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1. Lamont EB, Dias LE, Lauderdale DS: NSAIDs and colorectal cancer risk: do administrative data support a chemopreventive effect? J Gen Intern Med; 2007 Aug;22(8):1166-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Randomized trials show non-steroidal anti-inflammatory drugs (NSAIDs) reduce precancerous polyps.
  • METHODS: With National Ambulatory Medical Care Survey data, we find that patients with a diagnosis of osteoarthritis (OA) are 4.4 times more likely to concurrently have NSAID use documented than patients without such a diagnosis.

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  • (PMID = 17577606.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K07 CA093892; United States / NCI NIH HHS / CA / K07 CA93892
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Other-IDs] NLM/ PMC2305750
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2. Song J, Sohn KJ, Medline A, Ash C, Gallinger S, Kim YI: Chemopreventive effects of dietary folate on intestinal polyps in Apc+/-Msh2-/- mice. Cancer Res; 2000 Jun 15;60(12):3191-9
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  • [Title] Chemopreventive effects of dietary folate on intestinal polyps in Apc+/-Msh2-/- mice.
  • A recently developed murine model of intestinal tumorigenesis, which carries a heterozygous mutation in the Apc gene and a null mutation in the Msh2 gene (Apc+/-Msh2-/-), was used to determine the effect of dietary folate on intestinal tumorigenesis.
  • Microsatellite instability was determined in matched normal and polyp DNA from the small intestine and colon at 5 loci.
  • [MeSH-major] Colorectal Neoplasms / prevention & control. DNA-Binding Proteins. Diet. Folic Acid / therapeutic use. Intestinal Polyps / drug therapy. Intestinal Polyps / prevention & control
  • [MeSH-minor] Adenoma / prevention & control. Adenomatous Polyposis Coli Protein. Age Factors. Animals. Body Weight / drug effects. Colon / drug effects. CpG Islands / genetics. Cytoskeletal Proteins / genetics. Intestine, Small / drug effects. Methylation. Mice. Mice, Inbred C57BL. Microsatellite Repeats. MutS Homolog 2 Protein. Precancerous Conditions / drug therapy. Precancerous Conditions / prevention & control. Proto-Oncogene Proteins / genetics

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  • (PMID = 10866310.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 935E97BOY8 / Folic Acid; EC 3.6.1.3 / Msh2 protein, mouse; EC 3.6.1.3 / MutS Homolog 2 Protein
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3. Lal G, Ash C, Hay K, Redston M, Kwong E, Hancock B, Mak T, Kargman S, Evans JF, Gallinger S: Suppression of intestinal polyps in Msh2-deficient and non-Msh2-deficient multiple intestinal neoplasia mice by a specific cyclooxygenase-2 inhibitor and by a dual cyclooxygenase-1/2 inhibitor. Cancer Res; 2001 Aug 15;61(16):6131-6
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  • [Title] Suppression of intestinal polyps in Msh2-deficient and non-Msh2-deficient multiple intestinal neoplasia mice by a specific cyclooxygenase-2 inhibitor and by a dual cyclooxygenase-1/2 inhibitor.
  • COX-2 is overexpressed in adenomas and colorectal cancers, and COX-2-specific inhibitors have been shown to inhibit intestinal polyps in Apc(Delta716) mice more effectively than dual COX-1/COX-2 inhibitors such as sulindac.
  • Various Apc knockout mice, including the multiple intestinal neoplasia (Min) mouse and the Apc(Delta716) mouse, are limited by their lack of large numbers of colonic adenomas and aberrant crypt foci, the putative precursors of large-bowel polyps and cancers.
  • Weanling Apc+/-Msh2-/- and Min mice were fed diets containing no drug, sulindac, or a specific COX-2 inhibitor (MF-tricyclic).
  • Apc+/-Msh2-/- mice treated with MF-tricyclic had significantly fewer small-bowel polyps (mean +/- SD, 178 +/- 29) compared with mice on sulindac (278 +/- 80), or control diet (341 +/- 43; P < 0.001).
  • There was no difference in numbers of large-bowel polyps or aberrant crypt foci in mice in the three groups.
  • MF-tricyclic was also effective in reducing both small- and large-bowel polyps in Min mice.
  • Western analysis demonstrated COX-2 expression in both large- and small-bowel polyps from mice of both genotypes.
  • This study demonstrates that a specific COX-2 inhibitor is effective in preventing small-bowel polyps in mismatch-repair-deficient Min mice and both small- and large-bowel polyps in standard Min mice.
  • Therefore, specific COX-2 inhibitors may be useful as chemopreventive and therapeutic agents in humans at risk for colorectal neoplasia.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Cyclooxygenase Inhibitors / pharmacology. DNA-Binding Proteins. Intestinal Polyps / drug therapy. Isoenzymes / antagonists & inhibitors. Precancerous Conditions / drug therapy. Proto-Oncogene Proteins / physiology
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / enzymology. Adenoma / genetics. Animals. Crosses, Genetic. Cyclooxygenase 1. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. DNA Repair / genetics. Female. Furans / pharmacology. Genes, APC / genetics. Male. Membrane Proteins. Mice. Mice, Inbred C57BL. Mice, Knockout. MutS Homolog 2 Protein. Prostaglandin-Endoperoxide Synthases. Substrate Specificity. Sulindac / blood. Sulindac / pharmacology

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  • (PMID = 11507063.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / DNA-Binding Proteins; 0 / Furans; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 162011-83-8 / 3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl)phenyl)-2(5H)-furanone; 184SNS8VUH / Sulindac; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs1 protein, mouse; EC 3.6.1.3 / Msh2 protein, mouse; EC 3.6.1.3 / MutS Homolog 2 Protein
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4. Schmidt D, Horn LC: [Precancerous lesion of the endometrium and endometrial morphology in patients with tamoxifen therapy]. Zentralbl Gynakol; 2002 Jan;124(1):3-9
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  • [Title] [Precancerous lesion of the endometrium and endometrial morphology in patients with tamoxifen therapy].
  • [Transliterated title] Präkanzeröse Läsionen des Endometriums und Veränderungen unter Tamoxifen-Therapie.
  • The endometrioid type of endometrial adenocarcinoma,(type 1-carcinoma) is estrogen-dependent and frequently associated with endometrial hyperplasia.
  • In postmenopausal patients treatment should consist of abdominal hysterectomy.
  • The so-called type 2-carcinomas, serous-papillary and clear-cell type, do not demonstrate a similar association with precursor lesions.
  • Pathological findings in patients treated with Tamoxifen include endometrial atrophy and fibro-cystic endometrial polyps, sometimes with cellular metaplasias.
  • Patients with breast cancer and tamoxifen treatment have an increased risk of endometrial carcinoma.
  • In some of these patients it could be argued whether the carcinoma has developed in a proceeding endometrial hyperplasia.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Endometrial Neoplasms / pathology. Neoplasms, Hormone-Dependent / pathology. Precancerous Conditions / pathology. Tamoxifen / adverse effects
  • [MeSH-minor] Endometrium / drug effects. Endometrium / pathology. Female. Humans

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  • (PMID = 11873307.001).
  • [ISSN] 0044-4197
  • [Journal-full-title] Zentralblatt für Gynäkologie
  • [ISO-abbreviation] Zentralbl Gynakol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen
  • [Number-of-references] 38
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5. Zhang L, Ren X, Alt E, Bai X, Huang S, Xu Z, Lynch PM, Moyer MP, Wen XF, Wu X: Chemoprevention of colorectal cancer by targeting APC-deficient cells for apoptosis. Nature; 2010 Apr 15;464(7291):1058-61
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  • It holds promise for overcoming problems associated with the treatment of late-stage cancers.
  • To overcome these challenges, here we developed a new chemoprevention approach that specifically targets premalignant tumour cells for apoptosis.
  • In addition, we show that short-term and non-continuous TRAIL and RAc treatment induce apoptosis specifically in intestinal polyps, strongly inhibit tumour growth, and prolong survival in multiple intestinal neoplasms C57BL/6J-Apc(Min)/J (Apc(Min)) mice.
  • With our approach, we further demonstrate that TRAIL and RAc induce significant cell death in human colon polyps, providing a potentially selective approach for colorectal cancer chemoprevention by targeting APC-deficient cells for apoptosis.

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  • (PMID = 20348907.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI063063; United States / NIAID NIH HHS / AI / AI063063
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Cflar protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / beta Catenin; 11103-57-4 / Vitamin A; 3LE3D9D6OY / retinol acetate
  • [Other-IDs] NLM/ NIHMS396539; NLM/ PMC3425353
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6. Qiu YP, Su MM, Wu DZ, Zhao AH, Liu YM, Jia W: [Effect of jinfu kang to experimental precancerous colon lesions and urinary metabolites in rat]. Zhongguo Zhong Yao Za Zhi; 2008 Nov;33(22):2653-7
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  • [Title] [Effect of jinfu kang to experimental precancerous colon lesions and urinary metabolites in rat].
  • OBJECTIVE: : To profile urinary metabolite variations from 1, 2-dimethylhydrazine (DMH)-induced precancerous colon rats, Jinfu Kang treated rats and healthy controls.
  • RESULT: The time-dependent variations of metabolite profile showed a progressive deviation of the metabolism in the model group from the initial pattern over time and a systemic recovery of the metabolism in the treatment group, which is consistent with the histological results.
  • CONCLUSION: Metabolic study revealed that Jinfu Kang can effectively reverse metabolic departures in DMH-induced precancerous colon rat, which is consistent with pathological results.
  • [MeSH-major] Colonic Neoplasms / pathology. Colonic Polyps / drug therapy. Colonic Polyps / urine. Drugs, Chinese Herbal / pharmacology

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  • (PMID = 19216165.001).
  • [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 / Dimethylhydrazines; 0 / Drugs, Chinese Herbal
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7. Holt PR, Bresalier RS, Ma CK, Liu KF, Lipkin M, Byrd JC, Yang K: Calcium plus vitamin D alters preneoplastic features of colorectal adenomas and rectal mucosa. Cancer; 2006 Jan 15;106(2):287-96
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  • METHODS: In the current study, adenomatous polyps were transected, approximately 50% were removed for histologic examination, and the remnants tattooed before the administration of either calcium carbonate (1500 mg 3 times daily) plus vitamin D(3) 400 IU or a placebo for 6 months.
  • At study end, polyp remnants were resected completely and were used for histologic examination.
  • Immunohistochemical staining was performed in both flat mucosa and in polyp tissue.
  • RESULTS: Nineteen patients, including 11 patients in the treatment group and 8 patients in the control group, completed the study.
  • Proliferative indices fell both in flat mucosa and in polyps in the treatment group, and there were no significant changes in the control group.
  • Apoptosis and Bcl-2 immunostaining were unchanged in both groups, but the frequency of BAK-immunostained cells in the interior of polyps rose significantly.
  • Vitamin D receptor staining increased slightly and significantly in flat rectal tissue in the treatment group.
  • There were no significant changes in galectin-3 staining, but a striking reduction in MUC5AC mucin staining in polyps was observed after treatment with calcium plus vitamin D.
  • CONCLUSIONS: The administration of a calcium plus vitamin D chemopreventive regimen resulted in several changes in adenomatous tissue that may have contributed to reduced polyp formation.
  • [MeSH-major] Adenoma / drug therapy. Adenomatous Polyps / drug therapy. Calcium / administration & dosage. Colorectal Neoplasms / prevention & control. Precancerous Conditions / drug therapy. Vitamin D / administration & dosage
  • [MeSH-minor] Apoptosis. Biomarkers, Tumor / analysis. Cell Proliferation. Female. Humans. Intestinal Mucosa / drug effects. Intestinal Mucosa / pathology. Male. Middle Aged. Rectum / pathology

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  • (PMID = 16353199.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01CN25439-1; United States / NCI NIH HHS / CA / R01CA69480
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 1406-16-2 / Vitamin D; SY7Q814VUP / Calcium
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8. Smolka J, Mateasik A, Cunderlikova B, Sanislo L, Mlkvy P: In vivo fluorescence diagnostics and photodynamic therapy of gastrointestinal superficial polyps with aminolevulinic acid. A clinical and spectroscopic study. Neoplasma; 2006;53(5):418-23
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  • [Title] In vivo fluorescence diagnostics and photodynamic therapy of gastrointestinal superficial polyps with aminolevulinic acid. A clinical and spectroscopic study.
  • In the present study initial results of clinical study related to the treatment of patients having different types of precancerous lesions in the area of esophagus, stomach and intestine by photodynamic therapy (PDT) based on aminolevulinic acid (ALA-PDT) are reported.
  • The procedure was performed by laser fibre system with the light guides introduced through biopsy channel of an endoscope.
  • Each patient had a positive response to therapy.
  • It appears from the results of this study, that the treatment of precancerous lesions with ALA-PDT could be successful treatment modality.
  • [MeSH-major] Aminolevulinic Acid / therapeutic use. Intestinal Polyps / drug therapy. Photochemotherapy. Photosensitizing Agents / therapeutic use. Precancerous Conditions / drug therapy
  • [MeSH-minor] Endoscopy, Gastrointestinal. Esophageal Diseases / drug therapy. Esophageal Diseases / pathology. Female. Humans. Male. Middle Aged. Polyps / drug therapy. Polyps / pathology. Stomach Diseases / drug therapy. Stomach Diseases / pathology

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  • (PMID = 17013536.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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9. Niitsu Y, Takayama T, Miyanishi K, Nobuoka A, Hayashi T, Kukitsu T, Takanashi K, Ishiwatari H, Abe T, Kogawa T, Takahashi M, Matsunaga T, Kato J: Chemoprevention of colorectal cancer. Cancer Chemother Pharmacol; 2004 Sep;54 Suppl 1:S40-3
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  • Many chemopreventive trials have been performed, and several agents, including nonsteroidal antiinflammatory drugs, such as aspirin and sulindac, cyclooxygenase-2 selective inhibitors, such as celecoxib, vitamin D, folate, and calcium, have been shown to have some effect.
  • In these chemopreventive trials, the targeted lesions used for evaluation were mainly polyps.
  • However, the chemopreventive effects of some agents on polyps may require several years to evaluate.
  • Further, larger polyps may not be susceptible to chemopreventive agents.
  • [MeSH-minor] Animals. Clinical Trials as Topic. Glutathione S-Transferase pi. Glutathione Transferase / antagonists & inhibitors. Glutathione Transferase / metabolism. Humans. Intestinal Polyps / drug therapy. Isoenzymes / antagonists & inhibitors. Isoenzymes / metabolism. Mice. Precancerous Conditions / drug therapy

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  • (PMID = 15309513.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / Gstp1 protein, mouse
  • [Number-of-references] 33
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10. Guida M, Sanguedolce F, Bufo P, Di Spiezio Sardo A, Bifulco G, Nappi C, Pannone G: Aberrant DNA hypermethylation of hMLH-1 and CDKN2A/p16 genes in benign, premalignant and malignant endometrial lesions. Eur J Gynaecol Oncol; 2009;30(3):267-70
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  • METHODS: using nested methylation-specific PCR, we assessed the methylation of the promoter regions of two genes, hMLH1 and CDKN2A/p16, in tissue samples from endometrial polyps (EP), atypical hyperplasia (AH) and endometrial cancer (EC).
  • CONCLUSIONS: our preliminary findings seem to suggest that the association of the two genes hMLH1 and CDKN2A/p16 may allow a differential diagnosis between benign and premalignant/malignant endometrial lesions; this further supports the hypothesis that methylation of such DNA mismatch repair and tumour-suppressor genes may be associated with endometrial carcinogenesis thus representing a valuable target for selective pharmacologic therapy.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. DNA Methylation. Endometrial Neoplasms / genetics. Nuclear Proteins / genetics. Precancerous Conditions / genetics. Uterine Diseases / genetics
  • [MeSH-minor] Adult. Aged. DNA Mismatch Repair. Female. Humans. Middle Aged. Polyps / genetics. Promoter Regions, Genetic / genetics

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  • (PMID = 19697618.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / MLH1 protein, human; 0 / Nuclear Proteins
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11. Li JQ, Miki H, Ohmori M, Wu F, Funamoto Y: Expression of cyclin E and cyclin-dependent kinase 2 correlates with metastasis and prognosis in colorectal carcinoma. Hum Pathol; 2001 Sep;32(9):945-53
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  • To examine the roles of their expression in the progression of colorectal carcinoma, 21 normal mucosa, 9 hyperplastic polyps, 58 adenomas, 17 adenocarcinoma in adenomas, 203 primary cancers, 21 lymph node metastases, and 10 hepatic metastases were immunohistochemically stained with anti-cyclin E, anti-CDK2, and anti-Ki67 antibodies.
  • In primary carcinomas, the reduction of cyclin E was significantly associated with large tumor size, mucinous type, venous invasion, deep infiltration, lymph nodal metastasis, peritoneal metastasis, advanced stage, and poor prognosis.
  • Anti-cyclin E or anti-CDK2 chemotherapy should be targeted to the cancers with such overexpression.
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Aged. Antigens, Neoplasm / analysis. Biomarkers, Tumor / analysis. Colon / metabolism. Colon / pathology. Cyclin-Dependent Kinase 2. Disease-Free Survival. Humans. Hyperplasia. Immunoenzyme Techniques. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Intestinal Polyps / metabolism. Intestinal Polyps / pathology. Ki-67 Antigen / metabolism. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymphatic Metastasis. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Survival Rate

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  • [Copyright] Copyright 2001 by W.B. Saunders Company
  • (PMID = 11567224.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cyclin E; 0 / Ki-67 Antigen; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinases
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12. Half EE, Arber N: Chemoprevention of colorectal cancer: two steps forward, one step back? Future Oncol; 2006 Dec;2(6):697-704
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  • Chemoprevention aims to prevent the development or recurrence of precancerous lesions and cancers with the use of compounds that block the carcinogenic process.
  • Nonsteroidal anti-inflammatory drugs have drawn the most attention.
  • Sulindac and celecoxib were shown to be effective in promoting polyp regression in high-risk individuals with familial adenomatous polyposis.
  • In the more common sporadic setting, the Adenomatous Polyp PRevention On Vioxx (rofecoxib), Adenoma Prevention with Celecoxib and Prevention of Sporadic Adenomatous Polyps (celecoxib) trials have demonstrated a significant reduction in adenoma recurrence, but important concerns were raised regarding cardiovascular toxicity associated with selective cyclo-oxygenase-2 inhibitors.
  • [MeSH-major] Adenoma / prevention & control. Adenomatous Polyps / drug therapy. Anticarcinogenic Agents / therapeutic use. Colonic Polyps / drug therapy. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cyclooxygenase 2 Inhibitors / adverse effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Drug Therapy, Combination. Hormone Replacement Therapy. Humans

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  • (PMID = 17155896.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors
  • [Number-of-references] 59
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13. Pool-Zobel BL, Selvaraju V, Sauer J, Kautenburger T, Kiefer J, Richter KK, Soom M, Wölfl S: Butyrate may enhance toxicological defence in primary, adenoma and tumor human colon cells by favourably modulating expression of glutathione S-transferases genes, an approach in nutrigenomics. Carcinogenesis; 2005 Jun;26(6):1064-76
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  • Thus, we have investigated the gene expression of drug metabolism genes in primary human colon tissue, premalignant LT97 adenoma and HT29 tumor cells cultured in an appropriate medium+/-butyrate.
  • A total of 96 drug metabolism genes (including 12 GSTs) spotted on cDNA macroarrays (Superarray; n = 3) were hybridized with biotin-labeled cDNA probes.
  • Compared with fresh tissue, 13 genes were downregulated in primary cells cultivated ex vivo, whereas 8 genes were upregulated.
  • Several genes were less expressed in LT97 (40 genes) or in HT29 (41 and 17 genes, grown for 72 and 48 h, respectively) compared with primary colon tissue.
  • [MeSH-minor] Aged. Colonic Polyps / drug therapy. Colonic Polyps / metabolism. Dietary Fiber / metabolism. Enzyme Induction. Female. Gene Expression Profiling. Gene Expression Regulation, Enzymologic. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Precancerous Conditions / enzymology

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  • (PMID = 15746163.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Butyrates; EC 2.5.1.18 / Glutathione Transferase
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14. Telang N, Katdare M: Cell culture model for colon cancer prevention and therapy: an alternative approach to animal experimentation. ALTEX; 2007;24(1):16-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell culture model for colon cancer prevention and therapy: an alternative approach to animal experimentation.
  • Mouse models for colon cancer that harbor a germ line mutation in the tumor suppressor gene Adenomatous polyposis coli (Apc) exhibit a primary genetic defect that predisposes to a high incidence of adenomatous polyps in the small intestine rather than in the colon.
  • The newly developed colon epithelial cell lines 1638N COL-Cl(1) (clonal derivative of the parental Apc mutant cell line 1638N COL) and 1638N COL-Pr(1) (tumor derivative of the clone), established from an Apc1638N [+/-] mutant mouse, exhibit aberrant cell cycle progression, downregulated apoptosis, enhanced carcinogenic risk and tumor formation, indicating that aberrantly proliferative preneoplastic1638N COL-Cl(1) cells exhibit a quantifiable risk for carcinogenesis.
  • Treatment of these preneoplastic Apc mutant cells with a combination of celecoxib and 5-fluorouracil at clinically achievable low concentrations produced a 2.1 fold to 5.5 fold higher efficacy for cytostatic growth arrest and a 40.2% to 52.4% higher efficacy for inhibition of carcinogenic risk, relative to that obtained by these agents used individually.
  • These data validate a novel cell culture model and a rapid mechanism-based approach to prioritize efficacious drug combinations for animal studies and clinical trials on cancer prevention and, thereby, support the 3R concept by refining and/or reducing the use of animals in biomedical research relevant to prevention/therapy of colon cancer.
  • [MeSH-major] Animal Testing Alternatives. Colonic Neoplasms / drug therapy. Colonic Neoplasms / prevention & control. Genes, APC. Precancerous Conditions / prevention & control
  • [MeSH-minor] Animals. Anticarcinogenic Agents / pharmacology. Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Transformation, Neoplastic. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Humans. Mice. Mice, Inbred C57BL. Tumor Cells, Cultured

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  • (PMID = 17361317.001).
  • [ISSN] 1868-596X
  • [Journal-full-title] ALTEX
  • [ISO-abbreviation] ALTEX
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-29502-20; United States / NCI NIH HHS / CA / CA-29502-S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents
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15. Zheng W, Baker HE, Mutter GL: Involution of PTEN-null endometrial glands with progestin therapy. Gynecol Oncol; 2004 Mar;92(3):1008-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Involution of PTEN-null endometrial glands with progestin therapy.
  • OBJECTIVES: Loss of PTEN tumor suppressor gene function characterizes most (63%) endometrial precancerous lesions (endometrial intraepithelial neoplasia, EIN) and up to 83% of endometrioid endometrial cancers.
  • Because systemic progestins are known to promote involution of precancerous endometrial lesions, we tested the hypothesis that this therapy preferentially leads to clearance of immunohistochemically detected PTEN-null endometrial glands in a variety of histopathologic settings.
  • Intake biopsies were rediagnosed using EIN criteria as 5 normal (proliferative or secretory), 4 anovulatory, 3 polyps, and 5 EIN endometria.
  • RESULTS: Ten of 17 women prehormonal therapy had PTEN-null glands in the initial biopsy, and 90% (9/10) of these disappeared in the postprogestin sample.
  • CONCLUSIONS: We conclude that progestin therapy promotes involution, or disappearance, of PTEN-null endometrial glands relative to the persistence rate seen for normal cycling women.

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  • (PMID = 14984979.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA092301-01A1; United States / NCI NIH HHS / CA / CA092301-02; United States / NCI NIH HHS / CA / CA092301-03; United States / NCI NIH HHS / CA / 5 R01 CA92301
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Progestins; 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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16. Graham DY, Genta RM: Long-term proton pump inhibitor use and gastrointestinal cancer. Curr Gastroenterol Rep; 2008 Dec;10(6):543-7
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  • There is now sufficient experience with this class of drugs to allow reasonable estimation of their safety in terms of cancer development in humans.
  • It is thus recommended that patients being considered for long-term proton pump inhibitor therapy should be tested for H. pylori infection and, if present, this pathogen should be eradicated.
  • Oxyntic cell hyperplasia, glandular dilatations, and fundic gland polyps may develop in patients not infected with H. pylori, but these changes are believed to be reversible and without significant cancer risk.

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  • (PMID = 19006608.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK056338-07; United States / NIDDK NIH HHS / DK / P30 DK056338; United States / NIDDK NIH HHS / DK / DK56338; United States / NIDDK NIH HHS / DK / P30 DK056338-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 0 / Proton Pump Inhibitors
  • [Number-of-references] 42
  • [Other-IDs] NLM/ NIHMS177931; NLM/ PMC2838432
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17. Griffiths GJ: Exisulind Cell Pathways. Curr Opin Investig Drugs; 2000 Nov;1(3):386-91

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  • Cell Pathways has developed exisulind (Aptosyn), an oral apoptosis modulator and cGMP phosphodiesterase inhibitor, for the potential treatment of several oncologic indications including precancerous adenomatous polyposis coli (APC), also known as familial adenomatous polyposis (FAP), precancerous sporadic colonic polyps, cervical dysplasia and the prevention of tumor recurrence in prostate and breast cancer.
  • An NDA filing for the treatment of precancerous APC, for which the US FDA designated exisulind a Fast Track product in July 1998, was initially expected in March 1999 [291313].
  • The decision was based on unsatisfactory phase III data [308912], [313124].
  • An NDA was accepted for review by the FDA in October 1999 for the treatment of APC [328000], [338007], [344721], after data from three additional trials were submitted to the FDA in support of the NDA.
  • At this time phase II/III trials were also ongoing for prostate and breast cancer recurrence [287250], [326795].
  • Approval for the indication of FAP had been expected by the end of 2000 [365737] but in September 2000 the FDA completed its initial review and advised Cell Pathways that exisulind will not be approved at this time.
  • After 6 months of treatment with exisulind, 25 patients who had previously been taking placebo experienced a 50% reduction in polyp formation.
  • The patients continuing treatment with exisulind exhibited a further 50% reduction from their already reduced rate of polyp formation [344991].
  • As of October 1999, these patients were still on therapy and had been receiving exisulind for between 36 and 50 months.
  • They had all experienced statistically significant reductions in polyp formation rates [344991].
  • All patients exhibited a trend of reduced new polyp formation when compared to placebo.
  • The patents describe the mechanism of action of Cell Pathways' SAANDs, including exisulind, and use of that knowledge in screening for new drugs [374888].
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Drugs, Investigational / pharmacology. Sulindac / pharmacology

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  • (PMID = 11249724.001).
  • [ISSN] 1472-4472
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone
  • [Number-of-references] 57
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18. Shen R, Tao L, Xu Y, Chang S, Van Brocklyn J, Gao JX: Reversibility of aberrant global DNA and estrogen receptor-alpha gene methylation distinguishes colorectal precancer from cancer. Int J Clin Exp Pathol; 2009;2(1):21-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recently we have identified a new type of cancer cell called precancerous stem cells (pCSCs) and proposed that cancer may arise from a lengthy development process of tumor initiating cells (TICs) --> pCSCs --> cancer stem cells (CSCs) --> cancer, which is in parallel to histological changes of hyperplasia (TICs) --> precancer (pCSCs) --> carcinoma (CSCs/cancer cells), accompanied by clonal evolutionary epigenetic and genetic alterations.
  • Herein we show that global DNA hypomethylation and ER-alpha gene hypermethylation are progressively enhanced from hyperplastic polyps (HPs) --> adenomatous polyps (APs) --> adenomatous carcinoma (AdCa).
  • The aberrant methylation can be completely reversed in APs, but not in AdCa by a nonsteroidal anti-inflammatory drug (NSAID) celecoxib, which is a selective inhibitor of cyclooxygenase-2 (Cox-2), suggesting that the epigenetic alterations between colorectal precancer (AP) and cancer (AdCa) are fundamentally different in response to anti-cancer therapy.

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  • (PMID = 18830381.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; DNA methylation / Precancer / cancer progression / colorectal cancer / epigenetic / estrogen receptor-α / nonsteroidal anti-inflammatory drugs / tumor initiation
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19. McCluggage WG: My approach to the interpretation of endometrial biopsies and curettings. J Clin Pathol; 2006 Aug;59(8):801-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The increasing use of pipelle and other methods of biopsy not necessitating general anaesthesia has resulted in greater numbers of specimens with scant tissue, resulting in problems in assessing adequacy and in interpreting artefactual changes, some of which appear more common with outpatient biopsies.
  • Topics such as endometritis, endometrial polyps, changes that are induced by hormones and tamoxifen within the endometrium, endometrial metaplasias and hyperplasias, atypical polypoid adenomyoma, adenofibroma, adenosarcoma, histological types of endometrial carcinoma and grading of endometrial carcinomas are discussed with regard to endometrial biopsy specimens rather than hysterectomy specimens.
  • [MeSH-minor] Algorithms. Artifacts. Biopsy / methods. Curettage. Diagnosis, Differential. Endometrial Hyperplasia / pathology. Endometritis / diagnosis. Endometrium / drug effects. Estrogen Replacement Therapy. Female. Humans. Precancerous Conditions / pathology

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  • (PMID = 16873562.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 80
  • [Other-IDs] NLM/ PMC1860448
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20. Freedman AN, Slattery ML, Ballard-Barbash R, Willis G, Cann BJ, Pee D, Gail MH, Pfeiffer RM: Colorectal cancer risk prediction tool for white men and women without known susceptibility. J Clin Oncol; 2009 Feb 10;27(5):686-93
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Given the high incidence of colorectal cancer (CRC), and the availability of procedures that can detect disease and remove precancerous lesions, there is a need for a model that estimates the probability of developing CRC across various age intervals and risk factor profiles.
  • METHODS: The development of separate CRC absolute risk models for men and women included estimating relative risks and attributable risk parameters from population-based case-control data separately for proximal, distal, and rectal cancer and combining these estimates with baseline age-specific cancer hazard rates based on Surveillance, Epidemiology, and End Results (SEER) incidence rates and competing mortality risks.
  • RESULTS: For men, the model included a cancer-negative sigmoidoscopy/colonoscopy in the last 10 years, polyp history in the last 10 years, history of CRC in first-degree relatives, aspirin and nonsteroidal anti-inflammatory drug (NSAID) use, cigarette smoking, body mass index (BMI), current leisure-time vigorous activity, and vegetable consumption.
  • For women, the model included sigmoidoscopy/colonoscopy, polyp history, history of CRC in first-degree relatives, aspirin and NSAID use, BMI, leisure-time vigorous activity, vegetable consumption, hormone-replacement therapy (HRT), and estrogen exposure on the basis of menopausal status.
  • CONCLUSION: We developed absolute risk prediction models for CRC from population-based data, and a simple questionnaire suitable for self-administration.
  • [MeSH-minor] Aged. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Body Mass Index. Colonoscopy. Diet. European Continental Ancestry Group. Female. Humans. Intestinal Polyps. Leisure Activities. Male. Middle Aged. Models, Theoretical. Proportional Hazards Models. Risk Factors. Sigmoidoscopy

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  • (PMID = 19114701.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
  • [Other-IDs] NLM/ PMC2645090
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21. Exisulind: Aptosyn, FGN 1, Prevatac, sulindac sulfone. Drugs R D; 2004;5(4):220-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Exisulind [Aptosyn trade mark, FGN 1 trade mark, Prevatac trade mark, sulindac sulfone], the sulfone derivative of sulindac, is the lead compound in a series of selective apoptotic antineoplastic drugs (SAANDs) being developed by OSI Pharmaceuticals.
  • The compounds were originally developed by Cell Pathways, which was acquired by, and integrated into, OSI Pharmaceuticals in June 2003.
  • Exisulind inhibits the enzyme cyclic GMP phosphodiesterase (GMP-PDE), overexpressed in precancerous and cancerous colorectal cells, and induces apoptosis in such cells with minimal effects on normal cells.
  • The agreement allows Paladin exclusive rights to commercialise the drug in Canada.
  • In August 1999 Cell Pathways submitted an NDA application to the US FDA for exisulind (Aptosyn) for the treatment of familial adenomatous polyposis (FAP).
  • Cell Pathways then initiated another phase III study of the agent in combination with Aventis' docetaxel and comparing combination therapy with docetaxel alone.
  • Patients will be evaluated to determine whether polyp numbers have been reduced after 1 year relative to baseline.
  • In June 2000, Cell Pathways announced the results of a 1-year extension of a 1997-1999 phase III trial that showed that exisulind significantly reduced polyp formation in patients with FAP.
  • Enrollment of 282 patients in a multicentre, placebo-controlled phase III trial for the treatment of sporadic colonic polyps was completed in the US in May 1999.
  • The first study assessed the efficacy of exisulind in 15 patients who had undergone prostatectomy, were receiving LHRH-agonist hormone therapy and had increasing PSA levels (study EX1001).
  • This study compared the effect of exisulind + docetaxel on the rate of apoptosis and GMP-PDE expression in premalignant or malignant and normal prostate tissue.
  • Cell Pathways and Rhône-Poulenc Rorer (now Aventis) agreed to collaborate on clinical trials of exisulind in combination with docetaxel in the treatment of various solid tumours.
  • OSI Pharmaceuticals and Bristol-Myers Squibb are conducting a phase I/II trial (study EX 2002) of exisulind in combination with paclitaxel and carboplatin as first-line treatment for patients with NSCLC.
  • Cell Pathways and Glaxo Wellcome are cooperating in supporting a clinical trial (study EX 2004) of exisulind in combination with vinorelbine as first-line treatment for elderly patients with advanced NSCLC.
  • The objectives of the two studies are to determine the 12-month survival rate and response rates following treatment with the combination regimens.
  • Patents covering the mechanism of action of exisulind have been allowed in Europe and Japan, and extend to the methods of identifying compounds that selectively stimulate apoptosis in precancerous and cancerous cells.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasms / drug therapy. Sulindac / analogs & derivatives. Sulindac / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Clinical Trials as Topic. Humans

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  • (PMID = 15230629.001).
  • [ISSN] 1174-5886
  • [Journal-full-title] Drugs in R&D
  • [ISO-abbreviation] Drugs R D
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone
  • [Number-of-references] 21
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22. Exisulind shows positive results in the prevention of precancerous colon polyps. Oncology (Williston Park); 2000 May;14(5):772-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exisulind shows positive results in the prevention of precancerous colon polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Anticarcinogenic Agents / therapeutic use. Precancerous Conditions / prevention & control. Sulindac / analogs & derivatives. Sulindac / therapeutic use
  • [MeSH-minor] Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Clinical Trials, Phase III as Topic. Double-Blind Method. Humans. Treatment Outcome

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  • (PMID = 10853464.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] News
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone
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23. Kauh J, Umbreit J: Colorectal cancer prevention. Curr Probl Cancer; 2004 Sep-Oct;28(5):240-64
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.
  • [MeSH-major] Adenomatous Polyps / drug therapy. Chemoprevention. Colorectal Neoplasms / prevention & control. Precancerous Conditions / drug therapy
  • [MeSH-minor] Animals. Anticarcinogenic Agents / classification. Anticarcinogenic Agents / therapeutic use. Disease Progression. Drug Delivery Systems. Humans. Phenotype

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  • (PMID = 15375803.001).
  • [ISSN] 0147-0272
  • [Journal-full-title] Current problems in cancer
  • [ISO-abbreviation] Curr Probl Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents
  • [Number-of-references] 119
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