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1. Keller JJ, Offerhaus GJ, Drillenburg P, Caspers E, Musler A, Ristimäki A, Giardiello FM: Molecular analysis of sulindac-resistant adenomas in familial adenomatous polyposis. Clin Cancer Res; 2001 Dec;7(12):4000-7
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  • [Title] Molecular analysis of sulindac-resistant adenomas in familial adenomatous polyposis.
  • PURPOSE: Sulindac causes the reduction of adenomas in familial adenomatous polyposis (FAP) patients, but complete regression is unusual, and breakthrough of colorectal carcinoma during sulindac treatment has been described.
  • DESIGN: Fourteen baseline adenomas (removed before sulindac treatment) from six responsive patients were studied.
  • Also, 9 baseline adenomas and 34 resistant adenomas (removed during sulindac treatment) from three resistant patients were analyzed.
  • CONCLUSIONS: Sulindac-resistant adenomas display less alteration in beta-catenin staining and less epithelial Cox-2 expression when compared with adenomas removed before sulindac treatment.
  • [MeSH-major] Adenoma / drug therapy. Adenomatous Polyposis Coli / drug therapy. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Sulindac / therapeutic use. Trans-Activators
  • [MeSH-minor] Apoptosis. Biomarkers, Tumor / analysis. Codon. Cyclooxygenase 2. Cytoskeletal Proteins / analysis. Genes, ras. Humans. Immunohistochemistry. Isoenzymes / analysis. Loss of Heterozygosity. Membrane Proteins. Mutation. Prostaglandin-Endoperoxide Synthases / analysis. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins c-bcl-2 / analysis. Rectal Neoplasms / drug therapy. Tumor Suppressor Protein p53 / analysis. bcl-2-Associated X Protein. beta Catenin

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  • (PMID = 11751493.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 53801
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Codon; 0 / Cytoskeletal Proteins; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / beta Catenin; 184SNS8VUH / Sulindac; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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2. Kastritis E, Murray S, Kyriakou F, Horti M, Tamvakis N, Kavantzas N, Patsouris ES, Noni A, Legaki S, Dimopoulos MA, Bamias A: Somatic mutations of adenomatous polyposis coli gene and nuclear b-catenin accumulation have prognostic significance in invasive urothelial carcinomas: evidence for Wnt pathway implication. Int J Cancer; 2009 Jan 1;124(1):103-8
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  • [Title] Somatic mutations of adenomatous polyposis coli gene and nuclear b-catenin accumulation have prognostic significance in invasive urothelial carcinomas: evidence for Wnt pathway implication.
  • We searched for mutations in adenomatous polyposis coli (APC), a key regulator of the pathway, and studied b-catenin expression and interactions with the expression of other markers of apoptosis, angiogenesis, and proliferation in patients with invasive urothelial cancer.
  • The mutation cluster region of APC was directly sequenced in 70 patients with muscle invasive disease who were treated with surgery and adjuvant chemotherapy.
  • Further study of the role of the Wnt pathway, potential crosstalk with other pathways and potential candidate therapeutic targets in urothelial cancer is needed.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Carcinoma / genetics. Cell Nucleus / metabolism. Mutation. Urinary Bladder Neoplasms / genetics. Urothelium / pathology. Wnt Proteins / metabolism. beta Catenin / biosynthesis
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / pharmacology. Carboplatin / pharmacology. Chemotherapy, Adjuvant / methods. Female. Humans. Male. Middle Aged. Paclitaxel / pharmacology

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  • (PMID = 18844223.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [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 / Antineoplastic Agents; 0 / Wnt Proteins; 0 / beta Catenin; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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3. Voutsadakis IA: Pathogenesis of colorectal carcinoma and therapeutic implications: the roles of the ubiquitin-proteasome system and Cox-2. J Cell Mol Med; 2007 Mar-Apr;11(2):252-85
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  • [Title] Pathogenesis of colorectal carcinoma and therapeutic implications: the roles of the ubiquitin-proteasome system and Cox-2.
  • Pathways of the molecular pathogenesis of colorectal carcinoma have been extensively studied and molecular lesions during the development of the disease have been revealed.
  • High up in the list of colorectal cancer lesions are APC (adenomatous polyposis coli), K-ras, Smad4 (or DPC4-deleted in pancreatic cancer 4) and p53 genes.
  • Inhibition of Cox-2 by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce colon polyp formation in genetically predisposed populations and in the general population.
  • Targeted therapies, the result of increasingly understanding carcinogenesis in the molecular level, have entered the field of anti-neoplastic treatment and are used by themselves and in combination with chemotherapy drugs.
  • Combinations of targeted drugs have started also to be investigated.
  • This article reviews the molecular pathogenesis of colorectal cancer, the roles of UPS and Cox-2 in it and puts forward a rational for their combined inhibition in colorectal cancer treatment.
  • [MeSH-major] Carcinoma / therapy. Colorectal Neoplasms / therapy. Cyclooxygenase 2 / metabolism. Cyclooxygenase Inhibitors / therapeutic use. Proteasome Endopeptidase Complex / metabolism. Ubiquitin / metabolism

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  • (PMID = 17488476.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Ubiquitin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 298
  • [Other-IDs] NLM/ PMC3822826
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4. Stănciulea O, Preda C, Herlea V, Popa M, Ulmeanu D, Vasilescu C: [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis]. Chirurgia (Bucur); 2007 Mar-Apr;102(2):215-20
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  • [Title] [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis].
  • We present the case of a 52 years old man, with significant familial history, diagnosed with familial adenomatous polyposis-attenuated form, with no clinical and endoscopic surveillance until 2001 when he was admitted for an upper gastrointestinal haemorrhage episode.
  • The surgical procedure was followed by chemotherapy.
  • The patient underwent transverse colectomy (the histopathological exam--in situ carcinoma).
  • The surgical procedure recommended in patients with attenuated form of familial adenomatous polyposis and suspect periampullary lesions is duodenopancreatectomy.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Carcinoma / surgery. Duodenal Neoplasms / surgery. Gastrectomy. Neoplasms, Multiple Primary / surgery. Pancreaticoduodenectomy / methods
  • [MeSH-minor] Ampulla of Vater. Humans. Male. Middle Aged. Stomach Neoplasms / surgery. Treatment Outcome

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  • (PMID = 17615925.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Romania
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5. Zhang T, Fields JZ, Ehrlich SM, Boman BM: The chemopreventive agent sulindac attenuates expression of the antiapoptotic protein survivin in colorectal carcinoma cells. J Pharmacol Exp Ther; 2004 Feb;308(2):434-7
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  • [Title] The chemopreventive agent sulindac attenuates expression of the antiapoptotic protein survivin in colorectal carcinoma cells.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) such as sulindac have chemopreventive activity against colorectal tumors.
  • To test this hypothesis, we exposed HT-29 colon carcinoma cells to sulindac.
  • This is consistent with our earlier finding that inhibition of the beta-catenin:T-cell factor 4 (Tcf-4) pathway by the adenomatous polyposis coli protein down-regulates survivin expression and with recent evidence that sulindac induces beta-catenin degradation, which would reduce Tcf-4 activation.
  • This suggests that the beta-catenin:Tcf-4:survivin mechanism may be a useful target for therapy or chemoprevention of colon cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Gene Expression / drug effects. Microtubule-Associated Proteins / biosynthesis. Sulindac / pharmacology
  • [MeSH-minor] Colorectal Neoplasms / pathology. HT29 Cells. Humans. Inhibitor of Apoptosis Proteins. Neoplasm Proteins. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / drug effects. Tumor Cells, Cultured

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  • (PMID = 14610217.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 184SNS8VUH / Sulindac
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6. Penna Ch: [Management of familial polyposis coli]. J Chir (Paris); 2002 Oct;139(5):260-7
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  • [Title] [Management of familial polyposis coli].
  • Familial Multiple Polyposis Coli is an autosomal dominant hereditary illness characterized by the appearance in childhood of hundreds of colorectal polyps which inexorably undergo malignant transformation.
  • Subtotal Colectomy with ileorectal anastomosis is a well-tolerated procedure with quite acceptable functional results, but the need for eventual proctectomy is about 30% at 20 years and the risk of rectal cancer is about 10% at 20 years even with close endoscopic surveillance.
  • Total colectomy with ileal pouch-anal anastomosis is therefore the intervention of choice since it eliminates the risk of late rectal carcinoma albeit with more serious morbidity and less good functional results.
  • NSAID's, tamoxifen, and chemotherapy are used preventively and therapeutically; surgical excision is sometimes required.
  • Duodenal adenomas are present in almost 100% of these patients post-colectomy and the risk of duodenal cancer is 200 times higher than in the general population.
  • Endoscopic surveillance of the duodenum is essential and prophylactic duodenal resection should be considered when duodenal polyposis is extensive.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Colectomy
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / etiology. Adenoma / surgery. Adult. Anal Canal / surgery. Anastomosis, Surgical. Child. Colonic Pouches. Duodenal Neoplasms / diagnosis. Duodenal Neoplasms / etiology. Duodenal Neoplasms / surgery. Endoscopy. Fibromatosis, Abdominal / surgery. Follow-Up Studies. Humans. Intestinal Obstruction / surgery. Pancreaticoduodenectomy. Rectal Neoplasms / etiology. Rectal Neoplasms / surgery. Rectum / surgery. Risk Factors. Time Factors

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  • (PMID = 12410125.001).
  • [ISSN] 0021-7697
  • [Journal-full-title] Journal de chirurgie
  • [ISO-abbreviation] J Chir (Paris)
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 29
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7. Diegel CR, Cho KR, El-Naggar AK, Williams BO, Lindvall C: Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma. Cancer Res; 2010 Nov 15;70(22):9143-52
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  • [Title] Mammalian target of rapamycin-dependent acinar cell neoplasia after inactivation of Apc and Pten in the mouse salivary gland: implications for human acinic cell carcinoma.
  • To gain more insight into the interplay between Wnt and mTOR signaling in salivary gland tumorigenesis, we developed a mouse model in which both pathways are constitutively activated by the conditional inactivation of the Apc and Pten tumor suppressor genes.
  • However, deletion of both genes resulted in the formation of salivary gland tumors with 100% penetrance and short latency that showed a remarkable morphologic similarity to human acinic cell carcinoma.
  • Treatment of tumor-bearing mice using the mTOR inhibitor rapamycin led to complete regression of tumors, indicating that tumor growth was dependent on continued mTOR signaling.
  • Because rapamycin analogues are approved for treating other types of human malignancies, our findings suggest that rapamycin therapy should be evaluated for treating patients with salivary gland acinic cell carcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / deficiency. Carcinoma, Acinar Cell / metabolism. PTEN Phosphohydrolase / deficiency. Salivary Glands / metabolism. TOR Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Female. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Mice, 129 Strain. Mice, Knockout. Salivary Gland Neoplasms / genetics. Salivary Gland Neoplasms / metabolism. Salivary Gland Neoplasms / pathology. Signal Transduction / drug effects. Sirolimus / pharmacology. Tumor Burden / drug effects


8. de Campos FG, Perez RO, Imperiale AR, Seid VE, Nahas SC, Cecconello I: Evaluating causes of death in familial adenomatous polyposis. J Gastrointest Surg; 2010 Dec;14(12):1943-9
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  • [Title] Evaluating causes of death in familial adenomatous polyposis.
  • BACKGROUND: Familial adenomatous polyposis is a genetic syndrome associated with an increased risk of colorectal cancer (CRC) and different extracolonic manifestations.
  • At diagnosis, 57 patients (58.7%) already had CRC-associated polyposis.
  • Desmoid disease was the second cause of death (10.5% of all causes), leading to a fatal outcome 22% of all patients who developed DT during the study period.
  • (3) long-term survival was also strongly related to the development of extracolonic neoplasia, especially desmoid tumors and gastroduodenal carcinoma;.
  • [MeSH-major] Adenomatous Polyposis Coli / mortality

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  • (PMID = 20676788.001).
  • [ISSN] 1873-4626
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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9. Brasseur B, Dahan K, Beauloye V, Blétard N, Chantrain C, Dupont S, Guarin JL, Vermylen C, Brichard B: Multiple neoplasia in a 15-year-old girl with familial adenomatous polyposis. J Pediatr Hematol Oncol; 2009 Jul;31(7):530-2
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  • [Title] Multiple neoplasia in a 15-year-old girl with familial adenomatous polyposis.
  • A 15-year-old girl with adenomatous polyposis coli gene (APC) mutation and brain tumor-polyposis syndrome developed an unusual succession of cervicocephalic tumors (medulloblastoma, meningeal low-grade myxoid tumor, and papillary thyroid carcinoma), at the age of 5, 9, and 15 years, respectively.
  • We discuss the genetic profile of the thyroid tumor in which a large somatic deletion of APC gene was found and the physiopathology of thyroid carcinoma in patients with germline APC mutation.
  • We also point out the uncommon phenotype in this young girl with early multiple neoplasias and the difficulties of management of such familial adenomatous polyposis patients with occurrence of extracolonic cancers that require the use of potential trigger agents as radiotherapy or chemotherapy.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / genetics. Genes, APC. Neoplasms, Multiple Primary / complications. Neoplasms, Multiple Primary / genetics

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  • (PMID = 19564752.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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10. Peyrière H, Klouche K, Béraud JJ, Blayac JP, Hillaire-Buys D: Fatal systemic reaction after multiple doses of intravesical bacillus Calmette-Guérin for polyposis. Ann Pharmacother; 2000 Nov;34(11):1279-82
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  • [Title] Fatal systemic reaction after multiple doses of intravesical bacillus Calmette-Guérin for polyposis.
  • OBJECTIVE: To report a case of fatal systemic reaction after intravesical administrations of bacillus Calmette-Guérin (BCG) for polyposis.
  • CASE SUMMARY: A 72-year-old white man was treated by monthly injections of intravesical BCG immunotherapy for polyposis of the urinary bladder.
  • Results of a cerebral scan performed at this time were normal.
  • The patient required hemodialysis and symptomatic treatment.
  • DISCUSSION: The patient presented with symptoms compatible with a severe systemic reaction to BCG therapy, a rare but possible adverse effect.
  • CONCLUSIONS: BCG instillation is a valuable tool in the therapy of bladder carcinoma, but increasing reports of severe adverse reactions should continue to remind practicing urologists to be alert to the possibility of common and uncommon reactions after its use.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. BCG Vaccine / adverse effects. Hemolytic-Uremic Syndrome / chemically induced. Urinary Bladder Neoplasms / drug therapy

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  • (PMID = 11098343.001).
  • [ISSN] 1060-0280
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCG Vaccine
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11. Ferguson CB, Porter KG, Murphy SJ: Nine-year follow-up of a patient with attenuated familial adenomatous polyposis treated with cyclo-oxygenase-2 inhibitors. Scand J Gastroenterol; 2008;43(12):1534-6
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  • [Title] Nine-year follow-up of a patient with attenuated familial adenomatous polyposis treated with cyclo-oxygenase-2 inhibitors.
  • Familial adenomatous polyposis (FAP) is caused by germline mutations in the adenomatous polyposis coli (APC) gene with onset of florid polyposis in childhood and development of colorectal cancer by age 30.
  • Attenuated FAP (AFAP) is a variant of this condition with a later age of onset and milder clinical phenotype; however, colectomy is advised once polyposis develops and polyps cannot be managed endoscopically.
  • We report a case of a patient with AFAP and previously resected colonic carcinoma that was treated with chemoprophylaxis with long-term cyclooxygenase-2 (COX-2) inhibitors after declining colectomy.
  • After 9 years of follow-up, there was no evidence of colorectal cancer development or progression of polyposis.
  • This is the first case report on long-term treatment with COX-2 inhibition in a patient with AFAP and previous colonic carcinoma.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Colonic Neoplasms / drug therapy. Cyclooxygenase 2 Inhibitors / therapeutic use
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Middle Aged. Treatment Outcome

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  • (PMID = 18609144.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors
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12. Tonelli F, Valanzano R, Messerini L, Ficari F: Long-term treatment with sulindac in familial adenomatous polyposis: is there an actual efficacy in prevention of rectal cancer? J Surg Oncol; 2000 May;74(1):15-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term treatment with sulindac in familial adenomatous polyposis: is there an actual efficacy in prevention of rectal cancer?
  • BACKGROUND AND OBJECTIVES: Ileorectal anastomosis (IRA) is still used in the treatment of familial adenomatous polyposis (FAP).
  • Sulindac appears to induce regression of colorectal adenomas; however, its effects in long-term therapy and in preventing carcinoma remain unclear.
  • Number, size, and type of rectal polyps were assessed by endoscopic and histological evaluation every 6 months.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Rectal Neoplasms / prevention & control. Sulindac / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Colorectal Neoplasms / pathology. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Male. Middle Aged. Proctocolectomy, Restorative

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10861602.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 184SNS8VUH / Sulindac
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13. Achary MP, Jaggernauth W, Gross E, Alfieri A, Klinger HP, Vikram B: Cell lines from the same cervical carcinoma but with different radiosensitivities exhibit different cDNA microarray patterns of gene expression. Cytogenet Cell Genet; 2000;91(1-4):39-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell lines from the same cervical carcinoma but with different radiosensitivities exhibit different cDNA microarray patterns of gene expression.
  • Combining chemotherapy with radiotherapy has improved the cure rate among patients with cancers of the cervix.
  • Although one-half to two-thirds of the patients can be cured by radiation alone, such patients cannot be identified at present and must therefore suffer the burden of chemotherapy.
  • These were derived from the same tumor prior to treatment from a patient with squamous cell carcinoma of the cervix.
  • The genes that showed the greatest overexpression in the radioresistant cell line were metal-regulatory transcription factor-1, cytochrome P450 CYP1B1, adenomatosis polyposis coli, translation elongation factor-1, cytochrome-c oxidase, whereas in the sensitive cell line, transcription factor NF-kappa-B, metalloproteinase inhibitor-1 precursor, superoxide dismutase-2, insulin-like growth factor binding protein-3, guanine nucleotide-binding protein and transforming growth factor beta-induced protein were overexpressed.

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11173827.001).
  • [ISSN] 0301-0171
  • [Journal-full-title] Cytogenetics and cell genetics
  • [ISO-abbreviation] Cytogenet. Cell Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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14. Yu MK, Wade M, Fitzpatrick FA: Evaluating 2-chlorodeoxycytidine for its novel mechanism as a DNA methylation inhibitor. J Clin Oncol; 2004 Jul 15;22(14_suppl):3125

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although the adenomatous polyposis coli gene is frequently somatically mutated in colon carcinoma, methylation of the adenomatous polyposis coli gene is seen in early colon adenomas.
  • Further, reactivation of critical tumor suppressor genes in carcinomas may decrease chemotherapy resistance.
  • This drug has problems of DNA mutagenesis.
  • This time point is then used for future experiments.
  • Methylation sensitive endonuclease digested DNA will be amplified by real time polymerase chain reaction to assess for promoter methylation.

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  • (PMID = 28014866.001).
  • [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
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15. Lou PJ, Chen WP, Lin CT, Chen HC, Wu JC: Taxol reduces cytosolic E-cadherin and beta-catenin levels in nasopharyngeal carcinoma cell line TW-039: cross-talk between the microtubule- and actin-based cytoskeletons. J Cell Biochem; 2000 Sep 14;79(4):542-56
eagle-i research resources. PMID 10996845 (Special Collections) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Taxol reduces cytosolic E-cadherin and beta-catenin levels in nasopharyngeal carcinoma cell line TW-039: cross-talk between the microtubule- and actin-based cytoskeletons.
  • To obtain a better insight into possible cross-talk between the microtubule- and actin-based cytoskeletons, we studied the short-term effects of Taxol treatment on the expression of actin and the E-cadherin/catenin complex in the nasopharyngeal carcinoma cell line TW-039 using immunofluorescence, immunoprecipitation, and immunoblotting methods.
  • Levels of the detergent-soluble pool of alpha- and gamma-catenin and the detergent-insoluble pool of the E-cadherin/catenin complex were unchanged by Taxol treatment and no significant difference was seen in the levels of adenomatous polyposis coli or glycogen synthase-3beta or tyrosine phosphorylation patterns.
  • These results suggest that modulation of microtubule dynamics by Taxol may have effects on the expression of actin and the cytosolic E-cadherin and beta-catenin in nasopharyngeal carcinoma cells through pathways not involving the phosphorylation of beta-catenin.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Cadherins / metabolism. Cytoskeletal Proteins / metabolism. Nasopharyngeal Neoplasms / drug therapy. Nasopharyngeal Neoplasms / metabolism. Paclitaxel / pharmacology. Trans-Activators
  • [MeSH-minor] Actins / metabolism. Adenomatous Polyposis Coli Protein. Calcium-Calmodulin-Dependent Protein Kinases / metabolism. Cell Size / drug effects. Cytoskeleton / drug effects. Cytoskeleton / metabolism. Cytosol / drug effects. Cytosol / metabolism. Glycogen Synthase Kinase 3. Humans. Microtubules / drug effects. Microtubules / metabolism. Neoplasm Proteins / metabolism. Phosphorylation. Tumor Cells, Cultured. Tyrosine / metabolism. beta Catenin

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10996845.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Actins; 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents, Phytogenic; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Cytoskeletal Proteins; 0 / Neoplasm Proteins; 0 / Trans-Activators; 0 / beta Catenin; 42HK56048U / Tyrosine; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.26 / Glycogen Synthase Kinase 3; P88XT4IS4D / Paclitaxel
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16. Lakatos PL, Lakatos L: [Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of chemotherapy outcome]. Orv Hetil; 2006 Mar 12;147(10):449-55
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  • [Title] [Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of chemotherapy outcome].
  • In the 1990-ies the mutations responsible for the adenoma-carcinoma sequence were discovered on after the other.
  • In the second part of the review the authors discuss the genetic background of sporadic and IBD associated colorectal cancers as well as the role of genetics in the diagnosis, prognosis and prediction of therapy.
  • Similarly, genetic investigation may play an increasing role in the prediction of prognosis, therapy and complication of chemotherapy.
  • A more distant goal may be the individualization of the therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / genetics. Irritable Bowel Syndrome / complications
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Chromosomal Instability. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA Methylation. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Microsatellite Repeats. Mutation. Peutz-Jeghers Syndrome / genetics. Pharmacogenetics. Prognosis. Treatment Outcome

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  • (PMID = 16573174.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 50
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17. Lynch PM: Chemoprevention with special reference to inherited colorectal cancer. Fam Cancer; 2008;7(1):59-64
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  • Familial Adenomatous Polyposis (FAP) is a model for the adenoma-carcinoma sequence in several respects.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Chemoprevention / methods. Colorectal Neoplasms / genetics. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents. Ascorbic Acid / therapeutic use. Celecoxib. Clinical Trials as Topic. Curcumin / therapeutic use. Cyclooxygenase 2 Inhibitors / therapeutic use. Drug Therapy, Combination. Eflornithine / therapeutic use. Humans. Lactones / therapeutic use. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use. Sulfones / therapeutic use. Sulindac / therapeutic use. Vitamins / therapeutic use

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  • (PMID = 17680350.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Lactones; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Sulfones; 0 / Vitamins; 0QTW8Z7MCR / rofecoxib; 184SNS8VUH / Sulindac; IT942ZTH98 / Curcumin; JCX84Q7J1L / Celecoxib; PQ6CK8PD0R / Ascorbic Acid; ZQN1G5V6SR / Eflornithine
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18. Asano TK, McLeod RS: Non steroidal anti-inflammatory drugs (NSAID) and Aspirin for preventing colorectal adenomas and carcinomas. Cochrane Database Syst Rev; 2004;(2):CD004079
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non steroidal anti-inflammatory drugs (NSAID) and Aspirin for preventing colorectal adenomas and carcinomas.
  • BACKGROUND: There is evidence from experimental animals studies, prospective and retrospective observational studies that nonsteroidal anti-inflammatory drugs (NSAIDS) may reduce the development of sporadic colorectal adenomas (CRAs) and cancer (CRC) and may induce the regression of adenomas in familial adenomatous polyposis (FAP).
  • MAIN RESULTS: Nine trials with 150 familial adenomatous polyposis (FAP) and 24,143 population subjects met the inclusion criteria.
  • From the combined results of three trials, significantly fewer subjects in the low dose ASA group developed recurrent sporadic CRAs [RR 0.77 (95% CI 0.61, 0.96), (NNT 12.5 (95% CI 7.7, 25)] after one to three years.
  • [MeSH-major] Adenoma / drug therapy. Adenomatous Polyposis Coli / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Carcinoma / drug therapy. Colorectal Neoplasms / drug therapy

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  • (PMID = 15106236.001).
  • [ISSN] 1469-493X
  • [Journal-full-title] The Cochrane database of systematic reviews
  • [ISO-abbreviation] Cochrane Database Syst Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; R16CO5Y76E / Aspirin
  • [Number-of-references] 55
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19. Tan VP, Chan P, Hung IF, Pang R, Wong BC: Chemoprophylaxis in colorectal cancer: current concepts and a practical algorithm for use. Expert Opin Investig Drugs; 2010 Apr;19 Suppl 1:S57-66
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  • There is a 10 to 20 years lead time from normal mucosa to carcinoma which offers a window of opportunity to modify and prevent the outcome of CRC, with its incipient morbidity and mortality.
  • Currently, the role for chemoprophylaxis in CRC remains a niche area, with celecoxib the only recommended agent for use in patients with familial polyposis syndromes.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / drug therapy. Algorithms. Celecoxib. Clinical Trials as Topic. Cyclooxygenase 2 Inhibitors / pharmacology. Cyclooxygenase 2 Inhibitors / therapeutic use. Humans. Pyrazoles / pharmacology. Pyrazoles / therapeutic use. Risk Factors. Sulfonamides / pharmacology. Sulfonamides / therapeutic use

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  • (PMID = 20374032.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; JCX84Q7J1L / Celecoxib
  • [Number-of-references] 89
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20. Abir F, Alva S, Kaminski DL, Longo WE: The role of arachidonic acid regulatory enzymes in colorectal disease. Dis Colon Rectum; 2005 Jul;48(7):1471-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Nonsteroidal anti-inflammatory drugs have a wide ranging effect on diseases of the colon and rectum.
  • Interestingly, nonsteroidal anti-inflammatory drugs seem to play a beneficial role in colorectal cancer chemoprevention and adenoma regression, but may have a deleterious effect in inflammatory bowel disease.
  • Prostaglandin inhibition is central to both the beneficial and toxic effects of this class of drugs.
  • METHODS: A Medline search using "nonsteroidal anti-inflammatory drugs," "colon cancer," "inflammatory bowel disease," "colitis," "COX inhibitors," "arachidonic acid," and "chemoprevention" as key words was performed for English-language articles.
  • RESULTS: Based on numerous studies, nonsteroidal anti-inflammatory drugs have a beneficial role in colon cancer and colonic adenomas.
  • Nonsteroidal anti-inflammatory drugs work via multiple pathways, some well defined, and others unknown.
  • CONCLUSIONS: In the new millennium, nonsteroidal anti-inflammatory drugs may be used for chemoprevention of colorectal and other cancers.
  • In addition, they may be used in combination with surgery and chemotherapy to primarily treat colorectal carcinoma.
  • Undoubtedly, the use of novel cyclooxygenase inhibitors with less of a toxicity profile will allow more widespread use of nonsteroidal anti-inflammatory drugs for a variety of diseases.
  • The future of this class of drugs is promising.
  • [MeSH-minor] Adenoma / prevention & control. Adenomatous Polyposis Coli / prevention & control. Colorectal Neoplasms / prevention & control. Enterocolitis / parasitology. Humans. Inflammatory Bowel Diseases / prevention & control

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  • (PMID = 15868226.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase Inhibitors; 27YG812J1I / Arachidonic Acid; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 133
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21. Dvory-Sobol H, Sagiv E, Kazanov D, Ben-Ze'ev A, Arber N: Targeting the active beta-catenin pathway to treat cancer cells. Mol Cancer Ther; 2006 Nov;5(11):2861-71
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The adenomatous polyposis coli or beta-catenin genes are frequently mutated in colorectal cancer cells, resulting in oncogenic activation of beta-catenin signaling.
  • We used a recombinant adenovirus that carries a lethal gene [p53-up-regulated modulator of apoptosis (PUMA)] under the control of a beta-catenin/Tcf-responsive promoter (AdTOP-PUMA) to selectively target human colorectal cancer cells (SW480, HCT116, DLD-1, and LS174T), hepatocellular carcinoma (HepG2), and gastric cancer cells (AGS) in which the beta-catenin/Tcf pathway is activated, and compared its efficiency in killing cancer cells in which this pathway is inactive or only weakly active.
  • Chemotherapy synergistically enhanced the effect of AdTOP-PUMA.
  • A combination of the adenovirus system with standard therapy may improve the efficacy and reduce the toxicity of therapy in humans.
  • [MeSH-major] Colorectal Neoplasms / therapy. Signal Transduction. beta Catenin / metabolism
  • [MeSH-minor] Adenoviridae / genetics. Adenoviridae / metabolism. Animals. Antineoplastic Agents / therapeutic use. Apoptosis. Apoptosis Regulatory Proteins / genetics. Apoptosis Regulatory Proteins / metabolism. Apoptosis Regulatory Proteins / therapeutic use. HCT116 Cells. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Mice. Mice, Nude. Oncolytic Virotherapy. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins / therapeutic use. Stomach Neoplasms / drug therapy. Stomach Neoplasms / metabolism. TCF Transcription Factors / metabolism

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  • (PMID = 17121933.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / BBC3 protein, human; 0 / Proto-Oncogene Proteins; 0 / TCF Transcription Factors; 0 / beta Catenin
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22. Hsu HH, Cheng SF, Chen LM, Liu JY, Chu CH, Weng YJ, Li ZY, Lin CS, Lee SD, Kuo WW, Huang CY: Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells. Mol Cell Biochem; 2006 Sep;289(1-2):101-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Epidemiologic studies reported that the prevalence of hereditary non-polyposis colon cancer (HNPCC) in male is about 1.5-fold higher than that in female.
  • Patients that received E(2) replacement therapy were found to have a reduction in the incidence of colon adenoma and carcinoma.
  • The results clearly demonstrated that overexpressed ERalpha with or without E(2) (10(-8) M) treatment could activate caspase -8, -9, and 3 and induce DNA fragmentation in LoVo cell.
  • At the same time, overexpressed ERalpha plus E(2) significantly increases the expression and promoter activity of hTNF-alpha, and the DNA fragmentation effect induced by E(2) plus ERalpha were reduced by the addition of hTNF antibody (0.1 ng(ml).
  • Efforts aiming at enhancing ERalpha expression and(or activity may be proved to be an alternative therapy against colorectal cancer.
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / metabolism. Caspases / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. DNA Fragmentation. Down-Regulation / genetics. Estrogens / pharmacology. Female. Humans. Male. Middle Aged. Promoter Regions, Genetic / drug effects. Transfection. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / genetics. Wnt Proteins / metabolism

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  • (PMID = 16628468.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cell Cycle Proteins; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / TNF protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 0 / Wnt Proteins; 0 / beta Catenin; EC 3.4.22.- / Caspases
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23. Emami KH, Nguyen C, Ma H, Kim DH, Jeong KW, Eguchi M, Moon RT, Teo JL, Kim HY, Moon SH, Ha JR, Kahn M: A small molecule inhibitor of beta-catenin/CREB-binding protein transcription [corrected]. Proc Natl Acad Sci U S A; 2004 Aug 24;101(34):12682-7
The Lens. Cited by Patents in .

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  • Inherited and somatic mutations in the adenomatous polyposis coli occur in most colon cancers, leading to activation of beta-catenin-responsive genes.
  • ICG-001 selectively induces apoptosis in transformed cells but not in normal colon cells, reduces in vitro growth of colon carcinoma cells, and is efficacious in the Min mouse and nude mouse xenograft models of colon cancer.
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Animals. Apoptosis / physiology. Cell Line. Colon / anatomy & histology. Colonic Neoplasms / drug therapy. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Cyclin D1 / genetics. Cyclin D1 / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Epithelial Cells / cytology. Epithelial Cells / metabolism. Inhibitor of Apoptosis Proteins. Lymphoid Enhancer-Binding Factor 1. Male. Mice. Mice, Inbred C57BL. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Molecular Structure. Neoplasm Proteins. Signal Transduction / physiology. Transcription Factors / genetics. Transcription Factors / metabolism. beta Catenin

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  • (PMID = 15314234.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA105490
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / Bicyclo Compounds, Heterocyclic; 0 / CTNNB1 protein, mouse; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / ICG 001; 0 / Inhibitor of Apoptosis Proteins; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Pyrimidinones; 0 / Trans-Activators; 0 / Transcription Factors; 0 / beta Catenin; 136601-57-5 / Cyclin D1
  • [Other-IDs] NLM/ PMC515116
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24. Goh KL, Quek KF, Yeo GT, Hilmi IN, Lee CK, Hasnida N, Aznan M, Kwan KL, Ong KT: Colorectal cancer in Asians: a demographic and anatomic survey in Malaysian patients undergoing colonoscopy. Aliment Pharmacol Ther; 2005 Nov 1;22(9):859-64
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.
  • A total of 228 patients (7%) were diagnosed with carcinoma.
  • Four patients (0.1%) were diagnosed to have familial adenomatous polyposis coli.
  • Detailed records of treatment were available only in 176 patients.
  • A total of 147 of 176 patients (84%) underwent surgery and 50 (28%) also received adjuvant or palliative chemotherapy (28%).
  • [MeSH-minor] Aged. Cecal Neoplasms / epidemiology. Cecal Neoplasms / ethnology. Cecal Neoplasms / therapy. China / ethnology. Colonic Neoplasms / epidemiology. Colonic Neoplasms / ethnology. Colonic Neoplasms / therapy. Colonic Polyps / complications. Colonic Polyps / epidemiology. Colonoscopy / methods. Family Health. Female. Humans. India / ethnology. Malaysia / epidemiology. Male. Middle Aged. Neoplasm Staging. Neoplasms, Multiple Primary / epidemiology. Neoplasms, Multiple Primary / ethnology. Neoplasms, Multiple Primary / therapy. Population Surveillance / methods. Rectal Neoplasms / epidemiology. Rectal Neoplasms / ethnology. Rectal Neoplasms / therapy. Sex Distribution. Sigmoid Neoplasms / epidemiology. Sigmoid Neoplasms / ethnology. Sigmoid Neoplasms / therapy

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  • (PMID = 16225496.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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25. Boman BM, Huang E: Human colon cancer stem cells: a new paradigm in gastrointestinal oncology. J Clin Oncol; 2008 Jun 10;26(17):2828-38
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  • For the past half century, oncologists have had systemic drugs available, agents that are able to induce tumor responses in patients with colorectal cancer.
  • The recently introduced concept that cancer stem cells (SCs) drive tumor growth suggests a reason for these therapeutic failures--current chemotherapeutics target rapidly dividing cells but cancer SCs divide only slowly, and, they are relatively resistant to cytotoxic systemic therapies.
  • It also suggests a solution--development of therapeutics that target cancer SCs.
  • Our hypothesis, which has received recent experimental support, is that the mechanism that links abnormalities at the gene level (eg, APC mutations) and abnormalities at the tissue level (eg, proliferative shift, dysplasia, carcinoma) from cancer initiation to metastasis is SC overpopulation.
  • Finally, we discuss the concept that symmetric cancer SC division is an essential mechanism that drives tumor growth, and that development of a new generation of therapeutics that target colon cancer SCs by inhibiting symmetric SC division holds promise for truly curative approaches for patients with advanced colorectal cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colonic Neoplasms / drug therapy. Drug Resistance, Neoplasm. Gastroenterology. Intestinal Mucosa / drug effects. Medical Oncology. Neoplastic Stem Cells / drug effects
  • [MeSH-minor] Adenoma / pathology. Adenomatous Polyposis Coli / pathology. Biomarkers, Tumor / metabolism. Cell Differentiation. Cell Proliferation. Cell Separation / methods. Cell Transformation, Neoplastic / pathology. Colitis, Ulcerative / pathology. Gene Expression Regulation, Neoplastic. Humans. Mutation. Neoplasm Metastasis

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  • (PMID = 18539961.001).
  • [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; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
  • [Number-of-references] 114
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26. Gasser M, Gerstlauer C, Grimm M, Bueter M, Lebedeva T, Lutz J, Maeder U, Ribas C, Ribas C, Nichiporuk E, Thalheimer A, Heemann U, Thiede A, Meyer D, Waaga-Gasser AM: Comparative analysis of predictive biomarkers for therapeutical strategies in colorectal cancer. Ann Surg Oncol; 2007 Apr;14(4):1272-84
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  • BACKGROUND: Prognostic information regarding the risk of postoperative tumor recurrence defined by a profile of serological, morphological and/or molecular markers can have potential value, particularly for patients with colorectal carcinoma (CRC) of the International Union Against Cancer (UICC) stage II/III who may benefit from adjuvant chemotherapy after surgery.
  • In addition, protein and gene expression of p53, CEA, and adenomatous polyposis coli (APC) was assessed in the tumors of those patients.
  • CONCLUSION: Overall increased p53, CEA, and CA 19-9 serum levels and their marker expression in the tumor may be used at the time of primary tumor removal for defining patients at risk for tumor recurrence.
  • [MeSH-minor] Aged. Female. Humans. Immunoenzyme Techniques. Lymphatic Metastasis / pathology. Male. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Time Factors

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  • (PMID = 17211733.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 0 / Tumor Suppressor Protein p53
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27. Saha D, Roman C, Beauchamp RD: New strategies for colorectal cancer prevention and treatment. World J Surg; 2002 Jul;26(7):762-6
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  • [Title] New strategies for colorectal cancer prevention and treatment.
  • Surgical resection is an effective treatment for localized disease, achieving a 5-year survival rate of 90%; but chemotherapy and other novel treatments for metastatic disease remain ineffective.
  • There have been significant efforts to identify risk factors associated with the development of CRC and to explore potential preventive therapies.
  • Cooperative genetic aberrations involving APC (adenomatous polyposis coli), beta-catenine, K-ras, and p53 are involved in the multistep adenoma-carcinoma sequence of CRC.
  • Emerging data have implicated cyclooxygenase-2 (COX-2) and prostanoid production in the pathogenesis of colorectal carcinoma.
  • Several reports indicate a close relation between the intake of nonsteroidal antiinflammatory drugs (NSAIDs) and a decreased risk for developing colorectal cancer.
  • These developments may yield benefits in earlier detection and in the design of better antitumor interventions.
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cyclooxygenase 2. Humans. Isoenzymes / genetics. Isoenzymes / metabolism. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / genetics. Prostaglandin-Endoperoxide Synthases / metabolism. Prostaglandins / immunology. Prostaglandins / metabolism. Receptors, Cytoplasmic and Nuclear / metabolism. Transcription Factors / metabolism

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  • (PMID = 11948369.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-69457; United States / NCI NIH HHS / CA / CA-77839; United States / NIDDK NIH HHS / DK / DK-52334
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Prostaglandins; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Transcription Factors; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 46
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28. Hung KE, Maricevich MA, Richard LG, Chen WY, Richardson MP, Kunin A, Bronson RT, Mahmood U, Kucherlapati R: Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment. Proc Natl Acad Sci U S A; 2010 Jan 26;107(4):1565-70
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  • [Title] Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment.
  • Several of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent models for familial cancer predisposition syndromes.
  • We have developed a stochastic somatic mutation model for sporadic colon cancer that presents with isolated primary tumors in the distal colon and recapitulates the entire adenoma-carcinoma-metastasis axis seen in human colon cancer.
  • Because of the restricted location in the distal colon, the natural history of the tumors can be analyzed by serial colonoscopy.
  • As the mammalian target of rapamycin (mTOR) pathway is a critical component of the complex signaling network in colon cancer, we used this model to assess the efficacy of mTOR blockade through rapamycin treatment of mice with established tumors.
  • After treatment, Apc mutant tumors were more than 80% smaller than control tumors.
  • However, tumors that possessed both Apc and Kras mutations did not respond to rapamycin treatment.
  • These studies suggest that mTOR inhibitors should be further explored as potential colorectal cancer therapies in patients whose tumors do not have activating mutations in KRAS.

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  • (PMID = 20080688.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK078033; United States / NCI NIH HHS / CA / 5U01CA084301; United States / NCI NIH HHS / CA / U01 CA084301; United States / NCI NIH HHS / CA / 5P50CA127003; United States / NIDDK NIH HHS / DK / P30 DK043351; United States / NIBIB NIH HHS / EB / 5R01EB001872; United States / NIDDK NIH HHS / DK / 5K08DK078033; United States / NIBIB NIH HHS / EB / R01 EB001872; United States / NCI NIH HHS / CA / P50 CA127003
  • [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 / Antibiotics, Antineoplastic; 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2824379
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