[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 12 of about 12
1. Maiti S, Chen X, Chen G: All-trans retinoic acid induction of sulfotransferases. Basic Clin Pharmacol Toxicol; 2005 Jan;96(1):44-53
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Retinoids have been used clinically as therapeutic agents against a number of cancers.
  • Retinoids have been reported to induce the phase I drug metabolizing enzymes, cytochrome P-450s.
  • The present investigation evaluates the role of retinoic acid on the expression of aryl sulfotransferase IV and hydroxysteroid sulfotransferase a in male and female Sprague-Dawley rat liver and intestine.
  • Cultured human hepatic carcinoma cells (Hep G2) and intestinal carcinoma cells (Caco-2) were also used to study retinoic acid's effect on simple phenol sulfating sulfotransferase, dehydroepiandrosterone sulfotransferase and oestrogen sulfotransferase.
  • Retinoic acid induced aryl sulfotransferase IV in liver of female rats and sulfotransferase a in liver of male rats.
  • Intestinal rat aryl sulfotransferase IV and sulfotransferase a in male rats and intestinal aryl sulfotransferase IV in female rats were also induced after retinoic acid treatment.
  • In general, intestinal sulfotransferases were found to be more responsive than hepatic sulfotransferases to retinoic acid treatment. mRNA expressions were investigated using reverse transcription polymerase chain reaction with gene specific primers.
  • [MeSH-minor] Animals. Blotting, Western. Body Weight / drug effects. Caco-2 Cells. Cell Line, Tumor. Cytosol / drug effects. Cytosol / enzymology. Dehydroepiandrosterone Sulfate / metabolism. Dose-Response Relationship, Drug. Enzyme Induction / drug effects. Female. Gene Expression Regulation, Enzymologic / drug effects. Humans. Male. RNA / biosynthesis. Rats. Rats, Sprague-Dawley. Retinoid X Receptors / drug effects. Reverse Transcriptase Polymerase Chain Reaction

  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15667595.001).
  • [ISSN] 1742-7835
  • [Journal-full-title] Basic & clinical pharmacology & toxicology
  • [ISO-abbreviation] Basic Clin. Pharmacol. Toxicol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM59873
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Retinoid X Receptors; 5688UTC01R / Tretinoin; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 63231-63-0 / RNA; EC 2.8.2.- / Sulfotransferases
  •  go-up   go-down


2. Morozevich GE, Kozlova NI, Chubukina AN, Berman AE: Role of integrin alphavbeta3 in substrate-dependent apoptosis of human intestinal carcinoma cells. Biochemistry (Mosc); 2003 Apr;68(4):416-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of integrin alphavbeta3 in substrate-dependent apoptosis of human intestinal carcinoma cells.
  • Incubation of human intestinal carcinoma Caco-2 cells in suspension (i.e., in the absence of substrate contacts) leads to massive cell death by apoptosis.
  • Since this type of apoptosis has been referred to as anoikis, we designated these cells as anoikis-positive.
  • [MeSH-major] Apoptosis. Integrin alphaVbeta3 / physiology. Intestinal Neoplasms / pathology
  • [MeSH-minor] Anoikis. Caco-2 Cells. Cell Survival / drug effects. Cell Survival / genetics. Flow Cytometry / methods. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotides, Antisense / pharmacology. Polyhydroxyethyl Methacrylate / pharmacology. Signal Transduction / genetics. Staining and Labeling / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12765524.001).
  • [ISSN] 0006-2979
  • [Journal-full-title] Biochemistry. Biokhimii︠a︡
  • [ISO-abbreviation] Biochemistry Mosc.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Integrin alphaVbeta3; 0 / Oligonucleotides, Antisense; 25249-16-5 / Polyhydroxyethyl Methacrylate
  •  go-up   go-down


3. Perloff MD, von Moltke LL, Störmer E, Shader RI, Greenblatt DJ: Saint John's wort: an in vitro analysis of P-glycoprotein induction due to extended exposure. Br J Pharmacol; 2001 Dec;134(8):1601-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 1. Chronic use of Saint John's wort (SJW) has been shown to lower the bioavailability for a variety of co-administered drugs including indinavir, cyclosporin, and digoxin.
  • Decreases in intestinal absorption through induction of the multidrug resistance transporter, P-glycoprotein (P-gp), may explain decreased bioavailability.
  • Experiments were performed with 3 to 300 microg ml(-1) of methanol-extracted SJW and 0.03 to 3 microM HYP, representing low to high estimates of intestinal concentrations.
  • 3. In induction experiments, LS-180 intestinal carcinoma cells were exposed for 3 days to SJW, HYP, vehicle or a positive control (ritonavir).
  • Similar effects occurring in vivo may explain the decreased bioavailability of P-gp substrate drugs when co-administered with SJW.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VERAPAMIL HYDROCHLORIDE .
  • Hazardous Substances Data Bank. PERYLENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Pharmacol Ther. 1999 Oct;66(4):338-45 [10546917.001]
  • [Cites] Drug Metab Dispos. 1999 Oct;27(10):1187-93 [10497146.001]
  • [Cites] Lancet. 2000 Feb 12;355(9203):547-8 [10683007.001]
  • [Cites] Lancet. 2000 Feb 12;355(9203):548-9 [10683008.001]
  • [Cites] Int Clin Psychopharmacol. 2000 Mar;15(2):61-8 [10759336.001]
  • [Cites] Am J Health Syst Pharm. 2000 Apr 1;57(7):625-6 [10768811.001]
  • [Cites] Clin Ther. 2000 Apr;22(4):411-9 [10823363.001]
  • [Cites] Drug Metab Dispos. 2000 Jun;28(6):655-60 [10820137.001]
  • [Cites] Clin Pharmacol Ther. 2000 May;67(5):451-7 [10824623.001]
  • [Cites] Transplantation. 2000 May 27;69(10):2229-30 [10852634.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7500-2 [10852961.001]
  • [Cites] Lancet. 2000 May 27;355(9218):1912 [10866469.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Jul;294(1):88-95 [10871299.001]
  • [Cites] AIDS. 2000 Jun 16;14(9):1287-9 [10894301.001]
  • [Cites] BMJ. 2000 Sep 2;321(7260):536-9 [10968813.001]
  • [Cites] J Endocrinol. 2000 Sep;166(3):R11-6 [10974665.001]
  • [Cites] Clin Pharmacol Ther. 2000 Oct;68(4):345-55 [11061574.001]
  • [Cites] Int J Clin Pharmacol Ther. 2000 Oct;38(10):500-2 [11073292.001]
  • [Cites] Science. 2001 Jan 5;291(5501):37 [11192003.001]
  • [Cites] Clin Pharmacol Ther. 2000 Dec;68(6):598-604 [11180019.001]
  • [Cites] Transplantation. 2001 Jan 27;71(2):239-41 [11213066.001]
  • [Cites] Adv Drug Deliv Rev. 2001 Mar 1;46(1-3):89-102 [11259835.001]
  • [Cites] J Clin Pharmacol. 2001 Jul;41(7):708-14 [11452702.001]
  • [Cites] In Vitro. 1976 Mar;12(3):180-91 [1262041.001]
  • [Cites] Fundam Clin Pharmacol. 1991;5(7):567-82 [1778535.001]
  • [Cites] J Biol Chem. 1993 Feb 5;268(4):2946-52 [8094079.001]
  • [Cites] Cell. 1994 May 20;77(4):491-502 [7910522.001]
  • [Cites] Mol Carcinog. 1995 Jul;13(3):129-34 [7619215.001]
  • [Cites] Mol Pharmacol. 1996 Feb;49(2):311-8 [8632764.001]
  • [Cites] BMJ. 1996 Aug 3;313(7052):253-8 [8704532.001]
  • [Cites] Br J Pharmacol. 1996 Jul;118(6):1389-96 [8832062.001]
  • [Cites] Antimicrob Agents Chemother. 1996 Sep;40(9):2087-93 [8878586.001]
  • [Cites] Curr Opin Genet Dev. 1996 Oct;6(5):610-7 [8939727.001]
  • [Cites] Pharm Res. 1998 Mar;15(3):423-8 [9563072.001]
  • [Cites] J Pharmacol Exp Ther. 1999 Apr;289(1):149-55 [10086998.001]
  • [Cites] J Clin Invest. 1999 Jul;104(2):147-53 [10411543.001]
  • [Cites] Lancet. 2000 Jan 8;355(9198):134-8 [10675182.001]
  • (PMID = 11739235.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058496; United States / NIMH NIH HHS / MH / MH-34223; United States / NIDA NIH HHS / DA / DA-13209; United States / NIDDK NIH HHS / DK / DK/AI-58496; United States / NIDA NIH HHS / DA / R21 DA013209; United States / NIMH NIH HHS / MH / MH-01237; United States / NCRR NIH HHS / RR / RR-00054; United States / NIMH NIH HHS / MH / R01 MH058435; United States / NCRR NIH HHS / RR / M01 RR000054; United States / NIDA NIH HHS / DA / DA-05258; United States / NIMH NIH HHS / MH / MH-58435; United States / NIDA NIH HHS / DA / R01 DA005258
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antidepressive Agents; 0 / P-Glycoprotein; 1N3CZ14C5O / Rhodamine 123; 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin; CJ0O37KU29 / Verapamil; EC 2.7.11.13 / Protein Kinase C; O3J8G9O825 / Ritonavir
  • [Other-IDs] NLM/ PMC1572891
  •  go-up   go-down


Advertisement
4. Erba E, Bergamaschi D, Bassano L, Damia G, Ronzoni S, Faircloth GT, D'Incalci M: Ecteinascidin-743 (ET-743), a natural marine compound, with a unique mechanism of action. Eur J Cancer; 2001 Jan;37(1):97-105
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Both SW620 and LoVo human intestinal carcinoma cell lines exposed for 1 h to ET-743 progress through S phase more slowly than control cells and then accumulate in the G2M phase.
  • ET-743 induced a significant increase in p53 levels in cell lines expressing wild-type (wt) (p53).
  • However, the p53 status does not appear to be related to the ET-743 cytotoxic activity as demonstrated by comparing the drug sensitivity in p53 (-/-) or (+/+) mouse embryo fibroblasts and in A2780 ovarian cancer cells or the A2780/CX3 sub-line transfected with a dominant-negative mutant TP53.
  • The findings that G1 phase cells are hypersensitive and that NER-deficient cells are resistant to ET-743 indicate that the mode of action of ET-743 is unique and different from that of other DNA-interacting drugs.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Colonic Neoplasms / drug therapy. Dioxoles / therapeutic use. Isoquinolines / therapeutic use
  • [MeSH-minor] Cell Cycle / drug effects. Cell Division. Cyclins / metabolism. DNA Damage. DNA, Neoplasm / analysis. Drug Screening Assays, Antitumor. Humans. Tetrahydroisoquinolines. Tumor Cells, Cultured / drug effects. Tumor Suppressor Protein p53 / metabolism

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Eur J Cancer. 2001 Jan;37(1):8 [11165123.001]
  • (PMID = 11165136.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Cyclins; 0 / DNA, Neoplasm; 0 / Dioxoles; 0 / Isoquinolines; 0 / Tetrahydroisoquinolines; 0 / Tumor Suppressor Protein p53; 114899-77-3 / trabectedin
  •  go-up   go-down


5. Weaver SA, Ward SG: Phosphoinositide 3-kinases in the gut: a link between inflammation and cancer? Trends Mol Med; 2001 Oct;7(10):455-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Carcinoma of the gastrointestinal tract is the most common internal malignancy affecting men and women in Western countries.
  • Chronic intestinal inflammation, especially of the colon, is also a Western disease and correlates with a significantly increased risk of developing cancer.
  • Indeed, there is increasing evidence that phosphatidylinositol 3-kinases (PI 3-kinases) are involved in both the pathogenesis of colorectal carcinoma and intestinal inflammation.
  • Here, we discuss this rapidly progressing area of research, presenting evidence for a pivotal role of PI 3-kinase(s) in intestinal pathophysiology.
  • [MeSH-minor] Animals. Cell Division / drug effects. Chemokines / metabolism. Enzyme Inhibitors / pharmacology. Enzyme Inhibitors / therapeutic use. Gastrointestinal Motility / physiology. Humans. Inflammation / drug therapy. Inflammation / enzymology. Inflammation / pathology. Inflammation / physiopathology. Signal Transduction

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11597520.001).
  • [ISSN] 1471-4914
  • [Journal-full-title] Trends in molecular medicine
  • [ISO-abbreviation] Trends Mol Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chemokines; 0 / Enzyme Inhibitors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Number-of-references] 63
  •  go-up   go-down


6. Lowthers EL, Richard CL, Blay J: Differential sensitivity to short-chain ceramide analogues of human intestinal carcinoma cells grown in tumor spheroids versus monolayer culture. In Vitro Cell Dev Biol Anim; 2003 Sep-Oct;39(8-9):340-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential sensitivity to short-chain ceramide analogues of human intestinal carcinoma cells grown in tumor spheroids versus monolayer culture.
  • The cytotoxic activity of short-chain (C(2)) ceramide was evaluated in human intestinal carcinoma cells grown as multicellular tumor spheroids versus the same cells cultured as monolayers under closely comparable conditions.
  • The chemotherapeutic agents 5-fluorouracil and cisplatin were equally potent against spheroids and monolayer cultures, indicating that although drug access is a problem in conventionally grown tumor spheroids it is not a problem for spheroids grown under the conditions used in this study.
  • Our results suggest that although ceramide is capable of inducing cell death in intestinal carcinoma cells grown in spheroid culture, its cellular toxicity is constrained by influences that are independent of drug access and may be the consequence of the altered cellular relationships.
  • Carcinoma cell populations show an intrinsically decreased responsiveness to the effects of ceramide when they are grown in a three-dimensional culture format.
  • [MeSH-major] Antineoplastic Agents / toxicity. Carcinoma / metabolism. Cell Culture Techniques / methods. Ceramides / toxicity. Intestinal Neoplasms / metabolism. Spheroids, Cellular / metabolism. Tumor Cells, Cultured / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1998 Sep 1;58(17):3765-8 [9731480.001]
  • [Cites] Clin Cancer Res. 1999 Jun;5(6):1583-6 [10389947.001]
  • [Cites] Cancer Res. 1998 Apr 1;58(7):1408-16 [9537241.001]
  • [Cites] J Nutr. 1994 May;124(5):615-20 [8169652.001]
  • [Cites] Biochim Biophys Acta. 2002 Dec 30;1585(2-3):114-25 [12531544.001]
  • [Cites] Cancer Res. 1989 Dec 1;49(23):6449-65 [2684393.001]
  • [Cites] Exp Cell Res. 2002 May 15;276(1):90-100 [11978011.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5747-53 [11059769.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):878-84 [11895922.001]
  • [Cites] Exp Biol Med (Maywood). 2002 May;227(5):345-53 [11976405.001]
  • [Cites] Br J Cancer. 1995 Sep;72(3):607-14 [7669569.001]
  • [Cites] Lab Invest. 2003 Jan;83(1):87-98 [12533689.001]
  • [Cites] J Nutr. 2000 Mar;130(3):522-7 [10702579.001]
  • [Cites] Biochim Biophys Acta. 1998 Dec 8;1436(1-2):233-43 [9838138.001]
  • [Cites] Eur J Biochem. 2001 Jan;268(2):193-204 [11168352.001]
  • [Cites] Cancer Res. 1997 Jun 15;57(12):2388-93 [9192815.001]
  • [Cites] J Biol Chem. 1994 Feb 4;269(5):3125-8 [8106344.001]
  • [Cites] J Clin Invest. 2002 Jul;110(1):3-8 [12093880.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 2003 Jan-Feb;39(1-2):13-20 [12892522.001]
  • [Cites] Cancer Res. 1996 Nov 1;56(21):4936-41 [8895747.001]
  • [Cites] J Cell Physiol. 2000 Sep;184(3):285-300 [10911359.001]
  • [Cites] Cancer. 1986 Oct 15;58(8):1668-80 [3756789.001]
  • [Cites] Science. 1988 Apr 8;240(4849):177-84 [2451290.001]
  • [Cites] Electrophoresis. 2002 Apr;23(7-8):1174-84 [11981867.001]
  • [Cites] Anticancer Res. 1996 Mar-Apr;16(2):573-9 [8687100.001]
  • [Cites] J Natl Cancer Inst. 2001 Mar 7;93(5):347-57 [11238696.001]
  • [Cites] Biochem Pharmacol. 2003 Nov 1;66(9):1737-47 [14563484.001]
  • (PMID = 14640787.001).
  • [ISSN] 1071-2690
  • [Journal-full-title] In vitro cellular & developmental biology. Animal
  • [ISO-abbreviation] In Vitro Cell. Dev. Biol. Anim.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ceramides; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


7. Ohno R, Yoshinaga K, Fujita T, Hasegawa K, Iseki H, Tsunozaki H, Ichikawa W, Nihei Z, Sugihara K: Depth of invasion parallels increased cyclooxygenase-2 levels in patients with gastric carcinoma. Cancer; 2001 May 15;91(10):1876-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Depth of invasion parallels increased cyclooxygenase-2 levels in patients with gastric carcinoma.
  • BACKGROUND: Nonsteroidal anti-inflammatory drugs may reduce the incidence of intestinal carcinoma, presumably through inhibition of cyclooxygenase-2 (COX-2).
  • The authors correlated tumor expression of COX-2 with clinicopathologic features in tissues from patients with gastric carcinoma.
  • RESULTS: The COX-2 index in gastric carcinoma was significantly higher than in normal mucosa (3.4 +/- 0.7 vs. 2.2 +/- 0.7; P < 0.05).
  • COX-2 indices were significantly higher in gastric carcinoma tissues with deep invasion; indices for pT1, pT2, pT3, and pT4 carcinomas were 0.8 +/- 0.3, 2.8 +/- 0.5, 4.3 +/- 1.0, and 8.8 +/- 5.5, respectively (P < 0.05).
  • CONCLUSIONS: COX-2 mRNA expression in gastric carcinoma tissue is correlated closely with depth of invasion, indicating that COX-2 is involved in the growth of gastric carcinoma.
  • [MeSH-minor] Cyclooxygenase 2. DNA Primers / chemistry. Female. Gastrectomy. Gastric Mucosa / enzymology. Gastric Mucosa / pathology. Gastric Mucosa / surgery. Humans. Immunoenzyme Techniques. Lymphatic Metastasis. Lymphatic System / pathology. Male. Membrane Proteins. Middle Aged. Neoplasm Invasiveness. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2001 American Cancer Society.
  • (PMID = 11346869.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / RNA, Messenger; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  •  go-up   go-down


8. Perloff MD, Von Moltke LL, Marchand JE, Greenblatt DJ: Ritonavir induces P-glycoprotein expression, multidrug resistance-associated protein (MRP1) expression, and drug transporter-mediated activity in a human intestinal cell line. J Pharm Sci; 2001 Nov;90(11):1829-37
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ritonavir induces P-glycoprotein expression, multidrug resistance-associated protein (MRP1) expression, and drug transporter-mediated activity in a human intestinal cell line.
  • LS-180V intestinal carcinoma cells were exposed for 3 days to 1-100 microM RIT concurrently with controls.
  • Thus, RIT induced protein expression of P-gp and MRP1 and increased cellular drug exclusion of RH123, DOX, and CBF.
  • Similar in vivo phenomena may occur during anti-HIV drug therapy, explaining potential decrements in therapeutic efficacy due to decreases in bioavailability or alterations in drug distribution.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. HIV Protease Inhibitors / pharmacology. Membrane Transport Proteins / physiology. Multidrug Resistance-Associated Proteins. P-Glycoprotein / biosynthesis. Ritonavir / pharmacology. Tumor Cells, Cultured / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Colonic Neoplasms / metabolism. Dose-Response Relationship, Drug. Humans

  • COS Scholar Universe. author profiles.
  • SciCrunch. DrugBank: Data: Chemical .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2001 Wiley-Liss, Inc. and the American Pharmaceutical Association
  • (PMID = 11745741.001).
  • [ISSN] 0022-3549
  • [Journal-full-title] Journal of pharmaceutical sciences
  • [ISO-abbreviation] J Pharm Sci
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA-05258; United States / NIDA NIH HHS / DA / DA-13209; United States / NIDDK NIH HHS / DK / DK/AI-58496; United States / NIMH NIH HHS / MH / MH-01237; United States / NIMH NIH HHS / MH / MH-34223; United States / NIMH NIH HHS / MH / MH-58435; United States / NCRR NIH HHS / RR / RR-00054
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / HIV Protease Inhibitors; 0 / MSH3 protein, human; 0 / Membrane Transport Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / multidrug resistance-associated protein 1; O3J8G9O825 / Ritonavir
  •  go-up   go-down


9. Micu G, Stăniceanu F, Zurac S, Bastian A, Gramadă E, Popp C, Andrei R, Tudorică L, Slavnea A, Olariu M, Tebeică T, Ene A, Mateescu R, Rimbaş M, Voiosu R: E-cadherin and beta-catenin expression in gastric neoplastic and non-neoplastic lesions--correlations with H. pylori infection. Rom J Intern Med; 2010;48(3):271-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The variables of the study are the presence or absence of Helicobacter pylori, type I carcinogenetic agent for gastric carcinoma (especially intestinal type adenocarcinoma) and the presence of tumoral or non-tumoral gastric lesions.

  • MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21528754.001).
  • [ISSN] 1220-4749
  • [Journal-full-title] Romanian journal of internal medicine = Revue roumaine de médecine interne
  • [ISO-abbreviation] Rom J Intern Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Cadherins; 0 / beta Catenin
  •  go-up   go-down


10. Juopperi TA, Cesta M, Tomlinson L, Grindem CB: Extensive cutaneous metastases in a dog with duodenal adenocarcinoma. Vet Clin Pathol; 2003;32(2):88-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 6-year-old Rottweiler was presented to the North Carolina State University College of Veterinary Medicine for evaluation of multiple cutaneous nodules.
  • Cutaneous metastasis of intestinal carcinoma is rare in domestic animals.

  • MedlinePlus Health Information. consumer health - Intestinal Cancer.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12833224.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  •  go-up   go-down


11. Lin MC, Wang EJ, Lee C, Chin KT, Liu D, Chiu JF, Kung HF: Garlic inhibits microsomal triglyceride transfer protein gene expression in human liver and intestinal cell lines and in rat intestine. J Nutr; 2002 Jun;132(6):1165-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Garlic inhibits microsomal triglyceride transfer protein gene expression in human liver and intestinal cell lines and in rat intestine.
  • Fresh garlic extract (FGE) reduced MTP mRNA levels in both the human hepatoma HepG2 and intestinal carcinoma Caco-2 cells in dose-dependent fashion; significant reductions were detected with 3 g/L FGE.
  • To evaluate the in vivo effect of garlic on MTP gene expression, rats were given a single oral dose of fresh garlic homogenate (FGH), with hepatic and intestinal MTP mRNA measured 3 h after dosing.
  • Rats fed FGH had significantly (46% of the control) lower intestinal MTP mRNA levels compared with the control rats, whereas hepatic MTP mRNA levels were not affected.
  • Long-term dietary supplementation of fresh garlic may exert a lipid-lowering effect partly through reducing intestinal MTP gene expression, thus suppressing the assembly and secretion of chylomicrons from intestine to the blood circulation.
  • [MeSH-major] Carrier Proteins / antagonists & inhibitors. Garlic / chemistry. Gene Expression Regulation / physiology. Intestines / metabolism. Liver / metabolism. Plant Extracts / pharmacology
  • [MeSH-minor] Animals. Apolipoproteins B / secretion. Caco-2 Cells. Dose-Response Relationship, Drug. Humans. Rats. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12042427.001).
  • [ISSN] 0022-3166
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apolipoproteins B; 0 / Carrier Proteins; 0 / Plant Extracts; 0 / microsomal triglyceride transfer protein
  •  go-up   go-down


12. Peduto L, Reuter VE, Shaffer DR, Scher HI, Blobel CP: Critical function for ADAM9 in mouse prostate cancer. Cancer Res; 2005 Oct 15;65(20):9312-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here, we show that ADAM9 is similarly up-regulated in mouse models for prostate, breast, and intestinal carcinoma.
  • To assess whether ADAM9 is critical for the pathogenesis of prostate carcinoma, one of the most common cancers in men, we evaluated how loss of ADAM9 affects tumorigenesis in W(10) mice, a mouse model for this disease.
  • In the absence of ADAM9, most tumors in 50-week-old W(10) mice were well differentiated, whereas littermate controls expressing wild-type ADAM9 had predominantly poorly differentiated, and in some cases significantly larger, tumors.
  • Taken together, these results suggest that ADAM9 contributes to the pathogenesis of prostate cancer and potentially also other carcinomas, raising the possibility that ADAM9 might be a good target for antitumor drugs.
  • [MeSH-major] ADAM Proteins / metabolism. Membrane Proteins / metabolism. Prostatic Neoplasms / enzymology
  • [MeSH-minor] Animals. Cell Differentiation / physiology. Epidermal Growth Factor / metabolism. Female. Fibroblast Growth Factor 7 / metabolism. In Situ Hybridization. Intestinal Neoplasms / enzymology. Intestinal Neoplasms / genetics. Intestinal Neoplasms / pathology. Male. Mammary Neoplasms, Experimental / enzymology. Mammary Neoplasms, Experimental / genetics. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Inbred C57BL. Mice, Transgenic. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptor, Fibroblast Growth Factor, Type 2 / metabolism. Up-Regulation

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16230393.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM64750
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fgf7 protein, mouse; 0 / Membrane Proteins; 0 / RNA, Messenger; 126469-10-1 / Fibroblast Growth Factor 7; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / Adam9 protein, mouse
  •  go-up   go-down






Advertisement