [Cites] J Stud Alcohol. 1994 Mar;55(2):149-58 [8189735.001]
  • [Cites] Eur J Biochem. 1994 Sep 1;224(2):549-57 [7925371.001]
  • [Cites] Alcohol Alcohol. 1994 Nov;29(6):663-71 [7695781.001]
  • [Cites] Alcohol Alcohol. 1994 Nov;29(6):701-5 [7695787.001]
  • [Cites] Br J Psychiatry. 1996 Jun;168(6):762-7 [8773821.001]
  • [Cites] Am J Hum Genet. 2002 Feb;70(2):461-71 [11791213.001]
  • (PMID = 18331377.001).
  • [ISSN] 1530-0277
  • [Journal-full-title] Alcoholism, clinical and experimental research
  • [ISO-abbreviation] Alcohol. Clin. Exp. Res.
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / R01 AA011408; United States / Intramural NIH HHS / / Z01 AA000306-02; United States / NIAAA NIH HHS / AA / R01-AA-11408
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / ALDH1A1 protein, human; EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  • [Other-IDs] NLM/ NIHMS63621; NLM/ PMC2665790
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64. Toyama H, Chen ZW, Fukumoto M, Adachi O, Matsushita K, Mathews FS: Molecular cloning and structural analysis of quinohemoprotein alcohol dehydrogenase ADH-IIG from Pseudomonas putida HK5. J Mol Biol; 2005 Sep 9;352(1):91-104
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  • [Title] Molecular cloning and structural analysis of quinohemoprotein alcohol dehydrogenase ADH-IIG from Pseudomonas putida HK5.
  • Depending on the alcohols used as growth substrates, Pseudomonas putida HK5 produces two distinct quinohemoprotein alcohol dehydrogenases, ADH-IIB and ADH-IIG, both of which contain pyrroloquinoline quinone (PQQ) and heme c as the prosthetic groups but show different substrate specificities, especially for diol substrates.
  • Molecular cloning of the gene of ADH-IIB and its crystal structure are already reported.
  • Here, molecular cloning of the gene, qgdA, and solution of the three-dimensional structure of ADH-IIG are reported.
  • The crystal structure of ADH-IIG, determined at 2.2A resolution, shows that the overall structure and the amino acid residues involved in PQQ binding are quite similar to ADH-IIB and to another quinohemoprotein ADH, qhEDH from Comamonas testosteroni.
  • Apart from ADH-IIB and qhEDH, ADH-IIG has an extra 12-residue helix within loop 3 in the PQQ domain and an extra 3(10) helix in the C terminus of the cytochrome domain, and both helices appear parallel and linked by a hydrogen bond.
  • In the crystal structure of ADH-IIG with 1,2-propanediol, one of the hydroxyl groups of the substrate forms a hydrogen bond with O5 of PQQ and OD1 of Asp300, and the other interacts with a water molecule and with NE2 of Trp386, the corresponding residue of which is not found in ADH-IIB and qhEDH, and might be the residue responsible for making ADH-IIG prefer diol substrates.

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  • (PMID = 16061256.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB204833
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Isoenzymes; 9007-43-6 / Cytochromes c; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.2.8 / alcohol dehydrogenase (acceptor)
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65. Oota H, Dunn CW, Speed WC, Pakstis AJ, Palmatier MA, Kidd JR, Kidd KK: Conservative evolution in duplicated genes of the primate Class I ADH cluster. Gene; 2007 May 1;392(1-2):64-76
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  • [Title] Conservative evolution in duplicated genes of the primate Class I ADH cluster.
  • Humans have seven alcohol dehydrogenase genes (ADH) falling into five classes.
  • The three genes are tandemly arrayed within the ADH cluster on chromosome 4 and have very high nucleotide similarity to each other (exons: >90%; introns: >70%), suggesting the genes have been generated by duplication event(s).

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  • (PMID = 17204375.001).
  • [ISSN] 0378-1119
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB243573/ AB243574/ AB243575/ AB243576/ AB243577/ AB243578/ AB243579/ AB243580/ AB243581/ AB243582/ AB243583/ AB243584/ AB243585/ AB243586/ AB243587/ AB243588/ AB243589/ AB243590/ AB243591/ AB243592/ AB243593/ AB243594/ AB243595/ AB243596/ AB243597/ AB243598/ AB243599/ AB243600/ AB243601/ AB243602
  • [Grant] United States / NIAAA NIH HHS / AA / AA09379
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase
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66. Kalnenieks U, Galinina N, Toma MM: Physiological regulation of the properties of alcohol dehydrogenase II (ADH II) of Zymomonas mobilis: NADH renders ADH II resistant to cyanide and aeration. Arch Microbiol; 2005 Sep;183(6):450-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Physiological regulation of the properties of alcohol dehydrogenase II (ADH II) of Zymomonas mobilis: NADH renders ADH II resistant to cyanide and aeration.
  • The variable cyanide-sensitivity of the iron-containing alcohol dehydrogenase isoenzyme (ADH II) of the ethanol-producing bacterium Zymomonas mobilis was studied.
  • In aerobically grown permeabilized cells, cyanide caused gradual inhibition of ADH II, which was largely prevented by externally added NADH.
  • Cyanide-sensitivity of ADH II was highest in cells grown under conditions of vigorous aeration, in which intracellular NADH concentration was low.
  • Anaerobically grown bacteria, as well as those cultivated aerobically in the presence of cyanide, maintained higher intracellular NADH levels along with a more cyanide-resistant ADH II.
  • It was demonstrated that cyanide acted as a competitive inhibitor of ADH II, competing with nicotinamide nucleotides.
  • NADH increased both cyanide-resistance and oxygen-resistance of ADH II.

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  • (PMID = 16027951.001).
  • [ISSN] 0302-8933
  • [Journal-full-title] Archives of microbiology
  • [ISO-abbreviation] Arch. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cyanides; 0 / Enzyme Inhibitors; 0U46U6E8UK / NAD; EC 1.1.1.1 / Alcohol Dehydrogenase
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67. Jelski W, Chrostek L, Markiewicz W, Szmitkowski M: Activity of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in the sera of patients with breast cancer. J Clin Lab Anal; 2006;20(3):105-8
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  • [Title] Activity of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in the sera of patients with breast cancer.
  • Numerous experiments have shown that alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) play a significant role in the metabolism of many biological substances.
  • Some metabolic disorders that can lead to breast carcinogenesis may be the cause of changes in ADH and ALDH activity.
  • In previous experiments we found a changed level of class I ADH activity in breast cancer tissues.
  • Therefore, in this study we measured the activity of ADH isoenzymes and ALDH in the sera of patients with breast cancer.
  • Serum samples were taken for routine biochemical investigation from 45 women with breast cancer before treatment.
  • Among all tested classes of ADH isoenzymes, only class I had higher activity in the serum of patients with breast cancer in stage IV.
  • The total ADH and ALDH activities were not significantly higher in patients with breast cancer than in healthy controls.
  • The changes in activity, especially in class I ADH, appear to be caused by isoenzymes being released from the organ damaged by metastatic disease.
  • [MeSH-major] Alcohol Dehydrogenase / blood. Aldehyde Dehydrogenase / blood. Breast Neoplasms / enzymology. Carcinoma, Ductal, Breast / enzymology

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16721836.001).
  • [ISSN] 0887-8013
  • [Journal-full-title] Journal of clinical laboratory analysis
  • [ISO-abbreviation] J. Clin. Lab. Anal.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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68. Quigley R, Chu PY, Huang CL: Botulinum toxins inhibit the antidiuretic hormone (ADH)-stimulated increase in rabbit cortical collecting-tubule water Permeability. J Membr Biol; 2005 Apr;204(3):109-16
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  • [Title] Botulinum toxins inhibit the antidiuretic hormone (ADH)-stimulated increase in rabbit cortical collecting-tubule water Permeability.
  • The mammalian renal collecting duct increases its water permeability in response to antidiuretic hormone (ADH).
  • ADH causes cytoplasmic endosomes containing the water channel, aquaporin 2 (AQP 2), to fuse with the apical membrane so that the water permeability of the tubule increases many times above baseline.
  • In the present study, we examined the role of SNARE proteins in the insertion of water channels in the collecting-duct response to ADH by using botulinum toxins A, B and C.
  • ADH (200 pM) was then added to the bath after baseline measurements of osmotic water permeability (P(f)) and the change in P(f) was followed for one hour.
  • Thus, SNARE proteins are involved in the insertion of the water channels in the collecting duct.

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  • [Cites] Curr Opin Nephrol Hypertens. 2000 Sep;9(5):523-7 [10990372.001]
  • [Cites] Biochemistry. 1997 May 13;36(19):5719-28 [9153412.001]
  • [Cites] J Clin Invest. 1995 Oct;96(4):1834-44 [7560075.001]
  • [Cites] Am J Physiol. 1998 Jul;275(1 Pt 2):F131-42 [9689015.001]
  • [Cites] Am J Physiol. 1995 Mar;268(3 Pt 1):C792-7 [7900782.001]
  • [Cites] Nature. 1994 Nov 3;372(6501):55-63 [7969419.001]
  • [Cites] Neuron. 1994 Dec;13(6):1303-13 [7993624.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7363-8 [8692999.001]
  • [Cites] Nature. 1993 Mar 25;362(6418):318-24 [8455717.001]
  • [Cites] Am J Physiol. 1998 Sep;275(3 Pt 2):F328-31 [9729503.001]
  • [Cites] J Clin Invest. 1991 Aug;88(2):368-74 [1864951.001]
  • [Cites] J Membr Biol. 1977 Feb 24;31(1-2):103-29 [839529.001]
  • [Cites] Am J Physiol Renal Physiol. 2003 Dec;285(6):F1179-87 [12952855.001]
  • [Cites] Curr Opin Cell Biol. 1997 Aug;9(4):560-4 [9261056.001]
  • [Cites] J Clin Invest. 1996 Aug 15;98(4):906-13 [8770861.001]
  • [Cites] Mol Microbiol. 1994 Jul;13(1):1-8 [7527117.001]
  • [Cites] Am J Physiol. 1997 Jun;272(6 Pt 2):F817-22 [9227644.001]
  • [Cites] J Biol Chem. 1999 Sep 10;274(37):26518-22 [10473613.001]
  • [Cites] Kidney Int. 1972 Apr;1(4):224-31 [4671214.001]
  • [Cites] Am J Physiol. 1966 Jun;210(6):1293-8 [5923067.001]
  • [Cites] Ann N Y Acad Sci. 1981;372:106-17 [6951416.001]
  • [Cites] Am J Physiol. 1997 Dec;273(6 Pt 2):F1054-7 [9435696.001]
  • [Cites] Nature. 1995 Jun 22;375(6533):645-53 [7791897.001]
  • [Cites] Nature. 1993 Feb 11;361(6412):549-52 [8429910.001]
  • [Cites] Am J Physiol. 1994 Mar;266(3 Pt 2):F459-65 [8160795.001]
  • [Cites] J Biol Chem. 1997 Jun 6;272(23):14800-4 [9169447.001]
  • [Cites] FEBS Lett. 1995 May 29;365(2-3):209-13 [7540151.001]
  • [Cites] Am J Physiol. 1994 Dec;267(6 Pt 1):C1507-24 [7810592.001]
  • [Cites] J Biol Chem. 1996 May 31;271(22):13130-4 [8662834.001]
  • [Cites] J Biol Chem. 1997 Mar 7;272(10):6179-86 [9045631.001]
  • [Cites] Am J Physiol. 1997 Nov;273(5 Pt 2):F718-30 [9374835.001]
  • [Cites] Am J Physiol. 1995 Sep;269(3 Pt 1):C797-801 [7573412.001]
  • [Cites] Nature. 1997 Nov 20;390(6657):302-5 [9384384.001]
  • [Cites] J Clin Invest. 2000 Feb;105(3):377-86 [10675364.001]
  • [Cites] Am J Physiol. 1968 Oct;215(4):788-94 [5676377.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10972-7 [9724814.001]
  • [Cites] Am J Physiol. 1998 Nov;275(5 Pt 2):F752-60 [9815132.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 1999 Feb 28;354(1381):259-68 [10212474.001]
  • [Cites] Kidney Int. 1995 Oct;48(4):1057-68 [8569067.001]
  • (PMID = 16245033.001).
  • [ISSN] 0022-2631
  • [Journal-full-title] The Journal of membrane biology
  • [ISO-abbreviation] J. Membr. Biol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK54368
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aquaporin 2; 0 / Aquaporins; 0 / SNARE Proteins; 0 / Vesicular Transport Proteins; 059QF0KO0R / Water; 11000-17-2 / Vasopressins; EC 3.4.24.69 / Botulinum Toxins
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69. Katoh T, Nakaya D, Tamura K, Aotsuka T: Phylogeny of the Drosophila immigrans species group (Diptera: Drosophilidae) based on Adh and Gpdh sequences. Zoolog Sci; 2007 Sep;24(9):913-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phylogeny of the Drosophila immigrans species group (Diptera: Drosophilidae) based on Adh and Gpdh sequences.
  • To study the phylogeny of the immigrans group, we analyzed the nucleotide sequences of two nuclear genes, alcohol dehydrogenase (Adh) and glycerol-3-phosphate dehydrogenase (Gpdh), for 36 drosophilid species, including 12 species of the immigrans group.

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  • (PMID = 17960997.001).
  • [ISSN] 0289-0003
  • [Journal-full-title] Zoological science
  • [ISO-abbreviation] Zool. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA Primers; 9007-49-2 / DNA; EC 1.1.- / Glycerolphosphate Dehydrogenase; EC 1.1.1.1 / Alcohol Dehydrogenase
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70. Hense W, Anderson N, Hutter S, Stephan W, Parsch J, Carlini DB: Experimentally increased codon bias in the Drosophila Adh gene leads to an increase in larval, but not adult, alcohol dehydrogenase activity. Genetics; 2010 Feb;184(2):547-55
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  • [Title] Experimentally increased codon bias in the Drosophila Adh gene leads to an increase in larval, but not adult, alcohol dehydrogenase activity.
  • Previous work demonstrated that the experimental reduction of codon bias in the Drosophila alcohol dehydrogenase (Adh) gene led to a significant decrease in ADH protein expression.
  • In this study we performed the converse experiment: we replaced seven suboptimal leucine codons that occur naturally in the Drosophila melanogaster Adh gene with the optimal codon.
  • We then compared the in vivo ADH activities imparted by the wild-type and mutant alleles.
  • The introduction of optimal leucine codons led to an increase in ADH activity in third-instar larvae.
  • In adult flies, however, the introduction of optimal codons led to a decrease in ADH activity.
  • There is no evidence that other selectively constrained features of the Adh gene, or its rate of transcription, were altered by the synonymous replacements.

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  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3568-71 [12824367.001]
  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3406-15 [12824337.001]
  • [Cites] Genetics. 2004 Jan;166(1):237-42 [15020421.001]
  • [Cites] J Evol Biol. 2004 Jul;17(4):779-85 [15271077.001]
  • [Cites] Genetics. 2004 Aug;167(4):1791-9 [15342517.001]
  • [Cites] Genetics. 2004 Sep;168(1):559-61 [15454566.001]
  • [Cites] Trends Genet. 2004 Nov;20(11):534-8 [15475111.001]
  • [Cites] Biochem Genet. 1978 Jun;16(5-6):509-23 [104709.001]
  • [Cites] J Mol Biol. 1981 Sep 25;151(3):389-409 [6175758.001]
  • [Cites] Nucleic Acids Res. 1982 Nov 25;10(22):7261-72 [6296769.001]
  • [Cites] Nature. 1983 Aug 4-10;304(5925):412-7 [6410283.001]
  • [Cites] Nucleic Acids Res. 1986 Jul 11;14(13):5125-43 [3526280.001]
  • [Cites] J Mol Evol. 1986;24(1-2):28-38 [3104616.001]
  • [Cites] Genetics. 1988 Mar;118(3):461-70 [2835286.001]
  • [Cites] Genetics. 1991 Oct;129(2):481-8 [1743488.001]
  • [Cites] Genetics. 1991 Nov;129(3):897-907 [1752426.001]
  • [Cites] Nucleic Acids Res. 1992 Nov 11;20(21):5859-60 [1333590.001]
  • [Cites] Genetics. 1994 Mar;136(3):927-35 [8005445.001]
  • [Cites] Genetics. 1995 Feb;139(2):1067-76 [7713409.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9047-51 [7568070.001]
  • [Cites] Genetics. 1996 Oct;144(2):715-26 [8889532.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Feb 4;94(3):928-33 [9023359.001]
  • [Cites] J Mol Evol. 1997 Nov;45(5):514-23 [9342399.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15513-8 [9861000.001]
  • [Cites] Genetics. 1999 Feb;151(2):667-74 [9927459.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4482-7 [10200288.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] Cell. 2005 Jan 14;120(1):49-58 [15652481.001]
  • [Cites] Trends Genet. 2005 May;21(5):256-9 [15851058.001]
  • [Cites] Genetics. 2005 Aug;170(4):1691-700 [15937136.001]
  • [Cites] Genome Biol. 2005;6(9):R75 [16168082.001]
  • [Cites] J Mol Evol. 2005 Sep;61(3):306-14 [16044249.001]
  • [Cites] Genome Res. 2006 Jan;16(1):66-77 [16344558.001]
  • [Cites] PLoS Genet. 2006 Nov 3;2(11):e176 [17083275.001]
  • [Cites] BMC Bioinformatics. 2007;8:159 [17517127.001]
  • [Cites] Mol Biol Evol. 2007 Aug;24(8):1600-3 [17525472.001]
  • [Cites] Biol Cell. 2007 Sep;99(9):475-87 [17696878.001]
  • [Cites] Nature. 2007 Nov 8;450(7167):203-18 [17994087.001]
  • [Cites] Mol Biol Evol. 2007 Dec;24(12):2755-62 [17905999.001]
  • [Cites] BMC Evol Biol. 2007;7:226 [18005411.001]
  • [Cites] Science. 2008 Jun 27;320(5884):1784-7 [18583614.001]
  • [Cites] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W70-4 [18424795.001]
  • [Cites] Mol Biol Evol. 2008 Nov;25(11):2269-77 [18755761.001]
  • [Cites] Gene. 2008 Nov 15;424(1-2):102-7 [18755255.001]
  • [Cites] Science. 2009 Apr 10;324(5924):255-8 [19359587.001]
  • [Cites] Genetics. 2000 Feb;154(2):909-21 [10655240.001]
  • [Cites] Genes Genet Syst. 1999 Dec;74(6):271-86 [10791023.001]
  • [Cites] Genetics. 2000 Sep;156(1):219-27 [10978287.001]
  • [Cites] Genetics. 2001 Oct;159(2):623-33 [11606539.001]
  • [Cites] Curr Opin Genet Dev. 2001 Dec;11(6):660-6 [11682310.001]
  • [Cites] Genetics. 2002 May;161(1):389-410 [12019253.001]
  • [Cites] Science. 2002 Aug 9;297(5583):1007-13 [12114529.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13616-20 [12370444.001]
  • [Cites] Curr Opin Genet Dev. 2002 Dec;12(6):640-9 [12433576.001]
  • [Cites] Genetics. 2003 Jan;163(1):239-43 [12586711.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11499-504 [12972637.001]
  • (PMID = 19966063.001).
  • [ISSN] 1943-2631
  • [Journal-full-title] Genetics
  • [ISO-abbreviation] Genetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / Drosophila Proteins; EC 1.1.1.1 / ADH protein, Drosophila; EC 1.1.1.1 / Alcohol Dehydrogenase; GMW67QNF9C / Leucine
  • [Other-IDs] NLM/ PMC2828731
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71. Jelski W, Orywal K, Laniewska M, Szmitkowski M: The diagnostic value of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) measurement in the sera of gastric cancer patients. Clin Exp Med; 2010 Dec;10(4):215-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The diagnostic value of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) measurement in the sera of gastric cancer patients.
  • Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are present in gastric cancer cells (GC).
  • Moreover, the activity of total ADH and class IV isoenzymes is significantly higher in cancer tissue than in healthy mucosa.
  • The aim of this study was to investigate a potential role of ADH and ALDH as tumor markers for gastric cancer.
  • Total ADH activity and class III and IV isoenzymes were measured by photometric but ALDH activity and ADH I and II by the fluorometric method, with class-specific fluorogenic substrates.
  • There was significant increase in the activity of ADH IV isoenzyme and ADH total in the sera of gastric cancer patients compared to the control.
  • The diagnostic sensitivity for ADH IV was 73%, specificity 79%, positive and negative predictive values were 81 and 72% respectively.
  • Area under ROC curve for ADH IV was 0.67.
  • The results suggest a potential role for ADH IV as marker of gastric cancer.
  • [MeSH-major] Alcohol Dehydrogenase / blood. Aldehyde Dehydrogenase / blood. Stomach Neoplasms / diagnosis

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  • [Cites] FEBS Lett. 1989 Oct 23;257(1):105-9 [2806555.001]
  • [Cites] Clin Chim Acta. 2006 Dec;374(1-2):165-7 [16828725.001]
  • [Cites] Dig Dis Sci. 2007 Feb;52(2):531-5 [17211707.001]
  • [Cites] Clin Exp Med. 2006 Jun;6(2):89-93 [16820997.001]
  • [Cites] Anal Biochem. 1989 Apr;178(1):57-62 [2729580.001]
  • [Cites] Clin Chem Lab Med. 2009;47(9):1133-9 [19728856.001]
  • [Cites] Cancer. 2006 Oct 15;107(8):1711-42 [16958083.001]
  • [Cites] Anal Biochem. 1979 Oct 15;99(1):65-71 [231394.001]
  • [Cites] Oncology. 1999 Jul;57(1):55-62 [10394126.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Mar;25(3):421-6 [11290854.001]
  • [Cites] Hepatogastroenterology. 2007 Jun;54(76):1272-5 [17629087.001]
  • [Cites] Int J Biol Markers. 2003 Jan-Mar;18(1):21-7 [12699059.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Nov 2;216(1):216-22 [7488092.001]
  • [Cites] Dig Dis Sci. 2010 Oct;55(10):2953-7 [20069455.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Dec;20(9):1569-76 [8986205.001]
  • [Cites] Dig Dis Sci. 2008 Aug;53(8):2101-5 [18231859.001]
  • [Cites] Dig Dis Sci. 2002 Jul;47(7):1554-7 [12141816.001]
  • [Cites] BMJ. 2000 Feb 12;320(7232):424-7 [10669448.001]
  • (PMID = 20454995.001).
  • [ISSN] 1591-9528
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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72. Malherbe Y, Kamping A, van Delden W, van de Zande L: ADH enzyme activity and Adh gene expression in Drosophila melanogaster lines differentially selected for increased alcohol tolerance. J Evol Biol; 2005 Jul;18(4):811-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ADH enzyme activity and Adh gene expression in Drosophila melanogaster lines differentially selected for increased alcohol tolerance.
  • In Drosophila melanogaster, alcohol dehydrogenase (ADH) activity is essential for ethanol tolerance, but its role may not be restricted to alcohol metabolism alone.
  • Here we describe ADH activity and Adh expression level upon selection for increased alcohol tolerance in different life-stages of D. melanogaster lines with two distinct Adh genotypes: Adh(FF) and Adh(SS).
  • A slight constitutive increase in adult ADH activity for all selection regimes and genotypes was observed, that was not paralleled by Adh expression.
  • Larval Adh expression showed a constitutive increase, that was not reflected in ADH activity.
  • Increased ADH activity accompanies increased ethanol tolerance in D. melanogaster but this increase is not paralleled by expression of the Adh gene.

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  • (PMID = 16033552.001).
  • [ISSN] 1010-061X
  • [Journal-full-title] Journal of evolutionary biology
  • [ISO-abbreviation] J. Evol. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Drosophila Proteins; 3K9958V90M / Ethanol; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.1 / ADH protein, Drosophila; EC 1.1.1.1 / Alcohol Dehydrogenase
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73. Damelin LH, Mavri-Damelin D, Klaenhammer TR, Tiemessen CT: Plasmid transduction using bacteriophage Phi(adh) for expression of CC chemokines by Lactobacillus gasseri ADH. Appl Environ Microbiol; 2010 Jun;76(12):3878-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plasmid transduction using bacteriophage Phi(adh) for expression of CC chemokines by Lactobacillus gasseri ADH.
  • Modifying a previously established transduction model, which utilizes L. gasseri ADH and its prophage Phiadh, we show that mitomycin C induction of L. gasseri ADH transformants containing pGK12-based plasmids with CCL5 and CCL3 expression and secretion cassettes (under the control of promoters P6 and P59, respectively) and a 232-bp Phiadh cos site fragment results in the production of transducing particles which contain 8 to 9 copies of concatemeric plasmid DNA.

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  • [Cites] J Infect Dis. 1999 Dec;180(6):1950-6 [10558952.001]
  • [Cites] Appl Environ Microbiol. 2008 Aug;74(15):4626-35 [18539799.001]
  • [Cites] Plasmid. 2001 Sep;46(2):106-16 [11591136.001]
  • [Cites] J Appl Microbiol. 2002;92(3):451-9 [11872120.001]
  • [Cites] J Clin Microbiol. 2002 Aug;40(8):2746-9 [12149323.001]
  • [Cites] J Leukoc Biol. 2003 Sep;74(3):448-55 [12949249.001]
  • [Cites] Appl Environ Microbiol. 2004 Oct;70(10):6076-85 [15466553.001]
  • [Cites] Nihon Saikingaku Zasshi. 1971 Oct;26(10):482-7 [5169937.001]
  • [Cites] J Bacteriol. 1981 Jul;147(1):1-8 [6787022.001]
  • [Cites] Appl Environ Microbiol. 1984 Oct;48(4):726-31 [6095756.001]
  • [Cites] Appl Environ Microbiol. 1987 Oct;53(10):2452-7 [2447829.001]
  • [Cites] Appl Environ Microbiol. 1989 Sep;55(9):2206-13 [2508554.001]
  • [Cites] Mol Gen Genet. 1990 Sep;223(2):185-91 [2123518.001]
  • [Cites] Plasmid. 1991 Jul;26(1):55-66 [1840693.001]
  • [Cites] Gene. 1993 Apr 15;126(1):61-6 [8472961.001]
  • [Cites] Can J Microbiol. 1997 Jan;43(1):61-9 [9057296.001]
  • [Cites] FEBS Lett. 1999 Aug 27;457(2):219-22 [10471782.001]
  • [Cites] J Acquir Immune Defic Syndr. 2005 Dec 15;40(5):512-20 [16284525.001]
  • [Cites] J Immunol. 2006 May 1;176(9):5627-36 [16622032.001]
  • [Cites] Plasmid. 2006 May;55(3):184-93 [16458963.001]
  • [Cites] Biochem Pharmacol. 2006 Sep 14;72(6):739-48 [16844091.001]
  • [Cites] AIDS. 2006 Oct 3;20(15):1917-22 [16988512.001]
  • [Cites] J Appl Microbiol. 2007 May;102(5):1337-49 [17448169.001]
  • [Cites] Am J Reprod Immunol. 2008 Jan;59(1):44-54 [18154595.001]
  • [Cites] Appl Environ Microbiol. 2001 Mar;67(3):1253-61 [11229918.001]
  • (PMID = 20418431.001).
  • [ISSN] 1098-5336
  • [Journal-full-title] Applied and environmental microbiology
  • [ISO-abbreviation] Appl. Environ. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chemokines, CC; 0 / Recombinant Proteins
  • [Other-IDs] NLM/ PMC2893477
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74. Karabec M, Łyskowski A, Tauber KC, Steinkellner G, Kroutil W, Grogan G, Gruber K: Structural insights into substrate specificity and solvent tolerance in alcohol dehydrogenase ADH-'A' from Rhodococcus ruber DSM 44541. Chem Commun (Camb); 2010 Sep 14;46(34):6314-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural insights into substrate specificity and solvent tolerance in alcohol dehydrogenase ADH-'A' from Rhodococcus ruber DSM 44541.
  • The structure of the alcohol dehydrogenase ADH-'A' from Rhodococcus ruber reveals possible reasons for its remarkable tolerance to organic co-solvents and suggests new directions for structure-informed mutagenesis to produce enzymes of altered substrate specificity or improved selectivity.

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  • (PMID = 20676439.001).
  • [ISSN] 1364-548X
  • [Journal-full-title] Chemical communications (Cambridge, England)
  • [ISO-abbreviation] Chem. Commun. (Camb.)
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / W 901
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alcohols; 0 / Ketones; 0 / Solvents; EC 1.1.1.1 / Alcohol Dehydrogenase
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75. Holmes RS: Opossum alcohol dehydrogenases: Sequences, structures, phylogeny and evolution: evidence for the tandem location of ADH genes on opossum chromosome 5. Chem Biol Interact; 2009 Mar 16;178(1-3):8-15

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Opossum alcohol dehydrogenases: Sequences, structures, phylogeny and evolution: evidence for the tandem location of ADH genes on opossum chromosome 5.
  • BLAT (BLAST-Like Alignment Tool) analyses and interrogations of the recently published opossum genome were undertaken using previously reported rat ADH amino acid sequences.
  • Evidence is presented for six opossum ADH genes localized on chromosome 5 and organized in a comparable ADH gene cluster to that reported for human and rat ADH genes.
  • The predicted amino acid sequences and secondary structures for the opossum ADH subunits and the intron-exon boundaries for opossum ADH genes showed a high degree of similarity with other mammalian ADHs, and four opossum ADH classes were identified, namely ADH1, ADH3, ADH6 and ADH4 (for which three genes were observed: ADH4A, ADH4B and ADH4C).
  • Percentage substitution rates were examined for ADHs during vertebrate evolution which indicated that ADH3 is evolving at a much slower rate to that of the other ADH classes.

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  • (PMID = 18848532.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase
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76. de Gonzalo G, Lavandera I, Faber K, Kroutil W: Enzymatic reduction of ketones in "micro-aqueous" media catalyzed by ADH-A from Rhodococcus ruber. Org Lett; 2007 May 24;9(11):2163-6
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  • [Title] Enzymatic reduction of ketones in "micro-aqueous" media catalyzed by ADH-A from Rhodococcus ruber.
  • Mono- and biphasic aqueous-organic solvent systems (50% v v-1) as well as micro-aqueous organic systems (99% v v-1) were successfully employed for the biocatalytic reduction of ketones catalyzed by alcohol dehydrogenase ADH-A from Rhodococcus ruber via hydrogen transfer.

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  • (PMID = 17469836.001).
  • [ISSN] 1523-7060
  • [Journal-full-title] Organic letters
  • [ISO-abbreviation] Org. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ketones; 059QF0KO0R / Water; EC 1.1.1.1 / Alcohol Dehydrogenase
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77. Edegger K, Gruber CC, Poessl TM, Wallner SR, Lavandera I, Faber K, Niehaus F, Eck J, Oehrlein R, Hafner A, Kroutil W: Biocatalytic deuterium- and hydrogen-transfer using over-expressed ADH-'A': enhanced stereoselectivity and 2H-labeled chiral alcohols. Chem Commun (Camb); 2006 Jun 14;(22):2402-4
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  • [Title] Biocatalytic deuterium- and hydrogen-transfer using over-expressed ADH-'A': enhanced stereoselectivity and 2H-labeled chiral alcohols.
  • Employing the over-expressed highly organic solvent tolerant alcohol dehydrogenase ADH-'A' from Rhodococcus ruber DSM 44541, versatile building blocks, which were not accessible by the wild type catalyst, were obtained in > 99% e.e.

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  • (PMID = 16733594.001).
  • [ISSN] 1359-7345
  • [Journal-full-title] Chemical communications (Cambridge, England)
  • [ISO-abbreviation] Chem. Commun. (Camb.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alcohols; 0 / Ketones; 7YNJ3PO35Z / Hydrogen; AR09D82C7G / Deuterium; EC 1.1.1.1 / Alcohol Dehydrogenase
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78. Luo X, Kranzler HR, Zuo L, Wang S, Schork NJ, Gelernter J: Diplotype trend regression analysis of the ADH gene cluster and the ALDH2 gene: multiple significant associations with alcohol dependence. Am J Hum Genet; 2006 Jun;78(6):973-87
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diplotype trend regression analysis of the ADH gene cluster and the ALDH2 gene: multiple significant associations with alcohol dependence.
  • The relationships between some alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genes and alcohol dependence (AD) have long been studied in many populations, but not comprehensively.
  • In the present study, we genotyped 16 markers within the ADH gene cluster (including the ADH1A, ADH1B, ADH1C, ADH5, ADH6, and ADH7 genes), 4 markers within the ALDH2 gene, and 38 unlinked ancestry-informative markers in a case-control sample of 801 individuals.
  • We also found that several ADH genes and the ALDH2 gene were susceptibility loci for AD, and the associations were best explained by several independent risk genes.

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  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2004 Aug 15;129B(1):110-5 [15274051.001]
  • [Cites] Biol Psychiatry. 2004 Aug 15;56(4):217-24 [15312808.001]
  • [Cites] Ann Hum Genet. 1972 Mar;35(3):243-53 [5072686.001]
  • [Cites] Ann Hum Genet. 1973 Apr;36(4):401-14 [4748759.001]
  • [Cites] Proc Natl Acad Sci U S A. 1977 Oct;74(10):4378-81 [270680.001]
  • [Cites] Genet Epidemiol. 1984;1(3):215-28 [6544238.001]
  • [Cites] Exp Mol Pathol. 2003 Apr;74(2):183-9 [12710951.001]
  • [Cites] Am J Hum Genet. 2003 Jun;72(6):1492-1504 [12817591.001]
  • [Cites] Hum Genet. 2003 Sep;113(4):325-36 [12884000.001]
  • [Cites] Genetics. 2003 Aug;164(4):1567-87 [12930761.001]
  • [Cites] Am J Epidemiol. 2003 Sep 1;158(5):397-400 [12936892.001]
  • [Cites] Am J Hum Genet. 2003 Nov;73(5):1162-9 [14574645.001]
  • [Cites] Genet Epidemiol. 1990;7(3):177-85 [2369997.001]
  • [Cites] Biometrics. 1991 Mar;47(1):53-61 [2049513.001]
  • [Cites] Hum Genet. 1992 Dec;90(4):395-401 [1362387.001]
  • [Cites] Genet Epidemiol. 1993;10(6):581-6 [8314064.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Jun;18(3):640-3 [7943668.001]
  • [Cites] Proc Natl Sci Counc Repub China B. 1994 Jul;18(3):101-6 [7972542.001]
  • [Cites] J Biol Chem. 1995 Mar 3;270(9):4305-11 [7876191.001]
  • [Cites] Am J Hum Genet. 1999 Oct;65(4):1148-60 [10486334.001]
  • [Cites] Am J Med Genet. 2000 Oct 9;96(5):632-7 [11054770.001]
  • [Cites] Am J Hum Genet. 2001 Apr;68(4):978-89 [11254454.001]
  • [Cites] Ann Hum Genet. 2001 Mar;65(Pt 2):207-19 [11427179.001]
  • [Cites] Behav Genet. 2001 Mar;31(2):231-9 [11545539.001]
  • [Cites] Genome Res. 2001 Dec;11(12):2115-9 [11731502.001]
  • [Cites] Am J Hum Genet. 2002 Jan;70(1):157-69 [11741196.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Dec;25(12):1773-7 [11781511.001]
  • [Cites] Hum Hered. 2002;53(2):79-91 [12037407.001]
  • [Cites] Science. 2002 Jun 21;296(5576):2225-9 [12029063.001]
  • [Cites] Am J Psychiatry. 2002 Aug;159(8):1432-4 [12153842.001]
  • [Cites] Hum Mol Genet. 2002 Oct 1;11(20):2463-8 [12351582.001]
  • [Cites] Arukoru Kenkyuto Yakubutsu Ison. 1995 Feb;30(1):33-42 [7726757.001]
  • [Cites] Alcohol Clin Exp Res. 1995 Jun;19(3):564-6 [7573775.001]
  • [Cites] Hepatology. 1996 Feb;23(2):234-9 [8591846.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Feb;20(1):52-5 [8651462.001]
  • [Cites] Nat Genet. 1996 Aug;13(4):399-408 [8696333.001]
  • [Cites] Br J Psychiatry. 1996 Jun;168(6):762-7 [8773821.001]
  • [Cites] Am J Hum Genet. 1997 Mar;60(3):703-16 [9042931.001]
  • [Cites] Alcohol Clin Exp Res. 1997 Oct;21(7):1272-7 [9347089.001]
  • [Cites] Am J Hum Genet. 1997 Nov;61(5):1189-99 [9345092.001]
  • [Cites] Biometrics. 1997 Dec;53(4):1253-61 [9423247.001]
  • [Cites] J Stud Alcohol. 1998 Mar;59(2):133-9 [9500299.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):207-15 [9603606.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):216-21 [9603607.001]
  • [Cites] Ann Hum Genet. 1998 Jan;62(Pt 1):55-60 [9659978.001]
  • [Cites] Am J Hum Genet. 1998 Dec;63(6):1839-51 [9837836.001]
  • [Cites] Am J Hum Genet. 1998 Nov;63(5):1531-40 [9867708.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1147-57 [10090900.001]
  • [Cites] Hum Genet. 1999 Feb;104(2):177-87 [10190330.001]
  • [Cites] Am J Hum Genet. 1999 Sep;65(3):795-807 [10441588.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17316-21 [15563601.001]
  • [Cites] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300.001]
  • [Cites] Nat Genet. 2005 Apr;37(4):413-7 [15793588.001]
  • [Cites] Genet Epidemiol. 2005 May;28(4):302-12 [15782414.001]
  • [Cites] Am J Psychiatry. 2005 May;162(5):1005-7 [15863808.001]
  • [Cites] Am J Hum Genet. 2005 Jun;76(6):967-86 [15834813.001]
  • [Cites] Hum Mol Genet. 2005 Aug 15;14(16):2421-34 [16000316.001]
  • [Cites] Pharmacogenet Genomics. 2005 Nov;15(11):755-68 [16220108.001]
  • [Cites] Neuropsychopharmacology. 2006 May;31(5):1085-95 [16237392.001]
  • [Cites] Am J Hum Genet. 2000 Oct;67(4):947-59 [10954684.001]
  • [Cites] Genet Epidemiol. 1999;17 Suppl 1:S421-6 [10597473.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 2000;64:295-341 [10697413.001]
  • [Cites] Hepatology. 2000 Apr;31(4):984-9 [10733556.001]
  • [Cites] Mol Pathol. 1999 Oct;52(5):295-9 [10748880.001]
  • [Cites] Genetics. 2000 Jun;155(2):945-59 [10835412.001]
  • [Cites] Exp Clin Psychopharmacol. 2000 May;8(2):168-75 [10843299.001]
  • [Cites] Bioinformatics. 2000 Feb;16(2):182-3 [10842743.001]
  • [Cites] Am J Hum Genet. 2000 Jul;67(1):170-81 [10827107.001]
  • [Cites] Life Sci. 2000;67(10):1163-73 [10954050.001]
  • [Cites] Am J Hum Genet. 2003 Jan;72(1):115-24 [12478478.001]
  • [Cites] Am J Epidemiol. 2003 Nov 1;158(9):899-914 [14585768.001]
  • [Cites] Genet Epidemiol. 2004 Jan;26(1):22-30 [14691954.001]
  • [Cites] Biol Psychiatry. 2004 Jan 15;55(2):112-7 [14732589.001]
  • [Cites] Am J Hum Genet. 2004 Apr;74(4):765-9 [14997420.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2004 Apr 1;126B(1):19-22 [15048643.001]
  • [Cites] Stat Med. 2004 May 15;23(9):1439-53 [15116352.001]
  • (PMID = 16685648.001).
  • [ISSN] 0002-9297
  • [Journal-full-title] American journal of human genetics
  • [ISO-abbreviation] Am. J. Hum. Genet.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA012690; United States / NIAAA NIH HHS / AA / P50-AA12870; United States / NIDA NIH HHS / DA / K24-DA15105; United States / NIDA NIH HHS / DA / R01-DA12849; United States / NIDA NIH HHS / DA / R01 DA012849; United States / NCRR NIH HHS / RR / M01-RR06192; United States / NIDA NIH HHS / DA / K24 DA015105; United States / NIMH NIH HHS / MH / K02-MH01387; United States / NIAAA NIH HHS / AA / R01-AA11330; United States / NIAAA NIH HHS / AA / K24 AA013736; United States / NCRR NIH HHS / RR / M01 RR006192; United States / NIDA NIH HHS / DA / R01-DA12690; United States / NIAAA NIH HHS / AA / K08 AA013732; United States / NIAAA NIH HHS / AA / K08-AA13732; United States / NIAAA NIH HHS / AA / K24-AA13736; United States / NIAAA NIH HHS / AA / R01 AA011330; United States / NIAAA NIH HHS / AA / P50 AA012870
  • [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 / Genetic Markers; EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  • [Other-IDs] NLM/ PMC1474098
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79. Jelski W, Mroczko B, Szmitkowski M: The diagnostic value of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) measurement in the sera of colorectal cancer patients. Dig Dis Sci; 2010 Oct;55(10):2953-7
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The diagnostic value of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) measurement in the sera of colorectal cancer patients.
  • BACKGROUND: The activity of total alcohol dehydrogenase (ADH) and class I isoenzymes is significantly higher in colorectal cancer tissue than in healthy mucosa.
  • AIM: The aim of this study was to investigate a potential role of ADH and aldehyde dehydrogenase (ALDH) as tumor markers for colorectal cancer.
  • Total ADH activity and class III and IV isoenzymes were measured by photometric, but ALDH activity and ADH I and II by the fluorometric method, with class-specific fluorogenic substrates.
  • RESULTS: There was significant increase in the activity of ADH I isoenzyme and ADH total in the sera of colorectal cancer patients compared to the control.
  • The diagnostic sensitivity for ADH I was 76%, specificity 82%, AND positive and negative predictive values were 85 and 74%, respectively.
  • The sensitivity and specificity of ADH I increased with the stage of the carcinoma.
  • The area under ROC curve for ADH I was 0.72.
  • CONCLUSION: The results suggest a potential role for ADH I as marker for colorectal cancer.
  • [MeSH-major] Alcohol Dehydrogenase / blood. Aldehyde Dehydrogenase / blood. Biomarkers / blood. Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / metabolism. Isoenzymes / blood

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  • [Cites] FEBS Lett. 1989 Oct 23;257(1):105-9 [2806555.001]
  • [Cites] Clin Chem. 1993 Nov;39(11 Pt 1):2298-304 [8222224.001]
  • [Cites] Clin Exp Med. 2006 Jun;6(2):89-93 [16820997.001]
  • [Cites] Anal Biochem. 1989 Apr;178(1):57-62 [2729580.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):977-81 [15309886.001]
  • [Cites] Clin Exp Med. 2007 Dec;7(4):154-7 [18188528.001]
  • [Cites] Anal Biochem. 1979 Oct 15;99(1):65-71 [231394.001]
  • [Cites] Dig Dis Sci. 2005 Jun;50(6):1019-24 [15986847.001]
  • [Cites] Hematol Oncol Clin North Am. 2002 Aug;16(4):775-810 [12418049.001]
  • [Cites] Digestion. 1996;57(2):105-8 [8785998.001]
  • [Cites] Clin Chem Lab Med. 2008;46(10):1423-8 [18844497.001]
  • [Cites] Clin Chim Acta. 2006 Sep;371(1-2):143-7 [16603145.001]
  • [Cites] Clin Chim Acta. 2007 May 1;380(1-2):208-12 [17368603.001]
  • [Cites] Alcohol Clin Exp Res. 1996 May;20(3):551-5 [8727253.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Dec;20(9):1569-76 [8986205.001]
  • [Cites] Int J Colorectal Dis. 2007 Jan;22(1):33-8 [16520929.001]
  • [Cites] Clin Chem Lab Med. 2003 May;41(5):646-51 [12812262.001]
  • [Cites] BMJ. 2000 Feb 12;320(7232):424-7 [10669448.001]
  • (PMID = 20069455.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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80. Nishitani Y, Matsumoto H: Ethanol rapidly causes activation of JNK associated with ER stress under inhibition of ADH. FEBS Lett; 2006 Jan 9;580(1):9-14
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  • [Title] Ethanol rapidly causes activation of JNK associated with ER stress under inhibition of ADH.
  • Activations of JNK and Akt were enhanced by co-treatment with ethanol and a classical inhibitor of alcohol dehydrogenase (ADH).
  • Ethanol loading with ADH inhibition causes down-regulation of GRP78 mRNA levels.

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  • (PMID = 16343492.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Central Nervous System Depressants; 0 / Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / RNA, Messenger; 0 / molecular chaperone GRP78; 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / MAP Kinase Kinase 4
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81. Jelski W, Orywal K, Panek B, Gacko M, Mroczko B, Szmitkowski M: The activity of class I, II, III and IV of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in the wall of abdominal aortic aneurysms. Exp Mol Pathol; 2009 Aug;87(1):59-62

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  • [Title] The activity of class I, II, III and IV of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in the wall of abdominal aortic aneurysms.
  • OBJECTIVE: Human blood vessels contain a huge amount of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), which play a significant role in the metabolism of many biological substances and participate in various metabolic pathways.
  • The aim of this study was the investigation of the differences between the activities of ADH and ALDH in the wall of aortic aneurysm and wall of healthy aorta, that can explain the pathological background of aneurysm development.
  • METHODS: For the measurement of the activity of class I and II ADH isoenzymes and ALDH activity the fluorometric methods was employed.
  • The total ADH activity and activity of class III and IV isoenzymes was measured by the photometric method.
  • RESULTS: The activity of the class I ADH isoenzyme was significantly lower in the wall of aortic aneurysm than in healthy aorta.
  • The other tested classes of ADH showed the tendency to lower level of the activity in aneurysm tissue than that in wall of unchanged aorta.
  • The activities of total ADH and ALDH were also not significantly lower in the aneurysms.
  • CONCLUSION: The decrease of the activity of class I ADH isoenzymes in the wall of aortic aneurysm may be a factor of some disorders in metabolic pathways with participation of these isoenzymes.

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  • (PMID = 19332052.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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82. Jelski W, Zalewski B, Szmitkowski M: Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with liver cancer. J Clin Lab Anal; 2008;22(3):204-9
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  • [Title] Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with liver cancer.
  • The principal enzymes catalyzing the conversion of ethanol to acetate are alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).
  • In previous investigations we have found elevated levels of ADH, ALDH, and class I ADH activity in liver cancer cells.
  • In this work, the activity of ADH isoenzymes, and ALDH in the sera of patients with liver cancer was measured.
  • Total ADH activity was measured by photometric method with p-nitrosodimethylaniline (NDMA) as a substrate and ALDH activity by the fluorimetric method with 6-methoxy-2-naphtaldehyde as a substrate.
  • The activity of class III ADH was measured by the photometric method with formaldehyde and class IV with m-nitrobenzaldehyde as a substrate.
  • A statistically significant increase of class I ADH isoenzymes was found in the sera of cancer patients.
  • The activity of the class I ADH isoenzyme was significantly higher in the sera of patients with metastatic tumors than with primary cancers.
  • The total ADH activity was significantly higher (44%) among patients with cancer than healthy ones.
  • The activity of class I ADH isoenzymes was elevated only in the serum of patients with metastatic liver cancer.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18484658.001).
  • [ISSN] 0887-8013
  • [Journal-full-title] Journal of clinical laboratory analysis
  • [ISO-abbreviation] J. Clin. Lab. Anal.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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83. Li H, Gu S, Cai X, Speed WC, Pakstis AJ, Golub EI, Kidd JR, Kidd KK: Ethnic related selection for an ADH Class I variant within East Asia. PLoS One; 2008 Apr 02;3(4):e1881
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  • [Title] Ethnic related selection for an ADH Class I variant within East Asia.
  • BACKGROUND: The alcohol dehydrogenases (ADH) are widely studied enzymes and the evolution of the mammalian gene cluster encoding these enzymes is also well studied.
  • METHODOLOGY/PRINCIPAL FINDINGS: Here we report new data on 30 SNPs in the ADH7 and Class I ADH region in samples of 24 populations from China and Laos.

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  • [Cites] Hepatology. 2000 Apr;31(4):984-9 [10733556.001]
  • [Cites] Xenobiotica. 2000 Mar;30(3):285-95 [10752643.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):476-82 [15734975.001]
  • [Cites] Eur J Cardiovasc Prev Rehabil. 2005 Aug;12(4):355-62 [16079643.001]
  • [Cites] Jpn J Clin Oncol. 2003 Mar;33(3):111-21 [12672787.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):419-25 [12750236.001]
  • [Cites] Cancer Res. 2003 Jun 15;63(12):3092-100 [12810634.001]
  • [Cites] Am J Hum Genet. 2003 Sep;73(3):671-6 [12870132.001]
  • [Cites] Hum Genet. 2003 Sep;113(4):325-36 [12884000.001]
  • [Cites] Am J Hum Genet. 2003 Nov;73(5):1162-9 [14574645.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]
  • [Cites] Addict Behav. 2004 Sep;29(7):1295-309 [15345266.001]
  • [Cites] Nature. 2004 Sep 16;431(7006):302-5 [15372031.001]
  • [Cites] Neuropharmacology. 2004;47 Suppl 1:140-7 [15464133.001]
  • [Cites] Nat Genet. 2004 Nov;36(11 Suppl):S21-7 [15507999.001]
  • [Cites] World Rev Nutr Diet. 1990;63:143-60 [2197794.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1991;40:255-87 [2031085.001]
  • [Cites] Hum Genet. 1992 Jan;88(3):344-6 [1733836.001]
  • [Cites] Pharmacogenetics. 1992 Apr;2(2):48-62 [1302043.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Jun;18(3):640-3 [7943668.001]
  • [Cites] Nat Genet. 1995 Apr;9(4):341-2 [7795635.001]
  • [Cites] Am J Psychiatry. 1995 Aug;152(8):1219-21 [7625477.001]
  • [Cites] Hum Genet. 1995 Aug;96(2):151-4 [7635462.001]
  • [Cites] Mol Biol Evol. 1996 May;13(5):685-90 [8676743.001]
  • [Cites] Br J Psychiatry. 1996 Jun;168(6):762-7 [8773821.001]
  • [Cites] Gastroenterology. 1997 Mar;112(3):766-75 [9041238.001]
  • [Cites] Biol Psychiatry. 1997 Mar 15;41(6):703-9 [9066994.001]
  • [Cites] Proc Natl Sci Counc Repub China B. 1997 Jul;21(3):106-11 [9309874.001]
  • [Cites] Cancer Invest. 2005;23(6):497-504 [16203657.001]
  • [Cites] Bioinformatics. 2005 Oct 15;21(20):3938-9 [16131520.001]
  • [Cites] Hum Genet. 2005 Oct;117(6):511-9 [16028061.001]
  • [Cites] Alcohol Alcohol. 2006 Jan-Feb;41(1):14-7 [16239350.001]
  • [Cites] Int J Cancer. 2006 Apr 15;118(8):1998-2002 [16287084.001]
  • [Cites] Am J Hum Genet. 2000 Oct;67(4):947-59 [10954684.001]
  • [Cites] Am J Med Genet. 2000 Oct 9;96(5):632-7 [11054770.001]
  • [Cites] Hum Genet. 2000 Dec;107(6):582-90 [11153912.001]
  • [Cites] Nat Rev Genet. 2000 Nov;1(2):126-33 [11253652.001]
  • [Cites] Am J Hum Genet. 2001 Apr;68(4):978-89 [11254454.001]
  • [Cites] Alcohol Clin Exp Res. 2001 May;25(5 Suppl ISBRA):157S-163S [11391066.001]
  • [Cites] Pathol Biol (Paris). 2001 Nov;49(9):676-82 [11762128.001]
  • [Cites] Hum Genet. 2002 Jan;110(1):80-8 [11810301.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5261-6 [11959976.001]
  • [Cites] Am J Hum Genet. 2002 Jul;71(1):84-99 [12050823.001]
  • [Cites] Am J Psychiatry. 2002 Aug;159(8):1432-4 [12153842.001]
  • [Cites] Alcohol Clin Exp Res. 1997 Oct;21(7):1272-7 [9347089.001]
  • [Cites] J Stud Alcohol. 1998 Mar;59(2):133-9 [9500299.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):207-15 [9603606.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):216-21 [9603607.001]
  • [Cites] Alcohol Clin Exp Res. 1998 Oct;22(7):1463-9 [9802529.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1147-57 [10090900.001]
  • [Cites] Mol Biol Evol. 1999 Jan;16(1):37-48 [10331250.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Jul 22;261(1):100-7 [10405330.001]
  • [Cites] Am J Hum Genet. 1999 Sep;65(3):795-807 [10441588.001]
  • [Cites] Dig Dis. 2005;23(3-4):297-303 [16508294.001]
  • [Cites] PLoS Biol. 2006 Mar;4(3):e72 [16494531.001]
  • [Cites] Hum Mol Genet. 2006 May 1;15(9):1539-49 [16571603.001]
  • [Cites] Alcohol Clin Exp Res. 2006 Jun;30(6):928-37 [16737450.001]
  • [Cites] Int J Cancer. 2006 Sep 15;119(6):1447-54 [16596645.001]
  • [Cites] Hereditas. 2005 Feb;142(2005):103-11 [16970620.001]
  • [Cites] Am J Hum Genet. 2007 Mar;80(3):441-56 [17273965.001]
  • [Cites] Hum Mutat. 2007 May;28(5):506-10 [17285601.001]
  • [Cites] Thromb Res. 2007;120(5):679-84 [17289126.001]
  • [Cites] Am J Hum Genet. 2007 Oct;81(4):842-6 [17847010.001]
  • [Cites] Hum Genet. 2007 Nov;122(3-4):383-8 [17657509.001]
  • [Cites] Nature. 2007 Oct 18;449(7164):913-8 [17943131.001]
  • [Cites] Nature. 2002 Oct 24;419(6909):832-7 [12397357.001]
  • (PMID = 18382665.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / P01 GM057672; United States / NIAAA NIH HHS / AA / R01 AA009379; United States / NIAAA NIH HHS / AA / AA009379; United States / NIGMS NIH HHS / GM / GM057672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1B protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Other-IDs] NLM/ PMC2268739
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84. Luo X, Kranzler HR, Zuo L, Wang S, Schork NJ, Gelernter J: Multiple ADH genes modulate risk for drug dependence in both African- and European-Americans. Hum Mol Genet; 2007 Feb 15;16(4):380-90
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  • [Title] Multiple ADH genes modulate risk for drug dependence in both African- and European-Americans.
  • We previously reported associations of AD with seven alcohol dehydrogenase (ADH) genes.
  • We genotyped 16 markers within the ADH gene cluster and 38 unlinked ancestry-informative markers in a case-control sample of 718 individuals.

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  • [Cites] Pharmacogenet Genomics. 2005 Nov;15(11):755-68 [16220108.001]
  • [Cites] Psychopharmacology (Berl). 2005 Nov;183(1):41-53 [16163523.001]
  • [Cites] Hum Mol Genet. 2006 Mar 15;15(6):807-19 [16476706.001]
  • [Cites] Hum Mol Genet. 2006 May 1;15(9):1539-49 [16571603.001]
  • [Cites] Neuropsychopharmacology. 2006 May;31(5):1085-95 [16237392.001]
  • [Cites] Am J Hum Genet. 2006 May;78(5):759-69 [16642432.001]
  • [Cites] Am J Hum Genet. 2006 Jun;78(6):973-87 [16685648.001]
  • [Cites] Neuropsychopharmacology. 2006 Jul;31(7):1393-405 [16205781.001]
  • [Cites] Biol Psychiatry. 2007 Mar 1;61(5):599-608 [17069770.001]
  • [Cites] Genetics. 2000 Jun;155(2):945-59 [10835412.001]
  • [Cites] Am J Hum Genet. 2000 Jul;67(1):170-81 [10827107.001]
  • [Cites] Hum Mol Genet. 2000 Nov 22;9(19):2895-908 [11092766.001]
  • [Cites] J Biomed Sci. 2001 Jan-Feb;8(1):71-6 [11173978.001]
  • [Cites] Am J Hum Genet. 2001 Apr;68(4):978-89 [11254454.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5300-5 [11320258.001]
  • [Cites] Pharmacol Biochem Behav. 2001 Mar;68(3):455-9 [11325399.001]
  • [Cites] Neuroreport. 2001 May 8;12(6):1103-6 [11338173.001]
  • [Cites] Ann Hum Genet. 2001 Mar;65(Pt 2):207-19 [11427179.001]
  • [Cites] Genome Res. 2001 Dec;11(12):2115-9 [11731502.001]
  • [Cites] Mol Psychiatry. 2002;7(2):224-8 [11840318.001]
  • [Cites] J Neurosci. 2002 Nov 1;22(21):9595-603 [12417684.001]
  • [Cites] Am J Psychiatry. 2003 Apr;160(4):687-95 [12668357.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2003 Jul 1;120B(1):97-108 [12815747.001]
  • [Cites] Am J Epidemiol. 2003 Sep 1;158(5):397-400 [12936892.001]
  • [Cites] Am J Hum Genet. 2003 Nov;73(5):1162-9 [14574645.001]
  • [Cites] Drug Alcohol Depend. 2003 Nov 24;72(2):169-82 [14636972.001]
  • [Cites] Genet Epidemiol. 2004 Jan;26(1):22-30 [14691954.001]
  • [Cites] Neuromolecular Med. 2004;5(1):85-108 [15001815.001]
  • [Cites] Am J Hum Genet. 2004 Apr;74(4):765-9 [14997420.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 2004 Jun;369(6):576-82 [15138661.001]
  • [Cites] Eur J Pharmacol. 2004 Oct 19;502(3):221-31 [15476748.001]
  • [Cites] Eur J Pharmacol. 1976 Nov;40(1):45-56 [1033072.001]
  • [Cites] Arch Gen Psychiatry. 1978 Jul;35(7):837-44 [678037.001]
  • [Cites] Biochem Biophys Res Commun. 1986 Sep 30;139(3):1009-16 [2429655.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8908-12 [3466164.001]
  • [Cites] Psychol Rev. 1987 Oct;94(4):469-92 [3317472.001]
  • [Cites] Psychiatry Res. 1988 Mar;23(3):335-44 [3387505.001]
  • [Cites] Arch Gen Psychiatry. 1992 Aug;49(8):624-9 [1637252.001]
  • [Cites] J Med Chem. 1995 Jan 20;38(2):379-88 [7830281.001]
  • [Cites] Anesthesiology. 1996 Jan;84(1):143-54 [8572328.001]
  • [Cites] Pharmacol Toxicol. 1995 Nov;77(5):323-6 [8778744.001]
  • [Cites] Nat Genet. 1996 Aug;13(4):399-408 [8696333.001]
  • [Cites] Brain Res. 1996 Oct 14;736(1-2):287-96 [8930335.001]
  • [Cites] Biometrics. 1997 Dec;53(4):1253-61 [9423247.001]
  • [Cites] Arch Gen Psychiatry. 1998 Nov;55(11):967-72 [9819064.001]
  • [Cites] Am J Hum Genet. 1998 Nov;63(5):1531-40 [9867708.001]
  • [Cites] Eur J Biochem. 1999 Jun;262(2):324-9 [10336614.001]
  • [Cites] Nat Genet. 2005 Apr;37(4):413-7 [15793588.001]
  • [Cites] Am J Hum Genet. 2005 Jun;76(6):967-86 [15834813.001]
  • [Cites] Am J Med Genet B Neuropsychiatr Genet. 2005 Jul 5;136B(1):45-52 [15909294.001]
  • [Cites] Hum Mol Genet. 2005 Aug 15;14(16):2421-34 [16000316.001]
  • [Cites] Neuroscience. 2005;135(3):959-68 [16111825.001]
  • (PMID = 17185388.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA012690; United States / NIAAA NIH HHS / AA / P50-AA12870; United States / NIDA NIH HHS / DA / K24-DA15105; United States / NIDA NIH HHS / DA / R01-DA12849; United States / NIDA NIH HHS / DA / R01 DA012849; United States / NCRR NIH HHS / RR / M01-RR06192; United States / NIDA NIH HHS / DA / K24 DA015105; United States / NIMH NIH HHS / MH / K02-MH01387; United States / NIAAA NIH HHS / AA / R01-AA11330; United States / NIAAA NIH HHS / AA / K24 AA013736; United States / NCRR NIH HHS / RR / M01 RR006192; United States / NIDA NIH HHS / DA / R01-DA12690; United States / NIAAA NIH HHS / AA / K08 AA013732; United States / NIAAA NIH HHS / AA / K08-AA13732; United States / NIAAA NIH HHS / AA / K24-AA13736; United States / NIAAA NIH HHS / AA / R01 AA011330; United States / NIAAA NIH HHS / AA / R01-AA016015; United States / NIAAA NIH HHS / AA / P50 AA012870; United States / NIAAA NIH HHS / AA / R01 AA016015
  • [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] England
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Other-IDs] NLM/ NIHMS20098; NLM/ PMC1853246
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85. Jelski W, Zalewski B, Szmitkowski M: Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with pancreatic cancer. Dig Dis Sci; 2008 Aug;53(8):2276-80
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  • [Title] Alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) activity in the sera of patients with pancreatic cancer.
  • BACKGROUND: Numerous experiments have shown that alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are present in cells of various cancer and can play role in carcinogenesis.
  • Total ADH activity was measured by photometric method with p-nitrosodimethylaniline (NDMA) as a substrate, and ALDH activity by the fluorometric method with 6-methoxy-2-naphtaldehyde as a substrate.
  • The activities of other tested ADH isoenzymes and total ALDH were unchanged.
  • The activity of the class I ADH isoenzyme was significantly higher in the sera of drinkers with pancreatic cancer than non-drinkers.

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  • [Cites] Isozymes Curr Top Biol Med Res. 1983;8:219-44 [6354998.001]
  • [Cites] FEBS Lett. 1989 Oct 23;257(1):105-9 [2806555.001]
  • [Cites] Alcohol. 2005 Apr;35(3):205-11 [16054982.001]
  • [Cites] Dig Dis Sci. 2007 Feb;52(2):531-5 [17211707.001]
  • [Cites] Eur J Clin Chem Clin Biochem. 1994 Dec;32(12):881-4 [7696434.001]
  • [Cites] Gastroenterology. 2002 Jan;122(1):106-18 [11781286.001]
  • [Cites] Anal Biochem. 1989 Apr;178(1):57-62 [2729580.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):977-81 [15309886.001]
  • [Cites] Arch Med Res. 1997 Winter;28(4):453-71 [9428569.001]
  • [Cites] Anal Biochem. 1979 Oct 15;99(1):65-71 [231394.001]
  • [Cites] Digestion. 1996;57(2):105-8 [8785998.001]
  • [Cites] Dig Dis Sci. 2003 Jul;48(7):1230-3 [12870777.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Dec;20(9):1569-76 [8986205.001]
  • [Cites] Pancreas. 2007 Aug;35(2):142-6 [17632320.001]
  • [Cites] Dig Dis Sci. 2002 Jul;47(7):1554-7 [12141816.001]
  • (PMID = 18095160.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.1.1.284 / formaldehyde dehydrogenase (glutathione); EC 1.2.- / Aldehyde Oxidoreductases; EC 1.2.1.3 / Aldehyde Dehydrogenase
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86. Gonzàlez-Duarte R, Albalat R: Merging protein, gene and genomic data: the evolution of the MDR-ADH family. Heredity (Edinb); 2005 Sep;95(3):184-97
Saccharomyces Genome Database. Saccharomyces Genome Database .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Merging protein, gene and genomic data: the evolution of the MDR-ADH family.
  • Multiple members of the MDR-ADH (MDR: Medium-chain dehydrogenases/reductases; ADH: alcohol dehydrogenase) family are found in vertebrates, although the enzymes that belong to this family have also been isolated from bacteria, yeast, plant and animal sources.

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  • (PMID = 16121213.001).
  • [ISSN] 0018-067X
  • [Journal-full-title] Heredity
  • [ISO-abbreviation] Heredity (Edinb)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Number-of-references] 94
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87. Han Y, Gu S, Oota H, Osier MV, Pakstis AJ, Speed WC, Kidd JR, Kidd KK: Evidence of positive selection on a class I ADH locus. Am J Hum Genet; 2007 Mar;80(3):441-56
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence of positive selection on a class I ADH locus.
  • The alcohol dehydrogenase (ADH) family of enzymes catalyzes the reversible oxidation of alcohol to acetaldehyde.
  • Seven ADH genes exist in a segment of ~370 kb on 4q21.
  • Products of the three class I ADH genes that share 95% sequence identity are believed to play the major role in the first step of ethanol metabolism.
  • Data consisted of 54 single-nucleotide polymorphisms (SNPs) across the ADH clusters in a global sampling of 42 populations.
  • The ADH1B Arg47His functional polymorphism has the highest F(st) of the 54 SNPs in the ADH cluster, and it is significantly above the mean F(st) of 382 presumably neutral sites tested on the same 42 population samples.

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  • [Cites] Hepatology. 2000 Apr;31(4):984-9 [10733556.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):207-15 [9603606.001]
  • [Cites] Am J Med Genet. 2000 Oct 9;96(5):632-7 [11054770.001]
  • [Cites] Pathol Biol (Paris). 2001 Nov;49(9):676-82 [11762128.001]
  • [Cites] Am J Hum Genet. 2002 Jul;71(1):84-99 [12050823.001]
  • [Cites] Nature. 2002 Oct 24;419(6909):832-7 [12397357.001]
  • [Cites] Alcohol Clin Exp Res. 2002 Dec;26(12):1759-63 [12500098.001]
  • [Cites] Exp Mol Pathol. 2003 Apr;74(2):183-9 [12710951.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2003 May;12(5):419-25 [12750236.001]
  • [Cites] Hum Genet. 2003 Sep;113(4):325-36 [12884000.001]
  • [Cites] Ann Hum Genet. 2004 Mar;68(Pt 2):93-109 [15008789.001]
  • [Cites] Immunogenetics. 2004 Jul;56(4):225-37 [15185041.001]
  • [Cites] J Hered. 2004 Sep-Oct;95(5):406-20 [15388768.001]
  • [Cites] Neuropharmacology. 2004;47 Suppl 1:140-7 [15464133.001]
  • [Cites] Nat Genet. 2004 Nov;36(11 Suppl):S21-7 [15507999.001]
  • [Cites] In Vitro. 1984 Nov;20(11):856-8 [6519667.001]
  • [Cites] World Rev Nutr Diet. 1990;63:143-60 [2197794.001]
  • [Cites] Am J Med Genet. 1998 May 8;81(3):216-21 [9603607.001]
  • [Cites] Alcohol Clin Exp Res. 1998 Oct;22(7):1463-9 [9802529.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1147-57 [10090900.001]
  • [Cites] Genome Res. 1999 May;9(5):492-8 [10330129.001]
  • [Cites] Am J Hum Genet. 1999 Sep;65(3):795-807 [10441588.001]
  • [Cites] J Theor Biol. 2005 Jul 21;235(2):207-19 [15862590.001]
  • [Cites] PLoS Genet. 2005 Sep;1(3):e41 [16205789.001]
  • [Cites] Bioinformatics. 2005 Oct 15;21(20):3938-9 [16131520.001]
  • [Cites] Hum Genet. 2005 Oct;117(6):511-9 [16028061.001]
  • [Cites] Alcohol Alcohol. 2006 Jan-Feb;41(1):14-7 [16239350.001]
  • [Cites] Alcohol Clin Exp Res. 2005 Dec;29(12):2091-100 [16385178.001]
  • [Cites] Hum Genet. 2006 Mar;119(1-2):92-102 [16362345.001]
  • [Cites] PLoS Biol. 2006 Mar;4(3):e72 [16494531.001]
  • [Cites] Am J Hum Genet. 1991 Apr;48(4):677-81 [2014795.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1991;40:255-87 [2031085.001]
  • [Cites] Pharmacogenetics. 1992 Apr;2(2):48-62 [1302043.001]
  • [Cites] Lancet. 1994 Mar 19;343(8899):741-2 [7907720.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Jun;18(3):640-3 [7943668.001]
  • [Cites] Am J Psychiatry. 1995 Aug;152(8):1219-21 [7625477.001]
  • [Cites] Hum Genet. 1995 Aug;96(2):151-4 [7635462.001]
  • [Cites] J Hered. 1995 Sep-Oct;86(5):409-11 [7560877.001]
  • [Cites] Mol Biol Evol. 1996 May;13(5):685-90 [8676743.001]
  • [Cites] Br J Psychiatry. 1996 Jun;168(6):762-7 [8773821.001]
  • [Cites] Alcohol Alcohol Suppl. 1994;2:29-34 [8974313.001]
  • [Cites] Alcohol Clin Exp Res. 1997 Oct;21(7):1272-7 [9347089.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1460-5 [9465037.001]
  • [Cites] J Stud Alcohol. 1998 Mar;59(2):133-9 [9500299.001]
  • [Cites] J Hum Genet. 2000;45(3):127-32 [10807536.001]
  • (PMID = 17273965.001).
  • [ISSN] 0002-9297
  • [Journal-full-title] American journal of human genetics
  • [ISO-abbreviation] Am. J. Hum. Genet.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / P01 GM057672; United States / NIAAA NIH HHS / AA / R01 AA009379; United States / NIAAA NIH HHS / AA / AA09379; United States / NIGMS NIH HHS / GM / GM57672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Other-IDs] NLM/ PMC1821113
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88. Fredlund E, Beerlage C, Melin P, Schnürer J, Passoth V: Oxygen and carbon source-regulated expression of PDC and ADH genes in the respiratory yeast Pichia anomala. Yeast; 2006 Dec;23(16):1137-49
Hazardous Substances Data Bank. OXYGEN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxygen and carbon source-regulated expression of PDC and ADH genes in the respiratory yeast Pichia anomala.
  • Two ADH isogenes, PaADH1 and PaADH2, and one PDC gene, PaPDC1, were amplified from genomic P. anomala DNA by a two-step PCR approach, using degenerated primers against conserved regions of the respective genes for cloning core regions, and PCR-based gene walking for cloning the respective 5' and 3'-ends.

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  • [Copyright] Copyright 2006 John Wiley & Sons, Ltd.
  • (PMID = 17133621.001).
  • [ISSN] 0749-503X
  • [Journal-full-title] Yeast (Chichester, England)
  • [ISO-abbreviation] Yeast
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 4.1.1.1 / Pyruvate Decarboxylase; IY9XDZ35W2 / Glucose; S88TT14065 / Oxygen
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89. Jelski W, Kozlowski M, Laudanski J, Niklinski J, Szmitkowski M: The activity of class I, II, III, and IV alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in esophageal cancer. Dig Dis Sci; 2009 Apr;54(4):725-30
MedlinePlus Health Information. consumer health - Esophageal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The activity of class I, II, III, and IV alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in esophageal cancer.
  • Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the main enzymes involved in ethanol metabolism, which leads to generation of acetaldehyde.
  • In this study the activity of ADH isoenzymes and ALDH in esophageal cancer were compared with the activity in normal tissue.
  • METHODS: For measurement of the activity of class I and II ADH isoenzymes and ALDH activity fluorimetric methods were employed.
  • Total ADH activity and activity of class III and IV isoenzymes was measured by the photometric method.
  • RESULTS: The total activity of ADH and activity of class IV ADH were significantly higher in cancer cells than in healthy tissues.
  • The other tested classes of ADH showed a tendency toward higher activity in cancer than in normal cells.
  • CONCLUSION: Increased ADH IV activity may be a factor intensifying carcinogenesis, because of the increased ability to form acetaldehyde from ethanol.

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  • [Cites] FEBS Lett. 1989 Oct 23;257(1):105-9 [2806555.001]
  • [Cites] Gut. 2000 Dec;47(6):825-31 [11076882.001]
  • [Cites] J Gastroenterol Hepatol. 2006 Oct;21 Suppl 3:S26-9 [16958666.001]
  • [Cites] Dig Dis Sci. 2007 Feb;52(2):531-5 [17211707.001]
  • [Cites] Int J Cancer. 2008 Mar 15;122(6):1347-56 [18033686.001]
  • [Cites] Clin Exp Med. 2006 Jun;6(2):89-93 [16820997.001]
  • [Cites] Anal Biochem. 1989 Apr;178(1):57-62 [2729580.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):977-81 [15309886.001]
  • [Cites] Alcohol Clin Exp Res. 1993 Apr;17(2):376-81 [8488982.001]
  • [Cites] Anal Biochem. 1979 Oct 15;99(1):65-71 [231394.001]
  • [Cites] J Clin Lab Anal. 2003;17(3):93-6 [12696080.001]
  • [Cites] Nat Rev Cancer. 2007 Aug;7(8):599-612 [17646865.001]
  • [Cites] Clin Chem Lab Med. 2008;46(3):323-8 [18254707.001]
  • [Cites] Alcohol Alcohol. 1995 Mar;30(2):153-61 [7662033.001]
  • [Cites] Proc Nutr Soc. 2004 Feb;63(1):65-71 [15070439.001]
  • [Cites] Addict Biol. 2001 Sep;6(4):309-323 [11900609.001]
  • [Cites] Clin Liver Dis. 2005 Feb;9(1):1-35 [15763227.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Dec;20(9):1569-76 [8986205.001]
  • [Cites] Dig Dis. 2005;23(3-4):204-13 [16508284.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] Pancreas. 2007 Aug;35(2):142-6 [17632320.001]
  • [Cites] Nutr Cancer. 2008;60(3):354-63 [18444169.001]
  • [Cites] Gut. 2000 Dec;47(6):748-50 [11076870.001]
  • [Cites] Carcinogenesis. 2001 Mar;22(3):433-9 [11238183.001]
  • [Cites] Eur J Biochem. 2003 Jun;270(12):2652-62 [12787032.001]
  • (PMID = 18688716.001).
  • [ISSN] 1573-2568
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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90. Tomita M, Otsuka Y, Iida R, Kobayashi S, Kuriyama S, Hosoya T: [Syndrome of inappropriate ADH secretion (SIADH) induced by pramipexole in a patient with Parkinson's disease]. Nihon Jinzo Gakkai Shi; 2005;47(5):531-5
MedlinePlus Health Information. consumer health - Parkinson's Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Syndrome of inappropriate ADH secretion (SIADH) induced by pramipexole in a patient with Parkinson's disease].
  • Blood concentration of ADH measured at the onset was substantially higher(39.5 pg/ml) than normal (0.3-3.5 pg/ml under normal osmolarity).
  • Diseases causing hyponatremia, such as liver cirrhosis, congestive heart failure, hypotonic dehydration, and malignancy-associated inappropriate ADH secretion (SIADH), were all excluded.
  • Under the suspicion of SIADH due to pramipexole, the drug was discontinued and as a result, her consciousness level improved rapidly together with a prompt reduction in ADH level (9.2 pg/ml).
  • Since pramipexole is classified as a dopaminergic receptor agonist, this case may provide new insight into a link between ADH and the dopaminergic receptor in the central nervous system.

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  • (PMID = 16130408.001).
  • [ISSN] 0385-2385
  • [Journal-full-title] Nihon Jinzo Gakkai shi
  • [ISO-abbreviation] Nihon Jinzo Gakkai Shi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antiparkinson Agents; 0 / Benzothiazoles; 0 / Thiazoles; 83619PEU5T / pramipexole
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91. Shih HJ, Jones CD: Patterns of amino acid evolution in the Drosophila ananassae chimeric gene, siren, parallel those of other Adh-derived chimeras. Genetics; 2008 Oct;180(2):1261-3
FlyBase. FlyBase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of amino acid evolution in the Drosophila ananassae chimeric gene, siren, parallel those of other Adh-derived chimeras.
  • siren1 and siren2 are novel alcohol dehydrogenase (Adh)-derived chimeric genes in the Drosophila bipectinata complex. D. ananassae, however, harbors a single homolog of these genes.
  • Like other Adh-derived chimeric genes, siren evolved adaptively shortly after it was formed.

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  • [Cites] Genetics. 2000 May;155(1):431-49 [10790415.001]
  • [Cites] Genetics. 2000 Sep;156(1):219-27 [10978287.001]
  • [Cites] Syst Biol. 2002 Oct;51(5):786-805 [12396591.001]
  • [Cites] Proc Natl Acad Sci U S A. 1966 Jul;56(1):119-25 [5229841.001]
  • [Cites] Proc Natl Acad Sci U S A. 1968 Jan;59(1):102-9 [5242114.001]
  • [Cites] Nature. 1991 Jun 20;351(6328):652-4 [1904993.001]
  • [Cites] Genetics. 2007 Mar;175(3):1429-40 [17237518.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 16;101(46):16246-50 [15534206.001]
  • [Cites] Genetics. 2005 May;170(1):207-19 [15781692.001]
  • [Cites] Genet Res. 2005 Feb;85(1):23-46 [16089034.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 9;102(32):11373-8 [16076957.001]
  • [Cites] Genetics. 2005 Dec;171(4):1719-27 [16143626.001]
  • [Cites] Mol Phylogenet Evol. 2006 Jun;39(3):787-98 [16527496.001]
  • [Cites] Comput Appl Biosci. 1997 Oct;13(5):555-6 [9367129.001]
  • (PMID = 18780749.001).
  • [ISSN] 0016-6731
  • [Journal-full-title] Genetics
  • [ISO-abbreviation] Genetics
  • [Language] ENG
  • [Databank-accession-numbers] GENBANK/ EU877936/ EU877937/ EU877938/ EU877939/ EU877940/ EU877941/ EU877942/ EU877943/ EU877944/ EU877945/ EU880420/ EU880421/ EU880422/ EU880423/ EU880424/ EU880425/ EU880426/ EU880427/ EU880428/ EU880429
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK056350; United States / NIDDK NIH HHS / DK / DK56350
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Drosophila Proteins; EC 1.1.1.1 / ADH protein, Drosophila; EC 1.1.1.1 / Alcohol Dehydrogenase
  • [Other-IDs] NLM/ PMC2567373
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92. Macgregor S, Lind PA, Bucholz KK, Hansell NK, Madden PA, Richter MM, Montgomery GW, Martin NG, Heath AC, Whitfield JB: Associations of ADH and ALDH2 gene variation with self report alcohol reactions, consumption and dependence: an integrated analysis. Hum Mol Genet; 2009 Feb 1;18(3):580-93
SciCrunch. OMIM: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Associations of ADH and ALDH2 gene variation with self report alcohol reactions, consumption and dependence: an integrated analysis.
  • Alcohol dependence (AD) is a complex disorder with environmental and genetic origins.
  • This study tested for associations between nine polymorphisms in ALDH2 and 41 in the seven ADH genes, and alcohol-related flushing, alcohol use and dependence symptom scores in 4597 Australian twins.

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  • [Cites] Pharmacogenomics J. 2008 Jun;8(3):220-7 [17923853.001]
  • [Cites] Twin Res Hum Genet. 2008 Jun;11(3):287-305 [18498207.001]
  • [Cites] Alcohol Clin Exp Res. 1997 Jun;21(4):596-601 [9194910.001]
  • [Cites] Psychol Med. 1997 Nov;27(6):1381-96 [9403910.001]
  • [Cites] J Stud Alcohol. 1998 Mar;59(2):133-9 [9500299.001]
  • [Cites] J Abnorm Psychol. 1998 Aug;107(3):363-74 [9715572.001]
  • [Cites] Alcohol Clin Exp Res. 1998 Aug;22(5):1048-52 [9726271.001]
  • [Cites] Alcohol Clin Exp Res. 1998 Oct;22(7):1463-9 [9802529.001]
  • [Cites] Biol Psychiatry. 1999 Mar 1;45(5):518-21 [10088041.001]
  • [Cites] Biol Psychiatry. 1999 Mar 1;45(5):522-32 [10088042.001]
  • [Cites] Psychol Med. 1999 Sep;29(5):1069-81 [10576299.001]
  • [Cites] Addiction. 1999 Sep;94(9):1361-70 [10615721.001]
  • [Cites] Am J Hum Genet. 2000 Jan;66(1):279-92 [10631157.001]
  • [Cites] Hepatology. 2000 Apr;31(4):984-9 [10733556.001]
  • [Cites] Eur J Hum Genet. 2000 Jul;8(7):545-51 [10909856.001]
  • [Cites] Am J Med Genet. 2000 Oct 9;96(5):632-7 [11054770.001]
  • [Cites] J Stud Alcohol. 2000 Nov;61(6):827-35 [11188488.001]
  • [Cites] Behav Genet. 2001 Mar;31(2):231-9 [11545539.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Sep;25(9):1257-63 [11584143.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Sep;25(9):1264-9 [11584144.001]
  • [Cites] Nat Genet. 2002 Jan;30(1):97-101 [11731797.001]
  • [Cites] Alcohol Clin Exp Res. 2001 Dec;25(12):1773-7 [11781511.001]
  • [Cites] Am J Hum Genet. 2002 Jul;71(1):84-99 [12050823.001]
  • [Cites] Am J Hum Genet. 2002 Nov;71(5):1247-50; author reply 1250-1 [12452180.001]
  • [Cites] Alcohol Clin Exp Res. 2004 Jan;28(1):10-4 [14745297.001]
  • [Cites] Science. 1972 Jan 28;175(4020):449-50 [5007912.001]
  • [Cites] Behav Genet. 1985 Jul;15(4):305-47 [4041178.001]
  • [Cites] Hepatology. 1986 May-Jun;6(3):502-10 [3519419.001]
  • [Cites] Eur J Biochem. 1986 Sep 1;159(2):215-8 [3758060.001]
  • [Cites] Hum Genet. 1989 Apr;82(1):14-6 [2714775.001]
  • [Cites] Arch Gen Psychiatry. 1991 Jan;48(1):19-28 [1984758.001]
  • [Cites] Arukoru Kenkyuto Yakubutsu Ison. 1993 Feb;28(1):13-25 [8512495.001]
  • [Cites] Arch Gen Psychiatry. 1993 Sep;50(9):690-8 [8357294.001]
  • [Cites] Hepatology. 1994 Feb;19(2):360-6 [7904979.001]
  • [Cites] J Stud Alcohol. 1994 Mar;55(2):149-58 [8189735.001]
  • [Cites] Alcohol Clin Exp Res. 1994 Jun;18(3):640-3 [7943668.001]
  • [Cites] Am J Psychiatry. 1995 Aug;152(8):1219-21 [7625477.001]
  • [Cites] Alcohol Clin Exp Res. 1995 Jun;19(3):582-92 [7573778.001]
  • [Cites] J Clin Invest. 1995 Nov;96(5):2180-6 [7593603.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Feb;20(1):81-6 [8651467.001]
  • [Cites] Br J Psychiatry. 1996 Jun;168(6):762-7 [8773821.001]
  • [Cites] Hum Genet. 1996 Apr;97(4):409-13 [8834233.001]
  • [Cites] J Clin Invest. 1996 Nov 1;98(9):2027-32 [8903321.001]
  • [Cites] Alcohol Alcohol Suppl. 1994;2:113-9 [8974324.001]
  • [Cites] Biol Psychiatry. 1997 Mar 15;41(6):703-9 [9066994.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1147-57 [10090900.001]
  • [Cites] Am J Hum Genet. 1999 Sep;65(3):795-807 [10441588.001]
  • [Cites] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300.001]
  • [Cites] Psychol Med. 2004 Nov;34(8):1519-30 [15724882.001]
  • [Cites] Am J Psychiatry. 2005 May;162(5):1005-7 [15863808.001]
  • [Cites] J Stud Alcohol. 2005 Mar;66(2):196-204 [15957670.001]
  • [Cites] Am J Cardiol. 2005 Jul 15;96(2):227-32 [16018848.001]
  • [Cites] Bioinformatics. 2005 Aug 15;21(16):3445-7 [15947021.001]
  • [Cites] Ther Drug Monit. 2005 Dec;27(6):700-3 [16404797.001]
  • [Cites] Curr Psychiatry Rep. 2006 Apr;8(2):151-7 [16539893.001]
  • [Cites] Twin Res Hum Genet. 2006 Apr;9(2):194-7 [16611487.001]
  • [Cites] Hum Mol Genet. 2006 May 1;15(9):1539-49 [16571603.001]
  • [Cites] Neuropsychopharmacology. 2006 May;31(5):1085-95 [16237392.001]
  • [Cites] Am J Hum Genet. 2006 Jun;78(6):973-87 [16685648.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):1009-13 [16702384.001]
  • [Cites] Alcohol Clin Exp Res. 2006 Jul;30(7):1093-100 [16792555.001]
  • [Cites] Alcohol Clin Exp Res. 2006 Sep;30(9):1470-8 [16930209.001]
  • [Cites] Alcohol Clin Exp Res. 2007 Feb;31(2):216-20 [17250612.001]
  • [Cites] Hum Mutat. 2007 May;28(5):506-10 [17285601.001]
  • [Cites] Alcohol Clin Exp Res. 2007 Aug;31(8):1297-301 [17559546.001]
  • [Cites] Alcohol Clin Exp Res. 2008 May;32(5):785-95 [18331377.001]
  • (PMID = 18996923.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / AA13320; United States / NIAAA NIH HHS / AA / AA13321; United States / NIAAA NIH HHS / AA / AA013326; United States / NIAAA NIH HHS / AA / AA07728; United States / NIAAA NIH HHS / AA / AA11998; United States / NIAAA NIH HHS / AA / AA014041; United States / NIAAA NIH HHS / AA / AA07535
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Twin Study
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.1.1.1 / ADH1B protein, human; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / ALDH2 protein, human; EC 1.2.1.3 / Aldehyde Dehydrogenase
  • [Other-IDs] NLM/ PMC2722191
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93. Chen SH, Zhong GS, Li AL, Li SH, Wu LK: [Influence of Hovenia dulcis on alcohol concentration in blood and activity of alcohol dehydrogenase (ADH) of animals after drinking]. Zhongguo Zhong Yao Za Zhi; 2006 Jul;31(13):1094-6
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  • [Title] [Influence of Hovenia dulcis on alcohol concentration in blood and activity of alcohol dehydrogenase (ADH) of animals after drinking].
  • The activity of ADH in the liver in aqueous extract of H. dulcis group was increased in 2-3 h, while it was significantly increased in 1-1.5 h (P <0.05).
  • CONCLUSION: The aqueous extract of H. dulcis could reduce the alchol concentration in blood of animals and inrease the activity of ADH after given alcohol.

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  • (PMID = 17048612.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase
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94. Westerlund M, Galter D, Carmine A, Olson L: Tissue- and species-specific expression patterns of class I, III, and IV Adh and Aldh 1 mRNAs in rodent embryos. Cell Tissue Res; 2005 Nov;322(2):227-36
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  • [Title] Tissue- and species-specific expression patterns of class I, III, and IV Adh and Aldh 1 mRNAs in rodent embryos.
  • In the present study, the spatial and temporal expression patterns of Adh 1, Adh 3, Adh 4, and Aldh 1 mRNAs in embryonic C57BL/6 mice (E 9.5-E19.5) and Sprague-Dawley rats (E12.5-P0) have been investigated by using radioactive oligonucleotide in situ hybridization.
  • Expression of Adh 1 and Adh 4 mRNAs was observed in adrenal cortex and olfactory epithelium in mice.
  • Additionally, Adh 1 was expressed in epidermis, liver, conjunctival, and intestinal epithelium.
  • In rat embryos, expression was less extensive, with Adh 1 mRNA being found in liver and intestines.
  • Adh 3 expression was ubiquitous in both mouse and rat embryos, suggesting a housekeeping function of the gene.
  • Consistent with previous studies in adult rats and mice, our data suggest that Adh 3 is the only ADH class present in rodent brain.
  • Adh and Aldh gene activity in mouse and rat embryos indicate the possible involvement of the respective enzymes in retinoid metabolism and participation in defense against toxic insults, including those that may be involved in the pathogenesis of PD.

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  • (PMID = 16047160.001).
  • [ISSN] 0302-766X
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / RNA, Messenger; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; EC 1.2.1.- / aldehyde dehydrogenase 1; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 1.2.1.36 / Retinal Dehydrogenase
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95. Jelski W, Zalewski B, Szmitkowski M: The activity of class I, II, III, and IV alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in liver cancer. Dig Dis Sci; 2008 Sep;53(9):2550-5
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  • [Title] The activity of class I, II, III, and IV alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in liver cancer.
  • BACKGROUND: Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), which are most abundant in the liver, are the main enzymes involved in ethanol and acetaldehyde metabolism.
  • AIMS: The purpose of this study was to compare the activity of ADH isoenzymes and ALDH between liver carcinoma cells and healthy hepatocytes.
  • METHODS: Fluorimetric methods were used for measurement of the activity of class I and II ADH isoenzymes and ALDH activity.
  • Total ADH activity and activity of class III and IV isoenzymes were measured by a photometric method.
  • RESULTS: The activities of total ADH, ALDH, and class I ADH were significantly higher in cancer cells than in healthy tissues.
  • The other tested classes of ADH showed a tendency toward higher activity in cancer than in normal cells.
  • CONCLUSION: Differences in the activities of total ADH, ALDH and class I ADH isoenzyme between cancer liver tissues and healthy hepatocytes might be a factor in ethanol metabolism disorders, which can intensify carcinogenesis.

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  • [Cites] Recent Dev Alcohol. 1998;14:7-40 [9751941.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9247-51 [1409630.001]
  • [Cites] FEBS Lett. 1989 Oct 23;257(1):105-9 [2806555.001]
  • [Cites] Dig Dis Sci. 2007 Feb;52(2):531-5 [17211707.001]
  • [Cites] Clin Exp Med. 2006 Jun;6(2):89-93 [16820997.001]
  • [Cites] Alcohol Clin Exp Res. 2001 May;25(5 Suppl ISBRA):137S-143S [11391063.001]
  • [Cites] Anal Biochem. 1989 Apr;178(1):57-62 [2729580.001]
  • [Cites] Dig Dis Sci. 2004 Jun;49(6):977-81 [15309886.001]
  • [Cites] Ann Clin Biochem. 1993 Mar;30 ( Pt 2):146-51 [8385433.001]
  • [Cites] Anal Biochem. 1979 Oct 15;99(1):65-71 [231394.001]
  • [Cites] Histochem Cell Biol. 1999 May;111(5):391-7 [10403118.001]
  • [Cites] Cancer Lett. 1993 Feb;68(2-3):177-83 [8443790.001]
  • [Cites] J Clin Lab Anal. 2003;17(3):93-6 [12696080.001]
  • [Cites] Clin Liver Dis. 2001 Feb;5(1):87-107, vi [11218921.001]
  • [Cites] Gastroenterology. 1994 Apr;106(4):1085-105 [8143977.001]
  • [Cites] Alcohol. 2005 Apr;35(3):195-203 [16054981.001]
  • [Cites] Clin Liver Dis. 2005 Feb;9(1):1-35 [15763227.001]
  • [Cites] Alcohol Clin Exp Res. 1996 Dec;20(9):1569-76 [8986205.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] Clin Liver Dis. 2001 Feb;5(1):69-85 [11218920.001]
  • [Cites] Pancreas. 2007 Aug;35(2):142-6 [17632320.001]
  • [Cites] Carcinogenesis. 1985 Dec;6(12):1683-7 [4064245.001]
  • [Cites] Dig Dis Sci. 2002 Jul;47(7):1554-7 [12141816.001]
  • (PMID = 18224440.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.1.1.1 / alcohol dehydrogenase IV; EC 1.1.1.284 / formaldehyde dehydrogenase (glutathione); EC 1.2.- / Aldehyde Oxidoreductases; EC 1.2.1.3 / Aldehyde Dehydrogenase
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96. Husemoen LL, Fenger M, Friedrich N, Tolstrup JS, Beenfeldt Fredriksen S, Linneberg A: The association of ADH and ALDH gene variants with alcohol drinking habits and cardiovascular disease risk factors. Alcohol Clin Exp Res; 2008 Nov;32(11):1984-91
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  • [Title] The association of ADH and ALDH gene variants with alcohol drinking habits and cardiovascular disease risk factors.
  • In a Caucasian population, we examined the association of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genetic variants with alcohol drinking habits, biomarkers of alcohol exposure, and risk factors for cardiovascular disease.
  • ADH and ALDH gene variants were determined by standard techniques.

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  • (PMID = 18782342.001).
  • [ISSN] 1530-0277
  • [Journal-full-title] Alcoholism, clinical and experimental research
  • [ISO-abbreviation] Alcohol. Clin. Exp. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase; EC 1.2.1.3 / Aldehyde Dehydrogenase
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97. Jiang Q, Liu KY, Huang XJ, Lu WK: [Syndrome inappropriate ADH secretion after allogeneic hematopoietic stem cell transplantation: a case report and literature review]. Zhonghua Xue Ye Xue Za Zhi; 2006 Feb;27(2):78-81
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  • [Title] [Syndrome inappropriate ADH secretion after allogeneic hematopoietic stem cell transplantation: a case report and literature review].
  • OBJECTIVE: To study the syndrome of inappropriate ADH secretion (SIADH) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the possible etiology.
  • Early accurate diagnosis and treatment promptly is of great importance.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Inappropriate ADH Syndrome / etiology

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  • (PMID = 16732956.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
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98. Nishimura FT, Kimura Y, Abe S, Fukunaga T, Saijoh K: Effects of polymorphisms in untranslated regions of the class I alcohol dehydrogenase (ADH) genes on alcohol metabolism in Japanese subjects and transcriptional activity in HepG2 cells. Nihon Arukoru Yakubutsu Igakkai Zasshi; 2009 Jun;44(3):139-55
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  • [Title] Effects of polymorphisms in untranslated regions of the class I alcohol dehydrogenase (ADH) genes on alcohol metabolism in Japanese subjects and transcriptional activity in HepG2 cells.
  • Human class I ADH is a dimmer formed by the random association of three types of subunits (alpha, beta and gamma) encoded by ADH1A, ADH1B, and ADH1C, respectively.
  • In conclusion, polymorphisms in the untranslated regions of ADH class I genes were demonstrated to clearly affect individual differences in alcohol metabolism.

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  • (PMID = 19618839.001).
  • [ISSN] 1341-8963
  • [Journal-full-title] Nihon Arukōru Yakubutsu Igakkai zasshi = Japanese journal of alcohol studies & drug dependence
  • [ISO-abbreviation] Nihon Arukoru Yakubutsu Igakkai Zasshi
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Untranslated Regions; 3K9958V90M / Ethanol; EC 1.1.1.1 / Alcohol Dehydrogenase
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99. Ellsworth RE, Ellsworth DL, Weyandt JD, Fantacone-Campbell JL, Deyarmin B, Hooke JA, Shriver CD: Chromosomal alterations in pure nonneoplastic breast lesions: implications for breast cancer progression. Ann Surg Oncol; 2010 Jun;17(6):1688-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chromosomal alterations in pure nonneoplastic breast lesions: implications for breast cancer progression.
  • INTRODUCTION: Columnar cell lesions (CCL) and atypical ductal hyperplasia (ADH) frequently coexist and share molecular changes with in situ and invasive components, suggesting that CCL and ADH may be precursors to breast cancer.
  • These conclusions are largely based on studies examining CCL and/or ADH from patients diagnosed with more advanced disease.
  • We assessed allelic imbalance (AI) in pure CCL or ADH specimens to characterize molecular changes in nonneoplastic breast lesions.
  • METHODS: DNA samples were obtained from laser-microdissected pure CCL (n = 42) or ADH (n = 31).
  • AI was assessed at 26 chromosomal regions commonly altered in breast cancer.
  • RESULTS: The average AI frequency was 6.2% in CCL and 6.1% in ADH; approximately 33% of nonneoplastic lesions had no detectable genetic changes.
  • Levels of AI in CCL and ADH were significantly (P < 0.0001) lower than observed in either low- or high-grade ductal carcinoma in situ (DCIS) lesions.
  • CONCLUSIONS: Pure CCL and ADH lesions demonstrate lower levels of genetic alterations than DCIS, invasive carcinomas or CCL/ADH lesions from cancerous breasts; alterations of chromosomes 16q and 17p were not detected.
  • Pure CCL and ADH lesions are not genetically advanced, and molecular profiles do not support these lesions as obligatory precursors to more advanced disease.
  • [MeSH-major] Allelic Imbalance. Breast / pathology. Breast Diseases / genetics. Chromosome Aberrations. Precancerous Conditions / genetics. Precancerous Conditions / pathology
  • [MeSH-minor] Algorithms. Breast Neoplasms / genetics. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / genetics. Carcinoma, Ductal, Breast / pathology. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 17 / genetics. DNA / genetics. Disease Progression. Female. Humans. Hyperplasia / genetics. Risk. Statistics, Nonparametric

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  • (PMID = 20107913.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-49-2 / DNA
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100. Bigaillon C, El Jahiri Y, Garcia C, Hejl-Garcia C, Mayaudon H, Ceppa F, Burnat P: [Inappropriate ADH secretion-induced hyponatremia and associated with paroxetine use]. Rev Med Interne; 2007 Sep;28(9):642-4
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  • [Title] [Inappropriate ADH secretion-induced hyponatremia and associated with paroxetine use].
  • [Transliterated title] Hyponatrémie par sécrétion inappropriée d'ADH associée à la prise de paroxétine.
  • Serum investigations revealed hyponatremia (121 mmol/l) with low plasma osmolarity and normal natriuria consistent with diagnosis of SIADH.

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  • (PMID = 17499890.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Serotonin Uptake Inhibitors; 41VRH5220H / Paroxetine
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