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1. Chang JY, Kim HJ, Kim WJ, Jung YH, Lee BW, Han YS, Dong SH, Kim BH, Chang YW, Lee JI, Chang R: [A case of chronic pouchitis resistant to medical treatment]. Korean J Gastroenterol; 2003 Jul;42(1):72-6

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  • [Title] [A case of chronic pouchitis resistant to medical treatment].
  • Pouchitis, a non-specific acute inflammation occurring in the ileal pouch, is one of the most common complications developed after the restorative proctocolectomy and ileal pouch-anal anastomosis (IPAA) performed for the treatment for the patients with ulcerative colitis and familial adenomatous polyposis.
  • One to two percent of the cases are chronic and resistant to the drug therapy.
  • The effective treatment for this chronic resistant pouchitis is to remove the ileal pouch and perform the permanent ileostomy.
  • Hereby, we report one case of chronic pouchitis resistant to multiple drug therapy developed after IPAA performed for the treatment of ulcerative colitis in a patient.
  • [MeSH-major] Pouchitis / drug therapy
  • [MeSH-minor] Chronic Disease. Female. Humans. Middle Aged. Treatment Failure

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  • (PMID = 14532735.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
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2. Jaiswal AS, Narayan S: A novel function of adenomatous polyposis coli (APC) in regulating DNA repair. Cancer Lett; 2008 Nov 28;271(2):272-80
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  • [Title] A novel function of adenomatous polyposis coli (APC) in regulating DNA repair.
  • Prevailing literature suggests diversified cellular functions for the adenomatous polyposis coli (APC) gene.
  • Among them a recently discovered unique role of APC is in DNA repair.
  • The APC gene can modulate the base excision repair (BER) pathway through an interaction with DNA polymerase beta (Pol-beta) and flap endonuclease 1 (Fen-1).
  • Taken together with the transcriptional activation of APC gene by alkylating agents and modulation of BER activity, APC may play an important role in carcinogenesis and chemotherapy by determining whether cells with DNA damage survive or undergo apoptosis.
  • In this review, we summarize the evidence supporting this novel concept and suggest that these results will have implications for the development of more effective strategies for chemoprevention, prognosis and chemotherapy of certain types of tumors.

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  • (PMID = 18662849.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-100247; United States / NCI NIH HHS / CA / R01 CA100247-01; United States / NCI NIH HHS / CA / CA100247-01; United States / NCI NIH HHS / CA / R01 CA097031-01A1; United States / NCI NIH HHS / CA / CA-097031; United States / NCI NIH HHS / CA / CA097031-01A1; United States / NCI NIH HHS / CA / R01 CA097031; United States / NCI NIH HHS / CA / R01 CA100247
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Alkylating Agents; EC 2.7.7.- / DNA Polymerase beta; EC 3.1.- / Flap Endonucleases
  • [Number-of-references] 81
  • [Other-IDs] NLM/ NIHMS78341; NLM/ PMC2585005
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3. Chen T, Turner J, McCarthy S, Scaltriti M, Bettuzzi S, Yeatman TJ: Clusterin-mediated apoptosis is regulated by adenomatous polyposis coli and is p21 dependent but p53 independent. Cancer Res; 2004 Oct 15;64(20):7412-9
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  • [Title] Clusterin-mediated apoptosis is regulated by adenomatous polyposis coli and is p21 dependent but p53 independent.
  • To clarify the functional role of clusterin in regulating apoptosis, we examined its expression in human colon cancer tissues and in human colon cancer cell lines.
  • We additionally explored its expression and activity using models of adenomatous polyposis coli (APC)- and chemotherapy-induced apoptosis.
  • Clusterin RNA and protein levels were decreased in colon cancer tissues largely devoid of wild-type APC when compared with matched normal tissue controls, suggesting a means for invasive cancers to avoid apoptosis.
  • Conversely, induction of apoptosis by expression of wild-type APC or by treatment with chemotherapy led to increased clusterin RNA and protein levels localizing to apoptotic nuclei.
  • We found that transient transfection of clusterin to colon cancer cell lines directly enhanced basal and chemotherapy-induced apoptosis.
  • Clusterin-induced apoptosis was inhibited by antisense clusterin and was found to be highly dependent on p21 but not p53 expression, yet a deficit in p21 can be subverted by clusterin transfection.
  • Collectively, these data support the hypothesis that nuclear clusterin function is proapoptotic when induced by APC or chemotherapy in the context of p21 expression.
  • Absent of p21, clusterin in not induced, and apoptosis is significantly inhibited.
  • These data support a potential therapeutic role for clusterin in enhancing chemotherapy-induced apoptosis and in promoting apoptosis in cells deficient in p21.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Apoptosis / physiology. Colonic Neoplasms / pathology. Cyclins / physiology. Glycoproteins / physiology. Molecular Chaperones / physiology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Cell Nucleus / metabolism. Clusterin. Cyclin-Dependent Kinase Inhibitor p21. Down-Regulation. Gene Expression. Gene Expression Regulation, Neoplastic. Genes, APC. Humans. Oligonucleotides, Antisense / genetics. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Transfection. Up-Regulation

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  • (PMID = 15492264.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / CDKN1A protein, human; 0 / CLU protein, human; 0 / Clusterin; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Glycoproteins; 0 / Molecular Chaperones; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53
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4. Ma MK, McLeod HL: Lessons learned from the irinotecan metabolic pathway. Curr Med Chem; 2003 Jan;10(1):41-9
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  • Irinotecan has been widely used in the treatment of metastatic colorectal cancer, small cell lung cancer and several other solid tumors.
  • However, large inter-patient variability in irinotecan and SN-38 disposition, as well as severe but unpredictable diarrhea limits the clinical potential of irinotecan.
  • Intense clinical pharmacology studies have been conducted to elucidate its complicated metabolic pathways and to provide scientific rationale in defining strategies to optimize drug therapy.
  • Irinotecan is subjected to be shunted between CYP3A4 mediated oxidative metabolism to form two inactive metabolites APC or NPC and tissue carboxylesterase mediated hydrolysis to form SN-38 which is eventually detoxified via glucuronidation by UGT1A1 to form SN-38G.
  • The pharmacology of this compound is further complicated by the existence of genetic inter-individual differences in activation and deactivation enzymes of irinotecan (e.g., CYP3A4, CYP3A5, UGT1A1) and sharing competitive elimination pathways with many concomitant medications, such as anticonvulsants, St. John's Wort, and ketoconazole.
  • Efflux of the parent compound and metabolites out of cells by several drug transporters (e.g., Pgp, BCRP, MRP1, MRP2) also occurs.
  • This review highlights the latest findings in drug activation, transport mechanisms, glucuronidation, and CYP3A-mediated drug-drug interactions of irinotecan in order to unlock some of its complicated pharmacology and to provide ideas for relevant future studies into optimization of this promising agent.
  • [MeSH-minor] Animals. Aryl Hydrocarbon Hydroxylases / metabolism. Biotransformation. Carboxylic Ester Hydrolases / metabolism. Carrier Proteins / metabolism. Cytochrome P-450 CYP3A. Diarrhea / chemically induced. Glucuronides / metabolism. Humans. Oxidoreductases, N-Demethylating / metabolism

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  • (PMID = 12570720.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA091842; United States / NIGMS NIH HHS / GM / GM63340
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Carrier Proteins; 0 / Glucuronides; 7673326042 / irinotecan; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 1.5.- / Oxidoreductases, N-Demethylating; EC 3.1.1.- / Carboxylic Ester Hydrolases; XT3Z54Z28A / Camptothecin
  • [Number-of-references] 111
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5. Ramburan A, Oladiran F, Smith C, Hadley GP, Govender D: Microsatellite analysis of the adenomatous polyposis coli (APC) gene and immunoexpression of beta catenin in nephroblastoma: a study including 83 cases treated with preoperative chemotherapy. J Clin Pathol; 2005 Jan;58(1):44-50
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  • [Title] Microsatellite analysis of the adenomatous polyposis coli (APC) gene and immunoexpression of beta catenin in nephroblastoma: a study including 83 cases treated with preoperative chemotherapy.
  • AIMS: To determine whether microsatellite mutations of the adenomatous polyposis coli (APC) gene have pathological or prognostic significance in nephroblastomas and to correlate APC alterations with beta catenin immunoexpression.
  • METHODS: One hundred nephroblastomas were analysed, 83 of which received preoperative chemotherapy.
  • Normal and tumour DNA was isolated using standard proteinase K digestion and phenol/chloroform extraction from paraffin wax embedded tissue.
  • Polymerase chain reaction using four APC microsatellite markers-D5S210, D5S299, D5S82, and D5S346-was performed and the products analysed.
  • Although there was a significant correlation between the results for individual markers and the clinicopathological data, the overall results do not support a prognostic role for APC in nephroblastoma.
  • CONCLUSION: Microsatellite analysis of APC and immunoexpression of beta catenin did not provide significant pathological or prognostic information in this cohort of nephroblastomas.
  • [MeSH-major] Cytoskeletal Proteins / metabolism. Genes, APC. Kidney Neoplasms / genetics. Microsatellite Repeats / genetics. Trans-Activators / metabolism. Wilms Tumor / genetics
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / metabolism. Chemotherapy, Adjuvant. Child. Child, Preschool. Female. Humans. Infant. Loss of Heterozygosity. Male. Neoplasm Staging. Prognosis. Survival Analysis. beta Catenin

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  • (PMID = 15623481.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Trans-Activators; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC1770552
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6. Johnsen E, Svingen GF, Jørgensen HA: Practice regarding antipsychotic therapy: a cross-sectional survey in two Norwegian hospitals. Nord J Psychiatry; 2004;58(4):313-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Practice regarding antipsychotic therapy: a cross-sectional survey in two Norwegian hospitals.
  • Since the introduction of chlorpromazine, an increasing number of drugs have been added to the list of antipsychotics (neuroleptics).
  • These drugs can be further classified as either first-generation antipsychotics (FAPs) or second-generation antipsychotics (SAPs), depending on their ability to antagonize serotonine in addition to dopamine.
  • The efficacy of various drugs is generally equal, whereas both pharmacological profiles and side-effects differ.
  • Antipsychotic drug therapy recommendations are available both in Norway and internationally, and the purpose of this cross-sectional survey was to register the use of these drugs in representative mental hospitals (A and B), and compare our findings to the recommendations.
  • Eighty-two of these used one antipsychotic drug, and in this group, 65% received SAPs.
  • Antipsychotic combination therapy was received by 35 patients, and was associated with higher prescription rates of both anticholinergics and benzodiazepines.
  • SAPs were not associated with increased use of benzodiazepines, compared to FAPs.
  • Our findings in hospital A concerning therapy practices of antipsychotics, were confirmed in hospital B, where 64 patients' medical prescriptions were registered.
  • We conclude that FAPs are still commonly prescribed.
  • Antipsychotic combination therapy is used despite of lack of evidence for efficacy, and is associated with increased prescription rates of anticholinergics and benzodiazepines.
  • [MeSH-major] Antipsychotic Agents / therapeutic use. Drug Utilization / statistics & numerical data. Health Surveys. Practice Patterns, Physicians'. Psychotic Disorders / drug therapy

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  • (PMID = 15370781.001).
  • [ISSN] 0803-9488
  • [Journal-full-title] Nordic journal of psychiatry
  • [ISO-abbreviation] Nord J Psychiatry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antipsychotic Agents
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7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Wnt pathway signaling is crucial in many cancers and data indicate crosstalk with other key cancer pathways, however in urothelial carcinogenesis it has not been extensively studied.
  • 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.
  • Patients having either APC missense mutations or b-catenin nuclear accumulation had less frequent COX-2 overexpression (24% vs. 76%, p = 0.043) and more frequent lymph node involvement (75% vs. 38%, p = 0.023).
  • Patients with either APC mutations or b-catenin accumulation had shorter disease-free interval (13.4 vs. 28 months, p = 0.07), whereas in multivariate analysis they had shorter disease-specific survival (60.5 vs. 20.6 months, p = 0.048).
  • Somatic APC missense mutations are not rare in advanced urothelial neoplasms.
  • Either APC mutations and/or aberrant expression of b-catenin are associated with worse outcome.
  • 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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8. Imami N, Hardy G, Gotch F: Development of immunotherapeutic strategies for HIV-1. Expert Opin Biol Ther; 2001 Sep;1(5):803-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the majority of untreated patients, HIV-1 infection presents as a progressive disease of the immune system.
  • Emerging novel technologies, animal studies and detailed immunological studies have proven invaluable in defining the immune responses that are associated with a favourable clinical outcome.
  • Fully functional antigen-presenting cells (APC) are also essential in all stages of HIV-1 infection and possibly some (but not all) antibody responses contribute to beneficial immunity.
  • The availability of combination anti-retroviral drug therapy, which successfully controls viraemia, has enabled a beneficial outcome in many HIV-1 infected individuals.
  • Since no chronically HIV-1 infected patient has been shown to eradicate virus, novel approaches utilising therapeutic immunisation and various cytokines to manipulate immune responses and to induce and steer immunity towards a desired phenotype are required.
  • Here we review the immunopathogenesis of HIV-1 infection and discuss the promises of therapeutic immunisation and immunotherapy in general and their potential in the treatment of chronic HIV-1 disease.
  • [MeSH-major] HIV Infections / immunology. HIV Infections / therapy. HIV-1 / immunology. Immunotherapy / methods. Technology, Pharmaceutical / methods
  • [MeSH-minor] Animals. Drug Design. Humans

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  • (PMID = 11728216.001).
  • [ISSN] 1471-2598
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Number-of-references] 122
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9. Guimarães AP, Rocha RM, da Cunha IW, Guimarães GC, Carvalho AL, de Camargo B, Lopes A, Squire JA, Soares FA: Prognostic impact of adenomatous polyposis coli gene expression in osteosarcoma of the extremities. Eur J Cancer; 2010 Dec;46(18):3307-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of adenomatous polyposis coli gene expression in osteosarcoma of the extremities.
  • PURPOSE: To evaluate the impact of adjuvant chemotherapy on the outcome of osteosarcoma of the extremities, and to identify prognostic factors using the expression of adenomatous polyposis coli (APC), cadherin and β-catenin Wnt-signalling markers.
  • METHODS: The clinical, demographic, anatomic and pathological factors including a detailed analysis of the immunohistochemical expression of cadherin, β-catenin and APC were retrospectively examined in 97 patients with osteosarcoma of the extremities (metastatic and non-metastatic at diagnosis), treated with surgery and/or chemotherapy from 1985 to 2000.
  • RESULTS: APC immunoreactivity showed a statistically significant association with age and serum alkaline phosphatase levels (p = 0.025 and p = 0.038).
  • For overall survival, cadherin immunoreactivity and the interaction between APC expression and response to adjuvant chemotherapy were significant (p = 0.012 and p<0.001).
  • CONCLUSION: Lack of expression of cadherin was a significant variable to overall and disease-free survival.
  • Significantly, positive APC immunoreactivity and adjuvant chemotherapy were associated with a favourable treatment response.
  • Studies using newer immunohistochemical markers within the Wnt-signalling pathway may guide the development of more appropriate therapeutic targets for future individualised treatment.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Bone Neoplasms / genetics. Extremities. Genes, APC. Osteosarcoma / genetics

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20594821.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins
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10. Florent C, Meary N: [Cyclooxygenase 2 inhibitors and adenomatous polyposis coli]. Bull Cancer; 2004 May;91 Spec No:S85-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cyclooxygenase 2 inhibitors and adenomatous polyposis coli].
  • [Transliterated title] Inhibiteurs spécifiques de la cyclo-oxygénase 2 et polypose adénomateuse familiale.
  • Prolonged use of aspirin and/or non-steroidal anti-inflammatory drugs induces a partial regression of either sporadic adenomas or adenomas in adenomatous polyposis coli (APC), but also their emergence and colonic cancer development in sporadic adenomas.
  • Specific inhibitors of cyclooxygenase of type 2 (Cox2) induce less upper and lower digestive tract adverse events that non-specific anti-inflammatory drugs.
  • This better tolerance might allow a long-lasting use in patients with APC.
  • At time, we don't know if such treatments are able to prevent the development of cancer in the rectum or duodenum of these patients.
  • In this paper we will discuss the scientific proofs and potential interest of Cox2 inhibitors in the treatment of PAF.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors
  • [MeSH-minor] Anti-Inflammatory Agents / adverse effects. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Humans. Membrane Proteins. Prostaglandin-Endoperoxide Synthases

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  • (PMID = 15239335.001).
  • [ISSN] 0007-4551
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Neoplasm Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; R16CO5Y76E / Aspirin
  • [Number-of-references] 14
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11. Constantinidou A, Scurr M, Jones R, Al-Muderis O, Judson I: Treatment of aggressive fibromatosis with pegylated liposomal doxorubicin: The Royal Marsden Hospital experience. J Clin Oncol; 2009 May 20;27(15_suppl):10519

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of aggressive fibromatosis with pegylated liposomal doxorubicin: The Royal Marsden Hospital experience.
  • : 10519 Background: Aggressive fibromatosis (AF) or desmoid tumors are monoclonal proliferations which are locally invasive but do not metastasise.
  • Sporadic tumors are usually associated with mutations in the beta-catenin gene CTNNB1whereas those occurring in the context of familial adenomatous polyposis usually have inactivating mutations in APC.
  • When surgery and radiotherapy are not applicable or fail to control the disease, systemic treatment with anti-oestrogens, non steroidal anti-inflammatory drugs (NSAIDs) and chemotherapy can be used.
  • RESULTS: The female/male ratio was 9:1 and the median age at presentation was 39.5 years (range 18-53).
  • All but one had previous systemic therapy which comprised tamoxifen/toremifene (6), NSAIDs (1), chemotherapy (1) and imatinib (1).
  • One patient is currently receiving treatment and is too early to assess.
  • For the nine patients who have completed treatment the median number of C cycles was 6 (range 4-6).
  • Objective response according to RECIST was achieved in 4/10 patients and in 5 patients the best response was stable disease.
  • C as single agent therapy has acceptable toxicity and highly promising activity in unresectable AF and may provide long term clinical benefit in some patients.

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  • (PMID = 27963658.001).
  • [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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12. Silberstein PT, Jones D, Ternent C, Lynch H: Regression of colorectal adenomas with intravenous chemotherapy in a patient with familial adenomatous polyposis. J Clin Oncol; 2004 Jul 15;22(14_suppl):1021

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regression of colorectal adenomas with intravenous chemotherapy in a patient with familial adenomatous polyposis.
  • : 1021 Background Familial adenomatous polyposis (FAP) is an autosomally dominant disease.
  • This is a case of a 45 year old woman with FAP and colorectal cancer who showed marked regression of polyps after intravenous chemotherapy.
  • Search terms included polyps, regression, chemotherapy, colorectal adenomas, and polyposis.
  • Results The patient's colonoscopy in June 2002 revealed hundreds of colorectal adenomas throughout her colon.
  • The pathology showed tubular adenomas with metastatic disease in the pericolonic lymph nodes and liver (Stage IV, T3N1M1).
  • Her APC gene test was positive in April 2003.
  • There have been two published studies reporting the use of local chemotherapy (suppository 5-FU) for post-operative control of adenomas in the retained rectum in familial polyposis.
  • To our knowledge, this is the first reported case of intravenous chemotherapy causing the remission of colonic polyps.

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  • (PMID = 28014711.001).
  • [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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13. Hoimes CJ, Lamb L, Lok W, Elligers K, Carbone R, Keley K, Lansigan F, Liu SH, Cheng YC, Saif MW: Effect of PHY906 on capecitabine (CAP)-induced diarrhea in patients with GI malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):e20595

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e20595 Background: 15.4% of pts with GI cancers treated with CAP alone at 1250mg/m<sup>2</sup> BID D1-14 q 3 wks (14/7) develop G3/4 diarrhea (Hoff et al. JCO, 2001).
  • Preliminary studies showed synergistic activity of PHY906 with chemotherapeutics and reduction of chemotherapy-induced GI toxicities, especially chemotherapy-induced diarrhea (CID).
  • METHODS: We prospectively evaluated 44 pts treated on a clinical study with CAP plus PHY906 for diarrhea (experimental arm) and compared to historical data by Hoff et al., CAP 14/7 alone arm (control arm).
  • Experimental arm consisted of pts with refractory solid tumors in phase I and gemcitabine-refractory advanced pancreatic cancer (APC) in phase II.
  • Ph II treated pts with APC at 1500 mg/m<sup>2</sup> and PHY906 800mg BID D1-4.
  • Phase I pts had GI malignancies; 15 (63%) had APC and 6 (25%) colorectal.
  • One pt with APC who received 3 cycles at the 1500mg/m<sup>2</sup> dose level was diarrhea-free until he was removed from the study; he continued on single-agent CAP at 1000mg/m<sup>2</sup> BID and developed G3 diarrhea.
  • As an underlying mechanism of CID may include cytokine activation, evalation of cytokines is ongoing.

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  • (PMID = 27961165.001).
  • [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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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.
  • Thus, epigenetic silencing of tumor suppressor genes may play a role in the progression of colon polyps to carcinomas.
  • Further, reactivation of critical tumor suppressor genes in carcinomas may decrease chemotherapy resistance.
  • This drug has problems of DNA mutagenesis.
  • We are evaluating 2-chlorodeoxycytidine for its inhibitory properties of s-adenosylhomocysteine hydrolase.
  • This time point is then used for future experiments.
  • Genomic DNA is isolated and digested with a methylation sensitive restriction enzyme.
  • 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. Funakoshi A, Okusaka T, Ishii H, Sawaki A, Ohkawa S, Ishikawa O, Saitoh S: Phase II study of irinotecan (CPT-11) alone in patients (pts) with metastatic pancreatic cancer. J Clin Oncol; 2004 Jul 15;22(14_suppl):4102

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PATIENTS AND METHODS: Chemotherapy naive pts with metastatic pancreatic cancer who fulfilled the following criteria were registered: measurable metastatic disease, KPS≥50, age<75, ANC≥2000, Hgb≥10, Plts≥100K, AST&ALT≤2.5X nl, t-bili≤2.0, adequate organ function, and written informed consent.
  • The median survival time was 7.3 months.
  • Obstructive jaundice, elevated bilirubin and gastric variceal bleeding also occurred as drug unrelated SAE.
  • The AUC of CPT-11 was similar between pts with or without biliary drainage, but the metabolites (SN-38, APC, and SN-38 glucuronide) showed larger AUCs in the pts with drainage.

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  • (PMID = 28014506.001).
  • [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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16. Baker LH, Wathen K, Chugh R, Thomas D, Thall PF, Maki RG, Samuels BL, Meyers PA, Priebat DA, Benjamin RS: Activity of imatinib mesylate in desmoid tumors: Interim analysis of a Sarcoma Alliance for Research thru Collaboration (SARC) phase II trial. J Clin Oncol; 2004 Jul 15;22(14_suppl):9013

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of imatinib mesylate in desmoid tumors: Interim analysis of a Sarcoma Alliance for Research thru Collaboration (SARC) phase II trial.
  • : 9013 Background: Desmoid tumors (aggressive fibromatosis) are rare clonal neoplastic proliferations of connective tissues.
  • Standard treatment involves wide surgical resection and/or radiation therapy.
  • In cases of unresectable or recurrent disease, tamoxifen, chemotherapy, and NSAIDs have been used with varying success.
  • SARC, in association with the Connective Tissue Oncology Society, initiated a prospective phase II trial in patients with desmoid tumors, or one of nine sarcoma subtypes.
  • METHODS: Patients ≥ 10 years old with desmoid tumors that were not curable by surgical management or in whom curative surgery would lead to undesirable functional impairment were eligible.
  • Rules for early termination within each disease type were based on a hierarchical Bayesian probability model accounting for correlation of the responses of the 10 disease types.
  • Tissue specimens were analyzed by immunohistochemistry for expression of c-kit, PDGFRα, PDGFRß, AKT, PTEN, FKHR, and beta catenin.
  • Tumor DNA was analyzed for PDGFRα exon 18 and APC mutations by allelic discrimination PCR.

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  • (PMID = 28013675.001).
  • [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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17. Labianca R, Mandalà M, Barni S, Falanga A: Acquired and inherited risk factors for the developing of venous thromboembolism in cancer patients receiving adjuvant chemotherapy: A prospective trial. J Clin Oncol; 2009 May 20;27(15_suppl):9572

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired and inherited risk factors for the developing of venous thromboembolism in cancer patients receiving adjuvant chemotherapy: A prospective trial.
  • : 9572 Background: To assess the thrombogenic role of adjuvant chemotherapy, following radical surgical resection, in ambulatory cancer patients, is of particular interest, because of the little or no tumor burden.
  • The relation between adjuvant chemotherapy and thrombosis has been investigated in breast cancer.
  • Aim of this study was to investigate the acquired and inherited risk factors for VTE and the incidence of symptomatic VTE in patients on adjuvant chemotherapy for breast or GI cancer.
  • METHODS: In a prospective observational study (January 2003 and February 2006), 199 GI (82F/117M; age range, 26-84 years) and 182 breast (180F/2M; age range, 29-85 years) cancer patients were enrolled and followed-up for symptomatic VTE during adjuvant chemotherapy.
  • We prospectively evaluated the effect of acquired (i.e. age, chemotherapy, tumor hystotype, history of thrombosis, body mass index and smoke) and inherited risk factors (i.e. antithrombin, protein C, protein S, homocysteine, activated protein C [APC] resistance, factor V Leiden [FVL] and Prothrombin [PT] mutations).
  • RESULTS: Overall 30 VTE events (7.87%) were recorded: 28 (7.35%) during treatment and 2 (0.52%) during the subsequent follow-up.
  • At multivariate analysis thrombocytosis (HR 2.8; 95% CI, 1.13-7.30, P< 0.026) and a previous episode of thrombosis (HR 12.4; 95% CI, 2.48-62.6, P< 0.0026) were significantly associated to the development of VTE .
  • CONCLUSIONS: Our data demonstrate that, in the adjuvant setting, most VTE occur during therapy.

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  • (PMID = 27963660.001).
  • [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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18. Peethambaram P, Alberts S, Rinn K, Jones LA: Antigen presenting cell based immunotherapy targeting HER2/Neu positive solid tumors: Results of a phase 1 study of APC8024. J Clin Oncol; 2004 Jul 15;22(14_suppl):2528

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antigen presenting cell based immunotherapy targeting HER2/Neu positive solid tumors: Results of a phase 1 study of APC8024.
  • : 2528 Background: APC8024 is a cellular vaccine therapy derived from autologous antigen (Ag) presenting cells (APC) loaded ex vivo with the HER2/Neu tumor Ag HER500/GM-CSF, designated BA7072.
  • Autologous mononuclear cells were collected and APC precursors were isolated and then loaded with the fusion protein BA7072.
  • A total of 1 x 109 cells were reinfused at each time point.
  • Pts were followed without further therapy until either Week 52 or documented disease progression, whichever occurred first.
  • RESULTS: Ten pts (8 females, 2 males) received vaccine therapy and were evaluable.
  • All pts had advanced, metastatic disease and had received a mean of 3 prior chemotherapy regimens (range 0-6).
  • Cancer types included ovarian (4), colorectal (3), and breast (3).
  • The treatment was generally well tolerated.
  • The adverse events (AE) most frequently associated with APC8024 were fatigue (n=5), rigors (n=5), and pyrexia (n=2), all of which were Grade 1-2.
  • All higher grade and serious AEs were judged to be unrelated to the therapy.
  • An antigen specific T cell response, as measured by IFNγ ELISPOT and T cell proliferation, was induced after treatment compared to baseline (ELISPOT P=0.0153, Proliferation P<0.0001).
  • Based on the investigator's assessment, 2 subjects had stable disease for 16 and 24 weeks.
  • CONCLUSIONS: APC8024 was a safe and well tolerated cellular vaccine therapy in this Phase 1 study.
  • The robust T cell IR data supports further evaluation of administration of frozen/thawed product.

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  • (PMID = 28015011.001).
  • [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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19. Nemunaitis JJ, Cunningham CC, Senzer NN, Haltom E, Jones B, Vukelja SJ, Richards DA, Uprichard MJ: A phase 1 trial of PT-100 in patients receiving myelosuppressive chemotherapy. J Clin Oncol; 2004 Jul 15;22(14_suppl):2572

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase 1 trial of PT-100 in patients receiving myelosuppressive chemotherapy.
  • : 2572 Background: PT-100 is a small molecule which competitively inhibits dipeptidyl peptidase activity of fibroblast activation protein (FAP) and dipeptidyl peptidase IV (DPP-IV).
  • It rapidly increases cytokine (G-CSF, IL-8) production, accelerates neutrophil and erythrocyte regeneration, and causes tumor regression in mice via inhibition of FAP and DPP-IV.
  • This dose-escalation study was conducted to evaluate the safety of PT-100 in patients receiving myelosuppressive chemotherapy (a doxorubicin or taxane based regimen) and to assess its effects on neutrophil recovery.
  • METHODS: Patients received 2 cycles of chemotherapy: the first cycle (C1) served as each patient's individual control.
  • Most patients received PT-100 on Days 2-8 of chemotherapy in C2, except at 800mcg where one cohort was treated on a Day 5-11 schedule.
  • RESULTS: Five of 13 patients receiving PT-100 800mcg experienced a ≥ 2-day improvement in ≥ Grade 3 neutropenia, and a 62% improvement in median AUC in C2 vs. C1 was observed in patients treated on the Day 2-8 schedule.
  • An MTD was not reached.

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  • (PMID = 28015305.001).
  • [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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20. Chang HM, Kim TW, Ahn JH, Ryu MH, Lee JS, Kim WK, Kang YK: Phase II study of gemcitabine, capecitabine and cisplatin in patients with advanced pancreatic cancer. J Clin Oncol; 2004 Jul 15;22(14_suppl):4219

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 4219 Background: In advanced pancreatic cancer (APC), gemcitabine (G) monotherapy is considered as a standard chemotherapy.
  • However, the benefit of this treatment is needed to be improved.
  • We conducted phase II study with the combination of G, X and P (GXP) in pts with APC.
  • METHODS: Pts who were chemotherapy-naive with histologically confirmed, measurable APC were enrolled.
  • Twelve pts achieved partial response giving an overall response rate of 30.0% in intention-to-treat population (95% confidence interval (CI), 15.8-44.2%) and 14 pts (35.0%) had stable disease.
  • The median time to progression (TTP) of all patients was 5.1 months (mo) (95% CI, 3.8-6.3).
  • The median overall survival (OS) of all patients was 7.5 mo (95% CI, 6.7-8.3).
  • Grade 2/3 non-hematologic toxicities were asthenia (45.0 % of pts), diarrhea (12.5%), stomatitis (12.5%) and hand-foot syndrome (7.5%).
  • There was no treatment-related death.
  • CONCLUSIONS: The combination of gemcitabine, capecitabine and cisplatin is an active and tolerable regimen in pts with APC.

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  • (PMID = 28013986.001).
  • [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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21. Ch'ang H, Hwang T, Wang H, Chang M, Tien Y, Chen J, Hsieh R, Lin P, Shan Y, Cheng A, Chen L: A phase II study of gemcitabine-based chemoradiotherapy (CCRT) after triplet induction chemotherapy (ICT) for locally advanced pancreatic cancer (LAPC): A Taiwan Cooperative Oncology Group (TCOG) study. J Clin Oncol; 2009 May 20;27(15_suppl):e15562

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of gemcitabine-based chemoradiotherapy (CCRT) after triplet induction chemotherapy (ICT) for locally advanced pancreatic cancer (LAPC): A Taiwan Cooperative Oncology Group (TCOG) study.
  • Recently, we showed that triplet chemotherapy consisting of gemcitabine 800 mg/m<sup>2</sup> (10 mg/m<sup>2</sup>/min) followed by oxaliplatin 85 mg/m<sup>2</sup> and 48-hour infusion of 5-FU/LV 3,000 and 150 mg/m<sup>2</sup> Q 2 weeks, the GOFL regimen, is feasible and active for pts with APC.
  • Patients who did not experience disease progression (PD) after 6 cycles of GOFL would had CCRT consisting of weekly gemcitabine 400mg/m<sup>2</sup> plus 50.4Gy/28 fractions of radiation 4-6 weeks later.
  • After CCRT, pts were re-evaluated for surgical intervention and those with unresectable disease would continue GOFL until PD, unacceptable toxicity, patient's refusal or death.
  • Among the 34 (68%) with objective response or stable disease after 6 cycles of ICT, 27 (54%) who completed the assigned multimodality treatment are categorized as CCRT group; whiles 7 (14%) who either declined CCRT (in 5) or still on ICT (in 2) are categorized as non-CCRT group.
  • The median PFS and OS for the ITT population were 9.1 and 14.5 months, respectively.

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  • (PMID = 27962329.001).
  • [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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22. Del Giglio A, Pinto JF, Fonseca FA, Marsicano SR, Delgado PO, Coelho PG, Sant'Anna AL, Maeda P: Chemotherapy induces microssatelite instability (MIS) in plasma free DNA (pfDNA), peripheral blood mononuclear fraction (PBMNF) cells, and urine free DNA (ufDNA) of breast cancer (BC) patients as well as in normal PBMNF cells in vitro in the absence of amifostine (A). J Clin Oncol; 2009 May 20;27(15_suppl):e11505

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy induces microssatelite instability (MIS) in plasma free DNA (pfDNA), peripheral blood mononuclear fraction (PBMNF) cells, and urine free DNA (ufDNA) of breast cancer (BC) patients as well as in normal PBMNF cells in vitro in the absence of amifostine (A).
  • : e11505 Background: We have previously shown that alkylating agent based chemotherapy regimens (AQT) could induce MIS in the PBMNF of BC patients in parallel to a decrease in the expression of the protein hMSH2 in these cells (Fonseca et al., 2005, Breast Cancer Res, 7, R28-32).
  • Since plasma DNA derives mainly from tumor cells, we wanted to know if chemotherapy would also produce MIS in tumor DNA and if this phenomenon could be reproduced in vitro.
  • METHODS: 33 previously untreated female BC patients with a mean age of 51 years received AQT(16 ACT;3FAC;2 TAC;1FEC;10AC).
  • Samples from 3 additional patients who received Fulvestrant only as neoadjuvant therapy were also included.
  • Blood (pfDNA and PBMNNF) and urine (ufDNA) were evaluated at time 0,3 and 6 months with 6 MIS markers (BAT40,BAT26, MR2,TP53 PCR15.1, APC and ALU).
  • We incubated in vitro cultures of MCF- 7 cells and PBMNF cells with M at a dose of 0.7μg/ml for 30 minutes with and without A at 20% of the M dose and evaluated serially for 48 hours for MIS and hMH2 expression by immunohistochemistry.
  • Interestingly, fpDNA levels increased significantly in patients with measurable disease who responded to therapy (47.4 ± 13.34 vs 14.37± 5.32; p = 0.021).
  • In vitro, incubating MCF-7 cells and normal PBMNF cells with M ±A, we observed that we could induce MIS in both MCF-7 cells and normal PBMNF cells but A prevented MIS only in normal PBMNF cells.
  • CONCLUSIONS: We conclude that Chemotherapy as well as Fulvestran can induce MIS in normal and malignant cells and that in vitro these effects could be reproduced by treatment with M and prevented in normal cells by A.

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  • (PMID = 27964585.001).
  • [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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23. Riess H, Pelzer U, Deutschinoff G, Opitz B, Stauch M, Reitzig P, Hahnfeld S, Hilbig A, Stieler J, Oettle H: A prospective, randomized trial of chemotherapy with or without the low molecular weight heparin (LMWH) enoxaparin in patients (pts) with advanced pancreatic cancer (APC): Results of the CONKO 004 trial. J Clin Oncol; 2009 May 20;27(15_suppl):LBA4506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A prospective, randomized trial of chemotherapy with or without the low molecular weight heparin (LMWH) enoxaparin in patients (pts) with advanced pancreatic cancer (APC): Results of the CONKO 004 trial.

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  • (PMID = 27960826.001).
  • [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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24. O' Reilly EM, Abou-Alfa GK, Letourneau R, Harker WG, Modiano M, Hurwitz H, Tchekmedyian NS, Ackerman J, De Jager RL, Eckhardt SG: A randomized phase III trial of DX-8951f (Exatecan Mesylate; DX) and Gemcitabine (GEM) vs. Gemcitabine alone in advanced pancreatic cancer (APC). J Clin Oncol; 2004 Jul 15;22(14_suppl):4006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized phase III trial of DX-8951f (Exatecan Mesylate; DX) and Gemcitabine (GEM) vs. Gemcitabine alone in advanced pancreatic cancer (APC).
  • DX has single-agent and combination activity with GEM in APC (D'Adamo, et al. ASCO, 2001; O'Reilly, et al. ASCO, 2002).
  • A multicenter, randomized phase III trial comparing DX + GEM to GEM alone in APC was conducted.
  • METHODS: Eligibility included KPS ≥ 60%; locally advanced or metastatic pancreatic adenocarcinoma; no prior chemotherapy.
  • Radiation (RT) alone for locally advanced disease was permitted.
  • Patients (pts) were randomized on a 1: 1 basis to DX + GEM or GEM alone.
  • Pts were stratified by KPS, 60%, 70-80%, ≥ 90%, locally advanced vs metastatic disease, prior RT vs. no RT.
  • For the DX + GEM arm, DX was dosed at 2.0mg/m2; GEM at 1,000mg/m2 on a days 1 and 8, q 3 weeks.
  • Twenty-four pts (6.9%) were not treated.
  • The treatment arms were well-balanced for extent of disease, KPS, and prior RT.
  • The median survival time was 6.7 months for DX + GEM and 6.2 months for GEM alone (p=0.52).
  • There was an improvement in time-to-worsening of pain and analgesic consumption for DX + GEM compared to GEM alone.
  • However, time-to-worsening of KPS and weight were similar for both treatment arms.
  • CONCLUSIONS: DX + GEM was not superior to GEM alone with respect to overall survival in the front-line treatment of APC.
  • The results do not alter the standard of care for treatment of APC.

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  • (PMID = 28016360.001).
  • [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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25. Saif MW, Li J, Lamb L, Rosenberg A, Elligers K, Ruta S, Mezes M, Grant N, Liu SH, Chu E, Cheng Y: A phase II study of capecitabine (CAP) plus PHY906 in patients (pts) with advanced pancreatic cancer (APC). J Clin Oncol; 2009 May 20;27(15_suppl):e15508

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of capecitabine (CAP) plus PHY906 in patients (pts) with advanced pancreatic cancer (APC).
  • : e15508 Background: Gemcitabine (G) is regarded as the standard treatment for pts with APC.
  • However, a standard second-line chemotherapy regimen has yet to be defined after G.
  • Therefore, 1500mg/m<sup>2</sup> of CAP and PHY906 was further tested in a phase II study as second-line treatment in pts with APC.
  • METHODS: Pts with G-refractory APC with ECOG PS <2 were treated with CAP 1500mg/m<sup>2</sup> d1-7 with PHY906 800mg d1-4 q 2 wks.
  • Secondary objectives include overall RR, PFS and measurement of cytokines to assess inhibition of NF-kappa B, a possible mechanism responsible for PHY906's pharmacological activity.
  • At this point 5 pts are still in active treatment.
  • There were 7 deaths on/within 30 days of study treatment, 6 related to PD and 1 had acute MI.
  • CONCLUSIONS: This is the first clinical study to evaluate a botanical formulation PHY906 with CAP in G-refractory APC pts.
  • CAP + PHY906 regimen appears a safe and feasible salvage therapy in APC and warrants further investigation.
  • In addition, PHY906 may have a cytoprotective antidiarrheal and anti-HFS effect, making treatment with CAP more tolerable.

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  • (PMID = 27962238.001).
  • [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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26. Colucci G, Labianca R, Di Costanzo F, Gebbia V, Cartenì G, Massidda B, Frontini L, Falconi M, Gallo C, Di Maio M: A randomized trial of gemcitabine (G) versus G plus cisplatin in chemotherapy-naive advanced pancreatic adenocarcinoma: The GIP-1 (Gruppo Italiano Pancreas- GOIM/GISCAD/GOIRC) study. J Clin Oncol; 2009 May 20;27(15_suppl):4504

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized trial of gemcitabine (G) versus G plus cisplatin in chemotherapy-naive advanced pancreatic adenocarcinoma: The GIP-1 (Gruppo Italiano Pancreas- GOIM/GISCAD/GOIRC) study.
  • : 4504 Background: Single-agent gemcitabine (G) remains standard treatment for advanced pancreatic adenocarcinoma (APC).
  • The GIP-1 randomized phase III trial (clinicaltrials.gov ID NCT00813696 ) was performed to compare the combination of cisplatin (P) and G vs. G alone as 1st-line treatment.
  • In Arm B, P 25 mg/m2 weekly (with the exception of day 22) was added to G, same dose used in Arm A (Colucci et al, Cancer 2002; 94:902-10).
  • After a median follow-up of 38.2 months and 357 deaths, median OS was 8.3 vs 7.2 months in arm A and B, respectively (HR 1.10, 95% CI 0.89-1.35, p=0.38).
  • Median PFS was 3.9 vs 3.8 months in arm A and B, respectively (HR 0.97, 95% CI 0.80-1.19, p=0.80).
  • ORR was 10.1% in arm A and 12.9% in B (p=0.37).
  • CONCLUSIONS: Weekly combination of P and G, compared to single-agent G as 1st-line treatment of APC, failed to demonstrate any improvement in OS, PFS, ORR and clinical benefit.

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  • (PMID = 27962688.001).
  • [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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27. Cheverton P, Friess H, Andras C, Salek T, Geddes C, Bodoky G, Valle J, Humblet Y: Phase III results of exatecan (DX-8951f) versus gemcitabine (Gem) in chemotherapy-naïve patients with advanced pancreatic cancer (APC). J Clin Oncol; 2004 Jul 15;22(14_suppl):4005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase III results of exatecan (DX-8951f) versus gemcitabine (Gem) in chemotherapy-naïve patients with advanced pancreatic cancer (APC).
  • Ensiv has single-agent and combination activity with Gem in APC (D'Adamo, et al. ProcASCO, 2001; O'Reilly, et al. ProcASCO, 2002).
  • METHODS: A multi-centre randomised phase III trial comparing Ensiv with gemcitabine in APC has been completed.
  • Eligibility included KPS ≥ 60%; locally advanced or metastatic disease; no prior chemotherapy.
  • Patients (pts) were randomised in a 1:1 ratio to Ensiv (0.5 mg/m<sup>2</sup> daily x 5 q3w) or gemcitabine (1000 mg/m<sup>2</sup> weekly x 7 then 1 week rest, then weekly x 3 q4w).
  • Treatment continued until disease progression or intolerable toxicity.
  • Of these 330 (165 Ensiv; 165 Gem) received treatment.
  • Demographic factors were well balanced for age, sex, PS and disease extent.
  • Survival: Median Survival Times (MST) were Ensiv 151 days; Gem 197 days), 6-month Survival rates Ensiv 44.1%; Gem 51.1%, and 12-month Survival rates Ensiv 17.9%; Gem 22.1%.
  • Median Time to Tumor Progression (TTP) was; Ensiv 85 days; Gem 132 days.
  • Treatment emergent toxicities are tabulated below: Conclusions: Single agent Ensiv did not show the expected increase in survival or clinical benefit over gemcitabine in this study [Figure: see text] [Table: see text].

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  • (PMID = 28016361.001).
  • [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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28. Ohkawa S: Randomized controlled trial of gemcitabine in combination with UFT versus gemcitabine alone in patients with advanced pancreatic cancer. J Clin Oncol; 2004 Jul 15;22(14_suppl):4131

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 4131 Background: GEM is a standard drug for chemotherapy in patients with APC.
  • But they should be offered better therapy aimed more effective response and prolonging survival.
  • UFT is also available for treatment of APC.
  • METHODS: Eligibility: no pretreatment (chemotherapy and irradiation), good performance status (50-100 in Karnofsky Performance Status) and less than 75 years old in APC patients such as locally advanced or with distant metastasis.
  • Primary endpoints are response rate (RR) and survival time (MST).
  • Time to progression (TTP) and Clinical benefit response (CBR) were also evaluated.
  • RR (0/10 vs 3/9) and MST (5.0±0.6 months vs 7.6±2.1) were not significant (NS).
  • Toxicity (NCI-CTC grade 3/4); leucocytes (20.0%:33.3%), neutrophils (10.0%:11.1%), platelets (10.0%:0%), diarrhea (10.0%:0%), anorexia (40.0%:11.1%) Conclusions: The chemotherapy by GEM plus UFT in this method may not be effective compared with GEM alone.

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  • (PMID = 28014554.001).
  • [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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29. Lee S, Ryoo H, Bae S, Song H, Kim M, Lee K, Lee W, Park K, Kim J, Baek J: Fixed dose rate infusion of gemcitabine and UFT combination chemotherapy in patients with advanced biliary cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e15581

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fixed dose rate infusion of gemcitabine and UFT combination chemotherapy in patients with advanced biliary cancer.
  • Gemcitabine and UFT combination chemotherapy showed promising results in advanced pancreatic cancer(APC) and fixed dose- rate(FDR) infusion(10mg/m<sup>2</sup>/min) of gemcitabine is more effective than 30min-infusion in APC patients.
  • We conducted a prospective multicenter phase II study to evaluate the efficacy and toxicity of FDR gemcitabine and UFT combination chemotherapy in advanced biliary cancer(ABC) patients.
  • We evaluated the quality of life(QOL) and relationship between treatment outcome and polymorphisms of DNA repair gene such as RecQ1, RAD54L, XRCC1 and ATM.
  • Partial response was 24.2% and disease control rate was 51.5%.
  • The estimated median time to progression(TTP) was 87 days(95% CI 51-123).
  • Median overall survival was 243 days(95% CI 114-372).
  • Grade 3/4 neutropenia was observed in 12 of 33 patients(36.4%) and 17 times of 114 cycles of chemotherapy(14.9%).
  • Polymorphism of XRCC1 was related to TTP(TTP of wild, heterozygous variant and homozygous variant type was 162, 71 and 25 days, respectively. p=0.0039).
  • QOL as a secondary endpoint was not analyzed at this time.
  • CONCLUSIONS: FDR infusion of gemcitabine and UFT combination chemotherapy in chemo-naïve patients with ABC is a well-tolerated and effective regimen.

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  • (PMID = 27962362.001).
  • [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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30. Gerner EW, Ignatenko NA, Lance P, Hurley LH: A comprehensive strategy to combat colon cancer targeting the adenomatous polyposis coli tumor suppressor gene. Ann N Y Acad Sci; 2005 Nov;1059:97-105
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comprehensive strategy to combat colon cancer targeting the adenomatous polyposis coli tumor suppressor gene.
  • Somatic cells in the majority of colorectal polyps and cancers contain mutations/deletions in the adenomatous polyposis coli (APC) tumor suppressor gene.
  • APC is involved in normal intestinal development and acts to influence a variety of cellular processes.
  • Loss of APC function leads to intestinal neoplasia in both mice and humans.
  • APC influences expression of specific genes, including the c-Myc oncogene, which functions as a transcriptional activator.
  • Loss of APC function leads to alterations in c-Myc-regulated genes including ornithine decarboxylase (ODC), the first enzyme in polyamine synthesis.
  • A single nucleotide polymorphism (SNP) in the ODC promoter affecting c-Myc-dependent expression has been associated with risk of colorectal and other cancers.
  • Pharmaceuticals that target structural features of the c-Myc promoter, and suppress expression of c-Myc and other genes regulated by similar promoter elements, are being developed as potential colorectal cancer chemotherapies.
  • APC and APC-dependent genes, such as c-Myc and ODC, may be useful as genetic markers of risk and as targets for chemoprevention and therapy for colorectal cancer.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Colonic Neoplasms / drug therapy. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Aspirin / pharmacology. Base Sequence. Eflornithine / pharmacology. Humans. Models, Biological. Molecular Sequence Data. Neoplasms / metabolism. Polymorphism, Single Nucleotide. Proto-Oncogene Proteins c-myc / metabolism

  • Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ACETYLSALICYLIC ACID .
  • Hazardous Substances Data Bank. Eflornithine .
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  • (PMID = 16382048.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins c-myc; R16CO5Y76E / Aspirin; ZQN1G5V6SR / Eflornithine
  • [Number-of-references] 29
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31. Chen SP, Wu CC, Lin SZ, Kang JC, Su CC, Chen YL, Lin PC, Chiu SC, Pang CY, Harn HJ: Prognostic significance of interaction between somatic APC mutations and 5-fluorouracil adjuvant chemotherapy in Taiwanese colorectal cancer subjects. Am J Clin Oncol; 2009 Apr;32(2):122-6
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of interaction between somatic APC mutations and 5-fluorouracil adjuvant chemotherapy in Taiwanese colorectal cancer subjects.
  • OBJECTIVE: The correlations between adenomatous polyposis coli (APC) mutations and 5-fluorouracil (5-FU) adjuvant chemotherapy and colorectal cancer (CRC) patients' prognosis are not well known.
  • We performed an exploratory study to investigate the association between APC mutations and the survival of Taiwanese CRC subjects who received 5-FU adjuvant chemotherapy.
  • METHODS: Full-length APC gene isolated from tumor tissue and adjacent normal colon tissue from 117 CRC subjects was sequenced.
  • RESULTS: Although the subject survival rate was associated with the cancer stage, but not with the occurrence of APC mutations, we demonstrate a significant interaction between the somatic APC mutations and 5-FU adjuvant chemotherapy to the prognosis of CRC subjects.
  • Subjects carrying APC mutation(s) and receiving 5-FU adjuvant chemotherapy demonstrate increased hazards (vs. no APC mutation or chemotherapy) for all cause (hazard ratios = 5.565; P = 0.042) or CRC deaths (hazard ratios = 6.920; P = 0.043).
  • 5-FU adjuvant chemotherapy only decreases hazards in CRC subjects without APC mutation(s) for all cause death (hazard ratios = 0.257; P = 0.003) or CRC death (hazard ratios = 0.342; P = 0.028).
  • CONCLUSIONS: 5-FU adjuvant chemotherapy only prevents CRC subjects without somatic APC mutation(s) from all cause death or CRC death.
  • It needs further studies with larger sample size and longer follow-up time to confirm these results.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / genetics. Fluorouracil / therapeutic use. Genes, APC. Mutation / genetics
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Aged. Chemotherapy, Adjuvant. Chromatography, High Pressure Liquid. DNA / analysis. Female. Humans. Male. Neoplasm Staging. Prognosis. Survival Rate. Taiwan

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  • (PMID = 19307944.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 9007-49-2 / DNA; U3P01618RT / Fluorouracil
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32. Chen SP, Chiu SC, Wu CC, Lin SZ, Kang JC, Chen YL, Lin PC, Pang CY, Harn HJ: The association of methylation in the promoter of APC and MGMT and the prognosis of Taiwanese CRC patients. Genet Test Mol Biomarkers; 2009 Feb;13(1):67-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The association of methylation in the promoter of APC and MGMT and the prognosis of Taiwanese CRC patients.
  • AIMS: The purpose of this study was to investigate the association of methylation in the promoter regions of adenomatous polyposis coli (APC) and O(6)-methylguanine-DNA methyltransferase (MGMT) and the survival of Taiwanese colorectal cancer (CRC) subjects who received 5-fluorouracil (5-FU) adjuvant chemotherapy.
  • RESULTS: DNA isolated from tumor tissue of 117 CRC subjects was analyzed for the existence of methylation in the promoter regions of APC and MGMT by methylation-specific PCR.
  • Methylation in the promoter region is 62.4% (73/117) for APC and 60.7% (71/117) for MGMT in our CRC patients.
  • Subjects presenting methylation in the APC promoter demonstrate significantly lower hazards for all causes of death (hazard ratios=0.378, p=0.011) or CRC deaths (hazard ratios=0.426, p=0.039).
  • In addition, no interaction between 5-FU adjuvant chemotherapy and methylation of the two genes are observed.
  • CONCLUSIONS: Methylation in the APC promoter may serve as a predictor for the prognosis of Taiwanese CRC patients.
  • [MeSH-major] Colorectal Neoplasms / enzymology. Colorectal Neoplasms / genetics. DNA Methylation. DNA Modification Methylases / genetics. DNA Repair Enzymes / genetics. Genes, APC. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Aged. Antimetabolites, Antineoplastic / therapeutic use. Chemotherapy, Adjuvant. Female. Fluorouracil / therapeutic use. Humans. Male. Middle Aged. Prognosis. Promoter Regions, Genetic. Survival Analysis. Taiwan

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  • (PMID = 19309276.001).
  • [ISSN] 1945-0257
  • [Journal-full-title] Genetic testing and molecular biomarkers
  • [ISO-abbreviation] Genet Test Mol Biomarkers
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Tumor Suppressor Proteins; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes; U3P01618RT / Fluorouracil
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33. Quyn AJ, Steele RJ, Carey FA, Näthke IS: Prognostic and therapeutic implications of Apc mutations in colorectal cancer. Surgeon; 2008 Dec;6(6):350-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic and therapeutic implications of Apc mutations in colorectal cancer.
  • The adenomatous polyposis coli gene (Apc) is mutated in most colorectal cancers.
  • The multifunctional character of the Apc protein in the regulation of beta-catenin-mediated gene transcription and cytoskeletal proteins has been well described.
  • An important question is how this protein affects the behaviour of cells within a tumour and how its mutational status influences the prognosis for these tumours.
  • Here we provide an overview of the functions of Apc and examine how this information can be used in the prognosis and development of directed therapy in colorectal cancer.
  • [MeSH-major] Colorectal Neoplasms / genetics. Genes, APC / physiology
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Aspirin / pharmacology. Cytoskeleton / genetics. Humans. Prognosis. Signal Transduction / drug effects. Signal Transduction / genetics. Wnt Proteins / genetics. beta Catenin / metabolism

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  • [CommentIn] Surgeon. 2008 Dec;6(6):324 [19110817.001]
  • (PMID = 19110823.001).
  • [ISSN] 1479-666X
  • [Journal-full-title] The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland
  • [ISO-abbreviation] Surgeon
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Wnt Proteins; 0 / beta Catenin; R16CO5Y76E / Aspirin
  • [Number-of-references] 87
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34. Okuno SH, Edmonson JH: Combination chemotherapy for desmoid tumors. Cancer; 2003 Feb 15;97(4):1134-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination chemotherapy for desmoid tumors.
  • BACKGROUND: Desmoid tumor (aggressive fibromatosis) is an aggressive fibroblastic proliferation of well circumscribed, locally invasive, differentiated fibrous tissue.
  • For patients with desmoid tumors that are not amenable to surgery or radiation therapy, the use of hormonal agents and nonsteroidal antiinflammatory drugs (NSAIDs) have been attempted, with some success.
  • The use of chemotherapy also has been reported to have activity.
  • METHODS: Seven patients (5 males and 2 females) with a median age of 40 years (range, 17-66 years) who received cytotoxic chemotherapy (combinations of cyclophosphamide and doxorubicin; mitomycin, doxorubicin, and cisplatin; and ifosfamide and etoposide) for desmoid tumor were reviewed retrospectively.
  • Four patients had familial adenomatous polyposis.
  • Four patients had failed tamoxifen and six had failed NSAIDs prior to receiving cytotoxic chemotherapy.
  • RESULTS: Patients received a median number of six cycles of chemotherapy (range, two to eight cycles).
  • Objective disease regression occurred in 3 patients.
  • The chemotherapy was well tolerated and no treatment-related mortality was reported.
  • CONCLUSIONS: The results of the current study indicate that the use of combination chemotherapy for desmoid tumors may provide long-term clinical benefits.
  • [MeSH-major] Fibromatosis, Aggressive / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • [Copyright] Copyright 2003 American Cancer Society
  • (PMID = 12569616.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
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35. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemoprevention of colorectal cancer by targeting APC-deficient cells for apoptosis.
  • It holds promise for overcoming problems associated with the treatment of late-stage cancers.
  • However, the broad application of chemoprevention is compromised at present by limited effectiveness and potential toxicity.
  • To overcome these challenges, here we developed a new chemoprevention approach that specifically targets premalignant tumour cells for apoptosis.
  • We show that a deficiency in the adenomatous polyposis coli (APC) gene and subsequent activation of beta-catenin lead to the repression of cellular caspase-8 inhibitor c-FLIP (also known as CFLAR) expression through activation of c-Myc, and that all-trans-retinyl acetate (RAc) independently upregulates tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptors and suppresses decoy receptors.
  • Thus, the combination of TRAIL and RAc induces apoptosis in APC-deficient premalignant cells without affecting normal cells in vitro.
  • 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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36. Esaki M, Matsumoto T, Mizuno M, Kobori Y, Yoshimura R, Yao T, Iida M: Effect of sulindac treatment for attenuated familial adenomatous polyposis with a new germline APC mutation at codon 161: report of a case. Dis Colon Rectum; 2002 Oct;45(10):1397-402; discussion 1402-6
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  • [Title] Effect of sulindac treatment for attenuated familial adenomatous polyposis with a new germline APC mutation at codon 161: report of a case.
  • INTRODUCTION: Patients with familial adenomatous polyposis develop colorectal cancers if left untreated.
  • As indicated in patients with familial adenomatous polyposis, prophylactic colectomy has been recommended even in a milder colonic phenotype referred to as attenuated familial adenomatous polyposis.
  • However, therapeutic strategies in attenuated familial adenomatous polyposis are still controversial.
  • METHODS: We report a patient with attenuated familial adenomatous polyposis who has been treated with sulindac for five years.
  • Immunohistochemical study for cyclooxygenase-2 and genetic analysis in the adenomatous polyposis coli gene was also performed.
  • RESULTS: Continuous administration of sulindac resulted in obvious regression of both colorectal adenomatous polyps and gastric fundic gland polyps, and no cancers developed during the observation period.
  • Immunohistochemical study showed the decrease of cyclooxygenase-2-positive epithelial cells in colorectal polyps by the treatment.
  • The genetic analysis revealed a C to A substitution at nucleotide 481 of her germline adenomatous polyposis coli gene, which resulted in a nonsense mutation at codon 161.
  • CONCLUSIONS: Our case suggests that treatment with sulindac accompanied by intensive colonoscopic surveillance may be a choice of management for attenuated familial adenomatous polyposis.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Adenomatous Polyposis Coli / genetics. Antineoplastic Agents / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Germ-Line Mutation. Isoenzymes / metabolism. Prostaglandin-Endoperoxide Synthases / metabolism. Sulindac / therapeutic use
  • [MeSH-minor] Codon. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Female. Humans. Immunohistochemistry. Membrane Proteins. Middle Aged

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  • (PMID = 12394442.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Codon; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 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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37. Shimakawa T, Naritaka Y, Asaka S, Isohata N, Murayama M, Konno S, Yoshimatsu K, Shiozawa S, Katsube T, Ogawa K: Neoadjuvant chemotherapy (FAP) for advanced esophageal cancer. Anticancer Res; 2008 Jul-Aug;28(4C):2321-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neoadjuvant chemotherapy (FAP) for advanced esophageal cancer.
  • This study was performed to assess the usefulness and safety of neoadjuvant chemotherapy utilizing the FAP regimen consisting of 5-fluorouracil, cisplatin and adriamycin for the treatment of highly advanced esophageal cancer.
  • The patients generally received two cycles of FAP.
  • The results of this study therefore showed the usefulness and safety of FAP therapy, which is considered to be a treatment method worth aggressively trying for highly advanced esophageal cancer in which a curative resection can hardly be expected.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / surgery. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Cisplatin / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Humans. Male. Middle Aged. Neoadjuvant Therapy. Neoplasm Staging. Survival Rate

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  • (PMID = 18751413.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; FAP protocol
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38. Gould TD, Gray NA, Manji HK: Effects of a glycogen synthase kinase-3 inhibitor, lithium, in adenomatous polyposis coli mutant mice. Pharmacol Res; 2003 Jul;48(1):49-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of a glycogen synthase kinase-3 inhibitor, lithium, in adenomatous polyposis coli mutant mice.
  • Glycogen synthase kinase-3 (GSK-3) is an intermediary enzyme in various cellular pathways, and has been implicated in the pathophysiology and treatment of numerous diseases, including Alzheimer's disease, diabetes, and bipolar disorder.
  • There is therefore in developing potent, selective GSK-3 inhibitors for the treatment of these devastating illnesses.
  • It is thus of considerable importance to determine if GSK-3 inhibitors have tumorigenic potential in systems predisposed to developing tumors by virtue of mutations of the Wnt-signaling pathway.
  • We therefore investigated the effects of a GSK-3 inhibitor, lithium, in a murine model predisposed to the formation of tumors due to activation of the Wnt pathway-the adenomatous polyposis coli (APC) multiple intestinal neoplasia (min) mouse.
  • We found that 60 days of lithium treatment did not produce a significant increase in the number of tumors in these genetically predisposed mice.
  • Lithium treatment resulted in a modest overall increase in the tumor size.
  • The APC (min) mouse has previously been shown to be a robust indicator of tumorigenesis, with large increases in tumor number observed in response to a variety of agents; thus, our results suggest that lithium-and perhaps other inhibitors of GSK-3-pose a low risk for the development of cancers of the Wnt pathway.
  • These results are consistent with the available epidemiological evidence that long-term lithium therapy does not increase cancer morbidity or mortality, but rather is associated with reduced overall mortality in bipolar disorder.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Glycogen Synthase Kinase 3 / antagonists & inhibitors. Intestinal Neoplasms / chemically induced. Lithium / toxicity. Zebrafish Proteins
  • [MeSH-minor] Animals. Disease Models, Animal. Genes, APC. Male. Mice. Mice, Mutant Strains. Mutation. Proto-Oncogene Proteins / drug effects. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Signal Transduction / drug effects. Wnt Proteins

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  • (PMID = 12770514.001).
  • [ISSN] 1043-6618
  • [Journal-full-title] Pharmacological research
  • [ISO-abbreviation] Pharmacol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / Zebrafish Proteins; 9FN79X2M3F / Lithium; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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39. Radulescu S, Ridgway RA, Appleton P, Kroboth K, Patel S, Woodgett J, Taylor S, Nathke IS, Sansom OJ: Defining the role of APC in the mitotic spindle checkpoint in vivo: APC-deficient cells are resistant to Taxol. Oncogene; 2010 Dec 09;29(49):6418-27
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  • [Title] Defining the role of APC in the mitotic spindle checkpoint in vivo: APC-deficient cells are resistant to Taxol.
  • Mutations in the adenomatous polyposis coli (APC) tumour suppressor are the key initiating event of colorectal cancer.
  • Although the control of WNT signalling is well established as a central tumour-suppressive function, the significance of APC in regulating chromosome instability is less well established.
  • In this study, we test whether APC-deficient cells have a functional spindle assembly checkpoint (SAC) in vivo by examining the response of these cells to Taxol and Vinorelbine.
  • We also show for the first time that APC deficiency compromises the arrest response to Taxol in vivo.
  • This effect is independent of the role that APC has in WNT signalling.
  • At higher levels of Taxol, APC-deficient cells arrest as efficiently as wild-type cells.
  • Importantly, this dose of Taxol strongly suppresses intestinal tumourigenesis in models of benign (APC(Min/+) mouse) and invasive (AhCreER(+)APC(fl/+)PTEN(fl/fl)) cancer.
  • In contrast to intestinal enterocytes with a general SAC defect because of Bub1 (budding uninhibited by benzimidazole 1) deletion, APC-deficient enterocytes arrest equivalently to wild type when treated with Vinorelbine.
  • This suggests that the failed arrest in response to Taxol is because of a specific defect in microtubule stabilization following Taxol treatment rather than a general role of the APC protein in the mitotic spindle checkpoint.
  • In summary, this study clarifies the role of APC as a mitotic spindle checkpoint protein in vivo and shows that APC-deficient cells have a compromised response to Taxol.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Adenomatous Polyposis Coli Protein / physiology. Antineoplastic Agents, Phytogenic / therapeutic use. Drug Resistance, Neoplasm / genetics. Paclitaxel / therapeutic use. Spindle Apparatus / metabolism
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Chromosomal Instability / genetics. Enterocytes / drug effects. Enterocytes / pathology. Male. Mice. Mice, Inbred C57BL. Protein-Serine-Threonine Kinases / genetics. Sequence Deletion. Vinblastine / analogs & derivatives. Vinblastine / therapeutic use. Wnt Proteins / metabolism

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  • (PMID = 20729907.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A11243; Canada / Canadian Institutes of Health Research / / 12858; United Kingdom / Cancer Research UK / / 11243; United Kingdom / Cancer Research UK / / ; Canada / Canadian Institutes of Health Research / / 74711; United Kingdom / Cancer Research UK / / A7130; United Kingdom / Cancer Research UK / / 11913
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents, Phytogenic; 0 / Wnt Proteins; 5V9KLZ54CY / Vinblastine; EC 2.7.11.1 / Bub1 protein, mouse; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; P88XT4IS4D / Paclitaxel; Q6C979R91Y / vinorelbine
  • [Other-IDs] NLM/ PMC3016607; NLM/ UKMS31064
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40. Qiu ZF, Maruyama K, Sunayama K, Kashiwabara H, Shoji T, Nakamura T, Suzuki S, Konno H, Nakamura S: Piroxicam-induced regression of intestinal adenomatous polyps in APC(delta474) mice. J Invest Surg; 2003 Mar-Apr;16(2):71-81
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  • [Title] Piroxicam-induced regression of intestinal adenomatous polyps in APC(delta474) mice.
  • Mutation of adenomatous polyposis coli (APC) gene results in incidence or development of polyps and colorectal cancer.
  • It has been reported that nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cell growth, cause cell cycle arrest, and induce apoptosis.
  • All APC(delta474) mice have intestinal polyps.
  • Thirty-five APC(delta474) mice were divided into three groups: 0.005% solution of piroxicam in tap water was given for P group (n = 15) and 0.001% solution for P' group (n = 5), and water without piroxicam for C group (n = 15) from 4 weeks of age to 12 weeks, respectively.
  • Hematoxylin-eosin staining for number and size of polyps, immunohistochemical staining for cyclooxygenase (COX)-1 and -2, proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), TUNEL method, and Western blot analysis of COX-2 and VEGF were performed.
  • Polyps were divided into two types of large polyps of >or=300 microm in diameter and small polyps of <300 microm.
  • The number of large polyps in P group decreased significantly compared with C group (p <.0001), but without significant difference in small polyps.
  • There were no significant differences in PCNA index in both of large and small polyps among the three groups.
  • There was immunohistochemically no significant difference in COX-1 positivity of normal intestinal epithelia and adenomas among three groups.
  • Both numbers of VEGF-positive cells and COX-2 positive cells in the stroma of the small intestine were significantly downregulated in P group (p <.05).
  • There were no significant differences in VEGF expression between P' and C groups.
  • In conclusion, piroxicam suppressed the development of large polyps in APC(delta474) mice by inducing apoptosis and inhibiting VEGF expression in interstitial cells of polyps.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Adenomatous Polyposis Coli / genetics. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Genes, APC. Piroxicam / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cyclooxygenase 1. Cyclooxygenase 2. Female. Immunohistochemistry. Isoenzymes / metabolism. Male. Membrane Proteins. Mice. Mice, Inbred C57BL. Mice, Knockout. Mutation. Proliferating Cell Nuclear Antigen / metabolism. Prostaglandin-Endoperoxide Synthases / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 12746190.001).
  • [ISSN] 0894-1939
  • [Journal-full-title] Journal of investigative surgery : the official journal of the Academy of Surgical Research
  • [ISO-abbreviation] J Invest Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proliferating Cell Nuclear Antigen; 0 / Vascular Endothelial Growth Factor A; 13T4O6VMAM / Piroxicam; 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
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41. Roh H, Green DW, Boswell CB, Pippin JA, Drebin JA: Suppression of beta-catenin inhibits the neoplastic growth of APC-mutant colon cancer cells. Cancer Res; 2001 Sep 1;61(17):6563-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of beta-catenin inhibits the neoplastic growth of APC-mutant colon cancer cells.
  • Mutations involving the adenomatous polyposis coli (APC) tumor suppressorgene/beta-catenin signaling pathway have been identified in the majority of colon carcinomas.
  • However, the role of aberrant beta-catenin signaling in the neoplastic growth of APC-mutant colon cancer cells has not been directly studied.
  • To address this question, antisense oligonucleotides have been used to specifically down-regulate beta-catenin expression in APC-mutant human colon carcinoma cells.
  • Antisense-mediated suppression of beta-catenin inhibits the in vitro proliferation, anchorage-independent growth, and cellular invasiveness of APC-mutant human colon carcinoma cells.
  • The systemic administration of beta-catenin antisense oligonucleotides down-regulates beta-catenin expression in vivo in human colon cancer xenografts in nude mice.
  • Such treatment inhibits the tumorigenic growth of colon cancer xenografts and can completely eradicate tumors in some treated animals.
  • These studies formally demonstrate the critical role of beta-catenin signaling in the neoplastic growth of APC-mutant colon cancer cells and suggest that strategies targeting beta-catenin may be of use in the therapy of colon cancer.
  • [MeSH-major] Colonic Neoplasms / pathology. Cytoskeletal Proteins / antagonists & inhibitors. Genes, APC / genetics. Trans-Activators
  • [MeSH-minor] Animals. Cell Adhesion / physiology. Cell Division / physiology. Down-Regulation / drug effects. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Mutation. Neoplasm Transplantation. Oligonucleotides, Antisense / genetics. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Signal Transduction / physiology. Thionucleotides / genetics. Thionucleotides / pharmacology. Transplantation, Heterologous. Tumor Cells, Cultured. beta Catenin

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  • (PMID = 11522655.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA09621; United States / NCI NIH HHS / CA / CA79841
  • [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 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Thionucleotides; 0 / Trans-Activators; 0 / beta Catenin
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42. Hansen-Petrik MB, McEntee MF, Jull B, Shi H, Zemel MB, Whelan J: Prostaglandin E(2) protects intestinal tumors from nonsteroidal anti-inflammatory drug-induced regression in Apc(Min/+) mice. Cancer Res; 2002 Jan 15;62(2):403-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostaglandin E(2) protects intestinal tumors from nonsteroidal anti-inflammatory drug-induced regression in Apc(Min/+) mice.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are antitumorigenic in humans as well as in animal models of intestinal neoplasia, such as the adenomatous polyposis coli (Min/+) (Apc(Min/+)) mouse.
  • In the present study, we attempted to clarify this issue by treating Apc(Min/+) mice bearing established tumors with NSAIDs (piroxicam and sulindac, 0.5 and 0.6 mg/mouse/day, respectively) for 6 days and concomitantly bypassing COX inhibition by treatment with the E prostaglandin (EP) receptor agonists 16,16-dimethyl-prostaglandin E(2) (PGE(2)) and 17-phenyl-trinor-PGE(2) (10 microg each, three times daily) administered via gavage and/or i.p. routes.
  • Treatment with piroxicam and sulindac resulted in 95% and 52% fewer tumors, respectively, and a higher ratio of apoptosis:mitosis in tumors from sulindac-treated mice as compared with controls.
  • These effects were attenuated by concomitant EP receptor agonist treatment, suggesting PGE(2) is important in the maintenance of tumor integrity.
  • Immunological sequestration of PGE(2) with an anti-PGE(2) monoclonal antibody likewise resulted in 33% fewer tumors in Apc(Min/+) mice relative to untreated controls, additionally substantiating a role for PGE(2) in tumorigenesis.
  • The EP receptor subtype EP1 mediates the effects of PGE(2) by increasing intracellular calcium levels ([Ca(2+)](i)), whereas antagonism of EP1 has been shown to attenuate tumorigenesis in Apc(Min/+) mice.
  • We demonstrate that [Ca(2+)](i) is significantly elevated in tumors of Apc(Min/+) mice relative to the adjacent normal-appearing mucosa.
  • Furthermore, treatment with piroxicam results in significantly lower [Ca(2+)](i) in tumors, and this effect is attenuated by concomitant treatment with the EP1/EP3 receptor agonist 17-phenyl-trinor-PGE(2).
  • [MeSH-major] 16,16-Dimethylprostaglandin E2 / pharmacology. Adenomatous Polyposis Coli / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / antagonists & inhibitors. Dinoprostone / analogs & derivatives. Dinoprostone / pharmacology
  • [MeSH-minor] Animals. Antibodies, Monoclonal / pharmacology. Apoptosis / drug effects. Calcium / metabolism. Cyclooxygenase Inhibitors / pharmacology. Disease Models, Animal. Drug Interactions. Intestine, Small / drug effects. Intestine, Small / metabolism. Male. Mice. Mice, Inbred C57BL. Mitosis / drug effects. Piroxicam / antagonists & inhibitors. Piroxicam / pharmacology. Receptors, Prostaglandin E / agonists. Receptors, Prostaglandin E, EP1 Subtype. Receptors, Prostaglandin E, EP2 Subtype. Sulindac / antagonists & inhibitors. Sulindac / pharmacology

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  • (PMID = 11809688.001).
  • [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 / 17-phenyltrinorprostaglandin E2; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antibodies, Monoclonal; 0 / Cyclooxygenase Inhibitors; 0 / PTGER1 protein, human; 0 / PTGER2 protein, human; 0 / Ptger1 protein, mouse; 0 / Ptger2 protein, mouse; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP1 Subtype; 0 / Receptors, Prostaglandin E, EP2 Subtype; 13T4O6VMAM / Piroxicam; 184SNS8VUH / Sulindac; K7Q1JQR04M / Dinoprostone; M790V82VAC / 16,16-Dimethylprostaglandin E2; SY7Q814VUP / Calcium
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43. Chang WC, Everley LC, Pfeiffer GR 2nd, Cooper HS, Barusevicius A, Clapper ML: Sulindac sulfone is most effective in modulating beta-catenin-mediated transcription in cells with mutant APC. Ann N Y Acad Sci; 2005 Nov;1059:41-55
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sulindac sulfone is most effective in modulating beta-catenin-mediated transcription in cells with mutant APC.
  • Sulindac sulfone (FGN-1, Aptosyn), a metabolite of the nonsteroidal anti-inflammatory drug sulindac, lacks cyclooxygenase inhibitory activity.
  • Although its ability to inhibit tumorigenesis in both carcinogen-treated animals and patients with familial adenomatous polyposis has been attributed to the induction of apoptosis, its complete mechanism of action remains unclear.
  • The purpose of the present study was to determine the ability of sulindac metabolites to regulate cellular levels of beta-catenin and downstream targets of the adenomatous polyposis coli (APC)/beta-catenin pathway in vitro.
  • These data demonstrate that sulindac sulfone can modulate the APC/beta-catenin pathway in vitro and that its efficacy is dependent upon the mutational status of APC and beta-catenin.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Colonic Neoplasms / drug therapy. Sulindac / analogs & derivatives. Transcription, Genetic. beta Catenin / metabolism
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Line, Tumor. Colon / metabolism. Cyclin D1 / biosynthesis. Cyclooxygenase Inhibitors / pharmacology. Humans. Mutation. PPAR gamma / biosynthesis

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  • (PMID = 16382042.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-06927; United States / NCI NIH HHS / CA / CA-82624; United States / NCI NIH HHS / CA / CA-87817
  • [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 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents; 0 / Cyclooxygenase Inhibitors; 0 / PPAR gamma; 0 / beta Catenin; 136601-57-5 / Cyclin D1; 184SNS8VUH / Sulindac; K619IIG2R9 / sulindac sulfone
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44. Benoit L, Faivre L, Cheynel N, Ortega-Deballon P, Facy O, Marty M, Olschwang S, Fraisse J, Cuisenier J: 3' Mutation of the APC gene and family history of FAP in a patient with apparently sporadic desmoid tumors. J Clin Gastroenterol; 2007 Mar;41(3):297-300

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 3' Mutation of the APC gene and family history of FAP in a patient with apparently sporadic desmoid tumors.
  • Desmoid tumors may occur sporadically or as part of the extraintestinal manifestations of familial adenomatous polyposis.
  • Different phenotypes have been described and some genotype-phenotype correlations have been raised, associated with different sites of germline mutations in the adenomatous polyposis coli (APC) gene.
  • We report on a 42-year-old woman ascertained for a large desmoid tumor of the anterior chest wall with pleural involvement, which persistently recurred despite a decade of treatment including hormone therapy, chemotherapy, and surgery.
  • Spontaneous disappearance of the tumor was later noted after 1 year without any treatment and confirmed after 4 years of regular follow-up.
  • This mutation, located in the exon 15 at the 3' end of the APC gene, leads to an unusual and late onset phenotype.
  • The pedigree revealed other isolated or familial adenomatous polyposis-associated cases of desmoid tumors.
  • This family report shows that a molecular analysis of the APC gene should be performed in familial desmoid tumors for accurate genetic counseling and follow-up.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / genetics. Fibromatosis, Aggressive / complications. Fibromatosis, Aggressive / genetics. Genes, APC. Mutation. Thoracic Neoplasms / complications. Thoracic Neoplasms / genetics
  • [MeSH-minor] Adult. Female. Humans. Pedigree. Polymerase Chain Reaction. Tomography, X-Ray Computed

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  • (PMID = 17426470.001).
  • [ISSN] 0192-0790
  • [Journal-full-title] Journal of clinical gastroenterology
  • [ISO-abbreviation] J. Clin. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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45. Huang X, Guo B: Adenomatous polyposis coli determines sensitivity to histone deacetylase inhibitor-induced apoptosis in colon cancer cells. Cancer Res; 2006 Sep 15;66(18):9245-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenomatous polyposis coli determines sensitivity to histone deacetylase inhibitor-induced apoptosis in colon cancer cells.
  • Here, we report that the expression status of adenomatous polyposis coli (APC) protein determines the relative sensitivity of colon cancer cells to HDAC inhibitor-induced apoptosis.
  • HCA-7 cells (expressing wild-type beta-catenin and APC proteins) are more sensitive to apoptosis induced by HDAC inhibitors valproic acid (VPA) and suberoylanilide hydroxamic acid than SW620 or HT-29 cells (both expressing mutant APC).
  • When wild-type APC protein was expressed using an inducible expression system, HT-29 cells became sensitive to apoptosis in response to VPA.
  • Conversely, knocking down of endogenous APC protein by small interfering RNA (siRNA) blocked VPA-induced apoptosis in HCA-7 cells.
  • APC mediated VPA-induced apoptosis through down-regulation of survivin.
  • The level of survivin protein decreased in HCA-7 and HT-29/APC cells, but not in SW620 and HT-29/beta-Gal cells after VPA treatment.
  • VPA also induced proteasome-mediated degradation of survivin protein in HCA-7 cells.
  • Furthermore, we have shown that APC mutation-mediated resistance to apoptosis can be overcome by cotreatment with Flavopiridol, which promotes survivin degradation.
  • These results suggest that APC is a critical determinant of HDAC inhibitor-induced apoptosis in colon cancer cells and survivin is a potential target to enhance apoptotic response to HDAC inhibitors.

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  • (PMID = 16982769.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR015566; United States / NCRR NIH HHS / RR / 5P20RR015566-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / BIRC5 protein, human; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 0 / TCF Transcription Factors; 0 / TCF7L2 protein, human; 0 / Transcription Factor 7-Like 2 Protein; 0 / beta Catenin; 58IFB293JI / vorinostat; 614OI1Z5WI / Valproic Acid; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3
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46. Foreman JE, Sorg JM, McGinnis KS, Rigas B, Williams JL, Clapper ML, Gonzalez FJ, Peters JM: Regulation of peroxisome proliferator-activated receptor-beta/delta by the APC/beta-CATENIN pathway and nonsteroidal antiinflammatory drugs. Mol Carcinog; 2009 Oct;48(10):942-52
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  • [Title] Regulation of peroxisome proliferator-activated receptor-beta/delta by the APC/beta-CATENIN pathway and nonsteroidal antiinflammatory drugs.
  • Studies indicate that peroxisome proliferator-activated receptor-beta/delta (PPAR beta/delta) can either attenuate or potentiate colon cancer.
  • One hypothesis suggests that PPAR beta/delta is upregulated by the adenomatous polyposis coli (APC)/beta-CATENIN pathway and a related hypothesis suggests that PPAR beta/delta is downregulated by nonsteroidal antiinflammatory drugs (NSAIDs).
  • While APC/beta-CATENIN-dependent expression of CYCLIN D1 was observed in vivo and in vitro, expression of PPAR beta/delta was not different in colon or intestinal polyps from wild-type or Apc(min) heterozygous mice or in human colon cancer cell lines with mutations in APC and/or beta-CATENIN.
  • No difference in the level of PPAR beta/delta was found in colon from wild-type or Apc(min) heterozygous mice following treatment with NO-donating aspirin (NO-ASA).
  • NSAIDs inhibited cell growth in RKO (wild-type APC) and DLD1 (mutant APC) human colon cancer cell lines but expression of PPAR beta/delta was not downregulated in these cell lines in response to a broad concentration range of celecoxib, indomethacin, NS-398, or nimesulide.
  • However, indomethacin caused an increase in PPAR beta/delta mRNA and protein that was accompanied with increased expression of a known PPAR beta/delta target gene.
  • Interestingly, expression of PPAR alpha was also increased in the human colon cancer cell lines by several NSAIDs at the highest concentration examined.
  • Results from these studies provide additional evidence indicating that PPAR beta/delta is not upregulated by the APC/beta-CATENIN pathway.
  • Further, these studies suggest that increased PPAR beta/delta and/or PPAR alpha by NSAIDs in human colon cancer cell lines could contribute to the mechanisms underlying the chemopreventive effects of NSAIDs.

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
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  • (PMID = 19415698.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124533; United States / NCI NIH HHS / CA / CA97999; United States / NCI NIH HHS / CA / R21 CA129467; United States / NCI NIH HHS / CA / R01 CA097999; United States / NCI NIH HHS / CA / CA92423; United States / Intramural NIH HHS / / Z01 BC005708-17; United States / NCI NIH HHS / CA / CA129467; United States / NCI NIH HHS / CA / CA124533; United States / NCI NIH HHS / CA / R01 CA092423
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Nitrobenzenes; 0 / PPAR delta; 0 / PPAR-beta; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Sulfonamides; 0 / beta Catenin; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; JCX84Q7J1L / Celecoxib; V4TKW1454M / nimesulide; XXE1CET956 / Indomethacin
  • [Other-IDs] NLM/ NIHMS161535; NLM/ PMC2790141
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47. Poritz LS, Blackstein M, Berk T, Gallinger S, McLeod RS, Cohen Z: Extended follow-up of patients treated with cytotoxic chemotherapy for intra-abdominal desmoid tumors. Dis Colon Rectum; 2001 Sep;44(9):1268-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extended follow-up of patients treated with cytotoxic chemotherapy for intra-abdominal desmoid tumors.
  • BACKGROUND: Cytotoxic chemotherapy can achieve a good initial response in inoperable desmoid tumors that have caused progressive obstruction of the gastrointestinal and urinary tracts and have caused unrelenting pain.
  • METHODS: We have reviewed 8 patients (3 male) with desmoid tumors and familial adenomatous polyposis who underwent cytotoxic chemotherapy for inoperable gastrointestinal obstruction and/or uncontrolled pain.
  • RESULTS: Follow-up after cytotoxic chemotherapy in the 7 patients for whom it was available was a mean of 42 (range 24-54) months.
  • Two patients achieved complete remission after therapy.
  • Four patients achieved a partial remission after completing all or some of the chemotherapy regimen; of these, three remained in stable remission, whereas the other was lost to follow-up.
  • There were two recurrences that required further therapy; one of these patients was treated with further chemotherapy, which induced a second remission, and the other was treated with pelvic exenteration and has subsequently died.
  • CONCLUSIONS: Most patients had a substantial response to cytotoxic chemotherapy; however, two patients required additional therapy 24 and 30 months after cytotoxic chemotherapy, respectively.
  • Cytotoxic chemotherapy is effective in producing short-term and long-term remission in these difficult patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fibromatosis, Abdominal / drug therapy
  • [MeSH-minor] Adenomatous Polyposis Coli. Adult. Carboplatin / administration & dosage. Dacarbazine / administration & dosage. Doxorubicin / administration & dosage. Female. Follow-Up Studies. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 11584198.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin; BG3F62OND5 / Carboplatin
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48. Zhang ZH, Ma LW, Song SB, Xiu DR, Wang JJ, Yang XX, Jia YM: [Adjuvant chemotherapy after orthotopic liver transplantation for advanced hepatocellular carcinoma]. Zhonghua Zhong Liu Za Zhi; 2005 Jan;27(1):45-7
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  • [Title] [Adjuvant chemotherapy after orthotopic liver transplantation for advanced hepatocellular carcinoma].
  • OBJECTIVE: To investigate the feasibility, reliability and therapeutic effectiveness of adjuvant chemotherapy for advanced hepatocellular carcinoma (HCC) after orthotopic liver transplantation (OLT).
  • METHODS: The clinical data of adjuvant chemotherapy after OLT in 10 advanced HCC patients were studied retrospectively.
  • FAP chemotherapy regimen was adopted calcium folinate (CF) 200 mg/m(2) and 5-Fluorouracil 500 mg/m(2) iv on D1 to D5, and doxorubicin 40 mg/m(2), cisplatin 30 mg/m(2) iv on D1, with 28 days as a cycle.
  • The opportune time of chemotherapy, chemotherapy regimen, synergistic action between cytotoxic agent and immunosuppressive agent on liver and kidney and side-effects were preliminarily evaluated.
  • During the period of chemotherapy, the side-effects of adjuvant chemotherapy were moderate.
  • CONCLUSION: Chemotherapy which is able to prolong the life-span of patients with advanced HCC after orthotopic liver transplantation is feasible and effective, the side-effects were mild.
  • The choice of opportune time of chemotherapy might influence the outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. Liver Transplantation
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Female. Fluorouracil / administration & dosage. Follow-Up Studies. Humans. Leucovorin / administration & dosage. Male. Middle Aged. Neoplasm Staging. Postoperative Period. Retrospective Studies. Survival Rate

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  • (PMID = 15771799.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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49. Kikuyama S, Inada T, Shimizu K, Miyakita M, Ogata Y: p53, bcl-2 and thymidine phosphorylase as predictive markers of chemotherapy in patients with advanced and recurrent gastric cancer. Anticancer Res; 2001 May-Jun;21(3C):2149-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p53, bcl-2 and thymidine phosphorylase as predictive markers of chemotherapy in patients with advanced and recurrent gastric cancer.
  • PURPOSE: To study the relationship between expression of p53, bcl-2, thymidine phosphorylase and Ki-67 and the response to chemotherapy and survival in patients with recurrent and advanced gastric cancer.
  • MATERIALS AND METHODS: Protein expression was assessed immunohistochemically in 28 patients treated with 5-fluorouracil, pirarubicin and cisplatin (FAP).
  • The response rate was also reduced from 44% in patients negative for bcl-2 protein expression to 25% in bcl-2 positive patients.
  • Thymidine phosphorylase (dThdPase) expression was observed in 20 patients (71%), 50% of whom responded to chemotherapy, while patients negative for dThdPase expression did not respond to chemotherapy.
  • CONCLUSION: While dThdPase expression may be a useful predictor of response to chemotherapies that include 5-FU, p53 and bcl-2 expression may predict the outcome of patients with recurrent and advanced gastric cancer following chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Stomach Neoplasms / drug therapy. Stomach Neoplasms / metabolism. Thymidine Phosphorylase / biosynthesis. Tumor Suppressor Protein p53 / biosynthesis
  • [MeSH-minor] Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Female. Fluorouracil / administration & dosage. Humans. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / metabolism. Survival Rate

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  • (PMID = 11501839.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin; EC 2.4.2.4 / Thymidine Phosphorylase; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; FAP2 protocol
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50. Kimura Y, Yasuda T, Fujiwara Y, Takiguchi S, Miyata H, Nagano H, Yano M, Monden M: [Cases of postoperative hepatic metastasis from gastric cancer in which hepatic arterial infusion chemotherapy with 5-FU, adriamycin and cisplatin was performed after TS-1 chemotherapy]. Gan To Kagaku Ryoho; 2004 Oct;31(11):1825-7
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  • [Title] [Cases of postoperative hepatic metastasis from gastric cancer in which hepatic arterial infusion chemotherapy with 5-FU, adriamycin and cisplatin was performed after TS-1 chemotherapy].
  • The prognosis of patients with hepatic metastasis of gastric cancer is poor, and standard therapies for patients are not established.
  • In both cases, no other organ metastasis except the liver was confirmed, in which hepatic arterial infusion chemotherapy with 5-FU, adriamycin and cisplatin (FAP) were performed because TS-1 chemotherapy was not an effective chemotherapy.
  • Case 1: An 80-year-old man had distal gastrectomy for type 2 gastric cancer (Stage II) in January 2001.
  • After chemotherapy with TS-1 for 5 courses, a hepatic arterial infusion treatment was performed for 7 courses.
  • The effect was PR, but the treatment was canceled because of a catheter obstruction.
  • Case 2: This case was a 73-year-old man who had distal gastrectomy for type 0 IIc gastric cancer (Stage IA) in May 1999.
  • Multiple hepatic metastases recurred in the 32nd month post operation.
  • After chemotherapy with TS-1 for 2 courses, a hepatic arterial infusion treatment was performed for 10 courses.
  • The effect was CR, but a peritoneal recurrence was discovered, and a systemic chemotherapy was performed.
  • The hepatic arterial infusion chemotherapy with FAP was effective for gastric cancer patients with liver metastasis because TS-1 chemotherapy was not an effective chemotherapy.
  • It is necessary to consider combined chemotherapy in addition to systemic chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Fluorouracil / administration & dosage. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Silicates / therapeutic use. Stomach Neoplasms / pathology. Titanium / therapeutic use
  • [MeSH-minor] Aged. Hepatic Artery. Humans. Infusions, Intra-Arterial. Male

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  • (PMID = 15553728.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Silicates; 12067-57-1 / titanium silicide; 80168379AG / Doxorubicin; D1JT611TNE / Titanium; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; FAP protocol
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51. Wada H, Nagano H, Dono K, Kondo M, Yamamoto T, Ota H, Nakamura M, Yoshioka S, Damdinsuren B, Yubo Y, Marubashi S, Miyamoto A, Umeshita K, Nakamori S, Sakon M, Monden M: [Successful treatment for advanced cholangiocellular carcinoma with intrahepatic metastasis and/or portal vein tumor thrombi by intraarterial chemotherapy combined with 5-fluorouracil, adriamycin and cisplatin (FAP)--two cases report]. Gan To Kagaku Ryoho; 2004 Oct;31(11):1711-3
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  • [Title] [Successful treatment for advanced cholangiocellular carcinoma with intrahepatic metastasis and/or portal vein tumor thrombi by intraarterial chemotherapy combined with 5-fluorouracil, adriamycin and cisplatin (FAP)--two cases report].
  • From June 2003, he received hepatic arterial infusion chemotherapy (FAP: 5-fluorouracil 250 mg/day continuous infusion, day 1-5, adriamycin 10 mg/day, day 1, and CDDP 10 mg/day, day 1).
  • He received FAP arterial infusion chemotherapy that was a same regimen as with the case 1 patient.
  • After 5 courses were administered, Abdominal CT revealed that the size of the main tumor at S8 had not changed, and that portal vein tumor thrombus had disappeared.
  • In both cases, there was no complication related to the chemotherapy.
  • They are alive for more than 1 year after chemotherapy had started.
  • FAP hepatic arterial infusion chemotherapy might be promising as an effective therapy for non-resectable CCC without extra hepatic metastasis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bile Duct Neoplasms / drug therapy. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Fluorouracil / administration & dosage
  • [MeSH-minor] Aged. Bile Ducts, Intrahepatic. Cholangiocarcinoma / drug therapy. Drug Administration Schedule. Hepatic Artery. Humans. Infusions, Intra-Arterial. Male. Neoplastic Cells, Circulating / drug effects

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  • (PMID = 15553691.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; FAP protocol
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52. Schmelz EM, Roberts PC, Kustin EM, Lemonnier LA, Sullards MC, Dillehay DL, Merrill AH Jr: Modulation of intracellular beta-catenin localization and intestinal tumorigenesis in vivo and in vitro by sphingolipids. Cancer Res; 2001 Sep 15;61(18):6723-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of intracellular beta-catenin localization and intestinal tumorigenesis in vivo and in vitro by sphingolipids.
  • Sphingolipid consumption suppresses colon carcinogenesis, but the specific genetic defect(s) that can be bypassed by these dietary components are not known.
  • Colon tumors often have defect(s) in the adenomatous polyposis coli (APC)/beta-catenin regulatory system.
  • Therefore, C57Bl/6J(Min/+) mice with a truncated APC gene product were fed diets supplemented with ceramide, sphingomyelin, glucosylceramide, lactosylceramide, and ganglioside G(D3) (a composition similar in amount and type to that of dairy products) to determine whether tumorigenesis caused by this category of genetic defect is suppressed.
  • Sphingolipid feeding reduced the number of tumors in all regions of the intestine, and caused a marked redistribution of beta-catenin from a diffuse (cytosolic plus membrane) pattern to a more "normal" localization at mainly intercellular junctions between intestinal epithelial cells.
  • The major digestion product of complex sphingolipids is sphingosine, and treatment of two human colon cancer cell lines in culture (SW480 and T84) with sphingosine reduced cytosolic and nuclear beta-catenin, inhibited growth, and induced cell death.
  • Thus, dietary sphingolipids, presumably via their digestion products, bypass or correct defect(s) in the APC/beta-catenin regulatory pathway.
  • This may be at least one mechanism whereby dietary sphingolipids inhibit colon carcinogenesis, and might have implications for dietary intervention in human familial adenomatous polyposis and colon cancer.
  • [MeSH-major] Cytoskeletal Proteins / metabolism. Intestinal Neoplasms / prevention & control. Sphingolipids / pharmacology. Trans-Activators
  • [MeSH-minor] Adenomatous Polyposis Coli Protein. Animals. Cattle. Cell Division / drug effects. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Colonic Neoplasms / drug therapy. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Cytosol / drug effects. Cytosol / metabolism. Diet. Humans. Intestines / metabolism. Male. Mice. Mice, Inbred C57BL. Signal Transduction / physiology. Sphingosine / analogs & derivatives. Sphingosine / blood. Sphingosine / toxicity. Tumor Cells, Cultured. beta Catenin

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  • (PMID = 11559543.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA73327
  • [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 / Adenomatous Polyposis Coli Protein; 0 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / N-acetylsphingosine; 0 / Sphingolipids; 0 / Trans-Activators; 0 / beta Catenin; NGZ37HRE42 / Sphingosine
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53. Jing Z, Nan KJ, Zhang XZ, Ruan ZP, Guo H, Xu R: [Therapeutic effects of systemic chemotherapy on advanced pancreatic cancer patients]. Ai Zheng; 2004 Apr;23(4):439-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Therapeutic effects of systemic chemotherapy on advanced pancreatic cancer patients].
  • BACKGROUND & OBJECTIVE: Advanced,unresectable pancreatic cancer is an extremely aggressive disease.
  • Systemic chemotherapy is the most frequently administered treatment for the patients with advanced pancreatic cancer.
  • This clinical trial was designed to compare the efficacy, clinical benefit response (CBR), and toxicity profile of three regimens in treating advanced pancreatic cancer (APC).
  • Of 74 APC patients, 26 received 5-fluorouracil+leucovorin+cisplatin (Arm A), 23 received gemcitabine (Arm B) and 25 treated with gemcitabine+5-fluorouracil+leucovorin (Arm C).
  • There was no significant difference in the overall response rate(P=0.261,Chi-square test) and a significant difference in CBR among three groups(P< 0.05, Chi-square test).
  • The median survival time were 6.5 months for Arm A(95%CI 5.00,7.99 months),8.03 months for Arm B(95%CI 6.72,9.35 months) and 8.79 months for Arm C (95%CI 7.31,10.26 months).
  • There were significant differences among three groups in the median survival time(Breslow=8.85,P=0.0119).
  • CONCLUSION: The combination of gemcitabine,5-fluorouracil and leucovorin is a moderatedly active treatment with tolerable side effects.
  • Its treatment value is worth further studying.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostatic Neoplasms / drug therapy

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  • (PMID = 15087035.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CA-19-9 Antigen
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54. Javid SH, Moran AE, Carothers AM, Redston M, Bertagnolli MM: Modulation of tumor formation and intestinal cell migration by estrogens in the Apc(Min/+) mouse model of colorectal cancer. Carcinogenesis; 2005 Mar;26(3):587-95
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  • [Title] Modulation of tumor formation and intestinal cell migration by estrogens in the Apc(Min/+) mouse model of colorectal cancer.
  • Epidemiological studies suggest that post-menopausal hormone replacement therapy (HRT) reduces colorectal cancer (CRC) incidence.
  • Previous studies showed that ovariectomy induced a 77% increase in intestinal adenoma number in the C57BL/6J-Min/+ (Min/+) mouse, an animal model of adenomatous polyposis coli (APC)-associated CRC.
  • We hypothesized that the phytoestrogens genistein and coumestrol would inhibit intestinal tumorigenesis in ovariectomized Min/+ mice.
  • Min/+ and Apc(+/+) (WT) mice were ovariectomized and assigned to either a control diet or treatment with E(2), genistein or coumestrol.
  • Treatment of ovariectomized Min/+ (Min/+ OX) mice with genistein resulted in a non-significant reduction in tumor number.
  • Bromodeoxyuridine migration assays also demonstrated that treatment with E(2) or coumestrol improved enterocyte migration rate.
  • Immunoprecipitation and immunohistochemistry analyses showed that impaired association of the adherens junction proteins E-cadherin and beta-catenin in Min/+ mice was improved by treatment with either E(2) or coumestrol.
  • In conclusion, both coumestrol and E(2) prevent intestinal tumorigenesis and ameliorate enterocyte migration and intercellular adhesion in the Apc(Min/+) mouse model of CRC.
  • [MeSH-major] Cell Movement / drug effects. Colorectal Neoplasms / prevention & control. Coumestrol / pharmacology. Disease Models, Animal. Genes, APC. Genistein / pharmacology. Intestines / drug effects. Phytoestrogens / pharmacology

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  • (PMID = 15579483.001).
  • [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 / Phytoestrogens; 0 / Receptors, Estrogen; DH2M523P0H / Genistein; V7NW98OB34 / Coumestrol
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55. Seow-Choen F: The management of desmoids in patients with familial adenomatous polyposis (FAP). Acta Chir Iugosl; 2008;55(3):83-7
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  • [Title] The management of desmoids in patients with familial adenomatous polyposis (FAP).
  • Desmoids are rare in the general population but occurs in between 10 to 20% of patients with familial adenomatous polyposis (FAP).
  • This risk is about 852 times the risk for the population at large.
  • Desmoids are benign neoplasms that are capable of infiltrating locally with a high risk of recurrence (25-65%) even after extirpating surgery.
  • Desmoids in FAP may occur extra-abdominally, or within the abdominal wall or most commonly intra-abdominally within the mesentery or retroperitoneal.
  • Desmoids are a major problem in patients with FAP.
  • Simple drug treatment with tamoxifen or NSAIDS like sulindac should be used as first line treatment as it carries a response in 30-50% of patients.
  • Surgery for intra-abdominal desmoids should really only be attempted for intestinal obstruction or ureteric obstruction.
  • Dacarbazine-Doxorubicin chemotherapy may have dramatic response in some cases.
  • Genetic transfer may unlock this disease in future and may give patients with FAP and severe desmoids hope for the future.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Fibromatosis, Aggressive / therapy

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  • (PMID = 19069698.001).
  • [ISSN] 0354-950X
  • [Journal-full-title] Acta chirurgica Iugoslavica
  • [ISO-abbreviation] Acta Chir Iugosl
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Serbia
  • [Number-of-references] 21
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56. Bruserud Ø, Wendelboe Ø: Biological treatment in acute myelogenous leukaemia: how should T-cell targeting immunotherapy be combined with intensive chemotherapy? Expert Opin Biol Ther; 2001 Nov;1(6):1005-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biological treatment in acute myelogenous leukaemia: how should T-cell targeting immunotherapy be combined with intensive chemotherapy?
  • T-cell targeting immunotherapy is now considered as a possible strategy in the treatment of acute myelogenous leukaemia (AML).
  • Clinical importance of antileukaemic T-cell reactivity after allogeneic stem cell transplantation (SCT) is well established and the early experience from IL-2 therapy suggests that even autologous T-cells can mediate antileukaemic reactivity.
  • The clinical experience also indicates that immunotherapy should begin when the leukaemia cell burden is minimal, and the detection of an operative cellular immune system, even in patients with chemotherapy-induced cytopenia, further suggests that it is possible to begin T-cell targeting therapy early after chemotherapy while patients are still cytopenic.
  • However, adult patients in particular have a T-cell defect after chemotherapy that may last for several months.
  • For this reason immunotherapy should probably be continued or repeated until a maximal effect is achieved when the patients no longer have a T-cell defect.
  • This treatment approach may also be considered in combination with autologous SCT.
  • T-cell targeting regimens should include, if possible, several therapeutic components.
  • Firstly, native AML blasts can function as accessory cells during T-cell activation and in vivo therapy with T-cell growth factors (e.g., IL-2, IL-15) may then enhance antileukaemic reactivity or non-specific cytotoxicity against the AML cells; and secondly, a further enhancement of AML-specific reactivity may be achieved by vaccination with AML-specific peptides, immunisation with AML-blasts expressing a dendritic cell phenotype, or exposure to normal antigen-presenting cells (APC) pulsed with or expressing AML-specific peptide sequences.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunotherapy. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Combined Modality Therapy. Humans. Lymphocyte Activation. T-Lymphocytes / drug effects. T-Lymphocytes / immunology

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  • (PMID = 11728232.001).
  • [ISSN] 1471-2598
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 109
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57. Nagano H, Sakon M, Yasuda T, Dono K, Nakamori S, Yano M, Umeshita K, Shiozaki H, Okada A, Murakami T, Nakamura H, Monden M: [A case of postoperative multiple hepatic metastasis from esophageal cancer successfully treated by surgical resection and hepatic arterial infusion chemotherapy]. Gan To Kagaku Ryoho; 2001 Oct;28(11):1628-31
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  • [Title] [A case of postoperative multiple hepatic metastasis from esophageal cancer successfully treated by surgical resection and hepatic arterial infusion chemotherapy].
  • A 66-year-old male who underwent radical resection for esophageal cancer (stage IV) was diagnosed with multiple hepatic metastasis 1 year and 3 months after the surgery.
  • He underwent hepatic resection and received systemic chemotherapy (FAP: 5-FU, ADR, CDDP), as the post-operative adjuvant therapy.
  • One year and 3 months later, there was a huge recurrence in the residual liver and hepatic arterial infusion chemotherapy (FAP) was performed.
  • The recurrent lesion disappeared completely after 3 sessions of arterial infusion chemotherapy.
  • The arterial infusion chemotherapy was continued in the outpatient clinic and the recurrent lesion is well controlled.
  • The utility of hepatic arterial infusion chemotherapy and hepatectomy for postoperative multiple hepatic metastasis from esophageal cancer was shown in the present case.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / secondary. Carcinoma, Squamous Cell / therapy. Esophageal Neoplasms / pathology. Hepatectomy. Liver Neoplasms / secondary. Liver Neoplasms / therapy
  • [MeSH-minor] Aged. Cisplatin / administration & dosage. Combined Modality Therapy. Doxorubicin / administration & dosage. Drug Administration Schedule. Fluorouracil / administration & dosage. Hepatic Artery. Humans. Infusions, Intra-Arterial. Lymphatic Metastasis. Male

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  • (PMID = 11707996.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; FAP protocol
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58. Aretz S, Koch A, Uhlhaas S, Friedl W, Propping P, von Schweinitz D, Pietsch T: Should children at risk for familial adenomatous polyposis be screened for hepatoblastoma and children with apparently sporadic hepatoblastoma be screened for APC germline mutations? Pediatr Blood Cancer; 2006 Nov;47(6):811-8
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  • [Title] Should children at risk for familial adenomatous polyposis be screened for hepatoblastoma and children with apparently sporadic hepatoblastoma be screened for APC germline mutations?
  • Surgery combined with chemotherapy has resulted in dramatic improvements in prognosis.
  • However, even today, about one quarter of affected children do not survive the disease.
  • Compared to the general population, the risk of HB is 750-7,500 times higher in children predisposed to familial adenomatous polyposis (FAP), an autosomal-dominant cancer predispostion syndrome caused by germline mutations in the tumor suppressor gene APC.
  • Only limited data exist about the frequency of APC germline mutations in cases of apparently sporadic HB without a family history of FAP.
  • PROCEDURE: In our sample of 1,166 German FAP families, all known cases of HB were registered.
  • In addition, 50 patients with apparently sporadic HB were examined for APC germline mutations.
  • RESULTS: In the FAP families, seven unrelated cases of HB are documented; three had been detected at an advanced stage.
  • In patients with apparently sporadic HB, germline mutations in the APC gene were identified in 10%.
  • CONCLUSIONS: These data raise the issue of the appropriate screening for HB in children of FAP patients.
  • In Beckwith-Wiedemann syndrome (BWS), recent studies suggest an earlier detection of both Wilms tumor and HB by frequent screening.
  • We discuss the rationale and implications of a screening program; besides the examination procedure itself, screening for HB in children of FAP patients would have important consequences for the policy of predictive testing in FAP.
  • In a substantial fraction of sporadic HB, the disease is obviously the first manifestation of a de novo FAP.
  • These patients should be identified by routine APC mutation screening and undergo colorectal surveillance thereafter.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. Germ-Line Mutation. Hepatoblastoma / genetics. Liver Neoplasms / genetics
  • [MeSH-minor] DNA Mutational Analysis / methods. Disease Progression. Exons. Follow-Up Studies. Genetic Testing. Humans. Neoplasm Staging. Pedigree. Phenotype. Retrospective Studies. Risk Factors. Survival Rate


59. Hongoh S, Nomoto T, Kawakami M, Hanai K, Inatsuchi H, Terachi T: [Complete response to M-FAP chemotherapy for multiple lung metastases after segmental resection of urachal carcinoma : a case report]. Hinyokika Kiyo; 2010 Feb;56(2):107-10
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  • [Title] [Complete response to M-FAP chemotherapy for multiple lung metastases after segmental resection of urachal carcinoma : a case report].
  • Abdominal magnetic resonance imaging (MRI) and computed tomography(CT) demonstrated a tumor extending from the umbilicus to the bladder dome.
  • Chest CT and examination of the upper gastrointestinal did not reveal any abnormal findings.
  • About 10 months later, chest CT demonstrated multiple lung metastases.
  • After two courses of combination chemotherapy with methotrexate (MTX), 5-fluorouracil (5-FU), epirubicin (epiADM), and cisplatin (CDDP), the multiple lung metastases completely disappeared.
  • The patient has survived 23 months to date with no evidence of disease and is receiving adjuvant chemotherapy with tegafur uracil.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Urachus. Urinary Bladder Neoplasms / pathology. Urinary Bladder Neoplasms / surgery

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  • (PMID = 20185997.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 3Z8479ZZ5X / Epirubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate
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60. Lynch PM: Pharmacotherapy for inherited colorectal cancer. Expert Opin Pharmacother; 2010 May;11(7):1101-8
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  • [Title] Pharmacotherapy for inherited colorectal cancer.
  • This review is written in the interest of capturing the current state of chemoprevention in familial adenomatous polyposis (FAP).
  • WHAT THE READER WILL GAIN: The reader should gain an appreciation of the role that chemoprevention clinical trials in FAP has had in establishing a basis for clinically oriented use of selected drugs, mainly sulindac and celecoxib, as adjuncts to surgical and endoscopic treatment.
  • In addition, the reader will see how FAP trials can provide a foundation for similar trials in nonfamilial adenomas.
  • TAKE-HOME MESSAGE: As a proving ground for new, potential chemopreventive agents, trials in FAP involved short-term (3- to 12-month) administration of drug.
  • Endpoints generally involved measures of adenoma regression in the rectal segment retained post-colectomy.
  • [MeSH-minor] Adenomatous Polyposis Coli / complications. Adenomatous Polyposis Coli / genetics. Animals. Colorectal Neoplasms, Hereditary Nonpolyposis / prevention & control. Combined Modality Therapy. Humans. Randomized Controlled Trials as Topic. Risk Factors

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  • (PMID = 20345333.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 42
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61. Yasuda T, Yano M, Takiguchi S, Kimura Y, Fujiwara Y, Monden M: [A case of multiple advanced esophageal carcinomas with abdominal LN metastases showing complete response after chemoradiotherapy with concurrent cisplatin, 5-FU and adriamycin chemotherapy]. Gan To Kagaku Ryoho; 2003 Oct;30(11):1737-40
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  • [Title] [A case of multiple advanced esophageal carcinomas with abdominal LN metastases showing complete response after chemoradiotherapy with concurrent cisplatin, 5-FU and adriamycin chemotherapy].
  • The patient was a 66-year-old man who had double primary esophageal carcinomas: type o-IIc tumor of the cervical esophagus from the esophageal inlet to 23 cm from incisors and a 9 cm length type 3 tumor of the middle to lower thoracic esophagus with a 2 cm diameter cardiac lymph node metastasis.
  • Since he completely rejected surgical treatment, new definitive chemoradiotherapy with 2 courses of FAP chemotherapy (cisplatin 50 mg/m2 and adriamycin 20 mg/m2 on day 1 and 5-FU 700 mg/day from day 1 to 5 continuously) concurrent with a split course of radiotherapy to a total dose of 60 Gy in 30 fractions was devised and administered.
  • The treatment was completed and there was no severe toxicity except grade 3 leukocytopenia.
  • Just after treatment, cervical tumor and cardiac lymph node reached complete response but stenosis and wall thickness remained in the thoracic tumor.
  • Our new regimen of chemoradiotherapy concurrent with FAP chemotherapy seems to be effective and promising for advanced esophageal carcinoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Esophageal Neoplasms / drug therapy. Lymph Nodes / pathology
  • [MeSH-minor] Aged. Cisplatin / administration & dosage. Combined Modality Therapy. Doxorubicin / administration & dosage. Drug Administration Schedule. Fluorouracil / administration & dosage. Humans. Lymphatic Metastasis. Male. Remission Induction

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  • (PMID = 14619507.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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62. Kopjar N, Garaj-Vrhovac V, Milas I: Assessment of chemotherapy-induced DNA damage in peripheral blood leukocytes of cancer patients using the alkaline comet assay. Teratog Carcinog Mutagen; 2002;22(1):13-30
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  • [Title] Assessment of chemotherapy-induced DNA damage in peripheral blood leukocytes of cancer patients using the alkaline comet assay.
  • The alkaline comet assay was employed to assess the pre- and post-treatment levels of in vivo DNA damage in peripheral blood leukocytes of cancer patients.
  • During the study all patients were given antineoplastic drugs, mainly as polychemotherapy.
  • Our results indicate marked interindividual variations between baseline DNA damage in peripheral blood leukocytes recorded among cancer patients prior to the chemotherapy.
  • After intravenous administration of various antineoplastic drugs, a significantly increased level of DNA damage in all cancer patients compared to their pre-treatment values was recorded The highest level of DNA damage was seen following administration of 5-fluorouracil, adriamycin, and cisplatin (FAP protocol).
  • The results indicate that administration of antineoplastic drugs in standard protocols is accompanied by significant DNA damage in peripheral blood leukocytes.
  • In order to diminish the potential risks of developing second neoplasms, a continuous biomonitoring of cancer patients after the ending of chemotherapy becomes important.
  • Despite their limitations, present results confirm the usefulness of the alkaline comet assay as a sensitive biomarker of exposure that enables rapid and simple detection of primary DNA damage in peripheral blood leukocytes of cancer patients.
  • Together with standard cytogenetic endpoints, the comet assay provides a powerful technique for the routine detection of critical DNA lesions produced after administration of antineoplastic drugs in the clinical settings.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Comet Assay / methods. DNA Damage / drug effects. DNA, Neoplasm / drug effects. Lymphocytes / drug effects
  • [MeSH-minor] Adult. DNA Repair. Female. Humans. Male. Middle Aged. Neoplasms / drug therapy. Neoplasms / genetics

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 11754384.001).
  • [ISSN] 0270-3211
  • [Journal-full-title] Teratogenesis, carcinogenesis, and mutagenesis
  • [ISO-abbreviation] Teratog., Carcinog. Mutagen.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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63. Yuan P, Xu Y, Ouyang T, Wang TF, Fan ZQ, Fan T, Lin BY, Xie YT, Li JF: [Correlation of BRCA1 and APC aberrant methylation with the response to anthracycline-based neoadjuvant chemotherapy in primary breast cancer]. Zhonghua Zhong Liu Za Zhi; 2009 Apr;31(4):282-6
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  • [Title] [Correlation of BRCA1 and APC aberrant methylation with the response to anthracycline-based neoadjuvant chemotherapy in primary breast cancer].
  • OBJECTIVE: To investigate the correlation of hypermethylation of BRCA1 and APC gene promoters with the response to anthracycline-based neoadjuvant chemotherapy in primary breast cancer.
  • METHODS: One hundred and forty patients with primary breast cancer received anthracycline-based neoadjuvant chemotherapy, and pretreatment hypermethylation status of BRCA1 and APC genes promoters was detected by methylation-specific PCR.
  • RESULTS: Of the 140 patients, 30 (21.4%) achieved pathological complete response (pCR), and methylation rates of BRCA1 and APC gene promoters were 21.4% (30/140) and 18.3% (24/131), respectively.
  • Among the 110 patients with unmethylated BRCA1 gene, 28 (25.5%) achieved pCR, while in the 30 patients with methylated BRCA1 gene, only 2 (6.7%) had a pCR, with a significant difference between the two groups (chi(2) = 4.94, P = 0.026).
  • However, no statistically significant correlation was found between the methylation of APC gene and pCR to neoadjuvant chemotherapy in this cohort of patients (P > 0.05).
  • CONCLUSION: Primary breast cancer with an unmethylated BRCA1 gene is prone to achieve a pathological complete response to anthracycline-based neoadjuvant chemotherapy than those with a methylated BRCA1 gene.
  • BRCA1 methylation status may be a useful predictor for anthracycline-based neoadjuvant chemotherapy in primary breast cancer patients.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Anthracyclines / therapeutic use. BRCA1 Protein / genetics. Breast Neoplasms. DNA Methylation
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. CpG Islands / genetics. Cyclophosphamide / therapeutic use. Epirubicin / therapeutic use. Female. Fluorouracil / therapeutic use. Humans. Middle Aged. Neoadjuvant Therapy. Neoplasm Staging. Remission Induction. Young Adult

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  • (PMID = 19615284.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Anthracyclines; 0 / BRCA1 Protein; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; FEC protocol
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64. Dobbie Z, Muller PY, Heinimann K, Albrecht C, D'Orazio D, Bendik I, Müller H, Bauerfeind P: Expression of COX-2 and Wnt pathway genes in adenomas of familial adenomatous polyposis patients treated with meloxicam. Anticancer Res; 2002 Jul-Aug;22(4):2215-20
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  • [Title] Expression of COX-2 and Wnt pathway genes in adenomas of familial adenomatous polyposis patients treated with meloxicam.
  • BACKGROUND: Familial adenomatous polyposis (FAP) is an autosomal, dominantly inherited predisposition to colorectal cancer caused by germline mutations within the adenomatous polyposis coli (APC) gene, a key member of the Wnt signalling pathway.
  • A new class of non-steroidal anti-inflammatory drugs (NSAIDs), the specific cyclooxygenase 2 (COX-2) inhibitors, have recently been applied for the treatment of FAP patients.
  • PATIENTS AND METHODS: The expressions of the Wnt members and targets APC, c-myc, cyclin D1 and COX-2, as measured by real-time quantitative RT-PCR, have been evaluated in fresh samples of normal colorectal mucosa and matched adenoma tissue of six unrelated FAP patients before and after treatment with meloxicam.
  • RESULTS: A significant up-regulation of COX-2 in adenomas after treatment with meloxicam was found.
  • Furthermore, in adenomas, a down-regulation of APC after treatment and a tight correlation of the expressions of the two Wnt targets, c-myc and cyclin D1, in both stages of treatment were observed.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Antineoplastic Agents / therapeutic use. Isoenzymes / genetics. Prostaglandin-Endoperoxide Synthases / genetics. Proto-Oncogene Proteins / genetics. Thiazines / therapeutic use. Thiazoles / therapeutic use. Zebrafish Proteins
  • [MeSH-minor] Adolescent. Adult. Cyclin D1 / genetics. Cyclooxygenase 2. Female. Gene Expression Regulation, Neoplastic / drug effects. Genes, APC / drug effects. Genes, myc / drug effects. Genes, myc / genetics. Humans. Intestinal Mucosa / drug effects. Intestinal Mucosa / physiology. Male. Membrane Proteins. Middle Aged. Protein-Tyrosine Kinases / genetics. Rectal Neoplasms / drug therapy. Rectal Neoplasms / genetics. Reference Values. Reverse Transcriptase Polymerase Chain Reaction. Wnt Proteins

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  • (PMID = 12174906.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 0 / Thiazines; 0 / Thiazoles; 0 / Wnt Proteins; 0 / Zebrafish Proteins; 136601-57-5 / Cyclin D1; 71125-38-7 / meloxicam; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 2.7.10.1 / Protein-Tyrosine Kinases
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65. Lefevre JH, Parc Y, Kernéis S, Goasguen N, Benis M, Parc R, Tiret E: Risk factors for development of desmoid tumours in familial adenomatous polyposis. Br J Surg; 2008 Sep;95(9):1136-9
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  • [Title] Risk factors for development of desmoid tumours in familial adenomatous polyposis.
  • BACKGROUND: Desmoid tumours (DTs) are the primary cause of death of patients with familial adenomatous polyposis (FAP) following restorative proctocolectomy.
  • The aim of this study was to identify risk factors for DT in a French population.
  • METHODS: Clinical data for 442 patients with FAP from 1983 to 2004 were reviewed retrospectively.
  • DT sites were mesenteric (73 tumours), abdominal wall (44) and extra-abdominal (seven).
  • Female patients developed DT earlier than males.
  • Although DTs appeared after colectomy in 34 patients, the type of surgery did not influence the risk of DT.
  • An identified point mutation in the adenomatous polyposis coli (APC) gene after codon 1444 was a significant risk factor (hazard ratio 3.3 (95 per cent confidence interval 1.5 to 7.3)).
  • Belonging to a family affected by DT did not increase the individual's risk in this population.
  • CONCLUSION: No risk factor for life-threatening mesenteric DT could meaningfully modify the management of patients with FAP.
  • [MeSH-major] Abdominal Neoplasms / etiology. Adenomatous Polyposis Coli / complications. Fibromatosis, Abdominal / etiology. Fibromatosis, Aggressive / etiology. Proctocolectomy, Restorative
  • [MeSH-minor] Adolescent. Adult. Age of Onset. Aged. Child. Female. Genes, APC. Humans. Male. Mesentery. Middle Aged. Mutation / genetics. Pedigree. Retrospective Studies. Risk Factors

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  • (PMID = 18581438.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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66. 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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67. Naritaka Y, Ogawa K, Shimakawa T, Wagatsuma Y, Hamaguchi K, Konno S, Katsube T, Yagawa H, Aiba M, Ide H: Case report: a young woman with advanced esophageal cancer showing pathological complete response to neoadjuvant chemotherapy (CDDP, 5-FU and ADM). Anticancer Res; 2004 Jul-Aug;24(4):2385-9
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  • [Title] Case report: a young woman with advanced esophageal cancer showing pathological complete response to neoadjuvant chemotherapy (CDDP, 5-FU and ADM).
  • An upper gastrointestinal series revealed Borrmann type 2 esophageal cancer in the lower thoracic esophagus.
  • Because direct invasion of the thoracic aorta was suspected, FAP therapy (CDDP, 5-FU and ADM) was given as neoadjuvant chemotherapy.
  • Because the tumor had completely disappeared, the histological effect of chemotherapy was classified as grade 3, i.e., pathological complete response (PCR).
  • The response to FAP therapy was excellent and no serious adverse events occurred.
  • Therefore, this is one of the treatments that should be actively applied in patients who have advanced esophageal cancer with suspected lymph node metastasis and invasion of other organs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Esophageal Neoplasms / drug therapy
  • [MeSH-minor] Adult. Cisplatin / administration & dosage. Doxorubicin / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Neoadjuvant Therapy

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  • (PMID = 15330188.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; FAP protocol
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68. Humar B, D'Orazio D, Albrecht C, Bauerfeind P, Muller H, Dobbie Z, Bendik I: Expression of putative anticancer targets in familial adenomatous polyposis and its association with the APC mutation status. Int J Oncol; 2001 Dec;19(6):1179-86
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  • [Title] Expression of putative anticancer targets in familial adenomatous polyposis and its association with the APC mutation status.
  • Several substances interfering with colorectal carcinogenesis may reduce or prevent adenoma formation in familial adenomatous polyposis (FAP), an inherited predisposition to colorectal cancer.
  • This study determined the expression of genes coding for putative anticancer targets (COX-2, iNOS, MMP-7, ODC, PKCbeta, PPARgamma, RXRalpha, RXRbeta, RXRgamma) in FAP patients to provide one of the rationales for the design of chemotherapy and -prevention strategies.
  • Gene expression was assessed by TaqMan analysis in colonic tissue of 9 FAP patients with mutations in the APC gene (APCpos), 5 FAP patients without identified genetic defect (APCneg), and 3 healthy individuals.
  • Among the examined genes, PKCbeta and MMP-7 were most consistently altered in adenoma tissue relative to matched mucosa.
  • Intriguingly, ODC was clearly overexpressed in polyps from APCpos but not APCneg patients.
  • Furthermore, PKCbeta, MMP-7, ODC, and COX-2 as well as all RXRs displayed altered expression in apparently healthy FAP mucosa as opposed to that of healthy individuals.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli Protein / genetics. Genes, APC. Mutation. Neoplasm Proteins / genetics

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  • (PMID = 11713587.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Anticarcinogenic Agents; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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69. Kono T, Tomita I, Chisato N, Matsuda M, Kakisaka A, Kasai S: Successful low-dose chemotherapy using vinblastine and methotrexate for the treatment of an ileoanal pouch mesenteric desmoid tumor: report of a case. Dis Colon Rectum; 2004 Feb;47(2):246-9
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  • [Title] Successful low-dose chemotherapy using vinblastine and methotrexate for the treatment of an ileoanal pouch mesenteric desmoid tumor: report of a case.
  • The purpose of this report was to describe the first known case of ileoanal pouch salvage by a low-dose regimen of vinblastine and methotrexate chemotherapy for the treatment of desmoid tumor arising from the mesentery of the ileoanal pouch in a patient who had undergone ileal pouch-anal anastomosis for familial adenomatous polyposis.
  • The desmoid tumor response to the treatment was assessed at routine intervals by physical examination and magnetic resonance imaging.
  • Desmoid tumor was successfully treated with a low-dose regimen of vinblastine and methotrexate chemotherapy without significant side effects, and function of the ileoanal pouch was fully preserved.
  • This is a unique case highlighting the possibility of ileoanal pouch salvage by low-dose combination chemotherapy using vinblastine and methotrexate in a familial adenomatous polyposis patient with mesenteric desmoid tumor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonic Pouches / pathology. Fibromatosis, Aggressive / drug therapy. Mesentery / pathology. Peritoneal Neoplasms / drug therapy
  • [MeSH-minor] Adenomatous Polyposis Coli / surgery. Adult. Anal Canal / surgery. Anastomosis, Surgical. Female. Humans. Methotrexate / administration & dosage. Vinblastine / administration & dosage

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  • (PMID = 15043298.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine; YL5FZ2Y5U1 / Methotrexate
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70. Mukherjee SD, Swystun LL, Mackman N, Wang JG, Pond G, Levine MN, Liaw PC: Impact of chemotherapy on thrombin generation and on the protein C pathway in breast cancer patients. Pathophysiol Haemost Thromb; 2010;37(2-4):88-97
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  • [Title] Impact of chemotherapy on thrombin generation and on the protein C pathway in breast cancer patients.
  • Although thromboembolism is a problematic complication of chemotherapy, the pathogenic mechanisms by which chemotherapeutic agents exert prothrombotic effects in vivo are unclear.The objective of this study was to examine the effects of adjuvant chemotherapy on thrombin generation, the protein C anticoagulant pathway, and microparticle tissue factor (MP TF) activity in 26 breast cancer patients (stages I to III).
  • Plasma samples were collected on day 1 (baseline), day 2, and day 8 for the first 2 cycles of chemotherapy.
  • Levels of thrombin-antithrombin (TAT) complexes, MP TF activity, and components of the protein C anticoagulant pathway, including protein C, activated protein C (APC), soluble thrombomodulin (sTM), and soluble endothelial protein C receptor (sEPCR), were measured.
  • Compared to prechemotherapy baseline levels, plasma TAT, protein C, and APC were significantly different following the administration of chemotherapy (p < 0.01 for each).
  • Plasma protein C levels were lower in cycle 2, day 8, whereas plasma APC levels were lower in cycle 2, day 1, and cycle 2, day 8.
  • This study suggests that adjuvant chemotherapy in women with breast cancer increases thrombin generation and impairs the endothelium-based protein C anticoagulant pathway.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Breast Neoplasms / blood. Breast Neoplasms / drug therapy. Protein C / metabolism. Thrombin / metabolism
  • [MeSH-minor] Adult. Antigens, CD / blood. Antithrombin III. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Humans. Middle Aged. Neoplasm Staging. Peptide Hydrolases / blood. Receptors, Cell Surface / blood. Thrombomodulin / blood. Thromboplastin / metabolism. Thrombosis / blood. Thrombosis / chemically induced. Time Factors

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  • [Copyright] Copyright © 2011 S. Karger AG, Basel.
  • (PMID = 21430357.001).
  • [ISSN] 1424-8840
  • [Journal-full-title] Pathophysiology of haemostasis and thrombosis
  • [ISO-abbreviation] Pathophysiol. Haemost. Thromb.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-CTP79846
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / PROCR protein, human; 0 / Protein C; 0 / Receptors, Cell Surface; 0 / Thrombomodulin; 0 / antithrombin III-protease complex; 3Z8479ZZ5X / Epirubicin; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9000-94-6 / Antithrombin III; 9035-58-9 / Thromboplastin; EC 3.4.- / Peptide Hydrolases; EC 3.4.21.5 / Thrombin; U3P01618RT / Fluorouracil
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71. Nemunaitis J, Vukelja SJ, Richards D, Cunningham C, Senzer N, Nugent J, Duncan H, Jones B, Haltom E, Uprichard MJ: Phase I trial of PT-100 (PT-100), a cytokine-inducing small molecule, following chemotherapy for solid tumor malignancy. Cancer Invest; 2006 Oct;24(6):553-61
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  • [Title] Phase I trial of PT-100 (PT-100), a cytokine-inducing small molecule, following chemotherapy for solid tumor malignancy.
  • PT-100 upregulates cytokine expression competitively inhibiting the dipeptidyl peptidase activity of fibroblast activation protein (FAP) and dipeptidyl peptidase IV (DPP-IV).
  • This dose-escalation study was conducted to evaluate the safety of PT-100 in patients receiving myelosuppressive chemotherapy and to assess its effects on neutrophil recovery.PT-100 was administered orally for 7 days as a 200 microg, 400 microg, 800 microg, or 1,200 microg total daily dose (divided twice daily) to 6, 6, 17, and 5 patients, respectively.
  • Patients received 2 cycles of chemotherapy: The first cycle served as each individual patient's control.
  • Most patients received PT-100 on Days 2-8 of chemotherapy in Cycle 2, except at 800 microg where an additional cohort (n = 8) was treated on a Days 5-11 schedule.
  • A reduction in chemotherapy-related nausea, vomiting, fatigue, alopecia, and diarrhea was noted in patients receiving PT-100.
  • A maximum tolerated dose was not reached.
  • Given the accelerated neutrophil recovery, preclinical evidence of antitumor activity, and tolerable toxicities of PT-100, additional studies to optimize the PT-100 dosing schedule in patients receiving myelosuppressive chemotherapy are needed.
  • [MeSH-major] Boronic Acids / therapeutic use. Cytokines / metabolism. Dipeptides / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Dipeptidyl-Peptidases and Tripeptidyl-Peptidases / antagonists & inhibitors. Dose-Response Relationship, Drug. Female. Humans. Male. Maximum Tolerated Dose. Middle Aged. Salvage Therapy. Treatment Outcome

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  • (PMID = 16982458.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Cytokines; 0 / Dipeptides; 0 / PT-100 dipeptide; EC 3.4.14.- / Dipeptidyl-Peptidases and Tripeptidyl-Peptidases
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72. Raymond E, Fabbro M, Boige V, Rixe O, Frenay M, Vassal G, Faivre S, Sicard E, Germa C, Rodier JM, Vernillet L, Armand JP: Multicentre phase II study and pharmacokinetic analysis of irinotecan in chemotherapy-naïve patients with glioblastoma. Ann Oncol; 2003 Apr;14(4):603-14
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  • [Title] Multicentre phase II study and pharmacokinetic analysis of irinotecan in chemotherapy-naïve patients with glioblastoma.
  • PATIENTS AND METHODS: This multicentre phase II and pharmacokinetic study investigated the effects of irinotecan 350 mg/m(2) given as a 90-min infusion every 3 weeks either prior to (group A) or after relapse following radiotherapy (group B) in chemotherapy-naïve patients with glioblastoma.
  • Preferred concomitant medication for seizure prevention was valproic acid.
  • Pharmacokinetic analysis of irinotecan and its main metabolites (SN-38, SN-38-G, APC and NPC) was performed during cycle 1.
  • RESULTS: Fifty-two patients (25 patients in group A and 27 patients in group B) received a total of 191 cycles of irinotecan.
  • Forty-six patients (22 patients in group A and 24 patients in group B) were evaluable and externally reviewed for activity.
  • According to external review, one partial response (group B), seven minor responses (three in group A and four in group B), 12 disease stabilisations (seven in group A and five in group B) were observed.
  • The median time to tumour progression was 9 weeks in group A and 14.4 weeks in group B.
  • Six-month progression-free survival rates were 26% in group A and 43% in group B.
  • Grade 3-4 toxicities (percentage of patients in groups A and B) consisted of neutropenia (12.5% and 25.9%), diarrhoea (8.3% and 7.4%), asthenia (12.5% and 7.4%) and vomiting (0% and 7.4%).
  • The toxicity profile and plasma disposition of irinotecan and SN-38 were not strongly influenced by anticonvulsant valproic acid therapy.
  • Although the response rate of irinotecan as a single agent was limited, it remains an attractive drug for combination studies in patients with glioblastoma.

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  • (PMID = 12649109.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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73. Suzuki T, Izumi Y, Miura A, Kato T, Kawada K: [Successful management of the recurrent esophageal cancer following esophagectomy at a different time with combined local treatment of chemoradiotherapy and hepatic arterial infusion chemotherapy]. Gan To Kagaku Ryoho; 2008 Oct;35(10):1737-9
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  • [Title] [Successful management of the recurrent esophageal cancer following esophagectomy at a different time with combined local treatment of chemoradiotherapy and hepatic arterial infusion chemotherapy].
  • He was treated with concomitant chemoradiotherapy (CRT)with low-dose FP(5-FU, CDDP)and 60 Gy of irradiation.
  • He received systemic chemotherapy(5-FU, ADR, CDDP: FAP), but it was not effective, so hepatic arterial infusion chemotherapy(FAP)was performed.
  • Hepatic artery infusion therapy( 5-FU 1,000 mg/3.5 h x ADR 10 mg/1 h x CDDP 10 mg/1 h)was given for 1 day at an interval of 2 weeks for 18 months.
  • Since ADR reached the maximum dose, hepatic artery infusion of 5-FU(1,000 mg/3.5 h)and CDDP(10 mg/ 1 h)was continued for 14 months at an interval of 4 weeks.
  • The recurrent lesion disappeared completely 9 months after beginning hepatic artery infusion therapy.
  • Most cases with recurrent esophageal cancer have multiple metastases, and the treatment is mainly systemic therapy.
  • However, in a patient with recurrent tumors at different times, it is possible to achieve a complete response and long-time survival by local treatment with fewer side effects as in this case.
  • Combined local treatments could be the second treatment option after failed systemic chemotherapy for recurrent tumors in patients with esophageal cancer.
  • [MeSH-major] Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy. Esophagectomy. Hepatic Artery. Liver Neoplasms / secondary. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Humans. Infusions, Intra-Arterial. Male. Middle Aged. Time Factors


74. Kato H, Nagano H, Ota H, Nakamura M, Wada H, Yoshioka S, Noda T, Bazarragchaa D, Marubashi S, Miyamoto A, Takeda Y, Umeshita K, Dono K, Murakami T, Nakamura H, Monden M: [Successful treatment of combined intraarterial (5-fluorouracil and adriamycin and cisplatin) infusion chemotherapy for advanced hepatocellular carcinoma with multiple intrahepatic metastases and/or portal vein thrombosis--two case reports]. Gan To Kagaku Ryoho; 2005 Oct;32(11):1842-5
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  • [Title] [Successful treatment of combined intraarterial (5-fluorouracil and adriamycin and cisplatin) infusion chemotherapy for advanced hepatocellular carcinoma with multiple intrahepatic metastases and/or portal vein thrombosis--two case reports].
  • Hepatic arterial infusion chemotherapy has been often selected as a therapeutic option for advanced hepatocellular carcinoma with multiple intrahepatic metastases and/or portal vein thrombosis.
  • We successfully treated and obtained CR in the 2 cases of far advanced hepatocellular carcinoma with intraarterial infusion chemotherapy (FAP).
  • He received hepatic arterial infusion chemotherapy (FAP: 5-fluorouracil 500 mg/day: continuous infusion, day 1-5, adriamycin 10 mg/day, day 1, CDDP 10 mg/day, day 1).
  • This patient is still alive with no recurrence after 21 months from the beginning of this treatment.
  • He received FAP arterial infusion chemotherapy with the same protocol as case 1.
  • After 8 courses of this therapy, CT revealed that these lesions had disappeared (CR).
  • This patient is still alive with no recurrence after 9 months from the beginning of this treatment.
  • For 15 patients with advanced hepatocellular carcinoma using a same protocol, the response rate of this therapy was 33.3% (CR & PR).
  • These findings suggested that combined arterial infusion chemotherapy of FAP may be feasible and a promising modality for the advanced HCC with intrahepatic metastases and/or portal vein thrombosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. Neoplastic Cells, Circulating / pathology. Portal Vein / pathology

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  • (PMID = 16315958.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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75. Li J, Lv YM, Jin Z, Cui RL: [The effects of sulindac on the pathology of colorectal remnant polyps of familial adenomatous polyposis (FAP) patients]. Beijing Da Xue Xue Bao; 2005 Aug 18;37(4):371-3
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  • [Title] [The effects of sulindac on the pathology of colorectal remnant polyps of familial adenomatous polyposis (FAP) patients].
  • OBJECTIVE: To evaluate the long-term effectiveness of sulindac on the pathology of colorectal adenomas of familial adenomatous polyposis (FAP) patients.
  • METHODS: FAP patients were treated with sulindac 400 mg per day.
  • The type and dysplasia grade of biopsies were evaluated and compared with baseline.
  • RESULTS: Before the study, 90.8% of adenoma biopsies were tubular, while 9.2% was tubulovillous adenoma.
  • After sulindac treatment, 99.8% of adenoma biopsies were tubular, while 0.2% tubulovillous adenoma.
  • Minor flat elevation and erythema were found during the treatment, in which approximately 65% was adenoma.
  • CONCLUSION: Long-term use of sulindac seems to be effective in reducing dysplasia grade and tubulovillous adenoma of retained colorectal adenoma of FAP patients.
  • Minor flat elevation and erythema may be the lesions appearing during the regression of adenoma.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Colon / pathology. Rectum / pathology. Sulindac / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / therapeutic use. Biopsy. Colonoscopy. Female. Humans. Male. Middle Aged

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  • (PMID = 16086054.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 184SNS8VUH / Sulindac
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76. Tucker JM, Davis C, Kitchens ME, Bunni MA, Priest DG, Spencer HT, Berger FG: Response to 5-fluorouracil chemotherapy is modified by dietary folic acid deficiency in Apc(Min/+) mice. Cancer Lett; 2002 Dec 10;187(1-2):153-62
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  • [Title] Response to 5-fluorouracil chemotherapy is modified by dietary folic acid deficiency in Apc(Min/+) mice.
  • 5-Fluorouracil (5-FU) has been the foundation of advanced colorectal cancer treatment for over 40 years.
  • The Apc(Min/+) mouse, which is genetically predisposed to intestinal neoplasia, was used to examine the effects of 5-FU in this system and the impact of dietary folic acid on those effects.
  • 5-FU treatment resulted in a 60-80% reduction in tumor number.
  • Tumor numbers rebounded completely following termination of 5-FU therapy, indicating that the drug inhibits tumor growth but does not eradicate them.
  • In mice that were fed with a defined diet containing no folic acid (0 ppm), 5-FU not only induced regression of pre-existing tumors, but also inhibited tumor recovery following drug withdrawal.
  • Our data indicate that a dietary folic acid deficiency, in promoting tumor regression and inhibiting tumor recovery, may enhance the therapeutic effects of 5-FU.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Fluorouracil / therapeutic use. Folic Acid Deficiency / physiopathology. Intestinal Neoplasms / physiopathology. Intestinal Neoplasms / prevention & control
  • [MeSH-minor] Animals. DNA Primers / chemistry. Diet. Folic Acid / administration & dosage. Genes, APC / physiology. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. Polymerase Chain Reaction

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  • [ErratumIn] Cancer Lett. 2003 Dec 8;202(1):119
  • (PMID = 12359363.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 76560; United States / NCI NIH HHS / CA / CA 78651
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA Primers; 935E97BOY8 / Folic Acid; U3P01618RT / Fluorouracil
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77. Blanke CD: Celecoxib with chemotherapy in colorectal cancer. Oncology (Williston Park); 2002 Apr;16(4 Suppl 3):17-21
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  • [Title] Celecoxib with chemotherapy in colorectal cancer.
  • The expression of COX-2 is associated with a worse prognosis.
  • Regular consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) decreases the incidence of, and mortality rate resulting from, a number of types of gastrointestinal cancers.
  • The U.S. Food and Drug Administration has approved specific COX-2 inhibitors for the treatment of arthritis, pain, and familial adenomatous polyposis.
  • Preclinical studies show that these drugs block angiogenesis, suppress solid tumor metastases, and slow the growth of implanted gastrointestinal cancer cell lines.
  • Ongoing clinical trials are currently assessing the potential therapeutic role of COX-2 inhibitors in both prevention and treatment of a diverse range of human cancers.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / antagonists & inhibitors. Sulfonamides / therapeutic use
  • [MeSH-minor] Celecoxib. Clinical Trials as Topic. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / metabolism. Pyrazoles

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  • (PMID = 12014863.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Pyrazoles; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib
  • [Number-of-references] 32
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78. Koh PK, Loi C, Cao X, Cheah PY, Ho KS, Ooi BS, Tang CL, Eu KW: Mesenteric desmoid tumors in Singapore familial adenomatous polyposis patients: clinical course and genetic profile in a predominantly Chinese population. Dis Colon Rectum; 2007 Jan;50(1):75-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mesenteric desmoid tumors in Singapore familial adenomatous polyposis patients: clinical course and genetic profile in a predominantly Chinese population.
  • PURPOSE: This study examined the mutational profile of the adenomatous polyposis coli gene in relation to the development of desmoid tumors in familial adenomatous polyposis patients from a predominantly Chinese population.
  • METHODS: This is a retrospective review of all patients with familial adenomatous polyposis coli from the Singapore Polyposis Registry.
  • Identification of specific adenomatous polyposis coli gene mutation was performed and clinical course of associated desmoid disease obtained from case records and a computerized database.
  • RESULTS: Two hundred five patients from 75 families afflicted with familial adenomatous polyposis coli were reviewed, with gene mutations identified in 107 patients.
  • Of these, 23 (11.2 percent) developed desmoids.
  • Of the 92 patients with mutations 5' to codon 1444, 11 patients (12 percent) developed desmoids compared with 6 of 15 (40 percent) patients with adenomatous polyposis coli gene mutations 3' to codon 1444 (P<0.01).
  • Only 3 (13 percent) patients with aggressive tumor growth required chemotherapy.
  • Seventy-four percent of these desmoids (17/23) developed at a mean interval of 2.98 years after restorative proctocolectomy, while only 30 percent (7/23) were diagnosed preoperatively or discovered during the initial surgery.
  • The most common complications related to the mesenteric desmoids were intestinal obstruction (21.7 percent), ureteric obstruction (17.4 percent), and encasement of superior mesenteric vessels (13 percent).
  • CONCLUSION: The clinical course of desmoids in an individual familial adenomatous polyposis patient remains unpredictable and no reliable genetic marker is available for prognostication in desmoid disease.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Fibromatosis, Abdominal / genetics

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  • (PMID = 17082890.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon
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79. Gega M, Yanagi H, Yoshikawa R, Noda M, Ikeuchi H, Tsukamoto K, Oshima T, Fujiwara Y, Gondo N, Tamura K, Utsunomiya J, Hashimoto-Tamaoki T, Yamamura T: Successful chemotherapeutic modality of doxorubicin plus dacarbazine for the treatment of desmoid tumors in association with familial adenomatous polyposis. J Clin Oncol; 2006 Jan 1;24(1):102-5
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  • [Title] Successful chemotherapeutic modality of doxorubicin plus dacarbazine for the treatment of desmoid tumors in association with familial adenomatous polyposis.
  • PURPOSE: Desmoid tumors are locally aggressive and can be fatal in familial adenomatous polyposis (FAP) patients if they are not suitable for surgery or radiation therapy.
  • Here, we prospectively investigated the efficacy of a chemotherapeutic regimen involving doxorubicin (DOX) and dacarbazine (DTIC) for inoperable FAP-associated desmoid tumors.
  • PATIENTS AND METHODS: From an initial group of 120 FAP patients, seven of the 11 individuals with symptomatic unresectable desmoid tumors that were unresponsive to conventional hormone therapy were enrolled onto this study.
  • The general chemotherapy regimen comprised four or five cycles of DOX (20 mg/m2 daily) plus DTIC (150 mg/m2 daily) throughout 4 days of drip intravenous infusion (day 1 through 4) every 28 days, followed by the cyclooxygenase-2 inhibitor meloxicam (10 mg/m2).
  • The secondary end points included toxicity, clinical improvement, and tumor regression according to computed tomography.
  • Three patients showed grade 3 adverse events with no treatment-related mortality.
  • An adenomatous polyposis coli germline-mutation analysis revealed no mutations in the specified regions.
  • CONCLUSION: A chemotherapeutic regimen of DOX plus DTIC followed by meloxicam is an effective and safe treatment for FAP-associated desmoid tumors.
  • This modality should be considered for use as first-line chemotherapy in symptomatic desmoid tumors that are unresponsive to conventional medical therapy, due to the absence of useful presymptomatic markers.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fibromatosis, Aggressive / drug therapy
  • [MeSH-minor] Adult. Dacarbazine / administration & dosage. Doxorubicin / administration & dosage. Female. Genes, APC. Germ-Line Mutation. Humans. Male. Retrospective Studies. Thiazines / administration & dosage. Thiazoles / administration & dosage. Tomography, X-Ray Computed

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  • [CommentIn] J Clin Oncol. 2006 Jan 1;24(1):11-2 [16330666.001]
  • (PMID = 16382119.001).
  • [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 / Thiazines; 0 / Thiazoles; 71125-38-7 / meloxicam; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin
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80. Bhandari P, Shashidhara LS: Studies on human colon cancer gene APC by targeted expression in Drosophila. Oncogene; 2001 Oct 18;20(47):6871-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Studies on human colon cancer gene APC by targeted expression in Drosophila.
  • Mutations in human Adenomatous Polyposis Coli (APC) gene are associated with both familial and sporadic colorectal tumors.
  • APC is known to down regulate beta-catenin levels, a transducer of Wnt signaling.
  • The aim of this study is to provide transgenic Drosophila expressing either full-length or truncated forms of human APC (hAPC) protein and methods for using them in functional genomics and drug screening.
  • In addition, an anti-colon cancer drug, indomethacin, specifically enhanced hAPC-induced phenotypes.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Colorectal Neoplasms / drug therapy. Drosophila / genetics. Drosophila Proteins. Genes, APC. Trans-Activators
  • [MeSH-minor] Animals. Animals, Genetically Modified. Antineoplastic Agents / pharmacology. Armadillo Domain Proteins. Calcium-Calmodulin-Dependent Protein Kinases / metabolism. Cytoskeletal Proteins / physiology. Drug Screening Assays, Antitumor. Eye / anatomy & histology. Eye / embryology. Eye / ultrastructure. Gene Targeting. Genes, Insect. Glycogen Synthase Kinase 3. Humans. Indomethacin / pharmacology. Insect Proteins / physiology. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / physiology. Transcription Factors. Transfection. Wnt1 Protein. beta Catenin

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  • (PMID = 11687966.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Antineoplastic Agents; 0 / Armadillo Domain Proteins; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / Drosophila Proteins; 0 / Insect Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Wnt1 Protein; 0 / armadillo protein, Drosophila; 0 / beta Catenin; 0 / wg protein, Drosophila; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / shaggy protein, Drosophila; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.26 / Glycogen Synthase Kinase 3; XXE1CET956 / Indomethacin
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81. Giardiello FM, Casero RA Jr, Hamilton SR, Hylind LM, Trimbath JD, Geiman DE, Judge KR, Hubbard W, Offerhaus GJ, Yang VW: Prostanoids, ornithine decarboxylase, and polyamines in primary chemoprevention of familial adenomatous polyposis. Gastroenterology; 2004 Feb;126(2):425-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostanoids, ornithine decarboxylase, and polyamines in primary chemoprevention of familial adenomatous polyposis.
  • BACKGROUND & AIMS: Familial adenomatous polyposis because of germline mutation of the adenomatous polyposis coli gene is characterized by development of colorectal adenomas and, ultimately, colorectal cancer.
  • The usefulness of colorectal mucosal compounds to predict the effect on adenoma development of primary chemoprevention with the nonsteroidal anti-inflammatory drug sulindac was evaluated.
  • METHODS: A randomized, double-blind, placebo-controlled study of 41 subjects genotypically affected with familial adenomatous polyposis but phenotypically unaffected was conducted.
  • RESULTS: There were no statistically significant differences between treatment groups in baseline levels of prostanoids, ornithine decarboxylase, or polyamines.
  • Among the subset of patients taking sulindac, 3 of 5 prostaglandin levels were statistically significantly lower in patients who were polyp free than in those who developed polyps.
  • By contrast, there were no statistically significant differences in ornithine decarboxylase or polyamines between treatment groups or in those on sulindac who were polyp free compared with those who developed polyps.
  • CONCLUSIONS: Colorectal mucosal prostaglandin levels, but not ornithine decarboxylase or polyamines, may be valuable biomarkers to assess appropriate drug dosage and medication compliance in patients undergoing primary chemoprevention therapy with sulindac.

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  • (PMID = 14762779.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R24 DK064399-01; United States / NIDDK NIH HHS / DK / DK064399-01; United States / NCI NIH HHS / CA / CA 51085; United States / NCI NIH HHS / CA / CA 53801; United States / NIDDK NIH HHS / DK / R24 DK064399; United States / NCI NIH HHS / CA / CA 63721; United States / NCI NIH HHS / CA / P50 CA 93-16
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Polyamines; 0 / Prostaglandins; 184SNS8VUH / Sulindac; EC 4.1.1.17 / Ornithine Decarboxylase
  • [Other-IDs] NLM/ NIHMS38268; NLM/ PMC2225536
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82. Ignatenko NA, Besselsen DG, Stringer DE, Blohm-Mangone KA, Cui H, Gerner EW: Combination chemoprevention of intestinal carcinogenesis in a murine model of familial adenomatous polyposis. Nutr Cancer; 2008;60 Suppl 1:30-5
Hazardous Substances Data Bank. Eflornithine .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination chemoprevention of intestinal carcinogenesis in a murine model of familial adenomatous polyposis.
  • Familial adenomatous polyposis (FAP) is an autosomal dominantly inherited syndrome in humans.
  • The Apc(Min/+) mouse, which expresses a mutant homolog of the adenomatous polyposis coli gene, is a model of FAP in humans.
  • Treatment with the nonsteroidal anti-inflammatory drugs (NSAIDS) sulindac or celecoxib can suppress polyp development in FAP patients, but responses are generally transient and incomplete.
  • Combination chemoprevention with the ornithine decarboxylase inhibitor difluoromethylornithine (DFMO) and either celecoxib or sulindac was evaluated in the Apc(Min/+) mouse.
  • Combinations of DFMO and either NSAID reduced intestinal tumor number by more than 80% (P < 0.0001) compared to untreated controls.
  • In addition to the dramatic reduction in tumor number, the combination of DFMO and sulindac reduced the development of high-grade intestinal adenomas compared to sulindac alone (P = 0.003).
  • The fraction of high-grade intestinal adenomas remaining after treatment was similar for the combination of DFMO and celecoxib and celecoxib alone.
  • Only combinations of DFMO plus sulindac reduced total intestinal polyamine contents compared to untreated mice.
  • These data support the rationale for treatment of FAP patients postcolectomy with DFMO combined with either celecoxib or sulindac but indicate that sulindac may be more effective than celecoxib in reducing intestinal polyamine contents and the incidence of high-grade intestinal adenomas when combined with DFMO.
  • [MeSH-major] Adenoma / prevention & control. Adenomatous Polyposis Coli / drug therapy. Intestinal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Biogenic Polyamines / analysis. Celecoxib. Chemoprevention. Eflornithine / administration & dosage. Female. Genes, APC. Intestinal Polyps / prevention & control. Male. Mice. Mice, Inbred C57BL. Pyrazoles / administration & dosage. Sulfonamides / administration & dosage. Sulindac / administration & dosage

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  • (PMID = 19003578.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA123065; United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / CA72008; United States / NCI NIH HHS / CA / CA95060
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biogenic Polyamines; 0 / Pyrazoles; 0 / Sulfonamides; 184SNS8VUH / Sulindac; JCX84Q7J1L / Celecoxib; ZQN1G5V6SR / Eflornithine
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83. Telang N, Katdare M: Novel cell culture model for prevention of carcinogenic risk in familial adenomatous polyposis syndrome. Oncol Rep; 2009 Apr;21(4):1017-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel cell culture model for prevention of carcinogenic risk in familial adenomatous polyposis syndrome.
  • Clinical familial adenomatous polyposis (FAP) syndrome represents a high risk pre-invasive precursor for colon cancer, and is characterized by germ line mutation in the adenomatous polyposis coli (APC) tumor suppressor gene.
  • Cloned colon epithelial cell line from the Apc850 Min/+ mouse represented a model for FAP.
  • The Apc mutant 850Min COL-Cl1 cells exhibited decreased G0/G1:S+G2/M ratio, increased S+G2/M:subG0 ratio, and increased anchorage-independent colony formation, indicating loss of homeostatic growth control and gain of anchorage-independent growth.
  • Treatment with low dose combinations of synthetic enzyme inhibitor difluoro methylornithine (DFMO), synthetic non-steroidal anti-inflammatory drug sulindac (SUL), and naturally occurring epigallocatechin gallate (EGCG), and eicosapen-taenoic acid (EPA) produced cytostatic growth arrest and inhibited anchorage-independent colony formation.
  • These data identify a novel cell culture model and validate a mechanism-based approach to prioritize combinations of effective chemopreventive compounds for prevention/therapy of colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Colonic Neoplasms / prevention & control
  • [MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Catechin / analogs & derivatives. Catechin / therapeutic use. Cell Line. Eflornithine / therapeutic use. Eicosapentaenoic Acid / therapeutic use. Genes, APC. Mice. Mice, Inbred C57BL. Mutation

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  • (PMID = 19288003.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA29502-20; United States / NCI NIH HHS / CA / CA29502-S1; United States / NCI NIH HHS / CN / CN75029-63; United States / NCI NIH HHS / CA / R01 CA122394
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 8R1V1STN48 / Catechin; AAN7QOV9EA / Eicosapentaenoic Acid; BQM438CTEL / epigallocatechin gallate; ZQN1G5V6SR / Eflornithine
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84. Zhu P, Martin E, Mengwasser J, Schlag P, Janssen KP, Göttlicher M: Induction of HDAC2 expression upon loss of APC in colorectal tumorigenesis. Cancer Cell; 2004 May;5(5):455-63
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  • [Title] Induction of HDAC2 expression upon loss of APC in colorectal tumorigenesis.
  • We now identify faulty expression of a specific mediator of transcriptional repression in a solid tumor.
  • Loss of the adenomatosis polyposis coli (APC) tumor suppressor induces HDAC2 expression depending on the Wnt pathway and c-Myc.
  • Increased HDAC2 expression is found in the majority of human colon cancer explants, as well as in intestinal mucosa and polyps of APC-deficient mice.
  • Interference with HDAC2 by valproic acid largely diminishes adenoma formation in APC(min) mice.
  • These findings point toward HDAC2 as a particularly relevant potential target in cancer therapy.
  • [MeSH-major] Adenoma / enzymology. Adenomatous Polyposis Coli Protein / physiology. Colorectal Neoplasms / enzymology. Histone Deacetylases / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Transformation, Neoplastic. Cytoskeletal Proteins / metabolism. Enzyme Induction. Enzyme Inhibitors / pharmacology. Histone Deacetylase 2. Humans. Intestinal Mucosa / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Proto-Oncogene Proteins c-myc / metabolism. RNA, Small Interfering / pharmacology. Trans-Activators / metabolism. Up-Regulation. Valproic Acid / pharmacology. beta Catenin

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  • (PMID = 15144953.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [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 / CTNNB1 protein, human; 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / beta Catenin; 614OI1Z5WI / Valproic Acid; EC 3.5.1.98 / Hdac2 protein, mouse; EC 3.5.1.98 / Histone Deacetylase 2; EC 3.5.1.98 / Histone Deacetylases
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85. Niho N, Takahashi M, Kitamura T, Shoji Y, Itoh M, Noda T, Sugimura T, Wakabayashi K: Concomitant suppression of hyperlipidemia and intestinal polyp formation in Apc-deficient mice by peroxisome proliferator-activated receptor ligands. Cancer Res; 2003 Sep 15;63(18):6090-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Concomitant suppression of hyperlipidemia and intestinal polyp formation in Apc-deficient mice by peroxisome proliferator-activated receptor ligands.
  • Epidemiological studies have shown a positive association of colon cancer with hyperlipidemia.
  • In the present study, we assessed hyperlipidemia in Apc-deficient mice, model animals for human familial adenomatous polyposis, and examined the effects of pioglitazone and bezafibrate, respectively, PPARgamma and PPARalpha agonists, on both hyperlipidemia and intestinal polyposis.
  • Serum lipid levels in Apc(1309) mice and Min mice from 6 to 15 weeks of age were measured.
  • Although serum levels of triglyceride and cholesterol were low in both Apc(1309) and wild-type mice at 6 weeks, triglycerides were elevated 10-fold in Apc(1309) mice by the age of 12 weeks but not in their wild-type counterparts.
  • Cholesterol was also increased significantly, and marked centrilobular-restricted steatosis was observed in the livers of aged Apc(1309) mice.
  • Moreover, lipoprotein lipase mRNA levels in the liver and small intestine of Apc(1309) and Min mice were demonstrated to be lower than those in wild-type mice.
  • Treatment of Apc(1309) mice with 100 and 200 ppm pioglitazone or bezafibrate for 6 weeks from 6 weeks of age caused dose-dependent reduction in serum triglycerides and cholesterol, along with reduction in the numbers of intestinal polyps to 67% of the control value.
  • The present study clearly demonstrated a hyperlipidemic state in Apc gene-deficient mice and a potential of PPARalpha and PPARgamma ligands to suppress both hyperlipidemia and polyp formation.
  • Hyperlipidemia in these mice may thus be associated with their intestinal lesion development.
  • [MeSH-major] Bezafibrate / pharmacology. Genes, APC / physiology. Hyperlipidemias / drug therapy. Intestinal Polyposis / drug therapy. Receptors, Cytoplasmic and Nuclear / agonists. Thiazolidinediones / pharmacology. Transcription Factors / agonists
  • [MeSH-minor] Age Factors. Animals. Cholesterol / blood. Fatty Acids, Nonesterified / blood. Intestine, Small / enzymology. Ligands. Lipoprotein Lipase / biosynthesis. Lipoprotein Lipase / genetics. Lipoprotein Lipase / metabolism. Liver / enzymology. Mice. Mice, Inbred C57BL. Mice, Knockout. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Triglycerides / blood

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  • (PMID = 14522940.001).
  • [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 / Fatty Acids, Nonesterified; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Thiazolidinediones; 0 / Transcription Factors; 0 / Triglycerides; 97C5T2UQ7J / Cholesterol; EC 3.1.1.34 / Lipoprotein Lipase; X4OV71U42S / pioglitazone; Y9449Q51XH / Bezafibrate
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86. Mewhort-Buist TA, Liaw PC, Patel S, Atkinson HM, Berry LR, Chan AK: Treatment of endothelium with the chemotherapy agent vincristine affects activated protein C generation to a greater degree in newborn plasma than in adult plasma. Thromb Res; 2008;122(3):418-26
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  • [Title] Treatment of endothelium with the chemotherapy agent vincristine affects activated protein C generation to a greater degree in newborn plasma than in adult plasma.
  • INTRODUCTION: Activated protein C (APC) is well-established as a physiologically important anticoagulant.
  • During development, plasma concentrations of protein C and alpha(2)macroglobulin, factors involved in APC generation, differ from adult levels.
  • Chemotherapy drugs can perturb endothelial expression of PC-activating receptors.
  • This study examines the effect of chemotherapy treatment of endothelium on APC generation in newborn and adult plasma.
  • MATERIALS AND METHODS: APC generations were initiated on endothelial cells treated with vincristine or media by recalcifying defibrinated plasma with buffer containing thromboplastin.
  • APC generation was terminated by mixing timed subsamples into FFRCMK-EDTA or heparin, followed by EDTA.
  • APC-PCI and APC-alpha(1)AT were assayed by ELISA.
  • APC-alpha(2)M was measured chromogenically.
  • Since heparin converts free APC to APC-PCI, the difference between APC-PCI detected in heparin subsamples and APC-PCI detected in FFRCMK-EDTA subsamples gave the free APC.
  • RESULTS: Vincristine-treated endothelium decreased free APC generation in newborn plasma to a greater degree than in adult plasma.
  • APC-PCI levels in both adult and newborn plasma were unaffected by chemotherapy.
  • Vincristine treatment reduced levels of APC-alpha(1) AT and APC-alpha(2) M to a greater degree in newborn plasma versus adult plasma.
  • CONCLUSIONS: The differential response of newborn and adult plasma PC components to chemotherapy-mediated changes in cell surface components may be a factor in the increased risk of thrombosis in children receiving chemotherapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Blood Proteins / pharmacology. Endothelial Cells / drug effects. Protein C / metabolism. Thrombosis / prevention & control. Vincristine / pharmacology
  • [MeSH-minor] Adult. Age Factors. Cells, Cultured. Humans. Infant, Newborn. Membrane Proteins / metabolism. Plasma. Protein Binding / drug effects. Protein C Inhibitor / metabolism. Thrombomodulin / metabolism. Umbilical Veins / cytology. alpha 1-Antitrypsin / metabolism. alpha-Macroglobulins / metabolism

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  • (PMID = 18206217.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Blood Proteins; 0 / Membrane Proteins; 0 / Protein C; 0 / Protein C Inhibitor; 0 / Thrombomodulin; 0 / alpha 1-Antitrypsin; 0 / alpha-Macroglobulins; 5J49Q6B70F / Vincristine
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87. Bataille F, Rümmele P, Dietmaier W, Gaag D, Klebl F, Reichle A, Wild P, Hofstädter F, Hartmann A: Alterations in p53 predict response to preoperative high dose chemotherapy in patients with gastric cancer. Mol Pathol; 2003 Oct;56(5):286-92
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  • [Title] Alterations in p53 predict response to preoperative high dose chemotherapy in patients with gastric cancer.
  • AIMS: To evaluate the usefulness of molecular markers in predicting histopathological and clinical response to preoperative high dose chemotherapy (HDCT) and survival of patients with advanced gastric cancer.
  • METHODS: In a phase II trial, 25 patients with metastatic gastric cancer received preoperative tandem HDCT consisting of etoposide, cisplatin, and mitomycin, followed by autologous bone marrow transplantation to achieve surgical resectability.
  • Samples before and after treatment, from normal and tumour tissue, were characterised histopathologically, and both p53 and BAX expression was analysed by immunohistochemistry.
  • Pretreatment formalin fixed, paraffin wax embedded samples from normal and tumour tissue were microdissected, and the extracted DNA was preamplified using improved primer extension preamplification polymerase chain reaction.
  • Detection of microsatellite instability (MSI) or loss of heterozygosity (LOH) was performed using markers for p53, BAX, BAT25, BAT26, D2S123, D17S250, and APC.
  • RESULTS: Four parameters were significantly associated with response to chemotherapy and prolonged overall survival: positive p53 immunostaining, positive p53 mutation status before chemotherapy, strong histological regression induced by preoperative HDCT, and surgical treatment.
  • Patients's sex or age, tumour location or stage, lymph node status, Lauren classification, MSI, or LOH did not influence duration of survival significantly in this high risk population.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Genes, p53. Stomach Neoplasms / genetics. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Aged. Bone Marrow Transplantation. Chemotherapy, Adjuvant. Female. Genetic Markers. Humans. Male. Microsatellite Repeats. Middle Aged. Mutation. Neoplasm Metastasis. Preoperative Care / methods. Prognosis. Survival Analysis. Treatment Outcome

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  • (PMID = 14514923.001).
  • [ISSN] 1366-8714
  • [Journal-full-title] Molecular pathology : MP
  • [ISO-abbreviation] MP, Mol. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC1187340
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88. Bhatnagar N, Li X, Chen Y, Zhou X, Garrett SH, Guo B: 3,3'-diindolylmethane enhances the efficacy of butyrate in colon cancer prevention through down-regulation of survivin. Cancer Prev Res (Phila); 2009 Jun;2(6):581-9
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  • [Title] 3,3'-diindolylmethane enhances the efficacy of butyrate in colon cancer prevention through down-regulation of survivin.
  • Butyrate is an inhibitor of histone deacetylase (HDAC) and has been extensively evaluated as a chemoprevention agent for colon cancer.
  • We recently showed that mutations in the adenomatous polyposis coli (APC) gene confer resistance to HDAC inhibitor-induced apoptosis in colon cancers.
  • Here, we show that APC mutation rendered colon cancer cells resistant to butyrate-induced apoptosis due to the failure of butyrate to down-regulate survivin in these cells.
  • Another cancer-preventive agent, 3,3'-diindolylmethane (DIM), was identified to be able to down-regulate survivin in colon cancers expressing mutant APC.
  • DIM inhibited survivin mRNA expression and promoted survivin protein degradation through inhibition of p34(cdc2)-cyclin B1-mediated survivin Thr(34) phosphorylation.
  • Pretreatment with DIM enhanced butyrate-induced apoptosis in colon cancer cells expressing mutant APC.
  • DIM/butyrate combination treatment induced the expression of proapoptotic Bax and Bak proteins, triggered Bax dimerization/activation, and caused release of cytochrome c and Smac proteins from mitochondria.
  • Whereas overexpression of survivin blocked DIM/butyrate-induced apoptosis, knocking down of survivin by small interfering RNA increased butyrate-induced apoptosis in colon cancer cells.
  • We further showed that DIM was able to down-regulate survivin and enhance the effects of butyrate in apoptosis induction and prevention of familial adenomatous polyposis in APC(min/+) mice.
  • Thus, the combination of DIM and butyrate is potentially an effective strategy for the prevention of colon cancer.

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  • (PMID = 19470789.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA130062; United States / NCI NIH HHS / CA / 5R21CA111765; United States / NCRR NIH HHS / RR / 2P20RR015566; United States / NCI NIH HHS / CA / 1R03CA130062; United States / NCI NIH HHS / CA / R03 CA130062-02; United States / NIGMS NIH HHS / GM / P30 GM103332; United States / NCRR NIH HHS / RR / P20 RR015566; United States / NCRR NIH HHS / RR / P20 RR015566-08; United States / NCRR NIH HHS / RR / RR015566-08; United States / NCI NIH HHS / CA / R21 CA111765; United States / NCI NIH HHS / CA / CA130062-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / BIRC5 protein, human; 0 / Butyrates; 0 / DNA, Complementary; 0 / Histone Deacetylase Inhibitors; 0 / Indoles; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Fusion Proteins; SSZ9HQT61Z / 3,3'-diindolylmethane
  • [Other-IDs] NLM/ NIHMS209111; NLM/ PMC2901098
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89. Mutoh M, Niho N, Wakabayashi K: Concomitant suppression of hyperlipidemia and intestinal polyp formation by increasing lipoprotein lipase activity in Apc-deficient mice. Biol Chem; 2006 Apr;387(4):381-5
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  • [Title] Concomitant suppression of hyperlipidemia and intestinal polyp formation by increasing lipoprotein lipase activity in Apc-deficient mice.
  • Epidemiologically, a high-fat diet is associated with the risk of colon cancer.
  • In addition, serum levels of triglycerides (TGs) and cholesterol have been demonstrated to be positively associated with colon carcinogenesis.
  • We recently found that an age-dependent hyperlipidemic state (high serum TG levels) exists in Apc-deficient mice, an animal model for human familial adenomatous polyposis.
  • Moreover, treatment with a peroxisome proliferator-activated receptor (PPAR) alpha agonist, bezafibrate, or a PPARgamma agonist, pioglitazone, suppressed both hyperlipidemia and intestinal polyp formation in the mice, with induction of LPL mRNA.
  • One compound that also increases LPL expression levels but does not possess PPAR agnostic activity is NO-1886.
  • When given at 400 or 800 ppm in the diet, it suppresses both hyperlipidemia and intestinal polyp formation in Apc-deficient mice, with elevation of LPL mRNA.
  • In conclusion, a decrease in serum lipid levels by increasing LPL activity may contribute to a reduction in intestinal polyp formation with Apc deficiency.
  • PPARalpha and PPARgamma agonists, as well as NO-1886, could be useful as chemopreventive agents for colon cancer.
  • [MeSH-major] Genes, APC. Hyperlipidemias / drug therapy. Intestinal Polyps / prevention & control. Lipoprotein Lipase / metabolism
  • [MeSH-minor] Age Factors. Animals. Benzamides / metabolism. Benzamides / pharmacology. Bezafibrate / administration & dosage. Bezafibrate / metabolism. Bezafibrate / pharmacology. Cyclooxygenase 2 / metabolism. Humans. Membrane Proteins / metabolism. Mice. Organophosphorus Compounds / metabolism. Organophosphorus Compounds / pharmacology. PPAR alpha / metabolism. PPAR gamma / metabolism. Thiazolidinediones / administration & dosage. Thiazolidinediones / metabolism. Thiazolidinediones / pharmacology. Triglycerides / blood. Triglycerides / metabolism

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  • (PMID = 16606335.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzamides; 0 / Membrane Proteins; 0 / Organophosphorus Compounds; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Thiazolidinediones; 0 / Triglycerides; 133208-93-2 / 4-diethoxyphosphorylmethyl-N-(4-bromo-2-cyanophenyl)benzamide; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 3.1.1.34 / Lipoprotein Lipase; X4OV71U42S / pioglitazone; Y9449Q51XH / Bezafibrate
  • [Number-of-references] 30
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90. Eigenbrod T, Kullmann F, Klebl F: Resection of small bowel adenocarcinoma liver metastasis combined with neoadjuvant and adjuvant chemotherapy results in extended disease-free period--a case report. Int J Gastrointest Cancer; 2006;37(2-3):94-7
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  • [Title] Resection of small bowel adenocarcinoma liver metastasis combined with neoadjuvant and adjuvant chemotherapy results in extended disease-free period--a case report.
  • Small bowel adenocarcinoma (SBA) is a very rare tumor entity but occurs in up to 5% of patients suffering from familiar adenomatous polyposis (FAP).
  • Because of nonspecific symptoms, diagnosis is usually made with delay, which contributes to high rates of metastatic disease at the time of diagnosis.
  • For localized disease, complete surgical resection is the treatment of choice, whereas systemic chemotherapy is deemed indicated in tumors with metastatic spread.
  • The optimal regimen has not been defined as yet.
  • In October 2001, a 51-year-old woman with attenuated FAP, that had total proctocolectomy in 1994 was diagnosed with a jejunal adenocarcinoma.
  • Because a computed tomography (CT) scan in April 2002 revealed multiple liver metastases, chemotherapy with nine cycles FOLFOX6 was initiated.
  • Afterwards, a small residual lesion in segment VIII was seen in CT scan but could not be identified by PET and at laparotomy in November 2002.
  • Postoperatively, the patient received adjuvant chemotherapy with three cycles (with six applications in each cycle) 5-fluorouracil/folinic acid/irinotecan according to the AIO protocol.
  • Resection of liver metastases from SBA combined with neoadjuvant and adjuvant chemotherapy can result in extended disease-free survival and should undergo further investigation.
  • [MeSH-major] Adenocarcinoma / therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hepatectomy. Ileal Neoplasms / therapy. Jejunal Neoplasms / therapy. Liver Neoplasms / therapy. Neoadjuvant Therapy
  • [MeSH-minor] Adult. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Chemotherapy, Adjuvant. Combined Modality Therapy. Female. Fluorouracil / administration & dosage. Humans. Leucovorin / administration & dosage. Organoplatinum Compounds / administration & dosage. Prognosis

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  • (PMID = 17827529.001).
  • [ISSN] 1537-3649
  • [Journal-full-title] International journal of gastrointestinal cancer
  • [ISO-abbreviation] Int J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 0H43101T0J / irinotecan; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
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91. Knudsen AL, Bülow S: [Desmoid tumor in familial adenomatous polyposis]. Ugeskr Laeger; 2000 Oct 16;162(42):5628-31
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  • [Title] [Desmoid tumor in familial adenomatous polyposis].
  • [Transliterated title] Desmoid tumor ved familiaer adenomatøs polypose.
  • INTRODUCTION: Desmoid tumors (DT) are rare benign tumors that do not metastasize, but tend to invade locally.
  • DT are frequently seen in patients with familial adenomatous polyposis (FAP), and diagnosis and treatment are often difficult.
  • METHOD: The article presents the clinical picture, diagnosis and treatment of DT in patients registered in the Danish Polyposis Register by the end of 1999.
  • RESULTS: Twenty-seven of 486 patients (6%) had DT.
  • Eighteen patients were alive at the time of evaluation.
  • DT were found in the mesentery in 42%, in the abdominal wall in 40%, in the retroperitoneum in 8% and only 10% on the extremities.
  • Fifty percent of the patients had complications (intestinal obstruction, hydronephrosis or fistulas), and 2/9 deaths were caused by DT.
  • Ninety-three percent were treated with surgery, NSAIDs, antioestogenic drugs, chemotherapy or radiotherapy, but all modalities proved disappointing, except for treatment with a combination of the NSAID sulindac and tamoxifen.
  • DISCUSSION: Surgical excision is recommended in patients with DT in the abdominal wall.
  • First line treatment of mesenteric DT is Clinoril in combination with tamoxifen.
  • Elective surgery may be considered in patients with a small well-defined DT with no signs of invasion of vital structures, and in patients with imminent bowel ischaemia or obstruction.
  • The prognosis for mesenteric DT is grave, and improvement of the therapeutic strategy awaits current international studies.
  • [MeSH-major] Abdominal Neoplasms. Adenomatous Polyposis Coli. Fibromatosis, Aggressive. Peritoneal Neoplasms. Retroperitoneal Neoplasms
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Colectomy. Colonic Neoplasms / complications. Colonic Neoplasms / diagnosis. Colonic Neoplasms / surgery. Combined Modality Therapy. Female. Humans. Male. Prognosis. Registries

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  • (PMID = 11059301.001).
  • [ISSN] 0041-5782
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] DENMARK
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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92. Song Y, Zhang C: Hydralazine inhibits human cervical cancer cell growth in vitro in association with APC demethylation and re-expression. Cancer Chemother Pharmacol; 2009 Mar;63(4):605-13
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  • [Title] Hydralazine inhibits human cervical cancer cell growth in vitro in association with APC demethylation and re-expression.
  • PURPOSE: The tumor suppressor adenomatous polyposis coli (APC) is frequently silenced by promoter hypermethylation in human cervical cancer.
  • Clinically, it has been approved that DNA methylation inhibitors, such as 5-aza-2'-deoxycytidine (5-Aza-dC), can reverse APC promoter methylation, but widespread clinical use of these inhibitors is limited by their toxicity and instability in aqueous solution.
  • The purpose of this study was to evaluate the effects of hydralazine on APC reactivation and the inhibition of human cervical cancer cells in vitro.
  • METHODS: Expression of APC gene, and methylation status were analyzed by RT-PCR, quantitative real time RT-PCR, and methylation-specific PCR methods. beta-Catenin protein that correlates closely with APC was detected by immunohistochemistry method after treatment with hydralazine.
  • RESULTS: Methylated APC was not expressed in HeLa cell, hemimethylated APC was expressed in CaSki cells, and unmethylated APC was expressed normally in SiHa cells.
  • Hydralazine induces APC expression and promotes demethylation in HeLa and CaSki cells.
  • After treatment with 40 mumol/L hydralazine for 72 h, growth inhibitive rates (%) of HeLa, CaSki, and SiHa cell lines were 52.12 +/- 3.78, 44.31 +/- 2.59, and 47.73 +/- 4.73, respectively.
  • The expression of APC mRNA in HeLa, CaSki, and SiHa cell lines increased 10.35-, 11.40-, and 0.73-fold, respectively.
  • The expression of beta-catenin protein in the cell membrane was observed after the treatment with hydralazine.
  • CONCLUSIONS: Hydralazine, an effective inhibitor of APC methylation and promoter of APC re-expression, can inhibit cell growth in human cervical cancer in vitro and be potentially used for the clinical treatment of human cervical cancer.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / genetics. Antihypertensive Agents / pharmacology. Cell Proliferation / drug effects. DNA Methylation. Hydralazine / pharmacology. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoenzyme Techniques. Promoter Regions, Genetic / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. S Phase / drug effects. beta Catenin / metabolism


93. Jacoby RF, Cole CE, Tutsch K, Newton MA, Kelloff G, Hawk ET, Lubet RA: Chemopreventive efficacy of combined piroxicam and difluoromethylornithine treatment of Apc mutant Min mouse adenomas, and selective toxicity against Apc mutant embryos. Cancer Res; 2000 Apr 1;60(7):1864-70
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  • [Title] Chemopreventive efficacy of combined piroxicam and difluoromethylornithine treatment of Apc mutant Min mouse adenomas, and selective toxicity against Apc mutant embryos.
  • Genetic knockout or pharmacological inhibition of cyclooxygenase-2 decreases the number and size of adenomas in mouse models of familial adenomatous polyposis.
  • Epidemiological and clinical studies in humans indicate that the entire class of nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit both COX-1 and COX-2 enzymes are promising colon cancer chemopreventive agents.
  • We used the Apc mutant Min mouse model to test combinations of agents that might maximize preventive benefit with minimal toxicity because they act via different mechanisms.
  • Min mice (n = 144) were exposed to low doses of the nonselective COX inhibitor piroxicam and the ornithine decarboxylase (ODC) inhibitor difluoromethylornithine (DFMO), beginning at the time they were weaned and continuing throughout the duration of the experiment.
  • Piroxicam at 12, 25, and 50 ppm in the diet caused dose-dependent decreases in the number of tumors in the middle and distal portions of the small intestine.
  • This decrease in tumor multiplicity was associated with a striking decrease in the size of those tumors that did grow out.
  • In contrast, none of the doses of piroxicam alone decreased tumor multiplicity in the proximal portion of the intestine (duodenum).
  • Exposure to DFMO (0.5 or 1.0% in water) caused a dose-dependent decrease in tumor multiplicity in the middle and distal portions of the small intestine.
  • However, this decreased multiplicity was not associated with a striking decrease in the size of the tumors.
  • Combined treatment of mice with piroxicam plus DFMO was much more effective than either agent alone and resulted in a significant number of mice totally free of any intestinal adenomas (P < 0.001), in contrast to the 100% incidence and high multiplicity in control Min mice.
  • In addition to this profound effectiveness in reducing tumor number, the few residual tumors in mice treated with the combined drugs were markedly smaller in size than tumors that arose from control Min mice.
  • These experiments suggest that selective COX-2 inhibition combined with ODC inhibition is a very promising approach for colon cancer prevention.
  • These COX-2 and ODC inhibitor drugs were not overtly toxic at the doses used when administered to mice after weaning.
  • However, when treatment was begun in utero, the Mendelian expected progeny ratio of 1:1 that we routinely obtained in untreated control litters was no longer observed.
  • Apc(min)/+ progeny of pregnant dams treated with piroxicam and/or DFMO were reduced in number and their ratio to Apc+/+ progeny was decreased to approximately 0.28:1.
  • Thus, these agents are effective against adenomas that have homozygous mutation of the APC gene and also select against fetuses bearing a heterozygous mutation in the APC gene.
  • [MeSH-major] Adenoma / prevention & control. Anticarcinogenic Agents / therapeutic use. Cyclooxygenase Inhibitors / therapeutic use. Eflornithine / therapeutic use. Eflornithine / toxicity. Genes, APC. Intestinal Neoplasms / prevention & control. Piroxicam / therapeutic use. Piroxicam / toxicity
  • [MeSH-minor] Animals. Cyclooxygenase 1. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Drug Therapy, Combination. Embryo, Mammalian / drug effects. Female. Isoenzymes / metabolism. Male. Membrane Proteins. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Mutant Strains. Ornithine Decarboxylase Inhibitors. Pregnancy. Prostaglandin-Endoperoxide Synthases / metabolism

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  • (PMID = 10766173.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01 CN 65122
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Ornithine Decarboxylase Inhibitors; 13T4O6VMAM / Piroxicam; 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; ZQN1G5V6SR / Eflornithine
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94. Oikarinen SI, Pajari A, Mutanen M: Chemopreventive activity of crude hydroxsymatairesinol (HMR) extract in Apc(Min) mice. Cancer Lett; 2000 Dec 20;161(2):253-8
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  • [Title] Chemopreventive activity of crude hydroxsymatairesinol (HMR) extract in Apc(Min) mice.
  • We studied the effects of a lignan, hydroxymatairesinol (HMR), and rye bran on intestinal tumor development in adenomatous polyposis colimultiple intestinal neoplasia (Apc)(Min) mice.
  • HMR showed a strong chemopreventive effect in this animal model.
  • The mean number of adenomas in the small intestine was significantly lower (26.
  • HMR resulted in normalization of beta-catenin levels in adenoma tissue, indicating that HMR mediates its chemopreventive effect through the Apc-beta-catenin pathway.
  • In the cytosolic fraction, beta-catenin level in adenoma tissue was significantly elevated (P=0.008-0.013) in all the diet groups as compared with that of the surrounding mucosa.
  • In the nuclear fraction, beta-catenin in the inulin (3.15+/-2.9 relative units) and inulin/rye (5.17+/-6.94 relative units) groups was also significantly higher (P=0.003-0.009) in the adenoma tissue when compared with the surrounding mucosa (0.5+/-0.5 and 0.35+/-0.39 relative units).
  • However, HMR was able to restore nuclear beta-catenin level of the adenoma tissue (0.41+/-0.25 relative units) to the level found in the surrounding mucosa (0.36+/-0.28 relative units).
  • [MeSH-major] Furans / pharmacology. Intestinal Neoplasms / prevention & control. Lignans / pharmacology. Trans-Activators
  • [MeSH-minor] Adenoma / metabolism. Adenoma / prevention & control. Adenomatous Polyposis Coli / drug therapy. Adenomatous Polyposis Coli / metabolism. Animals. Body Weight / drug effects. Cell Nucleus / metabolism. Cytoskeletal Proteins / biosynthesis. Cytosol / metabolism. Intestinal Mucosa / metabolism. Intestine, Small / pathology. Inulin / pharmacology. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. Neoplasms, Experimental. Plant Extracts / pharmacology. Secale. beta Catenin

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  • (PMID = 11090976.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / Cytoskeletal Proteins; 0 / Furans; 0 / Lignans; 0 / Plant Extracts; 0 / Trans-Activators; 0 / beta Catenin; 9005-80-5 / Inulin
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95. Ikeda S: [Therapeutic strategy for familial amyloid polyneuropathy (FAP)]. Rinsho Shinkeigaku; 2009 Nov;49(11):953-5
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  • [Title] [Therapeutic strategy for familial amyloid polyneuropathy (FAP)].
  • Familial amyloid polyneuropathy (FAP) was long considered to be an incurable disease, but a new therapeutic approach was developed 15 years ago.
  • As the liver produces most of the transthyretin (TTR) in serum, it was assumed that the replacement of a liver expressing an abnormal TTR gene should stop the production of the variant TTR, the serum amyloid precursor in FAP.
  • Until now about 1,500 FAP patients underwent liver transplantation, and the 10-year-survival rate is about 77%.
  • After operation the progression of FAP symptoms certainly stopped, and patients who were in an early stage of the disease and underwent successful operations showed considerable improvement in their quality of life.
  • Electrophysiological study of peripheral nerve function has demonstrated that liver transplantation can halt the progression of peripheral neuropathy in FAP patients, and histopathological regression of amyloid deposits was seen on the patients with long post-transplatation courses.
  • Pharmacological therapies have been considered for FAP patients and among them, diflunisal, one of non-steroidal antiinflammatory drugs, is very promising.
  • TTR tetramer dissociation is an initial step for the process of TTR-derived amyloid fibril formation associated with FAP and diflinisal can inhibit this process by stabilization of the TTR tetramer.
  • Clinical trial of this drug for FAP patients is now going worldwide.
  • [MeSH-major] Amyloid Neuropathies, Familial / therapy. Liver Transplantation

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  • (PMID = 20030258.001).
  • [ISSN] 0009-918X
  • [Journal-full-title] Rinshō shinkeigaku = Clinical neurology
  • [ISO-abbreviation] Rinsho Shinkeigaku
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amyloid; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Prealbumin; 7C546U4DEN / Diflunisal
  • [Number-of-references] 15
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96. Nakamura K, Yamaguchi T, Sudo K, Ishihara T, Saisho H: [Combination chemotherapy with gemcitabine and S-1 for advanced pancreatic cancer]. Gan To Kagaku Ryoho; 2006 Jun;33 Suppl 1:219-23
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  • [Title] [Combination chemotherapy with gemcitabine and S-1 for advanced pancreatic cancer].
  • The five-year survival rate is still poor at less than 10%, because it is commonly considered to be linked to a high incidence of distant metastasis even at the initial diagnosis as well as to the tumor's resistance to anticancer agents.
  • Although gemcitabine has been the most widely used chemotherapeutic agent in patients with advanced pancreatic cancer (APC), gemcitabine monotherapy has obvious limitations.
  • Therefore, various combinations with other agents have been investigated to improving the survival of patients with APC.
  • Under these circumstances, we conducted a phase I /II trial of gemcitabine with S-1, an oral fluorouracil derivative, to determine the maximum tolerated dose and to evaluate the activity and toxicity of such a combination in patients with APC.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Aged. Anorexia / chemically induced. Deoxycytidine / administration & dosage. Deoxycytidine / adverse effects. Deoxycytidine / analogs & derivatives. Drug Administration Schedule. Drug Combinations. Humans. Maximum Tolerated Dose. Middle Aged. Nausea / chemically induced. Oxonic Acid / administration & dosage. Oxonic Acid / adverse effects. Survival Rate. Tegafur / administration & dosage. Tegafur / adverse effects. Thrombocytopenia / chemically induced

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  • (PMID = 16898006.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
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97. Loeffler M, Krüger JA, Niethammer AG, Reisfeld RA: Targeting tumor-associated fibroblasts improves cancer chemotherapy by increasing intratumoral drug uptake. J Clin Invest; 2006 Jul;116(7):1955-62
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  • [Title] Targeting tumor-associated fibroblasts improves cancer chemotherapy by increasing intratumoral drug uptake.
  • Tumor-associated fibroblasts are key regulators of tumorigenesis.
  • These cells are also the primary source of collagen type I, which contributes to decreased chemotherapeutic drug uptake in tumors and plays a significant role in regulating tumor sensitivity to a variety of chemotherapies.
  • To specifically kill tumor-associated fibroblasts, we constructed an oral DNA vaccine targeting fibroblast activation protein (FAP), which is specifically overexpressed by fibroblasts in the tumor stroma.
  • Through CD8+ T cell-mediated killing of tumor-associated fibroblasts, our vaccine successfully suppressed primary tumor cell growth and metastasis of multidrug-resistant murine colon and breast carcinoma.
  • Furthermore, tumor tissue of FAP-vaccinated mice revealed markedly decreased collagen type I expression and up to 70% greater uptake of chemotherapeutic drugs.
  • Most importantly, pFap-vaccinated mice treated with chemotherapy showed a 3-fold prolongation in lifespan and marked suppression of tumor growth, with 50% of the animals completely rejecting a tumor cell challenge.

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  • (PMID = 16794736.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA083856; United States / NCI NIH HHS / CA / CA83856
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Collagen Type I; 0 / Membrane Proteins; 0 / Recombinant Fusion Proteins; 0 / Vaccines, DNA; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC1481657
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98. Kosugi S, Kanda T, Nakagawa S, Ohashi M, Nishimaki T, Hatakeyama K: Efficacy and toxicity of fluorouracil, doxorubicin, and cisplatin/nedaplatin treatment as neoadjuvant chemotherapy for advanced esophageal carcinoma. Scand J Gastroenterol; 2005 Aug;40(8):886-92
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  • [Title] Efficacy and toxicity of fluorouracil, doxorubicin, and cisplatin/nedaplatin treatment as neoadjuvant chemotherapy for advanced esophageal carcinoma.
  • OBJECTIVE: Patients with advanced esophageal carcinoma including clinical T4 tumor, extensive lymph node metastasis, or intramural metastasis have a dismal prognosis, despite recent multimodality treatments.
  • The aim of this study was to evaluate the efficacy and toxicity of neoadjuvant chemotherapy using fluorouracil, doxorubicin, and cisplatin or nedaplatin (FAP/N) in these patients.
  • The first 9 patients received 600 mg/m2 fluorouracil on days 1-7 and days 29-35, and 30 mg/m2 doxorubicin and 60 mg/m2 cisplatin on days 1 and 29 (FAP).
  • The next 17 patients received modified FAP, in which 50 mg/m2 nedaplatin was given instead of cisplatin (FAN).
  • RESULTS: Grade 3 or 4 toxicities developed in 6 patients (23.1%) during chemotherapy, but there was no discontinuation of treatment.
  • The 1-year survival rates of 26 patients, 21 patients with resectable tumor, 16 with R0 resection, and 12 clinical responders, were 31.3%, 32.1%, 33.3%, and 45.5%, respectively, each with a median survival time of 9 months.
  • The median progression-free survival time of 26 patients was 6 months; in 16 patients with R0 resection progression-free survival was 6.5 months.
  • There was no correlation between the recurrence pattern and tumor spread before treatment.
  • CONCLUSIONS: FAP/N was found to have acceptable toxicities and the ability to control locoregional tumors, but made little contribution to patient survival.
  • The efficacy of this treatment for patients with advanced esophageal carcinoma, however, may not yet be apparent.
  • [MeSH-major] Carcinoma, Squamous Cell / therapy. Cisplatin. Doxorubicin. Esophageal Neoplasms / therapy. Esophagectomy. Fluorouracil. Organoplatinum Compounds
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Disease-Free Survival. Follow-Up Studies. Humans. Male. Middle Aged. Neoadjuvant Therapy. Neoplasm Recurrence, Local / mortality. Neoplasm Staging. Prospective Studies. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 16170897.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 80168379AG / Doxorubicin; 8UQ3W6JXAN / nedaplatin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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99. Suzuki T, Miura A, Kato T, Izumi Y, Monma K, Kawano T: [Usefulness of induction chemotherapy followed by chemo-radiotherapy for patients with advanced cervical esophageal cancer]. Gan To Kagaku Ryoho; 2010 Jan;37(1):71-5
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  • [Title] [Usefulness of induction chemotherapy followed by chemo-radiotherapy for patients with advanced cervical esophageal cancer].
  • It is reported that induction chemotherapy (ICT) followed by concurrent chemoradiotherapy (CRT) is useful.
  • The regimen of ICT was FAP therapy (fluorouracil 1,000 mg/day and cisplatin 20mg/day on days 1-5, and doxorubicin 50mg/day on day 1) every 4 weeks.
  • After 2-4 courses of FAP therapy, low-dose FP-CRT (fluorouracil 200mg/24 hours/day and cisplatin 5mg/day with radiation of 60-66 Gy, 2 Gy/day) were given.
  • The therapeutic effect of ICT and CRT was suggested to be useful for patients with advanced cervical esophageal cancer because it was performed safely with no serious adverse effect and the outcome of ICT predicted the effect of the subsequent CRT.
  • [MeSH-major] Esophageal Neoplasms / therapy
  • [MeSH-minor] Aged. Antibiotics, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Combined Modality Therapy. Doxorubicin / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Male. Middle Aged

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  • (PMID = 20087035.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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100. Dvory-Sobol H, Sagiv E, Liberman E, Kazanov D, Arber N: Suppression of gastric cancer cell growth by targeting the beta-catenin/T-cell factor pathway. Cancer; 2007 Jan 15;109(2):188-97
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  • BACKGROUND: Functional activation of beta-catenin/T-cell factor (Tcf) signaling plays an important role in the early events of carcinogenesis.
  • Recently, it was demonstrated that adenomatous polyposis coli or beta-catenin genes are mutated frequently in gastric cancer cells.
  • METHODS: 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) was used selectively to target gastric cancer cells (AGS) that posses an active beta-catenin/Tcf pathway.
  • Cell viability was measured by methylene blue assay, protein expression was measured by Western blot analysis, and cell cycle and apoptosis were evaluated by fluorescent-activated cell sorter analysis.
  • RESULTS.: The TOP-PUMA adenovirus inhibited AGS cell growth in a dose- and time-dependent fashion.
  • Growth inhibition was associated with the up-regulation of PUMA expression and the induction of apoptosis.
  • Chemotherapy synergistically enhanced the killing effect of AdTOP-PUMA.
  • CONCLUSIONS: Selective targeting of gastric cancer cells with the activated beta-catenin pathway may be a novel and effective therapy in gastric cancer.
  • Combination of this gene-therapy approach with standard therapy may improve efficacy and reduce toxicity.
  • [MeSH-minor] Adenoviridae / genetics. Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Apoptosis / genetics. Apoptosis / physiology. Apoptosis Regulatory Proteins / genetics. Apoptosis Regulatory Proteins / metabolism. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / genetics. Cell Survival / physiology. Doxorubicin / pharmacology. Flow Cytometry. Fluorouracil / pharmacology. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. HCT116 Cells. Humans. Microscopy, Fluorescence. Paclitaxel / pharmacology. Plasmids / genetics. Promoter Regions, Genetic / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Stomach Neoplasms / genetics. Stomach Neoplasms / pathology. Stomach Neoplasms / physiopathology

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  • (PMID = 17149756.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Apoptosis Regulatory Proteins; 0 / BBC3 protein, human; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF Transcription Factors; 0 / beta Catenin; 147336-22-9 / Green Fluorescent Proteins; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel; U3P01618RT / Fluorouracil
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