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1. Latruffe N, Delmas D, Jannin B, Cherkaoui Malki M, Passilly-Degrace P, Berlot JP: Molecular analysis on the chemopreventive properties of resveratrol, a plant polyphenol microcomponent. Int J Mol Med; 2002 Dec;10(6):755-60
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  • The biochemical mechanism by which resveratrol inhibits cell proliferation was provided by studies in numerous human cell lines including our work in hepatoblastoma HepG2 and colorectal tumor SW480 cells.
  • The results show that resveratrol strongly inhibits cell proliferation at the micromolar range in a time- and dose-dependent manner.
  • Our study reports a higher uptake of resveratrol in the human hepatic derived HepG2 cells than in colorectal derived SW480 cells.
  • In contrast, resveratrol is conjugated in these cells and derivatives are released in large amounts in the cell medium.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Cell Division / drug effects. Neoplasms / prevention & control. Stilbenes / pharmacology
  • [MeSH-minor] Colonic Neoplasms / drug therapy. Flow Cytometry. Genistein / pharmacology. Hepatoblastoma / drug therapy. Humans. In Vitro Techniques. S Phase / drug effects. Tumor Cells, Cultured

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  • (PMID = 12430003.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Stilbenes; DH2M523P0H / Genistein; Q369O8926L / resveratrol
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2. Raida M, Schwabe W, Häusler P, Van Kuilenburg AB, Van Gennip AH, Behnke D, Höffken K: Prevalence of a common point mutation in the dihydropyrimidine dehydrogenase (DPD) gene within the 5'-splice donor site of intron 14 in patients with severe 5-fluorouracil (5-FU)- related toxicity compared with controls. Clin Cancer Res; 2001 Sep;7(9):2832-9
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  • We developed a reverse transcription-PCR-based assay suitable for routine identification of the exon 14-skipping mutation and screened a control cohort of 851 Caucasian individuals as well as a cohort of 25 cancer patients reported by their physicians to have suffered from WHO grades 3-4 toxicity upon 5-FU chemotherapy.
  • Within the control cohort, in total, eight heterozygotes were detected (0.94%): one heterozygote in 51 healthy donors, (1.96%); five heterozygotes in 572 hospital patients (0.87%); and two heterozygotes in 228 colorectal tumor patients (0.88%).
  • We conclude that carriers of the DPD exon 14-skipping mutation are at significantly increased risk to experience life-threatening myelosuppression upon 5-FU treatment, even when the allelic status is heterozygous.
  • These data lead us to suggest routine testing for the exon 14-skipping mutation before 5-FU treatment.
  • [MeSH-minor] Adult. Aged. Alternative Splicing / genetics. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Breast Neoplasms / genetics. Colonic Neoplasms / drug therapy. Colonic Neoplasms / enzymology. Colonic Neoplasms / genetics. DNA, Complementary / genetics. Diarrhea / chemically induced. Diarrhea / pathology. Dihydrouracil Dehydrogenase (NADP). Exons / genetics. Female. Gene Frequency. Genotype. Heterozygote. Homozygote. Humans. Leukopenia / chemically induced. Leukopenia / pathology. Male. Middle Aged. Point Mutation. Rectal Neoplasms / drug therapy. Rectal Neoplasms / enzymology. Rectal Neoplasms / genetics. Reverse Transcriptase Polymerase Chain Reaction. Severity of Illness Index. Stomach Neoplasms / drug therapy. Stomach Neoplasms / enzymology. Stomach Neoplasms / genetics. Stomatitis / chemically induced. Stomatitis / pathology. Thrombocytopenia / chemically induced. Thrombocytopenia / pathology

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  • [CommentIn] Clin Cancer Res. 2002 May;8(5):1314; author reply 1315-6 [12006555.001]
  • (PMID = 11555601.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Complementary; EC 1.- / Oxidoreductases; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); U3P01618RT / Fluorouracil
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3. Capussotti L, Vigano' L, Ferrero A, Lo Tesoriere R, Ribero D, Polastri R: Timing of resection of liver metastases synchronous to colorectal tumor: proposal of prognosis-based decisional model. Ann Surg Oncol; 2007 Mar;14(3):1143-50
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  • [Title] Timing of resection of liver metastases synchronous to colorectal tumor: proposal of prognosis-based decisional model.
  • BACKGROUND: Timing of hepatectomy for synchronous metastases of colorectal cancer is still debated.
  • Patients with more than three metastases had a significantly worse survival in group A than in group B (3-year survival, 15.0% vs. 34.3%, P = .007); similarly, borderline significant difference was encountered in patients with T4 primary tumor (3-year survival, 16.7% vs. 60%, P = .064) CONCLUSIONS: Patients with liver metastases synchronous with colorectal cancer with T4 primary tumor, metastasis infiltration of neighboring structures, and especially with more than three metastases should receive neoadjuvant chemotherapy before liver resection.
  • [MeSH-major] Colorectal Neoplasms / surgery. Hepatectomy. Liver Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Middle Aged. Patient Selection. Prognosis. Retrospective Studies. Survival Rate. Time Factors. Treatment Outcome

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  • [CommentIn] Ann Surg Oncol. 2007 Sep;14(9):2435-6 [17562115.001]
  • (PMID = 17200913.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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4. Haase E, Yoo D, Sugarbaker PH: Management of appendiceal pseudomyxoma peritonei diagnosed during pregnancy. World J Surg Oncol; 2009;7:48
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  • The most common types encountered during pregnancy are cervical, breast and ovarian.
  • Epithelial tumors of the appendix on the other hand are rare and account for only approximately 1% of all colorectal neoplasms; the occurrence of this neoplasm during pregnancy is extremely rare.
  • CASE PRESENTATION: The medical history of a 30 year old woman diagnosed at 17 weeks gestation with an appendiceal mucinous tumor with large volume pseudomyxoma peritonei was presented.
  • At 2 1/2 weeks postpartum the patient underwent extensive cytoreductive surgery and intraperitoneal chemotherapy.
  • She remains disease-free 5 years after her initial diagnosis.
  • A literature review of this clinical situation and a discussion of treatment plans were presented.
  • CONCLUSION: The management of an appendiceal tumor with pseudomyxoma peritonei diagnosed during pregnancy requires full knowledge of the natural history of this disease to achieve a balance of concern for maternal survival and fetal health.
  • [MeSH-major] Appendiceal Neoplasms / surgery. Peritoneal Neoplasms / surgery. Pregnancy Complications, Neoplastic / surgery. Pseudomyxoma Peritonei / surgery

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  • (PMID = 19454019.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 18
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5. Lièvre A, Chapusot C, Bouvier AM, Zinzindohoué F, Piard F, Roignot P, Arnould L, Beaune P, Faivre J, Laurent-Puig P: Clinical value of mitochondrial mutations in colorectal cancer. J Clin Oncol; 2005 May 20;23(15):3517-25
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  • [Title] Clinical value of mitochondrial mutations in colorectal cancer.
  • PURPOSE: Prognostic factors that could select high-risk recurrence colorectal cancer patients and predict chemosensitivity are needed.
  • Since mutations of mitochondrial DNA (mtDNA) have been described in different types of cancers and since they may play a role in response to anticancer agents, we investigated in a population-based series of colorectal cancer patients the clinical value of mtDNA mutations.
  • RESULTS: D-loop mutations were found in 38.3% of the tumors.
  • The 3-year survival rate was 53.5% in patients with D-loop mutation versus 62.1% in patients without (P = .05).
  • After adjustment for age, stage, and microsatellite instability status, the relative risk of death in patients with D-loop mutation was 1.40 (95% CI, 1.02 to 1.93; P = .034) as compared with those without.
  • In stage III colon cancers, adjuvant chemotherapy was beneficial only for patients without D-loop mutation (3-year survival, 78.3% v 45.4%, P < .02).
  • In those with D-loop mutation who received adjuvant chemotherapy, the relative risk of death was 4.30 (95% CI, 1.23 to 15.00; P < .02).
  • CONCLUSION: The D-loop region is a hotspot for somatic mutations in colorectal tumors.
  • Moreover, presence of tumor D-loop mutation appears to be a factor of poor prognosis in colorectal patients and a factor of resistance to fluorouracil-based adjuvant chemotherapy in stage III colon cancers.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / genetics. DNA, Mitochondrial / genetics. Mutation
  • [MeSH-minor] Base Sequence. Case-Control Studies. Confidence Intervals. DNA Mutational Analysis. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Molecular Sequence Data. Multivariate Analysis. Pharmacogenetics. Polymerase Chain Reaction / methods. Prognosis. Proportional Hazards Models. Reference Values. Sampling Studies. Sensitivity and Specificity. Survival Analysis. Tissue Culture Techniques. Treatment Outcome

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  • (PMID = 15908662.001).
  • [ISSN] 0732-183X
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Mitochondrial
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6. Wendum D, Masliah J, Trugnan G, Fléjou JF: Cyclooxygenase-2 and its role in colorectal cancer development. Virchows Arch; 2004 Oct;445(4):327-33
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  • [Title] Cyclooxygenase-2 and its role in colorectal cancer development.
  • Cyclooxygenase 2 (COX-2), also called prostaglandin endoperoxide synthase 2, is involved in colorectal tumor development.
  • This review deals with particular questions raised in this field such as the mechanisms of COX-2 related tumor promotion, the role of the different types of cells (epithelial and interstitial) expressing COX-2, the factors that trigger COX-2 induction, and the clinical potential of selective COX-2 inhibitors to treat or prevent colorectal tumors.
  • Several mechanisms of COX-2 related tumor promotion have been identified.
  • COX-2 expression has been demonstrated in epithelial cells of colorectal cancers and adenomas and also in interstitial cells.
  • COX-2 expression in these interstitial cells participates in tumor development.
  • Finally, selective COX-2 inhibitors may be effective in preventing or treating colorectal adenomas or carcinomas.
  • [MeSH-major] Colorectal Neoplasms / etiology. Isoenzymes / physiology. Prostaglandin-Endoperoxide Synthases / physiology
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / therapeutic use. Dinoprostone / biosynthesis. Humans. Membrane Proteins

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  • (PMID = 15340847.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
  • [Number-of-references] 80
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7. Lin JT, Wang WS, Yen CC, Liu JH, Yang MH, Chao TC, Chen PM, Chiou TJ: Outcome of colorectal carcinoma in patients under 40 years of age. J Gastroenterol Hepatol; 2005 Jun;20(6):900-5
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  • [Title] Outcome of colorectal carcinoma in patients under 40 years of age.
  • AIMS: Colorectal carcinoma in patients under 40 years of age usually has a poor prognosis.
  • Controversies still exist regarding the features and the prognosis of colorectal cancer in young patients.
  • METHODS: The records of 45 patients with histologically confirmed colorectal carcinoma treated between 1992 and 2002 at the Division of Oncology at Taipei Veterans General Hospital were reviewed.
  • The relevance of sex, duration of symptoms, tumor site, histological type, lymph node involvement, Karnofsky performance status (KPS), carcinoembryonic antigen (CEA) and lactate dehydrogenase (LDH) levels at the diagnosis and tumor stage to overall survival (OS) were determined by univariate analysis, and their independent significance were tested by multivariate analysis.
  • RESULTS: Most patients presented with an advanced tumor stage (24% Dukes' C and 66% Dukes' D).
  • Colon carcinoma constituted 76% of the colorectal tumors.
  • Two patients were found to have colon carcinoma during pregnancy.
  • With aggressive treatment, patients with early stage carcinoma achieved longer survival.
  • Adjuvant chemotherapy with irinotecan/5-fluorouracil-based chemotherapy seemed to improve the OS in such patients, though the OS was still poorer than in patients with early stage tumors.
  • In univariate analysis, KPS (P = 0.0001), lymph node involvement (P = 0.0024), CEA (P = 0.0423) and LDH levels (P = 0.0126) at the diagnosis and tumor stage (P = 0.0122) proved to be significant predictors of overall survival.
  • Multivariate analyses revealed that KPS > or =70% (P = 0.007) and normal LDH levels at diagnosis (P = 0.004) were predictive of overall survival in this population.
  • CONCLUSIONS: The present study shows that performance status and preoperative LDH levels were the major determinants for survival in patients with colorectal carcinoma under 40 years of age and the present series also suggests that surgical resection of metastatic colorectal carcinoma followed by adjuvant chemotherapy might be beneficial in certain patients.
  • The data also suggests that current treatment modalities for young patients with advanced colorectal cancer might not be effective and more effective therapeutic regimens might be needed.
  • Thus, it is important for surgeons to recognize the potential for colorectal cancer in young patients and to take an aggressive approach to the diagnosis and early treatment of the disease.
  • [MeSH-major] Adenocarcinoma / mortality. Colorectal Neoplasms / mortality
  • [MeSH-minor] Adolescent. Age Factors. Carcinoembryonic Antigen / blood. Child. Female. Follow-Up Studies. Humans. Male. Neoplasm Staging. Pregnancy. Pregnancy Complications, Neoplastic / blood. Pregnancy Complications, Neoplastic / mortality. Pregnancy Complications, Neoplastic / pathology. Prognosis. Retrospective Studies. Risk Factors. Sex Factors. Survival Rate / trends. Taiwan / epidemiology

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  • [Copyright] (c) 2005 Blackwell Publishing Asia Pty Ltd.
  • (PMID = 15946138.001).
  • [ISSN] 0815-9319
  • [Journal-full-title] Journal of gastroenterology and hepatology
  • [ISO-abbreviation] J. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen
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8. Umekita N, Tanaka S, Abe H, Kitamura M: [Thymidylate synthase and dihydropyrimidine dehydrogenase activity in a metastatic liver tumor from colorectal cancer]. Gan To Kagaku Ryoho; 2000 Oct;27(12):1883-5
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  • [Title] [Thymidylate synthase and dihydropyrimidine dehydrogenase activity in a metastatic liver tumor from colorectal cancer].
  • The value of thymidylate synthase (TS) and dihydropyrimidine dehydrogenase (DPD) activity in metastatic liver tumor from colorectal cancer as predictive parameters for hepatic artery infusion (HAI) chemotherapy with 5-FU was investigated.
  • We measured TS and DPD activity in normal colonic mucosa, primary colon tumor, and metastatic liver tumor in these patients.
  • The TS (pmol/g-tissue) of primary tumor, metastatic tumor, and normal colonic mucosa was 6.6 +/- 1.40 (mean +/- SE), 3.2 +/- 0.83 and 2.5 +/- 0.83 respectively.
  • The DPD (pmol/min/mg/protein) of primary tumor, metastatic tumor, and normal colonic mucosa was 31.7 +/- 5.49, 82.1 +/- 12.5 and 50.6 +/- 8.46, respectively.
  • It is suggested that 5-FU catabolism in metastatic liver tumor was increased, and DPD activity may be a valuable predictive marker for tumor response to HAI therapy.
  • [MeSH-major] Colorectal Neoplasms / pathology. Liver Neoplasms / enzymology. Liver Neoplasms / secondary. Nucleoside-Phosphate Kinase / metabolism. Oxidoreductases / metabolism
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Colon / enzymology. Dihydrouracil Dehydrogenase (NADP). Fluorouracil / therapeutic use. Humans. Infusions, Intra-Arterial

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  • (PMID = 11086436.001).
  • [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 / Antimetabolites, Antineoplastic; EC 1.- / Oxidoreductases; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.7.4.4 / Nucleoside-Phosphate Kinase; EC 2.7.4.9 / dTMP kinase; U3P01618RT / Fluorouracil
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9. Hyde A, Fontaine D, Stuckless S, Green R, Pollett A, Simms M, Sipahimalani P, Parfrey P, Younghusband B: A histology-based model for predicting microsatellite instability in colorectal cancers. Am J Surg Pathol; 2010 Dec;34(12):1820-9
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  • [Title] A histology-based model for predicting microsatellite instability in colorectal cancers.
  • Identifying colorectal cancers (CRCs) with high levels of microsatellite instability (MSI-H) is clinically important.
  • MSI-H is a positive prognostic marker for CRC, a predictive marker for resistance to standard 5-fluorouracil-based adjuvant chemotherapy, and an important feature for identifying individuals and families with Lynch syndrome.
  • We tested 2 existing models used to predict MSI-H tumors, (1) Revised Bethesda Guidelines and (2) MsPath, in our population-based cohort of CRCs diagnosed less than 75 years from Newfoundland (N=710).
  • From this analysis, we developed a model for the prediction of MSI-H CRCs; Pathologic Role in Determination of Instability in Colorectal Tumors (PREDICT).
  • Tumor histology was a better predictor of MSI status than was personal and family history of cancer.
  • PREDICT included some new histology features, including peritumoral lymphocytic reaction and increased proportion of plasma cells in the tumor stroma.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Microsatellite Instability

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  • (PMID = 21107088.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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10. Herreros-Villanueva M, Muñiz P, García-Girón C, Cavia-Saiz M, del Corral MJ: TAp73 is one of the genes responsible for the lack of response to chemotherapy depending on B-Raf mutational status. J Transl Med; 2010;8:15
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  • [Title] TAp73 is one of the genes responsible for the lack of response to chemotherapy depending on B-Raf mutational status.
  • There is little research on the relationship between p73 gene transcription and its protein expression and the response to certain drugs such as oxaliplatin and cetuximab, which are drugs currently used in colorectal cancer.The purpose of this study was to evaluate the impact of TAp73 expression on oxaliplatin and cetuximab-based chemotherapy in colorectal cancer cell lines with different K-Ras and B-Raf mutational status.
  • METHODS: TAp73 was analyzed in three colorectal tumor cell lines HT-29, SW-480 and Caco-2. mRNA TAp73 was determined using Real time PCR; TAp73 protein by immunoblotting and cell viability was analyzed by the MTT method.
  • This was statistically significant and was also associated with higher cell viability after the treatment.
  • CONCLUSIONS: Here, for the first time we report, that there is a signaling loop between B-Raf activation and p73 function.Low expression of TAp73 in colorectal cancer cell lines with mutated B-Raf may be involved in the lack of response to oxaliplatin in monotherapy or combined with cetuximab.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colorectal Neoplasms. DNA-Binding Proteins / genetics. Mutation. Nuclear Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Cell Line, Tumor. Cetuximab. Humans. Organoplatinum Compounds / therapeutic use. RNA, Messenger / genetics. RNA, Messenger / metabolism. Signal Transduction / physiology

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  • (PMID = 20146801.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Organoplatinum Compounds; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73; 04ZR38536J / oxaliplatin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; PQX0D8J21J / Cetuximab
  • [Other-IDs] NLM/ PMC2841128
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11. Dylla SJ, Beviglia L, Park IK, Chartier C, Raval J, Ngan L, Pickell K, Aguilar J, Lazetic S, Smith-Berdan S, Clarke MF, Hoey T, Lewicki J, Gurney AL: Colorectal cancer stem cells are enriched in xenogeneic tumors following chemotherapy. PLoS One; 2008;3(6):e2428
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  • [Title] Colorectal cancer stem cells are enriched in xenogeneic tumors following chemotherapy.
  • BACKGROUND: Patients generally die of cancer after the failure of current therapies to eliminate residual disease.
  • A subpopulation of tumor cells, termed cancer stem cells (CSC), appears uniquely able to fuel the growth of phenotypically and histologically diverse tumors.
  • The subpopulation of human colorectal tumor cells with an ESA(+)CD44(+) phenotype are uniquely responsible for tumorigenesis and have the capacity to generate heterogeneous tumors in a xenograft setting (i.e. CoCSC).
  • We hypothesized that if non-tumorigenic cells are more susceptible to chemotherapeutic agents, then residual tumors might be expected to contain a higher frequency of CoCSC.
  • METHODS AND FINDINGS: Xenogeneic tumors initiated with CoCSC were allowed to reach approximately 400 mm(3), at which point mice were randomized and chemotherapeutic regimens involving cyclophosphamide or Irinotecan were initiated.
  • Data from individual tumor phenotypic analysis and serial transplants performed in limiting dilution show that residual tumors are enriched for cells with the CoCSC phenotype and have increased tumorigenic cell frequency.
  • Moreover, the inherent ability of residual CoCSC to generate tumors appears preserved.
  • CONCLUSIONS: CoCSC are enriched in colon tumors following chemotherapy and remain capable of rapidly regenerating tumors from which they originated.
  • By focusing on the biology of CoCSC, major resistance mechanisms to specific chemotherapeutic agents can be attributed to specific genes, thereby suggesting avenues for improving cancer therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Camptothecin / analogs & derivatives. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / pathology. Cyclophosphamide / therapeutic use. Neoplastic Stem Cells / cytology

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  • (PMID = 18560594.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7673326042 / irinotecan; 8N3DW7272P / Cyclophosphamide; EC 1.2.1.3 / Aldehyde Dehydrogenase; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC2413402
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12. Doi Y, Okada T, Matsumoto H, Ichihara M, Ishida T, Kiwada H: Combination therapy of metronomic S-1 dosing with oxaliplatin-containing polyethylene glycol-coated liposome improves antitumor activity in a murine colorectal tumor model. Cancer Sci; 2010 Nov;101(11):2470-5
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  • [Title] Combination therapy of metronomic S-1 dosing with oxaliplatin-containing polyethylene glycol-coated liposome improves antitumor activity in a murine colorectal tumor model.
  • Metronomic chemotherapy has been advocated recently as a novel chemotherapeutic regimen.
  • Polyethylene glycol (PEG)-coated liposomes are well known to accumulate in solid tumors by virtue of the highly permeable angiogenic blood vessels characteristic for growing tumor tissue, the so-called "enhanced permeability and retention (EPR) effect".
  • To expand the range of applications and investigate the clinical value of the combination strategy, the therapeutic benefit of metronomic S-1 dosing in combination with oxaliplatin (l-OHP)-containing PEG-coated liposomes was evaluated in a murine colon carcinoma-bearing mice model.
  • S-1 is an oral fluoropyrimidine formulation and metronomic S-1 dosing is a promising alternative to infused 5-FU in colorectal cancer therapy.
  • Therefore, the combination of S-1 with l-OHP may be an alternative to FOLFOX (infusional 5-FU/leucovorin (LV) in combination with l-OHP), which is a first-line therapeutic regimen of a colorectal carcinoma.
  • We confirmed that the synergistic antitumor effect is due to prolonged retention of l-OHP in the tumor on account of the PEG-coated liposomes, presumably via alteration of the tumor microenvironment caused by the metronomic S-1 treatment.
  • The combination regimen proposed here may be a breakthrough in treatment of intractable solid tumors and an alternative to FOLFOX in advanced colorectal cancer therapy with acceptable tolerance and preservation of quality of life (QOL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / drug therapy. Disease Models, Animal. Tumor Burden / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Combinations. Drug Synergism. Humans. Liposomes. Male. Mice. Mice, Inbred BALB C. Organoplatinum Compounds / administration & dosage. Oxonic Acid / administration & dosage. Polyethylene Glycols / chemistry. Tegafur / administration & dosage. Treatment Outcome

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  • [Copyright] © 2010 Japanese Cancer Association.
  • (PMID = 20731663.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Liposomes; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 30IQX730WE / Polyethylene Glycols; 5VT6420TIG / Oxonic Acid
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13. Medinger M, Steinbild S, Mross K: [Adjuvant and palliative anticancer treatment of colon carcinoma in 2004]. Praxis (Bern 1994); 2004 Sep 29;93(40):1633-44
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  • [Title] [Adjuvant and palliative anticancer treatment of colon carcinoma in 2004].
  • [Transliterated title] Die systemische Therapie des Kolonkarzinoms 2004.
  • This article reviews the available data regarding the acticity of postoperative adjuvant systemic therapy for colorectal cancer as first and second-line treatment in metastatic disease.
  • The efficacy of adjuvant treatment of patients with stage III colorectal cancer is well established.
  • The risk of relapse is low in stage II colon carcinoma and consequently the efficacy is relatively small compared to stage III.
  • New investigation indicate, Capecitabene has the potential to replace 5-FU/FS as standard treatment for patients with colon cancer.
  • In metastatic disease combination of 5-FU/folic acid plus CPT-11 or OXA are treatment of choice for the first-line therapy of metastatic colorectal carcinoma.
  • FOLFOX is high-dose intensity oxaliplatin added to the simplified bimonthly leucovorin and 5-fluorouracil regimen as second- line therapy for metastatic colorectal cancer.
  • New perspectives are novel chemotherapeutic and targeted agents in metastatic colorectal cancer: For the first time, there has been a targeted therapy shown convincingly to prolong survival for patients with unresectable metastatic colorectal cancer in a well-performed Phase III trial.
  • Results with bevacizumab should lead to rapid expansion of the number of strategies targeting tumour neovasculature.
  • Additionally, an antibody against the epidermal growth factor, cetuximab, has been shown to have both single-agent activity and the potential ability to partially reverse resistance to a chemotherapy drug.
  • These advancements, as well as data on other novel treatment agents that have been studied specifically in patients with colorectal neoplasms, are discussed in detail.
  • [MeSH-major] Colonic Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bevacizumab. Cetuximab. Chemotherapy, Adjuvant. Clinical Trials, Phase III as Topic. Colon / pathology. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / mortality. Colorectal Neoplasms / pathology. Colorectal Neoplasms / surgery. Combined Modality Therapy. Fluorouracil / administration & dosage. Fluorouracil / therapeutic use. Folic Acid / administration & dosage. Folic Acid / therapeutic use. Humans. Leucovorin / therapeutic use. Neoplasm Recurrence, Local. Neoplasm Staging. Organoplatinum Compounds. Palliative Care. Postoperative Care. Randomized Controlled Trials as Topic. Time Factors

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  • (PMID = 15495753.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antimetabolites, Antineoplastic; 0 / Organoplatinum Compounds; 2S9ZZM9Q9V / Bevacizumab; 935E97BOY8 / Folic Acid; PQX0D8J21J / Cetuximab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
  • [Number-of-references] 54
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14. Ishikawa H, Nakamura T, Kawano A, Gondo N, Sakai T: Chemoprevention of colorectal cancer in Japan: a brief introduction to current clinical trials. J Gastroenterol; 2009;44 Suppl 19:77-81
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  • [Title] Chemoprevention of colorectal cancer in Japan: a brief introduction to current clinical trials.
  • The rapidly increasing incidence of colorectal cancer in Japan poses a great challenge to researchers to develop preventive strategies against this disease.
  • Also, the Ministry of Health, Labour and Welfare of Japan recognizes the significance of cancer prevention studies, especially against colorectal cancer, including it as one of the pillars in the "Third Research Project on General Strategies against Cancer" and funding several large-scale projects.
  • Among them are two chemoprevention studies currently being performed: in patients with previous sporadic colorectal tumors (J-CAPP study) and in patients with familial adenomatous polyposis (J-FAPP study II).
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Aspirin / therapeutic use. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Chemoprevention / methods. Humans. Japan / epidemiology. Randomized Controlled Trials as Topic

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  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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15. McLornan DP, Barrett HL, Cummins R, McDermott U, McDowell C, Conlon SJ, Coyle VM, Van Schaeybroeck S, Wilson R, Kay EW, Longley DB, Johnston PG: Prognostic significance of TRAIL signaling molecules in stage II and III colorectal cancer. Clin Cancer Res; 2010 Jul 01;16(13):3442-51
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  • [Title] Prognostic significance of TRAIL signaling molecules in stage II and III colorectal cancer.
  • PURPOSE: We previously found that cellular FLICE-inhibitory protein (c-FLIP), caspase 8, and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (DR5) are major regulators of cell viability and chemotherapy-induced apoptosis in colorectal cancer.
  • In this study, we determined the prognostic significance of c-FLIP, caspase 8, TRAIL and DR5 expression in tissues from patients with stage II and III colorectal cancer.
  • EXPERIMENTAL DESIGN: Tissue microarrays were constructed from matched normal and tumor tissue derived from patients (n = 253) enrolled in a phase III trial of adjuvant 5-fluorouracil-based chemotherapy versus postoperative observation alone.
  • RESULTS: Colorectal tumors displayed significantly higher expression levels of c-FLIP (P < 0.001), caspase 8 (P = 0.01), and DR5 (P < 0.001), but lower levels of TRAIL (P < 0.001) compared with matched normal tissue.
  • In univariate analysis, higher TRAIL expression in the tumor was associated with worse overall survival (P = 0.026), with a trend to decreased relapse-free survival (RFS; P = 0.06), and higher tumor c-FLIP expression was associated with a significantly decreased RFS (P = 0.015).
  • Using multivariate predictive modeling for RFS in all patients and including all biomarkers, age, treatment, and stage, we found that the model was significant when the mean tumor c-FLIP expression score and disease stage were included (P < 0.001).
  • As regards overall survival, the overall model was predictive when both TRAIL expression and disease stage were included (P < 0.001).
  • CONCLUSIONS: High c-FLIP and TRAIL expression may be independent adverse prognostic markers in stage II and III colorectal cancer and might identify patients most at risk of relapse.
  • [MeSH-major] Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / metabolism. TNF-Related Apoptosis-Inducing Ligand / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism. Caspase 8 / metabolism. Chemotherapy, Adjuvant. Clinical Trials, Phase III as Topic. Eukaryotic Initiation Factor-3 / analysis. Female. Humans. Male. Middle Aged. Prognosis. Randomized Controlled Trials as Topic. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Signal Transduction

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  • (PMID = 20570920.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0600452; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / G0400302; United Kingdom / Cancer Research UK / / ; United Kingdom / Cancer Research UK / / A7402
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / EIF3A protein, human; 0 / Eukaryotic Initiation Factor-3; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 3.4.22.- / Caspase 8
  • [Other-IDs] NLM/ PMC2896551; NLM/ UKMS30270
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16. Taupin DR, Kinoshita K, Podolsky DK: Intestinal trefoil factor confers colonic epithelial resistance to apoptosis. Proc Natl Acad Sci U S A; 2000 Jan 18;97(2):799-804
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  • [Title] Intestinal trefoil factor confers colonic epithelial resistance to apoptosis.
  • Intestinal trefoil factor (ITF) is an essential regulator of colonic epithelial restitution, the rapid migration of colonocytes over mucosal wounds.
  • High levels of ITF are frequently present in colorectal cancers and derived cell lines.
  • Exogenous ITF also protected another human colonic carcinoma-derived cell line (HCT116) and a nontransformed rat intestinal epithelial cell line (IEC-6) from apoptosis.
  • These findings support a central role for ITF in the maintenance of intestinal mucosal continuity, and conversely demonstrate the potential for ITF expression to confer resistance of colorectal tumors to therapy.

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  • (PMID = 10639160.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P30 DK043351; United States / NIDDK NIH HHS / DK / R01 DK046906; United States / NIDDK NIH HHS / DK / DK 43351; United States / NIDDK NIH HHS / DK / DK 46906
  • [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 / Growth Substances; 0 / Mucins; 0 / Muscle Proteins; 0 / Neuropeptides; 0 / Peptides; 0 / Proto-Oncogene Proteins; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TFF3 protein, rat; 0 / Tumor Suppressor Protein p53; 146046-78-8 / trefoil factor; 63231-63-0 / RNA; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / 3-Phosphoinositide-Dependent Protein Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC15411
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17. Yanagisawa Y, Maruta F, Iinuma N, Ishizone S, Koide N, Nakayama J, Miyagawa S: Modified Irinotecan/5FU/Leucovorin therapy in advanced colorectal cancer and predicting therapeutic efficacy by expression of tumor-related enzymes. Scand J Gastroenterol; 2007 Apr;42(4):477-84
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  • [Title] Modified Irinotecan/5FU/Leucovorin therapy in advanced colorectal cancer and predicting therapeutic efficacy by expression of tumor-related enzymes.
  • OBJECTIVE: To evaluate the efficacy and safety of a regimen using Irinotecan, 5FU and Leucovorin for patients with advanced or recurrent colorectal cancer.
  • The mean survival time of all 21 patients was 15.7 months.
  • This regimen could be a valid option for patients with advanced colorectal cancer, especially those seeking a good QoL (quality of life) for the remainder of their lives.
  • We evaluated the expression of thymidylate synthase (TS), dihydropyrimidine dehydrogenase (DPD), thymidine phosphorylase (TP) and orotate phosphoribosyl transferase (OPRT) mRNAs, and sialyl Lewis X on formalin-fixed, paraffin-embedded colorectal tumor samples.
  • Expression of TS mRNA or sialyl Lewis X was negatively correlated with the response from chemotherapy.
  • Patients with low DPD mRNA expression in the tumor showed a significant longer survival than those with high expression.
  • CONCLUSIONS: Some predictive factors elucidated in this study could contribute to the progress of the tumor-biology based, individualized chemotherapy for colorectal cancer patients.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / enzymology
  • [MeSH-minor] Adult. Aged. Antigens, CD15 / analysis. Antigens, Tumor-Associated, Carbohydrate / analysis. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Dihydrouracil Dehydrogenase (NADP) / metabolism. Female. Fluorouracil / administration & dosage. Humans. Leucovorin / administration & dosage. Male. Middle Aged. Oligosaccharides / analysis. Orotate Phosphoribosyltransferase / analysis. Prognosis. Survival Rate. Thymidine Phosphorylase / metabolism. Thymidylate Synthase / metabolism. Vitamin B Complex / administration & dosage

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  • (PMID = 17454858.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / 5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine; 0 / Antigens, CD15; 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / Oligosaccharides; 0 / ST 439 antigen, human; 12001-76-2 / Vitamin B Complex; 7673326042 / irinotecan; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.1.1.45 / Thymidylate Synthase; EC 2.4.2.10 / Orotate Phosphoribosyltransferase; EC 2.4.2.4 / Thymidine Phosphorylase; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
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18. Takahashi K, Mori T, Yasuno M: [Indication for hepatic resection after hepatic arterial infusion chemotherapy for multiple liver metastases of colorectal cancer]. Gan To Kagaku Ryoho; 2000 Oct;27(12):1834-7
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  • [Title] [Indication for hepatic resection after hepatic arterial infusion chemotherapy for multiple liver metastases of colorectal cancer].
  • The indications for hepatic resection after hepatic arterial infusion chemotherapy (HAI) for unresectable metastatic liver tumor of colorectal cancer were analyzed from the surgical outcome of hepatic resections in 23 cases of hepatic resection after HAI.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Colorectal Neoplasms / pathology. Fluorouracil / administration & dosage. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary
  • [MeSH-minor] Combined Modality Therapy. Female. Hepatectomy. Hepatic Artery. Humans. Infusions, Intra-Arterial. Male. Prognosis. Survival Analysis

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  • (PMID = 11086424.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
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19. Lakatos PL, Lakatos L: [Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of chemotherapy outcome]. Orv Hetil; 2006 Mar 12;147(10):449-55
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  • [Title] [Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of chemotherapy outcome].
  • In the second part of the review the authors discuss the genetic background of sporadic and IBD associated colorectal cancers as well as the role of genetics in the diagnosis, prognosis and prediction of therapy.
  • Chromosomal instability (85%) and microsatellite instability with or without change in DNA methylation (15%) are the main mechanisms involved in the pathogenesis of sporadic colorectal cancers.
  • Most of neoplasms are genetically heterogeneous, independent pathways and simultaneous tumorigenesis may exist within the same organ, also in the colon.
  • Similar genetic mutations may be found in IBD associated colorectal cancers, however, the typical sequence and importance of mutations is different.
  • In future, fecal DNA testing may be an important screening tool for colorectal cancer; however, its routine use is still limited by its low sensitivity.
  • Similarly, genetic investigation may play an increasing role in the prediction of prognosis, therapy and complication of chemotherapy.
  • A more distant goal may be the individualization of the therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / genetics. Irritable Bowel Syndrome / complications
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Chromosomal Instability. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA Methylation. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Microsatellite Repeats. Mutation. Peutz-Jeghers Syndrome / genetics. Pharmacogenetics. Prognosis. Treatment Outcome


20. Carroll NM, Alexander HR Jr: Isolation perfusion of the liver. Cancer J; 2002 Mar-Apr;8(2):181-93
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  • Isolated hepatic perfusion (IHP) is a regional treatment strategy in which the vascular supply to the liver is isolated and perfused with a therapeutic regimen using an extracorporeal circuit consisting of a reservoir, heat exchanger, and oxygenator.
  • Drug doses that would cause severe toxicities if delivered systemically can be confined to the liver by isolated hepatic perfusion, resulting in the ability to intensify treatment to the cancer-burdened region of the body.
  • Agents and mechanisms commonly used in IHP include melphaIan, hyperthermia, and tumor necrosis factor.
  • IHP appears to be efficacious for patients with advanced disease, as reflected by large tumor size, high number of lesions, or significant overall tumor burden in the liver.
  • In addition, responses are observed for patients whose cancer is refractory to systemic and hepatic arterial infusion chemotherapy.
  • Recent clinical trials have demonstrated that IHP has anti-tumor efficacy against primary hepatic neoplasms and metastases from various primary tumors, such as colorectal carcinoma, ocular melanoma, and neuroendocrine tumors.
  • Current studies demonstrate that combining hepatic arterial infusion with floxuridine after IHP for patients with colorectal cancer metastases is associated with significant and durable response rates.
  • Continued clinical evaluation is warranted for the use of IHP in the treatment of unresectable liver metastases.
  • [MeSH-major] Chemotherapy, Cancer, Regional Perfusion / methods. Liver Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Eye Neoplasms / drug therapy. Humans. Hyperthermia, Induced. Melanoma / drug therapy. Tumor Necrosis Factor-alpha / administration & dosage

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  • (PMID = 12004803.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 72
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21. Tsoi KK, Ng SS, Leung MC, Sung JJ: Cost-effectiveness analysis on screening for colorectal neoplasm and management of colorectal cancer in Asia. Aliment Pharmacol Ther; 2008 Aug 1;28(3):353-63
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  • [Title] Cost-effectiveness analysis on screening for colorectal neoplasm and management of colorectal cancer in Asia.
  • BACKGROUND: Faecal occult blood testing (FOBT), flexible sigmoidoscopy (FS) and colonoscopy are recommended for subjects above 50 years of age for screening for colorectal cancer (CRC).
  • AIM: To evaluate the cost-effectiveness of FOBT, FS and colonoscopy on the basis of disease prevalence, compliance rate and cost of screening procedures in Asian countries.
  • The treatment cost of CRC, including surgery and chemotherapy, was evaluated.
  • The incremental cost-effectiveness ratio (ICER) for FOBT (US$6222 per life-year saved) is lower than FS (US$8044 per life-year saved) and colonoscopy (US$7211 per life-year saved).
  • [MeSH-major] Colonic Polyps / diagnosis. Colorectal Neoplasms / diagnosis. Occult Blood
  • [MeSH-minor] Aged. Aged, 80 and over. Asia. Biomarkers, Tumor / economics. Colonoscopy / economics. Cost-Benefit Analysis. Early Detection of Cancer. Female. Humans. Male. Mass Screening / economics. Middle Aged. Patient Compliance. Risk Factors. Sigmoidoscopy / economics

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  • (PMID = 18638075.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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22. Durand-Faucher K, Rabinovitch-Chable H, Dzugan H, Charret S, Aubry K, Genet D, Léobon S, Tubiana-Mathieu N, Cook-Moreau J, Rigaud M, Sturtz FG: A quantitative RT-PCR method to determine topoisomerase I mRNA levels in human tissue samples. Clin Chem Lab Med; 2005;43(7):707-14
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  • [Title] A quantitative RT-PCR method to determine topoisomerase I mRNA levels in human tissue samples.
  • Clinical interest has focused on Topo I as it is the molecular target of camptothecin (CPT), used in first and second lines of treatment for different cancer types.
  • Furthermore, it is well demonstrated that the patients who best responded to CPT-based chemotherapy were generally those with the greatest tumoral Topo I expression and/or activity.
  • We developed a sensitive, simple and reproducible method to measure Topo I mRNA expression in human cancer samples.
  • First, we checked the accuracy of the reverse transcription-polymerase chain reaction (RT-PCR) method by testing intra- and interassay reproducibility of Topo I and G6PDH gene amplification in different cell types.
  • We observed that crossing-points (Cps) were different, depending on the cell type, dilution or cDNA concentration, but that the intra- and interassay Cp standard deviation (SD) never exceeded 0.77% and 1.39% for Topo I amplification, or 1.63% and 2.9% for G6PDH amplification, respectively.
  • Secondly, we used our method to measure Topo I mRNA levels in primary tumor samples obtained from 27 patients with advanced colorectal cancer and 10 patients with pharyngeal/laryngeal cancer.
  • We found that the normalized Topo I/G6PDH mRNA ratios were significantly correlated with that of Topo I/PBGD in colorectal tumors (r(2)=0.47, p=0.02) but not in pharyngeal/laryngeal tumors (r(2)=0.35, p=0.3).
  • Neither ratio showed any significant association with clinicopathological parameters, such as gender, age, tumor size, or grade and lymph node status.

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  • (PMID = 16207129.001).
  • [ISSN] 1434-6621
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / RNA, Messenger; EC 1.1.1.49 / Glucosephosphate Dehydrogenase; EC 2.5.1.61 / Hydroxymethylbilane Synthase; EC 5.99.1.2 / DNA Topoisomerases, Type I
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23. Hiratsuka M, Yano T, Yamamoto M, Okazaki M, Kokufu I, Miyoshi H, Kimura F, Tanei T, Umemoto K, Miyashiro I, Sasaki Y, Ishikawa O: [Management of patients with hepatic metastases from gastric carcinoma]. Nihon Geka Gakkai Zasshi; 2003 Oct;104(10):711-6
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  • Many studies have reported the benefit of hepatic resection for metastatic tumors from colorectal cancer.
  • As systemic chemotherapy, S-1 + cisplatin results in a response rate of 50% in patients with metastases to the liver.
  • As arterial infusion chemotherapy, the 5-fluorouracil-doxorubicin-mitomycin (FAM) regimen yields a response rate of more than 70% including 15% complete response rate.
  • [MeSH-major] Liver Neoplasms / secondary. Liver Neoplasms / surgery. Stomach Neoplasms / pathology

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  • (PMID = 14579757.001).
  • [ISSN] 0301-4894
  • [Journal-full-title] Nihon Geka Gakkai zasshi
  • [ISO-abbreviation] Nihon Geka Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 34
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24. O'Dwyer PJ: The present and future of angiogenesis-directed treatments of colorectal cancer. Oncologist; 2006 Oct;11(9):992-8
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  • [Title] The present and future of angiogenesis-directed treatments of colorectal cancer.
  • The level of angiogenic activity in colorectal tumors has been shown to be a determinant of survival.
  • Recent trials established that, in both the first- and second-line treatment of metastatic colorectal cancer, the addition of the vascular endothelial growth factor (VEGF)-directed antibody bevacizumab to chemotherapy significantly prolongs survival compared to chemotherapy alone.
  • Those trials provided proof of principle that inhibition of angiogenesis has the potential to enhance the effectiveness of treatment of this disease.
  • Oral agents directed toward VEGF receptor signaling are in advanced development, but none to date has proven beneficial in phase III trials in advanced colorectal cancer.
  • Additional trials are needed to determine if improved pharmacological characteristics of the small molecules can be modified to replicate the activity of the antibody or if mechanistic differences require a more specific approach.
  • Since bevacizumab has minimal activity as a single agent, a key question for future therapeutic development relates to the interaction between antiangiogenic strategies and cytotoxic therapies.
  • We hypothesize that bevacizumab may potentiate the efficacy of cytotoxics not solely by alterations of tumor interstitial pressure but also by promoting sensitivity to proapoptotic signals consequent upon nutrient and oxygen withdrawal.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Colorectal Neoplasms / blood supply. Neovascularization, Pathologic / prevention & control. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 17030640.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  • [Number-of-references] 19
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25. Zidan J, Haim N, Beny A, Stein M, Gez E, Kuten A: Octreotide in the treatment of severe chemotherapy-induced diarrhea. Ann Oncol; 2001 Feb;12(2):227-9
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  • [Title] Octreotide in the treatment of severe chemotherapy-induced diarrhea.
  • BACKGROUND: Chemotherapy-induced diarrhea (CID) is a common side effect of a number of chemotherapeutic agents.
  • Conventional therapy for severe CID with opioids or loperamide is moderately effective.
  • A prospective trial was conducted using octreotide acetate for treatment of severe CID refractory to loperamide.
  • Previous chemotherapy consisted of regimens containing fluorouracil, leucovorin, CPT-11, cyclophosphamide, methotrexate and cisplatin.
  • Primary tumors were colorectal (n = 23), gastric (n = 3), and other cancers (n = 6).
  • RESULTS: Complete resolution of diarrhea was obtained in 30 of 32 patients (94%); 5 within 24 hours, 14 within 48 hours, and 11 within 72 hours of treatment.
  • Response was unaffected by age, gender, performance status, previous chemotherapy or primary tumor site.
  • CONCLUSIONS: Octreotide 100 microg subcutaneously 3x/day for three days is an effective, safe treatment for CID given primarily or as a second-line therapy after loperamide failure.

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  • (PMID = 11300329.001).
  • [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; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antidiarrheals; 0 / Antineoplastic Agents; RWM8CCW8GP / Octreotide
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26. Tsioulias GJ, Wood TF, Spirt M, Morton DL, Bilchik AJ: A novel lymphatic mapping technique to improve localization and staging of early colon cancer during laparoscopic colectomy. Am Surg; 2002 Jul;68(7):561-5
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  • [Title] A novel lymphatic mapping technique to improve localization and staging of early colon cancer during laparoscopic colectomy.
  • Encouraging results from our previous studies of sentinel lymph node (SLN) mapping in colorectal cancer (CRC) prompted investigation of its feasibility and accuracy during laparoscopic colectomy for early CRC.
  • Between 1996 and 2000, 14 patients with clinically localized colorectal neoplasms underwent colonoscopic tattooing of the primary site and SLN mapping.
  • In all 14 patients the primary neoplasm and an SLN were identified laparoscopically.
  • An average of 13.5 total lymph nodes and 1.7 SLNs per patient were identified.
  • The SLN correctly reflected the tumor status of the nodal basin in 93 per cent of the cases.
  • Lymphatic mapping caused no complications and added only 10 to 15 minutes to the overall operative time.
  • Comparison of results in this group with results for a matched group of 14 patients undergoing SLN mapping during open colon resection showed that the laparoscopic technique had similar rates of accuracy and success.
  • These preliminary findings indicate that colonoscopic/laparoscopic SLN mapping during laparoscopic colon resection is a feasible and technically simple means of identifying the primary colorectal neoplasm and its SLN.
  • Focused pathologic examination of this node can upstage CRC and thereby may improve selection of patients for adjuvant chemotherapy.
  • [MeSH-major] Colectomy / methods. Colorectal Neoplasms / pathology. Colorectal Neoplasms / surgery. Laparoscopy. Neoplasm Staging / methods. Sentinel Lymph Node Biopsy / methods

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  • (PMID = 12132733.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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27. Buck E, Eyzaguirre A, Barr S, Thompson S, Sennello R, Young D, Iwata KK, Gibson NW, Cagnoni P, Haley JD: Loss of homotypic cell adhesion by epithelial-mesenchymal transition or mutation limits sensitivity to epidermal growth factor receptor inhibition. Mol Cancer Ther; 2007 Feb;6(2):532-41
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  • Inhibitors of EGFR signaling have shown clinical utility; however, understanding response at the molecular level is important to define patient subsets most likely to benefit, as well as to support the rational design of drug combinations.
  • Pancreatic and colorectal tumor cell lines insensitive to EGFR inhibition were those that had lost or mutated the epithelial junction constituents E-cadherin and gamma-catenin, had lost homotypic adhesion, and often gained proteins associated with an epithelial to mesenchymal-like transition, such as vimentin, zeb1, or snail.
  • In matched pairs of colorectal tumor cells, the epithelial lines showed an average 7-fold greater sensitivity than mesenchymal-like lines.
  • In human pancreatic and colorectal tumor tissues, gain of mesenchymal characteristics and loss of epithelial characteristics correlated with advancing tumor stage.
  • These data indicate an especially sensitive patient subset as well as a rationale for the combination of EGFR antagonists with agents that affect the epithelial to mesenchymal-like transition process as a mechanism to enhance sensitivity for more advanced mesenchymal-like tumors.
  • [MeSH-major] Cell Adhesion. Colorectal Neoplasms / drug therapy. Drug Resistance, Neoplasm. Epithelial Cells / pathology. Mesoderm / pathology. Mutation / genetics. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cadherins / metabolism. Cell Line, Tumor. Erlotinib Hydrochloride. Humans. Immunoenzyme Techniques. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology. Tissue Array Analysis. Vimentin / metabolism

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  • (PMID = 17308052.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / Vimentin; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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28. Buess M, Terracciano L, Reuter J, Ballabeni P, Boulay JL, Laffer U, Metzger U, Herrmann R, Rochlitz C: Amplification of SKI is a prognostic marker in early colorectal cancer. Neoplasia; 2004 May-Jun;6(3):207-12
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  • [Title] Amplification of SKI is a prognostic marker in early colorectal cancer.
  • BACKGROUND: Improved risk stratification of early colorectal cancer might help to better select patients for adjuvant treatment.
  • Alterations in the transforming growth factor-beta (TGF-beta) pathway have frequently been found in colorectal cancer, but their impact on prognosis remains controversial.
  • We therefore analyzed two transcriptional corepressors of the TGF-beta signaling pathway with respect to prognosis and prediction of chemotherapy benefit in early colorectal cancer.
  • METHODS: The gene copy status of SKI and SNON was analyzed by use of quantitative real-time polymerase chain reaction in 179 colorectal tumor biopsies, which had been collected from a randomized multicenter trial of the Swiss Group for Clinical Cancer Research (SAKK).
  • CONCLUSION: Amplification of SKI is a negative prognostic marker in early-stage colorectal cancer.
  • This marker should help to improve risk stratification to better select patients for adjuvant therapy.
  • [MeSH-major] Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor. Early Diagnosis. Female. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 15153332.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 126648-96-2 / SKI protein, human
  • [Other-IDs] NLM/ PMC1502098
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29. Machado NO, Chopra PJ, Al Hamdani A: Pancreatic metastasis from colon carcinoma nine years after a hemicolectomy managed by distal pancreatectomy. A review of the literature regarding the role and outcome of pancreatic resection for colorectal metastasis. JOP; 2010;11(4):377-81
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  • [Title] Pancreatic metastasis from colon carcinoma nine years after a hemicolectomy managed by distal pancreatectomy. A review of the literature regarding the role and outcome of pancreatic resection for colorectal metastasis.
  • CONTEXT: Pancreatic metastasis from colorectal malignancy is rare and accounts for less than 2% of all pancreatic metastases.
  • A case of colonic metastasis to the pancreas is reported and the literature is reviewed to assess the role and outcome of pancreatic resection for metastatic tumors from colorectal malignancy.
  • CASE REPORT: A 58-year-old female underwent an emergency left hemicolectomy for an obstructing descending colon growth.
  • A postoperative staging CT scan showed no other metastases and she received 6 cycles of FOLFOX chemotherapy (folinic acid, 5-flurouracil and oxaliplatin).
  • She underwent a distal pancreatectomy, and histopathology of the resected specimen confirmed a metastatic tumor from colon cancer.
  • She then received 5 cycles of adjuvant chemotherapy.
  • She was symptom free for nine months and subsequently succumbed to recurrent disease.
  • CONCLUSION: Pancreatic metastasis from colorectal malignancy is rare.
  • The time-interval between the diagnosis of colorectal cancer and the detection of pancreatic metastasis varies widely but is approximately 24 months.
  • The median survival time for post-pancreatic resection is 16 months.
  • Pancreatic resection appears to offer good palliation until recurrence of the disease occurs and the possibility of long term cure is rare.
  • [MeSH-major] Carcinoma / surgery. Colectomy / methods. Colonic Neoplasms / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adult. Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / pathology. Colorectal Neoplasms / surgery. Female. Humans. Prognosis. Time Factors. Treatment Outcome

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  • [CommentIn] JOP. 2010;11(6):644-5; author reply 650 [21068505.001]
  • (PMID = 20601814.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 24
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30. Fournel C, Bertoletti L, Nguyen B, Vergnon JM: Endobronchial metastases from colorectal cancers: natural history and role of interventional bronchoscopy. Respiration; 2009;77(1):63-9
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  • [Title] Endobronchial metastases from colorectal cancers: natural history and role of interventional bronchoscopy.
  • The most frequent primary tumors associated with endobronchial involvement are breast, colon and renal cell carcinomas.
  • Metastases from colorectal cancers can be treated either surgically or with chemotherapy in order to improve survival.
  • OBJECTIVES: This paper aims to report the potential role of interventional bronchoscopy in patients with endobronchial metastases from colorectal cancer.
  • METHODS: This retrospective study included 24 patients who underwent an interventional bronchoscopy procedure between 1988 and 2006.
  • Assessment of the natural history of metastatic colorectal carcinoma, therapeutic options and survival associated with endobronchial metastases are reported.
  • RESULTS: Endobronchial metastases occurred at a median of 53 months (range 18-144) following the diagnosis of the primary tumor.
  • Atelectasis was a common radiological finding.
  • CONCLUSION: Endobronchial metastases occur relatively late in patients with a metastatic colorectal neoplasm.
  • Palliative treatment with interventional bronchoscopy to prevent asphyxia is a safe and effective method that may improve the quality of life in these patients.
  • [MeSH-major] Adenocarcinoma / therapy. Bronchial Neoplasms / therapy. Bronchoscopy. Colorectal Neoplasms / pathology

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18812690.001).
  • [ISSN] 1423-0356
  • [Journal-full-title] Respiration; international review of thoracic diseases
  • [ISO-abbreviation] Respiration
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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31. Curwen JO, Musgrove HL, Kendrew J, Richmond GH, Ogilvie DJ, Wedge SR: Inhibition of vascular endothelial growth factor-a signaling induces hypertension: examining the effect of cediranib (recentin; AZD2171) treatment on blood pressure in rat and the use of concomitant antihypertensive therapy. Clin Cancer Res; 2008 May 15;14(10):3124-31
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  • [Title] Inhibition of vascular endothelial growth factor-a signaling induces hypertension: examining the effect of cediranib (recentin; AZD2171) treatment on blood pressure in rat and the use of concomitant antihypertensive therapy.
  • PURPOSE: Inhibition of vascular endothelial growth factor-A (VEGF) signaling is a key therapeutic approach in oncology given the role of VEGF in angiogenesis and vascular permeability in solid tumors.
  • EXPERIMENTAL DESIGN: The ability of cediranib to induce hypertensive changes and the effect of giving antihypertensive therapy were investigated in conscious, unrestrained telemetered rats.
  • The antitumor activity of cediranib, alone and in combination with nifedipine, was also evaluated in a LoVo human colorectal tumor xenograft model in nude rats.
  • All treatments were given orally.
  • RESULTS: Administration of 0.1 to 1.5 mg/kg/d of cediranib for 4 consecutive days induced a relatively mild hypertensive effect, elevating diastolic blood pressure by 10 to 14 mmHg.
  • CONCLUSIONS: Hypertension is a direct consequence of inhibiting VEGF signaling but can be controlled with appropriately selected, standard antihypertensive medication.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Blood Pressure / drug effects. Hypertension / drug therapy. Quinazolines / pharmacology. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Antihypertensive Agents / pharmacology. Antineoplastic Agents / pharmacology. Captopril / pharmacology. Cell Line, Tumor. Colorectal Neoplasms / drug therapy. Humans. Mice. Nifedipine / pharmacology. Rats. Xenograft Model Antitumor Assays

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  • (PMID = 18483380.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antihypertensive Agents; 0 / Antineoplastic Agents; 0 / Quinazolines; 0 / Vascular Endothelial Growth Factor A; 9G64RSX1XD / Captopril; I9ZF7L6G2L / Nifedipine; NQU9IPY4K9 / cediranib
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32. Cusack JC Jr, Liu R, Baldwin AS Jr: Inducible chemoresistance to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothe cin (CPT-11) in colorectal cancer cells and a xenograft model is overcome by inhibition of nuclear factor-kappaB activation. Cancer Res; 2000 May 1;60(9):2323-30
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  • [Title] Inducible chemoresistance to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothe cin (CPT-11) in colorectal cancer cells and a xenograft model is overcome by inhibition of nuclear factor-kappaB activation.
  • Limited studies have indicated that some chemotherapy agents activate the transcription factor nuclear factor-kappaB (NF-kappaB), and that this leads to suppression of the apoptotic potential of the chemotherapy.
  • In contrast, it was reported recently that stable inhibition of NF-kappaB in four different cancer cell lines did not lead to augmentation of the chemotherapy-induced apoptosis.
  • In this study, we have focused on colorectal cancer, which is known to be highly resistant to genotoxic chemotherapy and gamma irradiation.
  • We show that the topoisomerase I inhibitor 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11) activates NF-kappaB in most colorectal cancer cell lines.
  • We then examine a therapeutic strategy that uses adenovirus-mediated transfer of the super-repressor IkappaBalpha to inhibit NF-kappaB activation as an adjuvant approach to promote chemosensitivity in colorectal tumor cells to treatment with CPT-11.
  • These data demonstrate that the protection from apoptosis induced in response to CPT-11 treatment is effectively inhibited by the transient inhibition of NF-kappaB in a variety of human colon cancer cell lines and in a tumor xenograft model, resulting in a significantly enhanced tumoricidal response to CPT-11 via increased induction of apoptosis.
  • These findings indicate that the activation of NF-kappaB by chemotherapy is an important underlying mechanism of inducible chemoresistance.
  • [MeSH-major] Camptothecin / analogs & derivatives. Colorectal Neoplasms / metabolism. Drug Resistance, Neoplasm. Enzyme Inhibitors / pharmacology. I-kappa B Proteins. NF-kappa B / metabolism
  • [MeSH-minor] Adenoviridae / metabolism. Animals. Apoptosis. Breast Neoplasms / metabolism. Cell Nucleus / metabolism. DNA-Binding Proteins / metabolism. Dose-Response Relationship, Drug. Enzyme Activation. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Mice. Mice, Nude. Time Factors. Transgenes / genetics. Tumor Cells, Cultured

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  • (PMID = 10811101.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA72771; United States / NCI NIH HHS / CA / CA75080; United States / NCI NIH HHS / CA / CA75528; etc
  • [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 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / I-kappa B Proteins; 0 / NF-kappa B; 139874-52-5 / NF-kappaB inhibitor alpha; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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33. Kodach LL, Bos CL, Durán N, Peppelenbosch MP, Ferreira CV, Hardwick JC: Violacein synergistically increases 5-fluorouracil cytotoxicity, induces apoptosis and inhibits Akt-mediated signal transduction in human colorectal cancer cells. Carcinogenesis; 2006 Mar;27(3):508-16
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  • [Title] Violacein synergistically increases 5-fluorouracil cytotoxicity, induces apoptosis and inhibits Akt-mediated signal transduction in human colorectal cancer cells.
  • Despite recent additions to the armory of chemotherapeutic agents for colorectal cancer (CRC) treatment, the results of chemotherapy remain unsatisfactory.
  • 5-Fluorouracil (5-FU) still represents the cornerstone of treatment and resistance to its actions is a major obstacle to successful chemotherapy.
  • Violacein, a pigment isolated from Chromobacterium violaceum in the Amazon river, has a diverse spectrum of biological activities, and represents a novel cytotoxic drug with known antileukemic properties.
  • Its underlying mechanisms of action were further investigated by studying its effects on the cell cycle, apoptosis and cell survival pathways [phosphatidylinositol-3-kinase/Akt, p44/42 mitogen activated protein kinase and nuclear factor kappaB (NF-kappaB)] in colon cancer cell lines.
  • Violacein inhibits the growth of all four colon cancer cell lines tested.
  • This leads to the increase in chemosensitivity to 5-FU in HCT116 colon cancer cells.
  • Taken together, our findings suggest that violacein will be active in the treatment of colorectal tumors and offers new prospects for overcoming 5-FU resistance.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Antimetabolites, Antineoplastic / toxicity. Colorectal Neoplasms / pathology. Fluorouracil / pharmacology. Fluorouracil / toxicity. Indoles / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Down-Regulation. Drug Interactions. Humans. NF-kappa B / biosynthesis. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. Tumor Cells, Cultured


34. Carethers JM: Systemic treatment of advanced colorectal cancer: tailoring therapy to the tumor. Therap Adv Gastroenterol; 2008 Jul;1(1):33-42
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  • [Title] Systemic treatment of advanced colorectal cancer: tailoring therapy to the tumor.
  • Colorectal cancer is a prevalent disease in Western countries.
  • While prevention through screening is the best approach to combat the development of colorectal cancer through the removal of precursor adenomas, many patients present with advanced disease that will require surgery and systemic therapy to improve survival.
  • With reference to systemic therapy, the median survival of patients with metastatic colorectal cancer (those with tumor spread to lymph nodes or distant sites) has improved over the past three decades due to the introduction of 5-fluorouracil (5-FU), its subsequent biomodulation, and the addition other chemotherapeutic agents.
  • There is now evidence that the biology of the colorectal tumor, in addition to the stage of colorectal cancer, may predict response to 5-FU-based therapy.
  • More recently, systemic biological therapies that target signaling processes for tumor growth, such as epidermal growth factor receptor, and vascular endothelial growth factor, are also effective in improving patient survival with metastatic colorectal cancer.
  • The use of a combination of systemic therapies that include chemotherapy and biologic therapy should continue to increase patient survival with metastatic colorectal cancer through appropriately designed clinical trials.
  • Treatments based on the biology of the colorectal tumor also need to be examined through clinical trials.

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  • (PMID = 21180512.001).
  • [ISSN] 1756-283X
  • [Journal-full-title] Therapeutic advances in gastroenterology
  • [ISO-abbreviation] Therap Adv Gastroenterol
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK067287; United States / NIDDK NIH HHS / DK / R24 DK080506
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3002487
  • [Keywords] NOTNLM ; 5-fluorouracil / bevacizumab / biologic therapy / cetuximab / chemotherapy / colorectal cancer / epidermal growth factor receptor / tyrosine kinase inhibitor / vascular endothelial growth factor
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35. Na HS, Lim YK, Jeong YI, Lee HS, Lim YJ, Kang MS, Cho CS, Lee HC: Combination antitumor effects of micelle-loaded anticancer drugs in a CT-26 murine colorectal carcinoma model. Int J Pharm; 2010 Jan 4;383(1-2):192-200
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  • [Title] Combination antitumor effects of micelle-loaded anticancer drugs in a CT-26 murine colorectal carcinoma model.
  • Experiments were designed to evaluate the in vitro cytotoxic interactions of anticancer drugs in combination, evaluate synergistic activity in vivo and utilize micelle-forming polymeric drugs as drug carriers in a murine cancer model.
  • Antitumor effects of 5-fluorouracil, cisplatin, CPT-11, oxaliplatin, etoposide, mitomycin-C, doxorubicin and paclitaxel were evaluated by determination of in vitro cytotoxicity to CT-26 colorectal tumor cells or in vivo following a subcutaneous transplant in BALB/c mice.
  • Single agent and combination in vivo studies were also performed using drug-loaded polymeric micelles composed of poly(gamma-benzyl L-glutamate) and poly(ethylene oxide) (GEG) or poly(L-lactide)/poly(ethylene glycol) (LE) diblock copolymer.
  • When tumor cells were exposed to doxorubicin concurrently with etoposide or paclitaxel, evidence of synergy was observed in CT-26 cells in vitro.
  • When tumor-bearing mice were treated in combination with doxorubicin-paclitaxel or doxorubicin-etoposide, substantial antitumor activity was evident compared with single therapy.
  • These data suggest that in vitro cytotoxicity of anticancer drugs is related to in vivo results, and chemotherapy using micelle-loaded anticancer drugs represents a promising potential as a carrier system in modulating drug delivery.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma / drug therapy. Colorectal Neoplasms / drug therapy. Disease Models, Animal. Micelles
  • [MeSH-minor] Animals. Cell Line, Tumor. Mice. Mice, Inbred BALB C. Survival Rate / trends

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  • (PMID = 19732817.001).
  • [ISSN] 1873-3476
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Micelles
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36. Ramadori G, Lindhorst A, Armbrust T: Colorectal tumors with complete obstruction--endoscopic recovery of passage replacing emergency surgery? A report of two cases. BMC Gastroenterol; 2007;7:14
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  • [Title] Colorectal tumors with complete obstruction--endoscopic recovery of passage replacing emergency surgery? A report of two cases.
  • BACKGROUND: Incomplete or complete obstructive ileus due to colorectal cancer is generally treated by emergency surgery that has higher morbidity and mortality than elective surgery.
  • CASE PRESENTATION: Here we describe an endoscopic technique by which a safe bowel decompression was performed instead of emergency surgery in two patients with complete tumorous obstruction of the colon.
  • By means of a polypectomy snare, a soft wire, an ERCP catheter, a set of endoscopes with different diameters (baby endoscope, gastroscope) and of argon plasma coagulation the tumor mass was reduced and the tumor stenosis was passed.
  • The patients recovered from symptoms of colon obstruction, no procedure-associated complications were observed.
  • One patient had surgery of the sigmoid tumor one week later (UICC-stage III), the other patient (UICC-stage IV) received systemic chemotherapy starting one week after endoscopic decompression.
  • CONCLUSION: Complete tumorous obstruction of the colon may be managed by endoscopic tumor debulking avoiding high risk emergency surgery and allowing immediate medical treatment of the primary tumor and of metastases.
  • [MeSH-major] Colonoscopy. Colorectal Neoplasms / complications. Intestinal Obstruction / surgery

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  • (PMID = 17391506.001).
  • [ISSN] 1471-230X
  • [Journal-full-title] BMC gastroenterology
  • [ISO-abbreviation] BMC Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1847445
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37. Choi JH, Ahn MJ, Rhim H, Lee HW, Oh HS, Lee YY, Choi IY, Kim IS: Radiofrequency ablation for metastatic hepatic tumor in colorectal carcinoma. Cancer Res Treat; 2004 Apr;36(2):128-31
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  • [Title] Radiofrequency ablation for metastatic hepatic tumor in colorectal carcinoma.
  • PURPOSE: The purpose of this study was to assess the efficacy and safety of radiofrequency ablation (RFA) to treat hepatic metastasis in patients with colorectal carcinoma.
  • MATERIALS AND METHODS: Between May 1999 and July 2002, a total of 45 tumors in 24 patients with colorectal cancer were treated with RFA.
  • Thirteen patients received systemic chemotherapy after the RFA procedure.
  • Complete tumor necrosis was achieved in 17 patients (70.8%) on an immediate (<24 hrs) CT scan.
  • In a univariate analysis, complete necrosis, tumor size and post-RFA chemotherapy were significant factors for survival.
  • Nineteen of the 24 patients developed a recurrence or progressed (79.2%).
  • There were no treatment related deaths or serious adverse effects, with the exception of one case of respiratory failure.
  • CONCLUSION: These results suggest that RFA is a well-tolerated and effective method to treat hepatic metastasis in colorectal carcinomas.

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  • (PMID = 20396552.001).
  • [ISSN] 2005-9256
  • [Journal-full-title] Cancer research and treatment : official journal of Korean Cancer Association
  • [ISO-abbreviation] Cancer Res Treat
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2855095
  • [Keywords] NOTNLM ; Colorectal neoplasm / Hepatic metastasis / Radiofrequency ablation
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38. Pitton MB, Herber S, Raab P, Mönch C, Wunsch M, Schneider J, Schweden F, Otto G, Thelen M: [Percutaneous radiofrequency ablation of liver tumors using the LeVeen 4 cm array probe]. Rofo; 2003 Nov;175(11):1525-31
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  • [Title] [Percutaneous radiofrequency ablation of liver tumors using the LeVeen 4 cm array probe].
  • METHODS: In 35 patients (age 63,9 +/- 12,6 years, range 22 - 83) a total of 65 liver tumors were percutaneously treated using a 200 watt radiofrequency generator and a LeVeen 4 cm array probe (RF3000, Boston Scientific).
  • Adapted to the tumor size, the LeVeen Probe was repositioned during the procedure with an additional safety margin of 1 cm.
  • Primary tumors were colorectal in 22, and mamma tumors (n = 4), zystic pancreas tumors (n = 2), gastric cancer (n = 1), zystadenocarcinoma of the liver (n = 1), lung cancer (n = 1), gastrointestinal stroma tumor (n = 1), duodenal carcinoma (n = 1), cholangiocellular carcinoma (n = 1) and hepatocellular carcinoma (n = 1).
  • RESULTS: One to 4 metastases were treated per patient during one or up to 4 procedure sessions.
  • Primary technical success with complete tumor ablation was reached in 60 of 65 lesions.
  • In 4 cases two treatment sessions were necessary in order to achieve the intended results.
  • In one case the procedure was aborted because of a close relationship between lesion and right colon.
  • 63 tumors were treated in sedation and local anesthesia.
  • One case with subcapsular tumor ablation suffered from a large subcapsular hematoma requiring a blood transfusion.
  • 21 of 35 patients showed no evidence of tumor recurrence.
  • One case is scheduled for a second treatment session for complete tumor ablation.
  • 13 of 35 patients suffered from tumor recurrence, either local recurrences and/or new metastases.
  • In three patients tumor recurrence was treated by means of a second RF-ablation.
  • The remaining 10 patients received chemotherapy.
  • CT follow-up is required every three months because of the tumor recurrence rate and reinterventions may be required.
  • [MeSH-major] Catheter Ablation / instrumentation. Catheter Ablation / methods. Liver Neoplasms / radiotherapy. Liver Neoplasms / secondary. Radio Waves / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Humans. Image Processing, Computer-Assisted. Middle Aged. Recurrence. Treatment Outcome

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  • (PMID = 14610704.001).
  • [ISSN] 1438-9029
  • [Journal-full-title] RöFo : Fortschritte auf dem Gebiete der Röntgenstrahlen und der Nuklearmedizin
  • [ISO-abbreviation] Rofo
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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39. Wajapeyee N, Kapoor V, Mahalingam M, Green MR: Efficacy of IGFBP7 for treatment of metastatic melanoma and other cancers in mouse models and human cell lines. Mol Cancer Ther; 2009 Nov;8(11):3009-14
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  • [Title] Efficacy of IGFBP7 for treatment of metastatic melanoma and other cancers in mouse models and human cell lines.
  • Restoration of IGFBP7 function by the addition of recombinant IGFBP7 (rIGFBP7) induces apoptosis in BRAF-positive human melanoma cell lines, and systemically administered rIGFBP7 markedly suppresses the growth of BRAF-positive primary tumors in xenografted mice.
  • Here we further evaluate the role of IGFBP7 in the treatment of BRAF-positive melanoma and other malignancies.
  • Using a murine experimental metastasis assay, we show that systemic administration of rIGFBP7 markedly suppresses the growth of metastatic disease and prolongs survival.
  • An analysis of the NCI60 panel of human cancer cell lines reveals that in addition to melanoma, IGFBP7 induces apoptosis in several other cancer types, in particular colorectal cancer cell lines.
  • Significantly, systemically administered rIGFBP7 blocks the growth of colorectal tumors containing an activating RAS or BRAF mutation in mouse xenografts.
  • [MeSH-major] Insulin-Like Growth Factor Binding Proteins / pharmacology. Melanoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Colorectal Neoplasms / drug therapy. Epigenesis, Genetic. Gene Silencing. HT29 Cells. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Proto-Oncogene Proteins B-raf / biosynthesis. Proto-Oncogene Proteins B-raf / genetics. Recombinant Proteins / pharmacology. Signal Transduction. Survival Rate. Xenograft Model Antitumor Assays. ras Proteins / biosynthesis. ras Proteins / genetics

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  • (PMID = 19861408.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Recombinant Proteins; 0 / insulin-like growth factor binding protein-related protein 1; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ HHMIMS150150; NLM/ PMC2783755
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40. Herráiz M, Muñoz-Navas M: Recognition and management of hereditary colorectal cancer syndromes. Rev Esp Enferm Dig; 2009 Feb;101(2):125-32
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  • [Title] Recognition and management of hereditary colorectal cancer syndromes.
  • Over 1,900 colorectal tumors will arise in association with a hereditary colorectal cancer syndrome in Spain in 2009.
  • Colonoscopy and prophylactic colectomy decrease colorectal cancer incidence and overall mortality in patients with hereditary colon cancer.
  • Extracolonic tumors are frequent in these syndromes, so specific surveillance strategies should be offered.
  • [MeSH-major] Colorectal Neoplasms / genetics. Neoplastic Syndromes, Hereditary / diagnosis
  • [MeSH-minor] Adenomatous Polyposis Coli / diagnosis. Adenomatous Polyposis Coli / drug therapy. Adenomatous Polyposis Coli / epidemiology. Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / surgery. Adolescent. Adult. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Child. Colectomy. Colonoscopy. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / drug therapy. Colorectal Neoplasms, Hereditary Nonpolyposis / epidemiology. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. Colorectal Neoplasms, Hereditary Nonpolyposis / surgery. Cyclooxygenase 2 Inhibitors / therapeutic use. Endometrial Neoplasms / genetics. Endometrial Neoplasms / surgery. Family Health. Female. Genes, Dominant. Genes, Neoplasm. Genes, Recessive. Genetic Testing. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 19335048.001).
  • [ISSN] 1130-0108
  • [Journal-full-title] Revista española de enfermedades digestivas : organo oficial de la Sociedad Española de Patología Digestiva
  • [ISO-abbreviation] Rev Esp Enferm Dig
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors
  • [Number-of-references] 71
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41. Zorcolo L: [Biomolecular prognostic factors in colorectal cancer]. Chir Ital; 2006 Nov-Dec;58(6):733-42
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  • [Title] [Biomolecular prognostic factors in colorectal cancer].
  • There is general agreement that staging of colorectal neoplasms based on classic anatomopathological parameters does not allow accurate selection of patients at higher risk of an adverse outcome.
  • Moreover, it would be useful to identify factors predictive of response to radiotherapy and chemotherapy.
  • At present, apart from CEA, whose prognostic value has been known for some time, we do not have sufficient data to definitively incorporate any of the other biomarkers in clinical practice.
  • In particular, growth factor receptors may play a role not only as prognostic factors but also in view of their therapeutic potential.
  • [MeSH-major] Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Adhesion. Genes, APC. Genes, DCC. Humans. Loss of Heterozygosity. Lymphatic Metastasis. Membrane Proteins / metabolism. Microsatellite Instability. Mutation. Neoplasm Invasiveness. Neoplasm Staging. Neoplastic Cells, Circulating. Prognosis. Receptors, Growth Factor / genetics

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  • (PMID = 17190278.001).
  • [ISSN] 0009-4773
  • [Journal-full-title] Chirurgia italiana
  • [ISO-abbreviation] Chir Ital
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / Receptors, Growth Factor
  • [Number-of-references] 94
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42. Gentner B, Wein A, Croner RS, Zeittraeger I, Wirtz RM, Roedel F, Dimmler A, Dorlaque L, Hohenberger W, Hahn EG, Brueckl WM: Differences in the gene expression profile of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) in primary colorectal tumors and their synchronous liver metastases. Anticancer Res; 2009 Jan;29(1):67-74
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  • [Title] Differences in the gene expression profile of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) in primary colorectal tumors and their synchronous liver metastases.
  • BACKGROUND: Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) have been strongly implicated in the pathogenesis of many types of human cancer.
  • We wanted to specifically define their role in established colorectal cancer liver metastases.
  • PATIENTS AND METHODS: The MMP/TIMP expression profiles of N=9 colorectal primary tumour liver metastasis tissue pairs were determined using oligonucleotide-based arrays.
  • Additionally, unsupervised clustering using the MMP/TIMP profile of N=25 colorectal cancer liver metastases was performed and the response to palliative 5-fluorouracil (5-FU)-based chemotherapy was assessed using radiological response criteria.
  • RESULTS: When comparing the primary tumors to their synchronous liver metastases, a statistically significant (p < 0.05) down-regulation of MMP1, -2, -3 and -12 was found in the metastases.
  • Unsupervised clustering using the MMP/TIMP profiles of 25 liver metastases revealed two distinct subgroups with different responses to palliative, 5-FU-based chemotherapy (response rates: 22% vs. 56%, respectively).
  • In particular, higher MMP7, TIMP1 and TIMP2 levels were found in the unfavourable group, while higher expression of MMP2, -9, -11 and -14 was associated with a more favourable response to chemotherapy.
  • CONCLUSION: Colorectal cancer liver metastases show a distinctive MMP/TIMP profile with predictive implications.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Liver Neoplasms / genetics. Liver Neoplasms / secondary. Matrix Metalloproteinases / biosynthesis. Tissue Inhibitor of Metalloproteinases / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Fluorouracil / therapeutic use. Gene Expression Profiling. Humans. Male. Middle Aged. Predictive Value of Tests. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19331134.001).
  • [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 / Tissue Inhibitor of Metalloproteinases; EC 3.4.24.- / Matrix Metalloproteinases; U3P01618RT / Fluorouracil
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43. Katayose Y, Unno M: Management of liver metastases from colorectal cancer. Clin J Gastroenterol; 2010 Jun;3(3):128-35
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  • [Title] Management of liver metastases from colorectal cancer.
  • About 50% of colorectal cancer patients develop liver metastasis, and liver resection is considered the only curative therapy.
  • Since surgical resection coverage has increased because of improved hepatectomy including portal vein embolization, tumors shrink because of the effectiveness of recent chemotherapy, such as FOLFOX and FOLFIRI, and it has become possible for many patients whose cancer was judged unresectable before to undergo resection.
  • Improvement of new anticancer drugs such as molecularly targeted biologics is greatly changing therapeutic systems of metastatic colorectal cancer, and it is time for us to innovate stage IV therapy.
  • In this report, we will review new treatment strategies for metastatic liver cancer from colorectal cancer, clinical trials of new anticancer drugs for liver metastasis, surgery and ablation as local therapy, and further clarify complex therapeutic systems for metastatic liver tumors from colorectal cancer.

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  • (PMID = 26190118.001).
  • [ISSN] 1865-7257
  • [Journal-full-title] Clinical journal of gastroenterology
  • [ISO-abbreviation] Clin J Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; Adjuvant / Chemotherapy / Colorectal / Neoadjuvant
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44. Scartozzi M, Bearzi I, Pierantoni C, Mandolesi A, Loupakis F, Zaniboni A, Catalano V, Quadri A, Zorzi F, Berardi R, Biscotti T, Labianca R, Falcone A, Cascinu S: Nuclear factor-kB tumor expression predicts response and survival in irinotecan-refractory metastatic colorectal cancer treated with cetuximab-irinotecan therapy. J Clin Oncol; 2007 Sep 1;25(25):3930-5
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  • [Title] Nuclear factor-kB tumor expression predicts response and survival in irinotecan-refractory metastatic colorectal cancer treated with cetuximab-irinotecan therapy.
  • PURPOSE: NF-kB expression has been shown to be responsible for resistance to antineoplastic agents and it also plays a part in the activation of the epidermal growth factor receptor downstream signaling pathway in colorectal tumors.
  • The aim of our analysis was to investigate a correlation between NF-kB expression, response rate, time to progression, and survival in advanced colorectal cancer patients receiving cetuximab and irinotecan.
  • Cetuximab and irinotecan were administered as second-line chemotherapy in 19 patients and after > or = two lines of chemotherapy in the remaining 57 patients.
  • Thirty-two patients (48%) experienced progressive disease; median time to progression (TTP) was 3.6 months and median overall survival was 10.3 months.
  • The response rate was 10% (four PRs) versus 48% (12 PRs; P = .0007) in NF-kB-positive and NF-kB-negative tumors, respectively.
  • Median overall survival was 9.5 v 15.8 months for NF-kB-positive and NF-kB-negative patients, respectively (P = .036) CONCLUSION: The difference in median TTP, overall survival, and response rate seem to confirm that NF-kB may play a crucial role in predicting the efficacy of cetuximab and irinotecan in advanced colorectal tumors.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Camptothecin / analogs & derivatives. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. NF-kappa B / metabolism
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Cetuximab. Disease Progression. Drug Eruptions / etiology. Drug Resistance, Neoplasm. Female. Humans. Immunohistochemistry. Male. Middle Aged. Survival Rate

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  • [CommentIn] J Clin Oncol. 2008 Mar 10;26(8):1388-9; author reply 1389-90 [18323566.001]
  • (PMID = 17761976.001).
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Biomarkers, Tumor; 0 / NF-kappa B; 7673326042 / irinotecan; PQX0D8J21J / Cetuximab; XT3Z54Z28A / Camptothecin
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45. Sugahara S, Kajiki M, Kuriyama H, Kobayashi TR: Complete regression of xenografted human carcinomas by a paclitaxel-carboxymethyl dextran conjugate (AZ10992). J Control Release; 2007 Jan 22;117(1):40-50
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  • To improve their pharmacological profiles, AZ10992 was synthesized based on the concept that a rational design of a polymer-drug conjugate would increase the efficacy of the parent drug.
  • Additionally, the comparative efficacy studies of AZ10992 and paclitaxel using a panel of human tumor xenografts in nude mice showed the advantages of drug-polymer conjugation.
  • Also, HT-29 colorectal tumor xenografts, which are highly refractory to paclitaxel, showed complete regression after AZ10992 administered at 30 mg/kg/day (seven injections for 4-days).
  • Pharmacokinetic studies showed that there were significant increases in the amount and the exposure time of total paclitaxel in the tumors after intravenous administration of AZ10992, which explains the enhanced efficacy of AZ10992.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma / drug therapy. Dextrans / therapeutic use. Paclitaxel / analogs & derivatives. Paclitaxel / therapeutic use
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Carbohydrate Sequence. Cell Line, Tumor. Chromatography, High Pressure Liquid. Colonic Neoplasms / drug therapy. Dose-Response Relationship, Drug. Humans. Injections, Intravenous. Male. Mice. Mice, Inbred BALB C. Molecular Sequence Data. Molecular Weight. Neoplasm Transplantation. Tissue Distribution

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  • (PMID = 17126446.001).
  • [ISSN] 0168-3659
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AZ 10992; 0 / Antineoplastic Agents, Phytogenic; 9044-05-7 / carboxymethyl dextran; K3R6ZDH4DU / Dextrans; P88XT4IS4D / Paclitaxel
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46. Fujii T, Tachibana M, Dhar DK, Ueda S, Kinugasa S, Yoshimura H, Kohno H, Nagasue N: Combination therapy with paclitaxel and thalidomide inhibits angiogenesis and growth of human colon cancer xenograft in mice. Anticancer Res; 2003 May-Jun;23(3B):2405-11
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  • [Title] Combination therapy with paclitaxel and thalidomide inhibits angiogenesis and growth of human colon cancer xenograft in mice.
  • BACKGROUND: Combination chemotherapy is increasingly practiced for treating malignancies with greater sensitivity and less toxicity.
  • Paclitaxel is a potent anti-tumor agent but has dose-limiting side-effects, whereas thalidomide is an orally active anti-angiogenic drug but less than sufficient to exert anti-tumor effect as a single agent.
  • MATERIALS AND METHODS: Nude mice bearing hypervascular (LS174T) and less vascular (HT29) colon carcinomas were challenged with either a non-cytotoxic dose of paclitaxel, thalidomide or a combination of paclitaxel and thalidomide.
  • RESULTS: Significant growth retardation was noticed only in the combination treatment group of LS174T tumors.
  • Microvessel density data indicated a significantly low count in the combination treatment group compared to the others.
  • Trends of decreased expression of angiogenic growth factors and increased apoptotic index were noticed in the combination treatment group.
  • CONCLUSION: The results of this study underscore the therapeutic efficacy of concomitant use of paclitaxel and thalidomide in the treatment of highly vascular colorectal tumors in a xenograft model.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Colonic Neoplasms / drug therapy. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Division / drug effects. Endothelial Growth Factors / biosynthesis. Endothelium, Vascular / drug effects. Fibroblast Growth Factor 2 / biosynthesis. Humans. Intercellular Signaling Peptides and Proteins / biosynthesis. Lymphokines / biosynthesis. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Paclitaxel / administration & dosage. Thalidomide / administration & dosage. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors. Xenograft Model Antitumor Assays

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  • (PMID = 12894521.001).
  • [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 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; 4Z8R6ORS6L / Thalidomide; P88XT4IS4D / Paclitaxel
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47. Warren RS, Kirn DH: Liver-directed viral therapy for cancer p53-targeted adenoviruses and beyond. Surg Oncol Clin N Am; 2002 Jul;11(3):571-88, vi
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  • [Title] Liver-directed viral therapy for cancer p53-targeted adenoviruses and beyond.
  • Both replication-incompetent (rAd.p53, or SCH58500) and replication-selective (dl1520, or Onyx-015) adenoviruses are being developed for the treatment of p53-deficient cancers.
  • Hepatic arterial infusion (HAI) has historically been used to selectively target colorectal tumors within the liver; consequently, regional therapy with adenovirus in this setting is an attractive approach.
  • [MeSH-major] Adenoviridae / genetics. Colorectal Neoplasms / pathology. Gene Transfer Techniques. Genes, p53 / genetics. Genetic Therapy / methods. Genetic Vectors / therapeutic use. Liver Neoplasms / secondary. Liver Neoplasms / therapy. Viral Vaccines / therapeutic use
  • [MeSH-minor] Animals. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Hepatic Artery. Humans. Infusions, Intra-Arterial. Maximum Tolerated Dose


48. Lin Q, Li Z, Zhang L, Zhang S, Xu G, Guo L, An D: [Effects on micro-vessel density after pre-operative intra-arterial infusion chemotherapy in colorectal cancer]. Zhonghua Zhong Liu Za Zhi; 2002 Jan;24(1):84-6
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  • [Title] [Effects on micro-vessel density after pre-operative intra-arterial infusion chemotherapy in colorectal cancer].
  • OBJECTIVE: To evaluate the effects of pre-operative intra-arterial infusion chemotherapy on colorectal cancer.
  • METHODS: Twenty-eight patients with colorectal cancer, treated by surgery from February to October 2000, were divided into two groups randomly.
  • There were 12 patients in group A (pre-operative intra-arterial infusion chemotherapy) and 16 in group B (control).
  • RESULTS: Micro-vessel density in the center, surface of the tumor and adjacent tissue around the tumor were 40.46 +/- 7.06, 52.27 +/- 18.40, 49.92 +/- 8.15 in group A, and 46.09 +/- 12.21, 73.44 +/- 22.06, 51.94 +/- 12.64 in group B.
  • Micro-vessel density on the surface in group A was significantly lower than that of group B (P < 0.05), with no significance between the center and the adjacent tissue.
  • CONCLUSION: Pre-operative intra-arterial infusion chemotherapy is able to reduce micro-vessel density on the surface of colorectal tumor.
  • [MeSH-major] Colorectal Neoplasms / drug therapy

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  • (PMID = 11977649.001).
  • [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] Clinical Trial; Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
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49. Cairns RA, Bennewith KL, Graves EE, Giaccia AJ, Chang DT, Denko NC: Pharmacologically increased tumor hypoxia can be measured by 18F-Fluoroazomycin arabinoside positron emission tomography and enhances tumor response to hypoxic cytotoxin PR-104. Clin Cancer Res; 2009 Dec 1;15(23):7170-4
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  • [Title] Pharmacologically increased tumor hypoxia can be measured by 18F-Fluoroazomycin arabinoside positron emission tomography and enhances tumor response to hypoxic cytotoxin PR-104.
  • PURPOSE: Solid tumors contain microenvironmental regions of hypoxia that present a barrier to traditional radiotherapy and chemotherapy, and this work describes a novel approach to circumvent hypoxia.
  • We propose to overcome hypoxia by augmenting the effectiveness of drugs that are designed to specifically kill hypoxic tumor cells.
  • EXPERIMENTAL DESIGN: We have constructed RKO colorectal tumor cells that express a small RNA hairpin that specifically knocks down the hypoxia-inducible factor 1a (HIF1a) transcription factor.
  • We have further used these cells in vivo in xenografted tumors to determine the role of HIF1 in regulating tumor hypoxia in response to DCA using (18)F-fluoroazomycin arabinoside positron emission tomography, and its role in regulating tumor sensitivity to the combination of DCA and PR-104.
  • DCA transiently increases cellular oxygen consumption in vitro and increases the extent of tumor hypoxia in vivo as measured with (18)F-fluoroazomycin arabinoside positron emission tomography.
  • This approach transiently increases tumor hypoxia and represents an important method to improve antitumor efficacy of hypoxia-targeted agents, without increasing toxicity to oxygenated normal tissue.
  • [MeSH-major] Cell Hypoxia. Fluorine Radioisotopes / pharmacology. Neoplasms / drug therapy. Neoplasms / pathology. Nitrogen Mustard Compounds / pharmacology. Nitroimidazoles / pharmacology. Positron-Emission Tomography / methods
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Humans. Mice. Mice, Nude. Mitochondria / metabolism. Neoplasm Transplantation. Oxygen Consumption. Radiopharmaceuticals / pharmacology

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  • (PMID = 19920111.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA131199; United States / NCI NIH HHS / CA / R01 CA131199-01
  • [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 / Fluorine Radioisotopes; 0 / Nitrogen Mustard Compounds; 0 / Nitroimidazoles; 0 / PR-104; 0 / Radiopharmaceuticals; 0 / fluoroazomycin arabinoside
  • [Other-IDs] NLM/ NIHMS168716; NLM/ PMC2810128
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50. O'Neil BH, Goldberg RM: Novel chemotherapeutic and targeted agents in metastatic colorectal cancer: the time has arrived. Expert Opin Investig Drugs; 2003 Dec;12(12):1939-49
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  • [Title] Novel chemotherapeutic and targeted agents in metastatic colorectal cancer: the time has arrived.
  • Colorectal cancer is a common disease with a high rate of mortality and very well-understood genetics.
  • Primary therapy still consists of relatively non-specific treatments: surgery, radiotherapy and chemotherapy.
  • In this article, recent data in the now fast-moving field of treatment of unresectable metastatic colorectal cancer are reviewed, beginning with new developments in conventional cytotoxic therapies.
  • A number of new cytotoxic agents appear to have at least some activity in this disease, including classes of drugs that have been effective to date.
  • The very rapidly growing area of targeted therapy will also be expanded upon.
  • This year, for the first time, there has been a targeted therapy shown convincingly to prolong survival for patients with unresectable metastatic colorectal cancer in a well-performed Phase III trial.
  • Results with bevacizumab should lead to rapid expansion of the number of strategies targeting tumour neovasculature.
  • Additionally, an antibody against the epidermal growth factor, cetuximab, has been shown to have both single-agent activity and the potential ability to partially reverse resistance to a chemotherapy drug.
  • These advancements, as well as data on other novel treatment agents that have been studied specifically in patients with colorectal neoplasms, are discussed in detail.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Animals. Antibodies / therapeutic use. Drug Delivery Systems. Genes, erbB-2. Humans. Immunotherapy. Neoplasm Metastasis. Receptor, Epidermal Growth Factor / antagonists & inhibitors


51. Qutob SS, Proulx D, Mesak FM, Ng CE: Effects of N1, N13-diethylnorspermine (DENSPM) and X-radiation treatment on human colorectal tumor clones with varying X-radiation and drug responses. Radiat Res; 2005 Apr;163(4):357-63
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  • [Title] Effects of N1, N13-diethylnorspermine (DENSPM) and X-radiation treatment on human colorectal tumor clones with varying X-radiation and drug responses.
  • This study was designed to examine the effects of treatment with N1, N13-diethylnorspermine (DENSPM), a spermine analog, and X radiation on survival and on the polyamine and spermidine/spermine N1-acetyltransferase (SSAT) levels in closely related human colorectal tumor (HCT116) clones exhibiting a wide range of X-radiation and drug responses.
  • After treatment with DENSPM and X radiation, clonogenic cell survival was measured.
  • DENSPM enhanced the efficacy of radiation treatment in HCT116, HCT116-Clone2 (a radiation-resistant clone) and HCT116-Clone10 (a clone with similar X-radiation response as the parental HCT116 cells) but not in HCT116-CloneK (an X-radiation-sensitive but relatively drug-resistant clone).
  • Treatment with DENSPM without X radiation caused the most significant increase in SSAT activity (approximately 22-fold) and an almost complete depletion of SPD levels in HCT116-CloneK.
  • Our results suggest that (a) the lack of sensitization of X-radiation treatment by DENSPM in HCT116-CloneK was likely due to the prior depletion of SPD levels by DENSPM alone, (b) natural polyamine contents and/or inducibility of SSAT may be important factors influencing cellular response to combined X-radiation and DENSPM treatments, and (c) more importantly, there may be a potentially novel role for combining polyamine analogs such as DENSPM with X rays.
  • [MeSH-major] Cell Survival / drug effects. Cell Survival / radiation effects. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / radiotherapy. Spermine / administration & dosage. Spermine / analogs & derivatives
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Cloning, Molecular / methods. Combined Modality Therapy. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Drug Resistance, Neoplasm / radiation effects. Humans. Radiation Tolerance / drug effects. Treatment Outcome. X-Ray Therapy / methods

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  • (PMID = 15799689.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 121749-39-1 / N(1),N(11)-diethylnorspermine; 2FZ7Y3VOQX / Spermine
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52. Morimoto LM, Newcomb PA, Ulrich CM, Bostick RM, Lais CJ, Potter JD: Risk factors for hyperplastic and adenomatous polyps: evidence for malignant potential? Cancer Epidemiol Biomarkers Prev; 2002 Oct;11(10 Pt 1):1012-8
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  • Recent studies have suggested that hyperplastic polyps may be benign precursor lesions for a distinct subset of colorectal tumors.
  • Cases with hyperplastic polyps (n = 219), adenomas (n = 437), and both types of polyps (n = 138), along with colonoscopy-negative controls (n = 708), were identified at a gastroenterology practice in the Minneapolis area during 1991-1994.
  • Risk factors for hyperplastic and adenomatous polyps were generally similar to those for colorectal cancer.
  • Male sex, smoking, and alcohol consumption were associated with increased risk of all polyp groups; nonsteroidal anti-inflammatory drug use, hormone replacement therapy use, and calcium intake were associated with reduced risk.
  • The OR estimate for individuals diagnosed with both polyp types was 4.2 (95% CI, 1.9-9.3).
  • To the contrary, individuals with both polyp types may be expressing a phenotype distinct from those who have only adenomas and should be considered separately.
  • Overall, the similarity of the risk profiles of colorectal hyperplastic polyps, adenoma, and cancer provides additional support for the growing body of evidence that some hyperplastic polyps may have neoplastic potential.
  • [MeSH-major] Adenomatous Polyps / etiology. Colonic Neoplasms / etiology. Colonic Polyps / etiology. Smoking / adverse effects
  • [MeSH-minor] Adult. Aged. Alcohol Drinking / adverse effects. Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Case-Control Studies. Female. Hormone Replacement Therapy / adverse effects. Humans. Hyperplasia. Male. Middle Aged. Phenotype. Risk Factors. Sex Factors

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  • (PMID = 12376501.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5-T32-CA09168; United States / NIEHS NIH HHS / ES / ES-07033; United States / NCI NIH HHS / CA / P01 CA 50405; United States / NCI NIH HHS / CA / T32 CA09661
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal
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53. Matsunaga N, Yamada N, Ohira M, Tachimori A, Nishiguchi Y, Nishino H, Seki S, Hirakawa K: Combined treatment with selective cyclooxygenase-2 inhibitor and fluorinated pyrimidines for liver metastasis of colon cancer. Oncol Rep; 2004 Jan;11(1):167-71
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  • [Title] Combined treatment with selective cyclooxygenase-2 inhibitor and fluorinated pyrimidines for liver metastasis of colon cancer.
  • Liver metastasis is a major contributor to mortality in patients with colorectal cancer.
  • Hence, it is essential to establish preventive therapy to control liver metastasis.
  • Recently, it has become widely accepted that cyclooxygenase (COX)-2 inhibitors possess anti-cancer activity for various types of tumor, especially colorectal.
  • In this study, we have developed a combined treatment with a selective COX-2 inhibitor and fluorinated pyrimidines for liver metastasis of colorectal cancer, and examined the effect of these agents on proliferation and invasion of a highly metastatic human colon cancer cell line, LM-H3.
  • Combined treatment with etodolac and UFT markedly reduced liver metastasis.
  • In conclusion, combined treatment with etodolac and UFT might be a promising preventive therapy for liver metastasis of colon cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonic Neoplasms / drug therapy. Liver Neoplasms / drug therapy. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / administration & dosage. Dose-Response Relationship, Drug. Etodolac / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Isoenzymes / antagonists & inhibitors. Membrane Proteins. Mice. Mice, Inbred BALB C. Neoplasm Invasiveness. Prostaglandin-Endoperoxide Synthases

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  • (PMID = 14654921.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 2M36281008 / Etodolac; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; U3P01618RT / Fluorouracil
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54. Rubinfeld B, Upadhyay A, Clark SL, Fong SE, Smith V, Koeppen H, Ross S, Polakis P: Identification and immunotherapeutic targeting of antigens induced by chemotherapy. Nat Biotechnol; 2006 Feb;24(2):205-9
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  • [Title] Identification and immunotherapeutic targeting of antigens induced by chemotherapy.
  • Cancer cells differ from normal cells in their response to chemotherapy.
  • We exploited this dissimilarity by identifying and targeting tumor-specific, cell-surface proteins whose expression is induced by the chemotherapeutic irinotecan (CPT-11; Camptosar).
  • A cytotoxin-armed antibody reactive with one of these drug-induced surface proteins, the LY6D/E48 antigen, originally identified as the target of a monoclonal antibody reactive with squamous cell carcinomas, caused complete regression of colorectal tumor xenografts in mice treated with CPT-11, whereas either agent alone was less effective.
  • These results suggest that a positive therapeutic index may be generated for other drug combinations by immunotherapeutic targeting of chemotherapy-induced antigens.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, Neoplasm / immunology. Camptothecin / analogs & derivatives. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / immunology. Drug Delivery Systems / methods. Immunotherapy / methods
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Base Sequence. Cell Line, Tumor. Female. Humans. Membrane Proteins / immunology. Mice. Mice, Nude. Molecular Sequence Data. Treatment Outcome

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  • [CommentIn] Nat Biotechnol. 2006 Feb;24(2):163-4 [16465160.001]
  • (PMID = 16444269.001).
  • [ISSN] 1087-0156
  • [Journal-full-title] Nature biotechnology
  • [ISO-abbreviation] Nat. Biotechnol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ U58516
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Membrane Proteins; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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55. Yuan F, Zhou W, Zhang J, Zhang Z, Zou C, Huang L, Zhang Y, Dai Z: Anticancer drugs are synergistic with freezing in induction of apoptosis in HCC cells. Cryobiology; 2008 Aug;57(1):60-5
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  • [Title] Anticancer drugs are synergistic with freezing in induction of apoptosis in HCC cells.
  • Cryotherapy has been shown to be an important therapeutic alternative to surgery in the treatment of hepatocellular carcinoma (HCC).
  • Here, the influence of cryo-chemotherapy on HCC was examined in vitro using the human HCC cell line Bel-7402, a drug-resistant HCC cell line originating from Bel-7402 cells (Bel-7402/R), as well as two control cell lines, the HCC cell line SMMC-7721 and a colorectal tumor cell line HIC-251.
  • Cells were treated with either exposure to different freezing temperatures (ranging from -15 to -80 degrees C for 20 min), exposure to sub-lethal concentrations of anticancer chemotherapy drugs or a combination of cryotherapy and chemotherapy.
  • We found that the combined treatment resulted in increases in both cell death and apoptosis compared to either treatment alone.
  • The increased level of apoptosis observed in Bel-7402 cells after cryo-chemotherapy was inhibited in the presence of caspase inhibitors.
  • Furthermore, Bax expression was increased 2- to 3-fold in cells exposed to the combination treatment compared with cells treated by freezing or drugs alone.
  • Although Bel-7402/R cells originated from the Bel-7402 cell line, they were more sensitive to the freezing procedure than the parental cell line.
  • In conclusion, our data show that in HCC cells, apoptosis induced by cryotherapy can be synergistically enhanced using anticancer drugs.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis. Carcinoma, Hepatocellular / therapy. Cryotherapy. Liver Neoplasms / therapy
  • [MeSH-minor] Annexin A5 / metabolism. Cell Death. Cell Line, Tumor. Cell Survival. Combined Modality Therapy. Freezing. Humans. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. RNA, Messenger / metabolism. Up-Regulation. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

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  • (PMID = 18586021.001).
  • [ISSN] 1090-2392
  • [Journal-full-title] Cryobiology
  • [ISO-abbreviation] Cryobiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein
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56. Baker SD: Pharmacology of fluorinated pyrimidines: eniluracil. Invest New Drugs; 2000 Nov;18(4):373-81
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  • The pharmacological inactivation of dihydropyrimidine dehydrogenase (DPD) represents one strategy to improve 5-FU therapy, which historically has been associated with unpredictable pharmacological behavior and toxicity.
  • By inactivating DPD and suppressing the catabolism of 5-FU, eniluracil has dramatically altered the pharmacological profile of 5-FU.
  • Administration of eniluracil 10 to 20 mg twice daily completely inactivates DPD activity both in peripheral blood mononuclear cells and in colorectal tumor tissue, and prolonged inhibition of DPD after discontinuation of eniluracil treatment has been noted.
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / pharmacokinetics. Dihydrouracil Dehydrogenase (NADP). Drug Synergism. Fluorouracil / pharmacokinetics. Humans. Oxidoreductases / antagonists & inhibitors

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  • (PMID = 11081573.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 2E2W0W5XIU / eniluracil; 56HH86ZVCT / Uracil; EC 1.- / Oxidoreductases; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); U3P01618RT / Fluorouracil
  • [Number-of-references] 43
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57. Yegüez JF, Martinez SA, Sands DR, Sands LR, Hellinger MD: Colorectal malignancies in HIV-positive patients. Am Surg; 2003 Nov;69(11):981-7
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  • [Title] Colorectal malignancies in HIV-positive patients.
  • Due to the development of more effective medications, those infected with HIV are living longer.
  • Consequently, more tumors and infections have been added to the AIDS-defining criteria in the last decade.
  • Our aim was to review the occurrence and clinical course of colorectal (CR) malignancies in HIV infected/AIDS patients from a single institution.
  • A retrospective review of HIV/AIDS patients with colorectal malignant tumors was undertaken.
  • We included adult patients, with ELISA and Western blot test positive for HIV, and primary malignant tumors located in the colon or rectum.
  • Malignant neoplasms of the anus were excluded for the purposes of this study.
  • Twelve patients (9 males and 3 females), mean age 41 years, were identified with the following neoplasm: 6 adenocarcinomas (ACA), 5 non-Hodgkin lymphomas (NHL), and 1 small-cell carcinoma.
  • Intravenous drug abuse was the main risk factor for HIV.
  • No patient had identified risk factors for colorectal neoplasm.
  • Five out of six patients with ACA had metastatic disease at the time of diagnosis.
  • One patient with stage II ACA developed early liver metastases after colonic resection.
  • This is the largest series of cases of colorectal cancer in the HIV/AIDS patient population published in the English language and the largest number of colorectal ACA reported in this unique population.
  • Early in our experience, tumors frequently found in immunoincompetent patients were detected (NHL).
  • More recently, we have only treated patients with colorectal ACA; none of them had no risk factors for colorectal cancer (family history, IBD, FAP, HNPCC).
  • These patients developed tumors at earlier ages and were diagnosed at an advanced stage.
  • Therefore, these tumors may be associated with the grade of immunosuppression induced during the course of the HIV infection and with a tumorigenic effect of the HIV on the colonic epithelium.
  • The use of the new antiretroviral therapy regimens should be further evaluated to know its impact in the survival.
  • [MeSH-major] Colorectal Neoplasms / complications. HIV Infections / complications


58. Saif MW, Sandoval A: Atypical hand-and-foot syndrome in an African American patient treated with capecitabine with normal DPD activity: is there an ethnic disparity? Cutan Ocul Toxicol; 2008;27(4):311-5
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  • Fluoropyrimidines constitute the backbone of chemotherapy regimens for gastrointestinal tumors, especially colorectal cancer (CRC).
  • Comparison of oral and intravenous fluoropyrimidine treatments in patients with CRC has shown that hand-and-foot syndrome (HFS) (all grades) has the most frequently reported association with toxicity from capecitabine, an oral fluoropyrimidine.
  • This article presents the case of a 69-year-old African American man with a gastric adenocarcinoma status post gastrectomy who received 5-fluorouracil (5-FU) plus leucovorin for 5 days, to be followed by radiation plus capecitabine given 5 days per week for 5 weeks, and then 8 weeks of capecitabine monotherapy.
  • He developed discoloration of his palms consistent with HFS, contrary to the pattern and degree of HFS reported in the current guidelines as proposed in the drug insert.
  • This finding becomes more important as our recent findings suggest that DPD deficiency may be more common among African Americans.
  • This case also suggests that severe toxicity to infusional 5-FU might not be indicative of severe toxicity to oral fluoropyrimidine drugs.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Aged. Antimetabolites, Antineoplastic / adverse effects. Capecitabine. Humans. Male. Stomach Neoplasms / drug therapy

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  • (PMID = 19037763.001).
  • [ISSN] 1556-9535
  • [Journal-full-title] Cutaneous and ocular toxicology
  • [ISO-abbreviation] Cutan Ocul Toxicol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); U3P01618RT / Fluorouracil
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59. Marsh S, McKay JA, Cassidy J, McLeod HL: Polymorphism in the thymidylate synthase promoter enhancer region in colorectal cancer. Int J Oncol; 2001 Aug;19(2):383-6
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  • [Title] Polymorphism in the thymidylate synthase promoter enhancer region in colorectal cancer.
  • Thymidylate synthase (TS) is an important target for chemotherapy drugs such as 5-fluorouracil and raltitrexed.
  • Over-expression of TS has been linked to chemotherapy resistance.
  • The presence of a triple tandem repeat (TSER*3) increases in vitro TS expression compared to a double tandem repeat (TSER*2) and is associated with higher in vivo tumor TS activity.
  • In this study, PCR analysis of genomic DNA from 121 patients with colorectal cancer demonstrated 29% of patients were homozygous for TSER*3, 16% were homozygous for TSER*2 and 55% were heterozygous.
  • In 44/45 microdissected tumors the TS enhancer genotype was identical between paired samples of colorectal tumor and normal tissue.
  • In 24 patients receiving a bolus/infusion 5-fluorouracil (5FU) regimen for metastatic colorectal cancer, 22% of non-responders to chemotherapy were homozygous for TSER*2 compared with 40% of responders.
  • [MeSH-major] Colorectal Neoplasms / genetics. Enhancer Elements, Genetic / genetics. Promoter Regions, Genetic / genetics. Thymidylate Synthase / genetics
  • [MeSH-minor] DNA, Neoplasm / chemistry. DNA, Neoplasm / genetics. Gene Frequency. Genotype. Humans. Polymorphism, Genetic. Tandem Repeat Sequences / genetics

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  • (PMID = 11445856.001).
  • [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 / DNA, Neoplasm; EC 2.1.1.45 / Thymidylate Synthase
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60. Afrem G, Crăiţoiu S, Mărgăritescu C, Mogoantă SS: The study of p53 and CA19-9 prognostic molecular markers in colorectal carcinomas. Rom J Morphol Embryol; 2010;51(3):473-81
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  • [Title] The study of p53 and CA19-9 prognostic molecular markers in colorectal carcinomas.
  • Immunohistochemistry represents a relatively new identification technique of cellular and tissular antigens due to an antigen-antibody binding interactions, applied more and more in the pathology laboratories for positive and differential diagnosis of premalignant and malignant lesions and also for evolutive prognosis of tumoral formations.
  • The present study is based on the immunohistochemical investigation of some molecular markers with a prognosis value in colorectal cancers (CCR), like the antibody p53 immune expression and of some factors supposed to have prognosis value, such as CA19-9 (carcinoembryonic antigen, carbohydrate antigen or Lewis antigen).
  • In the last decade, the studies have tried to define the prognosis of the molecular markers that allow the identification of the patients with recurrent risk after surgical treatment and who can benefit from chemotherapy in an efficient way.
  • The purpose of the study on immunohistochemical markers is to aim towards the treatment based on molecular phenotypes of colorectal tumors.
  • In 2000, according to the Consensus Conference of the Colorectal Working Group of the American Joint Committee on Cancer Prognostic Factors (AJC), there were established four categories of prognosis factors in colorectal cancers based on the practical importance and the number of studies referring to them.
  • [MeSH-major] Biomarkers, Tumor / metabolism. CA-19-9 Antigen / metabolism. Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 20809023.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen; 0 / Tumor Suppressor Protein p53
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61. Bruin SC, Verwaal VJ, Vincent A, van't Veer LJ, van Velthuysen ML: A clinicopathologic analysis of peritoneal metastases of colorectal and appendiceal origin. Ann Surg Oncol; 2010 Sep;17(9):2330-40
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  • [Title] A clinicopathologic analysis of peritoneal metastases of colorectal and appendiceal origin.
  • OBJECTIVE: To predict clinical outcome by classification of peritoneal metastases (PM) of colorectal or appendiceal origin.
  • BACKGROUND: This study investigates whether standardized histological classification can predict outcome for PM of colorectal or appendiceal origin treated with cytoreduction and hyperthermic intraperitoneal chemotherapy (HIPEC).
  • For overall survival (OS) and disease-free survival (DFS) Cox proportional-hazard models were constructed.
  • Covariates included tumor, patient, and treatment characteristics.
  • RESULTS: PM could be categorized into four groups: low-grade, well-differentiated mucinous tumor (DPAM); intermediated-grade mucinous carcinoma (PMCA-i); high-grade mucinous carcinoma (PMCA); and high-grade nonmucinous carcinoma (PCA).
  • Multivariate analysis showed that histological classification, gender, number of segments affected, completeness of cytoreduction, and HIPEC as primary treatment were significant related to OS and DFS.
  • Of PM originating from an appendix tumor, 29% were of non-DPAM type.
  • Of primary colorectal tumors, 37% resulted in mucinous PM, and another 26% of PM of colorectal origin had partly mucinous histology.
  • [MeSH-major] Adenocarcinoma, Mucinous / secondary. Appendiceal Neoplasms / pathology. Colorectal Neoplasms / pathology. Peritoneal Neoplasms / secondary
  • [MeSH-minor] Aged. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 20232161.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
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62. Coss A, Tosetto M, Fox EJ, Sapetto-Rebow B, Gorman S, Kennedy BN, Lloyd AT, Hyland JM, O'Donoghue DP, Sheahan K, Leahy DT, Mulcahy HE, O'Sullivan JN: Increased topoisomerase IIalpha expression in colorectal cancer is associated with advanced disease and chemotherapeutic resistance via inhibition of apoptosis. Cancer Lett; 2009 Apr 18;276(2):228-38
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  • [Title] Increased topoisomerase IIalpha expression in colorectal cancer is associated with advanced disease and chemotherapeutic resistance via inhibition of apoptosis.
  • The influence of topoisomerase IIalpha gene (TOP2A) or protein alterations on disease progression and treatment response in colorectal cancer (CRC) is unknown.
  • Topoisomerase IIalpha levels, proliferation index, and HER2 expression were examined in 228 colorectal tumors by immunohistochemistry.
  • Cell growth inhibition and apoptosis were quantified using the crystal violet assay and flow cytometry, respectively, in response to drug treatment.
  • Amplification of TOP2A was identified in 3 (7.7%) tumors using array CGH and confirmed using FISH.
  • At the protein level, topoisomerase IIalpha staining was observed in 157 (69%) tumors, and both staining and intensity levels were associated with an aggressive tumor phenotype (p values 0.04 and 0.005, respectively).
  • Using logistic regression analysis, topoisomerase IIalpha remained significantly associated with advanced tumor stage when corrected for tumor proliferation (p=0.007) and differentiation (p=0.001).
  • In vitro, overexpression of topoisomerase IIalpha was associated with resistance to irinotecan (p=0.001) and etoposide chemotherapy (p=0.03), an effect mediated by inhibition of apoptosis.
  • Topoisomerase IIalpha overexpression is significantly associated with alterations in tumor behavior and response to drug treatment in CRC.
  • [MeSH-major] Antigens, Neoplasm / physiology. Apoptosis. Colorectal Neoplasms / enzymology. DNA Topoisomerases, Type II / physiology. DNA-Binding Proteins / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Proliferation. Chromosomal Instability. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Receptor, ErbB-2 / analysis

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  • (PMID = 19111388.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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63. Martinez-Balibrea E, Martínez-Cardús A, Musulén E, Ginés A, Manzano JL, Aranda E, Plasencia C, Neamati N, Abad A: Increased levels of copper efflux transporter ATP7B are associated with poor outcome in colorectal cancer patients receiving oxaliplatin-based chemotherapy. Int J Cancer; 2009 Jun 15;124(12):2905-10
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  • [Title] Increased levels of copper efflux transporter ATP7B are associated with poor outcome in colorectal cancer patients receiving oxaliplatin-based chemotherapy.
  • Recently, the copper efflux transporters ATP7B and ATP7A have been implicated in the transport of and resistance to platinum drugs in breast and ovarian cancers.
  • Because of the extensive use of oxaliplatin in colorectal cancer (CRC), we examined the expression of both transporters in tumors from CRC patients treated with oxaliplatin/5FU and sought to determine whether their expression can predict clinical outcome in these patients.
  • ATP7B and ATP7A levels were determined by quantitative real-time PCR in 50 primary tumors of previously untreated patients with advanced colorectal adenocarcinoma who were subsequently treated with oxaliplatin/5FU.
  • Additionally, ATP7B protein expression was assessed by immunohistochemical staining using a tissue microarray.
  • Patients with the lowest mRNA expression levels of ATP7B had a significantly longer time to progression (TTP) (p = 0.0009) than patients with the highest levels (12.14 months vs. 6.43 months) who also had an increased risk of progression (HR = 3.56; 95% CI, 1.6-7.9; p = 0.002).
  • In conclusion, ATP7B mRNA and protein expression in colorectal tumors is associated with clinical outcome to oxaliplatin/5FU.
  • Prospective studies are required to evaluate the role of this marker in tailoring chemotherapy.
  • [MeSH-major] Adenosine Triphosphatases / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cation Transport Proteins / metabolism. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Chemotherapy, Adjuvant. Female. Fluorouracil / administration & dosage. Follow-Up Studies. Humans. Immunoenzyme Techniques. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Invasiveness. Organoplatinum Compounds / administration & dosage. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tissue Array Analysis. Treatment Outcome

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  • [Copyright] Copyright 2008 UICC.
  • (PMID = 19296535.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cation Transport Proteins; 0 / Organoplatinum Compounds; 0 / RNA, Messenger; 04ZR38536J / oxaliplatin; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.3.4 / ATP7A protein, human; EC 3.6.3.4 / Wilson disease protein; U3P01618RT / Fluorouracil
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64. Mentha G, Roth AD, Terraz S, Giostra E, Gervaz P, Andres A, Morel P, Rubbia-Brandt L, Majno PE: 'Liver first' approach in the treatment of colorectal cancer with synchronous liver metastases. Dig Surg; 2008;25(6):430-5
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  • [Title] 'Liver first' approach in the treatment of colorectal cancer with synchronous liver metastases.
  • BACKGROUND: In patients with synchronous colorectal liver metastases, an approach reversing the traditional therapeutic order - i.e. starting with chemotherapy first, doing the liver surgery second, and performing the colorectal surgery last - is theoretically appealing as it avoids the risk of metastatic progression during treatment of the primary tumor.
  • PATIENTS AND METHODS: 35 patients with advanced synchronous colorectal metastases and nonobstructive colorectal tumors were treated with the reversed approach.
  • Five patients could not complete the program (one death from sepsis during chemotherapy, 3 cases of progressive disease under treatment, and one case of vanishing liver metastases).
  • One patient needed a Hartmann's procedure for obstruction after a first-step hepatectomy, and 1 patient had a rectal anastomotic leak.
  • Potential problems, in particular regrowth of vanishing metastases and primary tumors, chemotherapy-associated liver damage, and large bowel obstruction, can be minimized by careful multidisciplinary selection, planning and execution.
  • [MeSH-major] Colorectal Neoplasms / pathology. Colorectal Neoplasms / therapy. Hepatectomy / methods. Liver Neoplasms / secondary. Liver Neoplasms / therapy. Neoadjuvant Therapy
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Colectomy / methods. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Pilot Projects. Prospective Studies. Risk Assessment. Survival Analysis. Time Factors. Treatment Outcome


65. Loeffler-Ragg J, Mueller D, Gamerith G, Auer T, Skvortsov S, Sarg B, Skvortsova I, Schmitz KJ, Martin HJ, Krugmann J, Alakus H, Maser E, Menzel J, Hilbe W, Lindner H, Schmid KW, Zwierzina H: Proteomic identification of aldo-keto reductase AKR1B10 induction after treatment of colorectal cancer cells with the proteasome inhibitor bortezomib. Mol Cancer Ther; 2009 Jul;8(7):1995-2006
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  • [Title] Proteomic identification of aldo-keto reductase AKR1B10 induction after treatment of colorectal cancer cells with the proteasome inhibitor bortezomib.
  • Targeting the ubiquitin-proteasome pathway with the proteasome inhibitor bortezomib has emerged as a promising approach for the treatment of several malignancies.
  • The cellular and molecular effects of this agent on colorectal cancer cells are poorly characterized.
  • This study investigated the antiproliferative effect of bortezomib on colorectal cancer cell lines (Caco-2 and HRT-18).
  • The in vitro efficacy of bortezomib as a single agent in colorectal cancer cell lines was confirmed.
  • This study shows for the first time a bortezomib-induced up-regulation of AKR1B10.
  • Small interfering RNA-mediated inhibition of this enzyme with known intracellular detoxification function sensitized HRT-18 cells to therapy with the proteasome inhibitor.
  • To further characterize the relevance of AKR1B10 for colorectal tumors, immunohistochemical expression was shown in 23.2% of 125 tumor specimens.
  • These findings indicate that AKR1B10 might be a target for combination therapy with bortezomib.
  • [MeSH-major] Aldehyde Reductase / biosynthesis. Boronic Acids / pharmacology. Colorectal Neoplasms / drug therapy. Protease Inhibitors / pharmacology. Proteome / analysis. Pyrazines / pharmacology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Blotting, Western. Bortezomib. Cell Cycle / drug effects. Cohort Studies. Cyclooxygenase 2 / metabolism. Electrophoresis, Gel, Two-Dimensional. HSP72 Heat-Shock Proteins / metabolism. Humans. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Survival Rate. Tissue Array Analysis. Tumor Cells, Cultured

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  • (PMID = 19567817.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Boronic Acids; 0 / HSP72 Heat-Shock Proteins; 0 / Protease Inhibitors; 0 / Proteome; 0 / Pyrazines; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 69G8BD63PP / Bortezomib; EC 1.1.1.- / AKR1B10 protein, human; EC 1.1.1.21 / Aldehyde Reductase; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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66. Wang Y, Bansal V, Zelikin AN, Caruso F: Templated synthesis of single-component polymer capsules and their application in drug delivery. Nano Lett; 2008 Jun;8(6):1741-5
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  • [Title] Templated synthesis of single-component polymer capsules and their application in drug delivery.
  • The general applicability of this approach is demonstrated by the preparation of nanocapsules using various polymers, including synthetic polyelectrolytes, polypeptides, and polypeptide-drug conjugates.
  • The potential of doxorubicin (Dox)-loaded poly(L-glutamic acid) nanocapsules in tumor therapy applications is demonstrated via in vitro degradation experiments, which show a near-linear release of the Dox in the presence of a lysosomal hydrolase, nanocapsule uptake by human colorectal tumor cells, and delivery of the anticancer drug into the tumor cells, leading to tumor cell death.
  • [MeSH-major] Cell Survival / drug effects. Colorectal Neoplasms / metabolism. Doxorubicin / administration & dosage. Doxorubicin / pharmacokinetics. Drug Carriers / chemistry. Polyglutamic Acid / chemistry

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  • (PMID = 18489168.001).
  • [ISSN] 1530-6984
  • [Journal-full-title] Nano letters
  • [ISO-abbreviation] Nano Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Capsules; 0 / Drug Carriers; 25513-46-6 / Polyglutamic Acid; 80168379AG / Doxorubicin
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67. Koshiishi H, Yoshimura T, Okamura T, Tamamoto F, Takahashi E, Hayashi N, Koshiishi Y: [Evaluation of bronchial arterial infusion (BAI) for metastatic lung tumor from colorectal cancer]. Gan To Kagaku Ryoho; 2004 Oct;31(11):1838-41
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  • [Title] [Evaluation of bronchial arterial infusion (BAI) for metastatic lung tumor from colorectal cancer].
  • Three cases of metastatic lung tumor from colorectal cancer with an ineffectual systemic chemotherapy were examined based on the therapeutic effectiveness and safety of bronchial infusion (BAI) as a symptomatic therapy.
  • Two out of three cases were rectal cancer and the third case being ascending colon cancer.
  • The lung metastases became large in size and thoracic symptoms (severe cough, chest pain) appeared in spite of the systemic chemotherapy of CPT-11, 5-FU and CDDP.
  • A low dosage of BAI was administered by using CPT-11 (40 mg/m2) + CDDP (40 mg/m2) as one shot, and was repeated (three and six times respectively) for the two cases.
  • All three patients were stable and showed improvement in the condition of the disease.
  • BAI using low dosage of anti-cancer agents was effective, as means of improving the chest condition and quality of life in patients with metastatic lung tumor from colorectal cancer, with an ineffectual systemic chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Camptothecin / analogs & derivatives. Colorectal Neoplasms / pathology. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary
  • [MeSH-minor] Aged. Bronchial Arteries. Cisplatin / administration & dosage. Disease Progression. Female. Humans. Infusions, Intra-Arterial. Length of Stay. Male. Middle Aged


68. Vincenzi B, Santini D, Loupakis F, Addeo R, Rojas Llimpe FL, Baldi GG, Di Fabio F, Del Prete S, Pinto C, Falcone A, Tonini G: Cigarettes smoking habit may reduce benefit from cetuximab-based treatment in advanced colorectal cancer patients. Expert Opin Biol Ther; 2009 Aug;9(8):945-9
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  • [Title] Cigarettes smoking habit may reduce benefit from cetuximab-based treatment in advanced colorectal cancer patients.
  • There are reports showing that NF-kappaB expression and activity is enhanced after nicotine treatment.
  • Some data demonstrated that NF-kappaB activation plays a role in the induction of resistance to cetuximab and irinotecan in advanced colorectal tumors.
  • The aim of this study was to evaluate the effect of cigarette smoking on cetuximab efficacy in advanced colorectal cancer patients.
  • METHODS: We retrospectively analysed the smoking habits of 200 patients treated with a variety of anticancer regimens containing cetuximab for advanced colorectal cancer.
  • All patients were irinotecan-resistant and received an oxaliplatin-based first line treatment.
  • RESULTS: Out of 200 patients 58 declared a history of cigarette smoking, 108 patients never smoked and the remaining 44 patients were cigarette smokers during cetuximab-based anticancer therapy.
  • Of the 44 smokers, 18 smoked more than 10 cigarettes per day.
  • No statistically significant differences in terms of response rate (RR) and time to progression (TTP) were identified between previous smokers and never smokers.
  • Comparing smokers of more than 10 cigarettes per day and smokers of less than 10 cigarettes per day no differences were detected in RR, TTP or OS.
  • CONCLUSIONS: Our results suggest that cigarette smoking during anticancer treatment with a cetuximab-based regimen may be responsible for a decrease in RR and lead to a lower TTP.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Colorectal Neoplasms / drug therapy. Smoking / adverse effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Cetuximab. Disease Progression. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Organoplatinum Compounds / pharmacology. Retrospective Studies. Risk. Treatment Outcome

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  • (PMID = 19534585.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 7673326042 / irinotecan; PQX0D8J21J / Cetuximab; XT3Z54Z28A / Camptothecin
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69. Messersmith W, Oppenheimer D, Peralba J, Sebastiani V, Amador M, Jimeno A, Embuscado E, Hidalgo M, Iacobuzio-Donahue C: Assessment of Epidermal Growth Factor Receptor (EGFR) signaling in paired colorectal cancer and normal colon tissue samples using computer-aided immunohistochemical analysis. Cancer Biol Ther; 2005 Dec;4(12):1381-6
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  • [Title] Assessment of Epidermal Growth Factor Receptor (EGFR) signaling in paired colorectal cancer and normal colon tissue samples using computer-aided immunohistochemical analysis.
  • The Epidermal Growth Factor Receptor (EGFR) plays a role in multiple tumor cell processes and is targeted by several anticancer therapies.
  • Although EGFR mutations may determine tumor susceptibility in a small proportion of patients, knowledge of the EGFR signaling pathway status in tumors may help guide further drug development and hypothesis-driven combination studies.
  • We aimed to validate and apply a novel computer-aided immunohistochemical (IHC) technique to characterize the status of EGFR signaling in matched colorectal tumor and normal colon tissue samples.
  • Tissue Microarrays (TMA)were made from both cancerous and normal colorectal tissue in 18 patients and stained with antibodies against EGFR, phospho-EGFR (pEGFR), Akt, pAkt, MAPK, and pMAPK.
  • A post-scan "image microdissection" technique of analyzing heterogeneous human samples showed good correlation between paired human samples [Pearson correlation for tumors, 0.922 (p < .001)].
  • We conclude that ACIS IHC of human tissue samples is quantitative, reproducible, and correlates with Western blots and ELISA in cell line pellets as well as pathologist's scores of human samples.
  • Colorectal tumors show higher staining of pEGFR and downstream effectors compared to matched normal colorectal tissues.
  • [MeSH-major] Colon / chemistry. Colorectal Neoplasms / chemistry. Image Processing, Computer-Assisted / methods. Receptor, Epidermal Growth Factor / analysis. Signal Transduction


70. Kim YJ, Hong KS, Chung JW, Kim JH, Hahm KB: Prevention of colitis-associated carcinogenesis with infliximab. Cancer Prev Res (Phila); 2010 Oct;3(10):1314-33
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  • The emergence of infliximab was an epochal event in the treatment of inflammatory bowel disease (IBD).
  • Multiple colorectal tumors developed in 75% to 80% of control mice, whereas only 16.7% of mice treated with infliximab on the 1st, 3rd, and 7th weeks developed colon tumors.
  • Significant decreases in tumor necrosis factor-α level, mast cell number, and the expression of inflammatory cytokines were observed in top-down strategy using infliximab.
  • Conclusively, earlier and intensive therapy with infliximab should be considered for either mitigating clinical course or preventing ultimate development of colitic cancer in high-risk IBD patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Colitis / complications. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Animals. Anti-Inflammatory Agents / therapeutic use. Apoptosis / drug effects. Blotting, Western. Cytokines / biosynthesis. Dextran Sulfate / toxicity. Disease Models, Animal. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inflammation / complications. Inflammation / metabolism. Infliximab. Jurkat Cells. Matrix Metalloproteinases / biosynthesis. Matrix Metalloproteinases / drug effects. Mice. Mice, Inbred C57BL. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] ©2010 AACR.
  • (PMID = 20736334.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Cytokines; 9042-14-2 / Dextran Sulfate; B72HH48FLU / Infliximab; EC 3.4.24.- / Matrix Metalloproteinases
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71. McKay JA, Lloret C, Murray GI, Johnston PG, Bicknell R, Ahmed FY, Cassidy J, McLeod HL: Application of the enrichment approach to identify putative markers of response to 5-fluorouracil therapy in advanced colorectal carcinomas. Int J Oncol; 2000 Jul;17(1):153-8
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  • [Title] Application of the enrichment approach to identify putative markers of response to 5-fluorouracil therapy in advanced colorectal carcinomas.
  • A wide range of tumor response is seen amongst patients with the same stage of colorectal cancer, even with the use of uniform chemotherapy.
  • The significant economic and personal impact of chemotherapy provides the impetus for the identification of markers of response for use in guiding patient treatment.
  • However, practical constraints prevent evaluation of all putative markers in a definitive manner.
  • In this study, the enrichment approach was evaluated by examining the expression of a panel of putative response markers in selected patient populations with advanced colorectal cancer (i.e., those demonstrating the best and the poorest clinical response to a standardized 5-fluorouracil/folinic acid chemotherapy regimen).
  • Bcl-2 overexpression in primary colorectal tumor specimens was found to correlate with clinical response of metastatic deposits to chemotherapy (P=0.044), as did the site of the primary tumor (P=0.011).
  • However, no clear association was observed between response status and the other examined factors (p53, PCNA, TP, MMPs 1, 2 or 9, TIMPs 1 or 2, TS, Dukes' stage at initial diagnosis, histological grade, sex or age).
  • This approach has allowed prioritization of markers of clinical response on which larger, statistically definitive studies will be performed.
  • [MeSH-major] Biomarkers, Tumor / analysis. Colonic Neoplasms / drug therapy. Colorectal Neoplasms / drug therapy. Rectal Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Female. Humans. Leucovorin / therapeutic use. Liver Neoplasms / drug therapy. Liver Neoplasms / pathology. Liver Neoplasms / secondary. Male. Matrix Metalloproteinase 1 / analysis. Matrix Metalloproteinase 2 / analysis. Middle Aged. Neoplasm Metastasis. Predictive Value of Tests. Proliferating Cell Nuclear Antigen / analysis. Proto-Oncogene Proteins c-bcl-2 / analysis. Survival Rate. Thymidylate Synthase / analysis. Tissue Inhibitor of Metalloproteinases / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 10853033.001).
  • [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 / Biomarkers, Tumor; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tissue Inhibitor of Metalloproteinases; 0 / Tumor Suppressor Protein p53; EC 2.1.1.45 / Thymidylate Synthase; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.7 / Matrix Metalloproteinase 1; Q573I9DVLP / Leucovorin
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72. Hirata A, Hosoi F, Miyagawa M, Ueda S, Naito S, Fujii T, Kuwano M, Ono M: HER2 overexpression increases sensitivity to gefitinib, an epidermal growth factor receptor tyrosine kinase inhibitor, through inhibition of HER2/HER3 heterodimer formation in lung cancer cells. Cancer Res; 2005 May 15;65(10):4253-60
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  • Gefitinib (Iressa), an epidermal growth factor receptor targeting drug, has been clinically useful for the treatment of patients with non-small cell lung cancer (NSCLC).
  • Gefitinib is currently being applied in clinical studies as either a monotherapy, or as part of a combination therapy against prostate, head and neck, gastric, breast, and colorectal tumors.
  • However, success rates vary between different tumor types, and thus it is important to understand which molecular target(s) are responsible for limiting the therapeutic efficacy of the drug.
  • Treatment with 0.5 to 1 micromol/L gefitinib specifically blocked Akt activation in both HER2-transfectant lines, but not in the parental LK2 cells.
  • Treatment of LK2/HER2 cells with gefitinib markedly decreased the formation of HER2/HER3 heterodimers, HER3 basal phosphorylation, and the association of p85alpha with HER3.
  • [MeSH-major] Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, ErbB-2 / antagonists & inhibitors. Receptor, ErbB-3 / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Cycle Proteins / biosynthesis. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p27. Dose-Response Relationship, Drug. G1 Phase / drug effects. Humans. Phosphorylation / drug effects. Protein Kinase Inhibitors / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Transfection. Tumor Suppressor Proteins / biosynthesis


73. Ellis LM: Angiogenesis and its role in colorectal tumor and metastasis formation. Semin Oncol; 2004 Dec;31(6 Suppl 17):3-9
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  • [Title] Angiogenesis and its role in colorectal tumor and metastasis formation.
  • Advances in our comprehension of cancer biology and metastasis formation have led to the development of new therapeutic approaches that target tumor biology.
  • In phase I trials, targeting VEGF with single-agent therapy did not produce clinical benefit for patients, despite promise in preclinical trials.
  • However, the recent data showing that anti-VEGF therapy can enhance the effects of chemotherapy demonstrate the utility in targeting angiogenic factors as a component of antineoplastic regimens.
  • This article will highlight what is known about colorectal cancer angiogenesis, and will discuss how therapy targeting VEGF may enhance the effects of chemotherapy (and radiation therapy).
  • [MeSH-major] Angiogenesis Inducing Agents. Angiogenesis Inhibitors. Colorectal Neoplasms / blood supply. Neovascularization, Pathologic
  • [MeSH-minor] Angiopoietins. Animals. Humans. Integrins. Neoplasm Metastasis. Platelet-Derived Growth Factor. Receptor, TIE-2. Receptors, Vascular Endothelial Growth Factor. Ribonuclease, Pancreatic. Thrombospondins. Thymidine Phosphorylase. Vascular Endothelial Growth Factors

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  • (PMID = 15696024.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16672
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Angiogenesis Inhibitors; 0 / Angiopoietins; 0 / Integrins; 0 / Platelet-Derived Growth Factor; 0 / Thrombospondins; 0 / Vascular Endothelial Growth Factors; EC 2.4.2.4 / Thymidine Phosphorylase; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 3.1.27.- / angiogenin; EC 3.1.27.5 / Ribonuclease, Pancreatic
  • [Number-of-references] 82
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74. Lassmann S, Hennig M, Rosenberg R, Nährig J, Schreglmann J, Krause F, Poignee-Heger M, Nekarda H, Höfler H, Werner M: Thymidine phosphorylase, dihydropyrimidine dehydrogenase and thymidylate synthase mRNA expression in primary colorectal tumors-correlation to tumor histopathology and clinical follow-up. Int J Colorectal Dis; 2006 Apr;21(3):238-47
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  • [Title] Thymidine phosphorylase, dihydropyrimidine dehydrogenase and thymidylate synthase mRNA expression in primary colorectal tumors-correlation to tumor histopathology and clinical follow-up.
  • AIM: Evaluation of thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD), and thymidylate synthase (TS) mRNA levels in formalin-fixed, and paraffin-embedded tissues of patients with colorectal cancer and their prognostic and/or predictive value.
  • MATERIALS AND METHODS: Total RNA was isolated from microdissected, formalin-fixed, and paraffin-embedded tissues (controls and tumor) and subjected to quantitative RT-PCR (QRT-PCR) in the LightCycler system.
  • Resulting mRNA levels correlated to tumor histology (n=102) and the clinical follow-up in patients treated by resection alone (n=40) and by resection plus adjuvant 5-FU-based chemotherapy (n=52).
  • RESULTS: Correlation to histopathological parameters revealed a significant association between tumor stage and the TP mRNA level (T and N category and UICC) as well as the TP:DPD (T and N category and UICC) and TS:DPD (T category) ratio.
  • In addition, tumor differentiation was correlated to the TS mRNA level and the TS:DPD ratio.
  • Moreover, a high TP:DPD ratio (>8.1; p=0.002) and, marginally, low DPD (<8.2; p=0.05) mRNA levels significantly correlated to disease-free survival.
  • CONCLUSION: We present a novel, standardized approach for TP, DPD, and TS mRNA quantification in archival tissue specimens and applied this to a large series of primary colorectal tumors.
  • Correlations to histopathological parameters and clinical follow-up revealed an association of TP, DPD and TS mRNA expression patterns with tumor stage and suggested new prognostic and predictive markers for patients with colorectal cancer.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Dihydrouracil Dehydrogenase (NADP) / genetics. RNA, Messenger / genetics. Thymidine Phosphorylase / genetics. Thymidylate Synthase / genetics
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonic Neoplasms / enzymology. Colonic Neoplasms / genetics. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Rectal Neoplasms / enzymology. Rectal Neoplasms / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16132996.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.1.1.45 / Thymidylate Synthase; EC 2.4.2.4 / Thymidine Phosphorylase
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75. Ciccolini J, Evrard A, Cuq P: Thymidine phosphorylase and fluoropyrimidines efficacy: a Jekyll and Hyde story. Curr Med Chem Anticancer Agents; 2004 Mar;4(2):71-81
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  • Thymidine phosphorylase (TP) is markedly upregulated in many solid tumors such as colorectal, breast and kidney cancers.
  • Some studies have shown that high tumoral TP expression was associated indeed with poor clinical response and tumor aggressiveness.
  • Conversely, other reports demonstrated that tumoral TP could be considered as a good response factor in patients exposed to fluoropyrimidine drugs.
  • As a result, TP-targeting as a rationale for anticancer therapy remains unclear.
  • TP inhibitors are being synthesized as an attempt to fight neoangiogenesis, whereas promising new strategies such as taxotere/capecitabine or radiotherapy/fluoropyrimidines associations aim at nothing but boosting TP activity to optimize drug activation in tumors.
  • Such a discrepancy illustrates the complexity of understanding and predicting the exact role of TP in the clinical outcome of patients exposed to fluoropyrimidines, a group of major drugs extensively used in oncology.
  • [MeSH-minor] Angiogenesis Inhibitors / chemistry. Angiogenesis Inhibitors / pharmacology. Angiogenesis Inhibitors / therapeutic use. Animals. Clinical Trials as Topic. Fluorouracil / analogs & derivatives. Fluorouracil / pharmacology. Fluorouracil / therapeutic use. Humans. Neoplasms / blood supply. Neoplasms / drug therapy. Neoplasms / enzymology. Structure-Activity Relationship. Transfection. Up-Regulation

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  • (PMID = 15032715.001).
  • [ISSN] 1568-0118
  • [Journal-full-title] Current medicinal chemistry. Anti-cancer agents
  • [ISO-abbreviation] Curr Med Chem Anticancer Agents
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Pyrimidines; EC 2.4.2.4 / Thymidine Phosphorylase; U3P01618RT / Fluorouracil
  • [Number-of-references] 165
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76. Nijkamp MW, Hoogwater FJ, Steller EJ, Westendorp BF, van der Meulen TA, Leenders MW, Borel Rinkes IH, Kranenburg O: CD95 is a key mediator of invasion and accelerated outgrowth of mouse colorectal liver metastases following radiofrequency ablation. J Hepatol; 2010 Dec;53(6):1069-77
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  • [Title] CD95 is a key mediator of invasion and accelerated outgrowth of mouse colorectal liver metastases following radiofrequency ablation.
  • CD95 is best known for its ability to induce apoptosis but can also promote tumorigenesis in apoptosis-resistant tumor cells.
  • Therefore, we tested whether CD95 signaling plays a role in accelerated outgrowth of colorectal liver metastases following RFA.
  • METHODS: Hypoxia-induced invasion was assessed in three-dimensional EGFP-expressing C26 tumor cell cultures by confocal microscopy.
  • Invasion and outgrowth of liver metastases following RFA were analyzed by post-mortem confocal microscopy and by morphometric assessment of tumor load.
  • Hypoxia-induced tumor cell invasion in vitro increased the expression of CD95 and CD95L and induced translocation of CD95 to the invasive front.
  • In vitro invasion, metastasis invasion, and accelerated tumor growth in the transition zone were strongly suppressed by neutralizing CD95L or by suppressing tumor cell CD95.
  • CONCLUSIONS: Hypoxia causes autocrine activation of CD95 on colorectal tumor cells, thereby promoting local invasion and accelerated metastasis outgrowth in the hypoxic transition zone following RFA.
  • Further pre-clinical work is needed to assess the role of CD95L neutralization, either alone or in combination with chemotherapy, in limiting aggressive recurrence of liver metastases following RFA.
  • [MeSH-major] Antigens, CD95 / physiology. Colorectal Neoplasms. Liver Neoplasms, Experimental / immunology. Liver Neoplasms, Experimental / secondary
  • [MeSH-minor] Animals. Anoxia / immunology. Anoxia / pathology. Catheter Ablation. Cell Line, Tumor. Fas Ligand Protein / antagonists & inhibitors. Fas Ligand Protein / deficiency. Fas Ligand Protein / genetics. In Vitro Techniques. Male. Mice. Mice, Inbred BALB C. Mice, Knockout. Neoplasm Invasiveness / immunology. RNA Interference. Signal Transduction / immunology

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  • [Copyright] Copyright © 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20832890.001).
  • [ISSN] 1600-0641
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Fas Ligand Protein
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77. Di Nicolantonio F, Mercer SJ, Knight LA, Gabriel FG, Whitehouse PA, Sharma S, Fernando A, Glaysher S, Di Palma S, Johnson P, Somers SS, Toh S, Higgins B, Lamont A, Gulliford T, Hurren J, Yiangou C, Cree IA: Cancer cell adaptation to chemotherapy. BMC Cancer; 2005;5:78
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  • [Title] Cancer cell adaptation to chemotherapy.
  • BACKGROUND: Tumor resistance to chemotherapy may be present at the beginning of treatment, develop during treatment, or become apparent on re-treatment of the patient.
  • The mechanisms involved are usually inferred from experiments with cell lines, as studies in tumor-derived cells are difficult.
  • Studies of human tumors show that cells adapt to chemotherapy, but it has been largely assumed that clonal selection leads to the resistance of recurrent tumors.
  • METHODS: Cells derived from 47 tumors of breast, ovarian, esophageal, and colorectal origin and 16 paired esophageal biopsies were exposed to anticancer agents (cisplatin; 5-fluorouracil; epirubicin; doxorubicin; paclitaxel; irinotecan and topotecan) in short-term cell culture (6 days).
  • Real-time quantitative PCR was used to measure up- or down-regulation of 16 different resistance/target genes, and when tissue was available, immunohistochemistry was used to assess the protein levels.
  • RESULTS: In 8/16 paired esophageal biopsies, there was an increase in the expression of multi-drug resistance gene 1 (MDR1) following epirubicin + cisplatin + 5-fluorouracil (ECF) chemotherapy and this was accompanied by increased expression of the MDR-1 encoded protein, P-gp.
  • Exposure to topotecan in vitro, resulted in >4-fold down-regulation of TOPOIIalpha in 6/7 colorectal tumors and 8/10 ovarian tumors.
  • CONCLUSION: This study suggests that up-regulation of resistance genes or down-regulation in target genes may occur rapidly in human solid tumors, within days of the start of treatment, and that similar changes are present in pre- and post-chemotherapy biopsy material.
  • The molecular processes used by each tumor appear to be linked to the drug used, but there is also heterogeneity between individual tumors, even those with the same histological type, in the pattern and magnitude of response to the same drugs.
  • Adaptation to chemotherapy may explain why prediction of resistance mechanisms is difficult on the basis of tumor type alone or individual markers, and suggests that more complex predictive methods are required to improve the response rates to chemotherapy.
  • [MeSH-major] Drug Therapy / methods. Gene Expression Regulation, Neoplastic. Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Biopsy. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Cell Line, Tumor. Cisplatin / pharmacology. Down-Regulation. Doxorubicin / pharmacology. Drug Resistance, Neoplasm. Epirubicin / pharmacology. Fluorouracil / pharmacology. Humans. Immunohistochemistry. P-Glycoprotein / metabolism. Paclitaxel / pharmacology. Recurrence. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Topotecan / pharmacology. Treatment Outcome. Up-Regulation

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  • (PMID = 16026610.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 3Z8479ZZ5X / Epirubicin; 7673326042 / irinotecan; 7M7YKX2N15 / Topotecan; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC1199589
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78. Jo WS, Carethers JM: Chemotherapeutic implications in microsatellite unstable colorectal cancer. Cancer Biomark; 2006;2(1-2):51-60
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  • [Title] Chemotherapeutic implications in microsatellite unstable colorectal cancer.
  • Chemotherapy for colorectal cancer is currently offered to patients based on the stage of their cancer, and there is evidence to show an overall survival benefit with 5-fluorouracil-based (5-FU) therapy for patients with lymph node metastasis who receive it.
  • The pathogenesis of colorectal cancer involves genomic instability, with about 15% of tumors demonstrating a form of genomic instability called high-frequency microsatellite instability (MSI-H) and due to loss of DNA mismatch repair function, and the remainder of colorectal tumors lacking MSI-H with retained DNA mismatch repair function and called microsatellite stable (MSS), with a large proportion of these tumors demonstrating another form of genomic instability called chromosomal instability.
  • There is now evidence to show that the form of genomic instability that is present in a patient's colorectal cancer may predict a survival benefit from 5-FU.
  • In particular, patients whose colorectal tumors have MSI-H do not gain a survival benefit with 5-FU as compared to patients with MSS tumors.
  • In vitro evidence supports these findings, as MSI-H colon cancer cell lines are more resistant to 5-FU compared to MSS cell lines.
  • The binding and subsequent cell death events would be absent in colorectal tumors with MSI-H, which have lost intact DNA mismatch repair function.
  • These findings suggest that: (a) tumor cytotoxicity of 5-FU is mediated by DNA mechanisms in addition to well-known RNA mechanisms, and (b) patients whose tumors demonstrate MSI-H may not benefit from 5-FU therapy.
  • Future studies should include a better understanding of the cellular mechanisms of the DNA recognition of 5-FU, multi-centered prospective trials investigating the survival benefit of 5-FU based on genomic instability, and the investigation of alternative chemotherapeutic regimens for patients with MSI-H tumors to improve survival.

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  • (PMID = 17192059.001).
  • [ISSN] 1574-0153
  • [Journal-full-title] Cancer biomarkers : section A of Disease markers
  • [ISO-abbreviation] Cancer Biomark
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK067287; United States / NIDDK NIH HHS / DK / DK067287-01A2; United States / NIDDK NIH HHS / DK / DK067287; United States / NCI NIH HHS / CA / R01 CA090231; United States / NIDDK NIH HHS / DK / R01 DK067287-01A2; United States / NCI NIH HHS / CA / CA90231
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 87
  • [Other-IDs] NLM/ NIHMS209550; NLM/ PMC4948976
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79. Sharma RI, Smith TA: Colorectal tumor cells treated with 5-FU, oxaliplatin, irinotecan, and cetuximab exhibit changes in 18F-FDG incorporation corresponding to hexokinase activity and glucose transport. J Nucl Med; 2008 Aug;49(8):1386-94
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  • [Title] Colorectal tumor cells treated with 5-FU, oxaliplatin, irinotecan, and cetuximab exhibit changes in 18F-FDG incorporation corresponding to hexokinase activity and glucose transport.
  • The purpose of this study was to determine therapy-induced changes in 18F-FDG incorporation at the colorectal tumor cell level in response to conventional and novel chemotherapy agents and examine how these changes relate to factors involved in 18F-FDG incorporation.
  • 18F-FDG incorporation, glucose transport, hexokinase (HK) activity, adenosine triphosphate (ATP) content, annexin V binding, and cell cycle distribution were determined after 24-, 48-, and 72-h treatments.
  • Eight-hour treatments with and without subsequent incubation in drug-free medium were also examined.
  • A clonogenic assay was used to determine the tumor-forming ability of treated cells.
  • RESULTS: Apoptosis was evident in SW620 cells, especially after treatment with irinotecan and 5-FU.
  • 18F-FDG incorporation was increased in SW620 cells after 24- or 48-h treatments with some agents and in HCT-8 cells after irinotecan treatment but was decreased in all 72-h treatments or cell-line combinations including cetuximab.
  • Treatment of SW620 cells for 8 h followed by 64 h in drug-free medium also resulted in decreased 18F-FDG incorporation.
  • ATP levels were decreased by oxaliplatin treatment and increased at 48 or 72 h after irinotecan treatment.
  • CONCLUSION: 18F-FDG incorporation is modulated by therapy-induced changes in both glucose transport and HK activity depending on the tumor cell.
  • Colorectal cells treated with IC50 doses of cetuximab also exhibit decreased 18F-FDG.
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Biological Transport. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Cetuximab. Colorectal Neoplasms. Drug Interactions. Fluorouracil / pharmacology. Humans. Organoplatinum Compounds / pharmacology. Radiopharmaceuticals / metabolism

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  • (PMID = 18632807.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 0 / Radiopharmaceuticals; 04ZR38536J / oxaliplatin; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 7673326042 / irinotecan; EC 2.7.1.1 / Hexokinase; IY9XDZ35W2 / Glucose; PQX0D8J21J / Cetuximab; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
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80. Chong G, Lee FT, Hopkins W, Tebbutt N, Cebon JS, Mountain AJ, Chappell B, Papenfuss A, Schleyer P, U P, Murphy R, Wirth V, Smyth FE, Potasz N, Poon A, Davis ID, Saunder T, O'keefe GJ, Burgess AW, Hoffman EW, Old LJ, Scott AM: Phase I trial of 131I-huA33 in patients with advanced colorectal carcinoma. Clin Cancer Res; 2005 Jul 1;11(13):4818-26
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  • [Title] Phase I trial of 131I-huA33 in patients with advanced colorectal carcinoma.
  • PURPOSE: Humanized monoclonal antibody A33 (huA33) targets the A33 antigen which is expressed on 95% of colorectal cancers.
  • A previous study has shown excellent tumor-targeting of iodine-131 labeled huA33 (131I-huA33).
  • EXPERIMENTAL DESIGNS: Fifteen patients with pretreated metastatic colorectal carcinoma each received two i.v. doses of 131I-huA33.
  • The first was an outpatient trace-labeled "scout" dose for biodistribution assessment, followed by a second "therapy" dose.
  • There were no acute infusion-related adverse events, and gastrointestinal toxicity was not observed despite uptake of 131I-huA33 in bowel.
  • Seven patients developed pruritus or rash, which was not related to 131I dose.
  • There was excellent tumor-targeting of 131I-huA33 shown in all patients.
  • The mean absorbed tumor dose was 6.49 +/- 2.47 Gy/GBq.
  • Four patients developed human anti-human antibodies.
  • At restaging, 4 patients had stable disease, whereas 11 patients had progressive disease.
  • CONCLUSION: Radioimmunotherapy using 131I-huA33 shows promise in targeting colorectal tumors, and is deliverable at a maximum tolerated dose of 40 mCi/m2.
  • Further studies of 131I-huA33 in combination with chemotherapy are planned.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Colorectal Neoplasms / radiotherapy. Iodine Radioisotopes / therapeutic use. Membrane Glycoproteins / immunology. Radioimmunotherapy / methods
  • [MeSH-minor] Adult. Aged. Exanthema / etiology. Female. Humans. Male. Middle Aged. Neutropenia / etiology. Pruritus / etiology. Radiotherapy Dosage. Tissue Distribution. Treatment Outcome

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  • (PMID = 16000579.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / GPA33 protein, human; 0 / Iodine Radioisotopes; 0 / Membrane Glycoproteins
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81. Sanborn R, Blanke CD: Cyclooxygenase-2 inhibition in colorectal cancer: boom or bust? Semin Oncol; 2005 Feb;32(1):69-75
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  • [Title] Cyclooxygenase-2 inhibition in colorectal cancer: boom or bust?
  • Currently, combination chemotherapy represents the standard of care treatment for patients with metastatic colorectal cancer in the United States.
  • Despite recent improvements with the addition of biologic agents, novel treatment approaches are needed to further benefit patients.
  • COX-2 is highly expressed in colorectal tumor neovasculature and nodal and liver metastases, and expression of COX-2 correlates with tumor stage and patient survival in selected series.
  • COX-2 may be related to colorectal cancer development and propagation through multiple mechanisms, including stimulation of growth, migration, and invasiveness, resistance to apoptosis, and enhancement of angiogenesis.
  • Epidemiologic data suggest nonsteroidal anti-inflammatory drugs (NSAIDs) might prevent development of colorectal cancers, and preclinical data suggest selective COX-2 inhibitors might be additive or synergistic with specific chemotherapeutic agents used in the treatment of colorectal cancer.
  • Despite the lack of published phase I data and the limited, preliminary results of phase II studies, combinations of celecoxib and standard colorectal cancer chemotherapy have entered randomized trials.
  • It is too early to definitively state whether COX-2 inhibition represents a major breakthrough in the treatment of colorectal cancer.
  • Pending the results of ongoing and planned phase III studies, use of COX-2 inhibitors as single agents or incorporation of COX-2 inhibition into combined modality therapy of colorectal cancer should be limited to the setting of clinical trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Cyclooxygenase Inhibitors / therapeutic use. Prostaglandin-Endoperoxide Synthases / metabolism
  • [MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Clinical Trials as Topic. Colonic Polyps / drug therapy. Colonic Polyps / metabolism. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Humans. Membrane Proteins. Protein Isoforms

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  • (PMID = 15726508.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Membrane Proteins; 0 / Protein Isoforms; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 71
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82. Kobayashi K, Matsumoto S, Morishima T, Kawabe T, Okamoto T: Cimetidine inhibits cancer cell adhesion to endothelial cells and prevents metastasis by blocking E-selectin expression. Cancer Res; 2000 Jul 15;60(14):3978-84
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  • Although the beneficial effect of cimetidine on survival in cancer has been clinically demonstrated in colorectal cancer patients, the mode of action of cimetidine has not been elucidated.
  • In this report, we have demonstrated for the first time that cimetidine can block the adhesion of a colorectal tumor cell line to the endothelial cell monolayer in cell culture and that it can suppress the metastasis of the tumor cell in a nude mouse model.
  • We also demonstrated that these antimetastasis effects of cimetidine might occur through down-regulation of the cell surface expression of E-selectin on endothelial cells, a ligand for sialyl Lewis antigens on tumor cells.
  • We found that the cimetidine-mediated down-regulation of E-selectin did not involve down-regulation of E-selectin mRNA or blocking of the nuclear translocation of nuclear factor kappaB, a transcriptional activator of E-selectin gene expression.
  • Because two other histamine type 2 receptor antagonists, famotidine and ranitidine, did not show any similar effect, these actions of cimetidine probably do not occur via blocking of the histamine receptor.
  • These observations support the idea that cancer metastasis can be blocked by cimetidine administration through blocking the adhesion of tumor cells to the endothelium when an interaction between E-selectin and sialyl-Lewis antigens plays a role.
  • [MeSH-major] Cimetidine / pharmacology. E-Selectin / metabolism. Endothelium, Vascular / drug effects. Endothelium, Vascular / metabolism. Histamine H2 Antagonists / pharmacology
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Nucleus / metabolism. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Enzyme Inhibitors / pharmacology. Enzyme-Linked Immunosorbent Assay. Famotidine / pharmacology. Humans. Interleukin-1 / metabolism. Liver Neoplasms / prevention & control. Liver Neoplasms / secondary. Mice. Mice, Nude. Microscopy, Confocal. NF-kappa B / metabolism. Neoplasm Transplantation. Oligosaccharides / metabolism. RNA, Messenger / metabolism. Ranitidine / pharmacology. Transcriptional Activation. Tumor Cells, Cultured. Umbilical Veins / drug effects. Umbilical Veins / metabolism

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  • (PMID = 10919677.001).
  • [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 / 5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine; 0 / E-Selectin; 0 / Enzyme Inhibitors; 0 / Histamine H2 Antagonists; 0 / Interleukin-1; 0 / NF-kappa B; 0 / Oligosaccharides; 0 / RNA, Messenger; 5QZO15J2Z8 / Famotidine; 80061L1WGD / Cimetidine; 884KT10YB7 / Ranitidine
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83. Bendardaf R, Lamlum H, Ristamäki R, Pyrhönen S: CD44 variant 6 expression predicts response to treatment in advanced colorectal cancer. Oncol Rep; 2004 Jan;11(1):41-5
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  • [Title] CD44 variant 6 expression predicts response to treatment in advanced colorectal cancer.
  • CD44 variant 6 (CD44v6) has been postulated to be involved in both carcinogenesis and tumor progression.
  • Therefore, we have examined CD44v6 expression in tumors from 57 patients with advanced colorectal cancer who received one of two chemotherapy regimes (either irinotecan alone or irinotecan and 5-flurouracil with folinic acid).
  • CD44v6 expression was determined immunohistochemically in 57 paraffin-embedded primary tumor sections and assessed using image analysis software.
  • Strong expression levels of CD44v6 were seen in 24/57 (42%) of tumors, moderate levels in 17/57 (30%), weak levels in 9/57 (16%) and no expression was seen in 7/57 (12%).
  • The pattern of staining was predominantly cytoplasmic, 7/57 tumors also exhibited membrane specific expression.
  • A significant association was found between tumor CD44v6 expression and treatment response (Fisher's exact test p=0.01).
  • Only 1/12 patients with no or weak tumor expression of CD44v6 showed a response to treatment whereas 20/41 (49%) patients with moderate or strong CD44v6 expression responded to treatment.
  • Evaluation of CD44v6 expression of locally advanced and metastatic colorectal tumors may enable the clinician to identify and select patients that will show the best response to irinotecan based chemotherapy.
  • [MeSH-major] Antigens, CD44 / biosynthesis. Colorectal Neoplasms / pathology. Glycoproteins / biosynthesis
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Fluorouracil / administration & dosage. Follow-Up Studies. Humans. Immunohistochemistry. Leucovorin / administration & dosage. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Survival Analysis


84. Buck E, Eyzaguirre A, Haley JD, Gibson NW, Cagnoni P, Iwata KK: Inactivation of Akt by the epidermal growth factor receptor inhibitor erlotinib is mediated by HER-3 in pancreatic and colorectal tumor cell lines and contributes to erlotinib sensitivity. Mol Cancer Ther; 2006 Aug;5(8):2051-9
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  • [Title] Inactivation of Akt by the epidermal growth factor receptor inhibitor erlotinib is mediated by HER-3 in pancreatic and colorectal tumor cell lines and contributes to erlotinib sensitivity.
  • Signaling through the receptor for epidermal growth factor receptor (EGFR) is frequently deregulated in solid tumors.
  • Herein, we have sought to understand the signaling pathways that mediate erlotinib sensitivity for pancreatic and colorectal cancers.
  • In a panel of 12 pancreatic tumor cell lines, we find that EGFR is coexpressed with HER-3 in all cell lines sensitive to erlotinib but not in insensitive cell lines.
  • Knockdown of HER-3 in BxPC3, an erlotinib-sensitive pancreatic tumor cell line, results in inhibition of the phosphorylation for both Akt and S6 and is associated with a decrease in cell proliferation and reduced sensitivity to erlotinib.
  • Therefore, EGFR transactivation of HER-3 mediates Akt signaling and can contribute to erlotinib sensitivity for pancreatic tumors.
  • We extended our analysis to a panel of 13 colorectal tumor cell lines and find that, like pancreatic, HER-3 is coexpressed with EGFR in the most erlotinib-sensitive cell lines but not in erlotinib-insensitive cell lines.
  • These studies suggest that HER-3 could be used as a biomarker to select patients who are most likely to respond to erlotinib therapy.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Pancreatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-akt / drug effects. Quinazolines / pharmacology. Receptor, ErbB-3 / metabolism
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Erlotinib Hydrochloride. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Phosphorylation. Protein Kinase Inhibitors / pharmacology. Protein Kinases / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Ribosomal Protein S6 Kinases / drug effects. Ribosomal Protein S6 Kinases / metabolism. Signal Transduction. TOR Serine-Threonine Kinases


85. Busemann C, Schmidt CA, Fendrich K, Hoffmann W: [Lung metastases of colorectal tumors: clinical background and development of care supply]. Radiologe; 2004 Jul;44(7):711-4
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  • [Title] [Lung metastases of colorectal tumors: clinical background and development of care supply].
  • [Transliterated title] Lungenmetastasen kolorektaler Tumoren: klinischer Hintergrund und Entwicklung des Versorgungsbedarfs.
  • The incidence of most cancers increases with age, including colorectal-, lung- and breast carcinomas.
  • Each year, approximately 50,000 new cases of colorectal carcinoma (CRC) are diagnosed in Germany with a peak incidence around the age of 65.
  • At diagnosis, 50% of CRC-cases show already metastases.
  • Cure of metastatic disease with chemotherapy, radiology or surgery alone or in combination can be rarely achieved in this situation.
  • However, palliative therapy regimens can significantly prolong life in most cases.
  • Besides systemic therapy, minimal invasive techniques for tumor reduction are an interesting option in the palliative situation, especially in elderly patients.
  • [MeSH-major] Colorectal Neoplasms / epidemiology. Lung Neoplasms / epidemiology. Lung Neoplasms / secondary. Minimally Invasive Surgical Procedures / trends. Palliative Care / trends

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  • (PMID = 15221153.001).
  • [ISSN] 0033-832X
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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86. Paradisi A, Mehlen P: Netrin-1, a missing link between chronic inflammation and tumor progression. Cell Cycle; 2010 Apr 1;9(7):1253-62
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  • [Title] Netrin-1, a missing link between chronic inflammation and tumor progression.
  • Netrin-1 discovered as a neuronal navigation cue, has been recently proposed to play a crucial role during colorectal tumorigenesis by regulating apoptosis.
  • The netrin-1 receptors, DCC (for Deleted in Colorectal Cancer) and UNC5H (UNC5 homologues), indeed belong to the functional family of dependence receptors that share the ability to induce apoptosis in the absence of their ligands and such a trait has been hypothesized to confer these receptors a tumor suppressor activity as their presence render cell survival dependent on ligand availability.
  • As a consequence, human tumors show either a loss of dependence receptors or a gain of netrin-1, allowing tumors to escape this safeguard mechanism.
  • We recently found that netrin-1 is a direct transcriptional target of the transcription factor NFκB, and that a fraction of colorectal tumors show a netrin-1 gain parallel to NFκB activation.
  • Moreover, colorectal cancers from patients affected by inflammatory bowel diseases (IBD) show upregulation of netrin-1.
  • We propose that induction of netrin-1 expression via NFκB in IBD patients could affect colorectal tumor promotion and progression and that inhibition of netrin-1 could be an innovative target for drug therapy in inflammation-driven colorectal cancers.
  • [MeSH-major] Inflammation / metabolism. Neoplasms / immunology. Neoplasms / metabolism. Nerve Growth Factors / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. Apoptosis / physiology. Humans. Inflammatory Bowel Diseases / metabolism. Models, Biological. NF-kappa B / metabolism. Receptors, Cell Surface / metabolism

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  • (PMID = 20305387.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Nerve Growth Factors; 0 / Receptors, Cell Surface; 0 / Tumor Suppressor Proteins; 0 / netrin receptors; 158651-98-0 / netrin-1
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87. Díaz GD, Paraskeva C, Thomas MG, Binderup L, Hague A: Apoptosis is induced by the active metabolite of vitamin D3 and its analogue EB1089 in colorectal adenoma and carcinoma cells: possible implications for prevention and therapy. Cancer Res; 2000 Apr 15;60(8):2304-12
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  • [Title] Apoptosis is induced by the active metabolite of vitamin D3 and its analogue EB1089 in colorectal adenoma and carcinoma cells: possible implications for prevention and therapy.
  • Vitamin D3 is believed to reduce the risk of colon cancer, and serum levels inversely correlate with colorectal cancer incidence.
  • The active metabolite, 1alpha,25-dihydroxyvitamin D3, has previously been shown to inhibit growth and promote differentiation of colon cancer cells.
  • In this study we examined the effects of alpha,25-dihydroxyvitamin D3 and EB1089 on five colorectal tumor cell lines (two adenoma and three carcinoma) to determine the mechanism of growth inhibition and to ascertain whether premalignant adenoma cells were responsive to these agents.
  • The ability of EB1089 to induce apoptosis in colorectal carcinoma cells suggests that this or other vitamin D analogues may prove clinically effective for the treatment of colorectal cancer.
  • Furthermore, the fact that it induces cell cycle arrest and apoptosis in the premalignant adenoma cells may suggest an application in colorectal cancer chemoprevention.
  • [MeSH-major] Apoptosis / drug effects. Calcitriol / analogs & derivatives. Calcitriol / pharmacology. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / prevention & control
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / prevention & control. Adenoma / drug therapy. Adenoma / metabolism. Adenoma / pathology. Adenoma / prevention & control. Alkaline Phosphatase / metabolism. Blotting, Western. Cell Adhesion / drug effects. Cell Differentiation / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. G1 Phase / drug effects. Genes, p53 / physiology. Humans. Membrane Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Cells, Cultured. bcl-2 Homologous Antagonist-Killer Protein

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  • (PMID = 10786699.001).
  • [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 / BAK1 protein, human; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2 Homologous Antagonist-Killer Protein; EC 3.1.3.1 / Alkaline Phosphatase; FXC9231JVH / Calcitriol; Q0OZ0D9223 / seocalcitol
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88. Ong CW, Kim LG, Kong HH, Low LY, Iacopetta B, Soong R, Salto-Tellez M: CD133 expression predicts for non-response to chemotherapy in colorectal cancer. Mod Pathol; 2010 Mar;23(3):450-7
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  • [Title] CD133 expression predicts for non-response to chemotherapy in colorectal cancer.
  • In this study, we examined both the prognostic and predictive significance of putative cancer stem cell markers in colorectal cancer.
  • In this study, immunohistochemistry for three candidate cancer stem cell markers (CD133, Oct-4 and Sox-2) and for six other postulated prognostic markers (CK7, CK20, Cox-2, Ki-67, p27 and p53) were performed using tissue microarrays containing 501 primary colorectal cancer cases.
  • Multivariate analysis revealed that positive expression for CD133 and Oct-4 was associated with significantly worse survival in patients treated by surgery alone (P=0.023 and P<0.001, respectively) and in patients treated with 5-fluorouracil-based chemotherapy (P=0.001 and P=0.021, respectively).
  • Stage III patients with negative CD133 expression showed an apparent survival benefit from 5-fluorouracil treatment (P=0.002), but not those with positive CD133 expression.
  • Positive expression of CD133 was also associated with poorer clinical response to chemotherapy in stage IV patients (P=0.006).
  • In summary, the putative cancer stem cell markers CD133 and Oct-4 showed strong prognostic significance in colorectal cancer.
  • Our results show for the first time that CD133+ colorectal tumors are more resistant to 5-fluorouracil-based chemotherapy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antigens, CD / metabolism. Antimetabolites, Antineoplastic / therapeutic use. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / drug therapy. Fluorouracil / therapeutic use. Glycoproteins / metabolism. Peptides / metabolism
  • [MeSH-minor] Chemotherapy, Adjuvant. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Octamer Transcription Factor-3 / metabolism. Prognosis. Survival Rate. Tissue Array Analysis

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  • (PMID = 20081809.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Octamer Transcription Factor-3; 0 / Peptides; U3P01618RT / Fluorouracil
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89. Buess M, Terracciano L, Reuter J, Ballabeni P, Boulay JL, Laffer U, Metzger U, Herrmann R, Rochlitz C: STRAP is a strong predictive marker of adjuvant chemotherapy benefit in colorectal cancer. Neoplasia; 2004 Nov-Dec;6(6):813-20
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  • [Title] STRAP is a strong predictive marker of adjuvant chemotherapy benefit in colorectal cancer.
  • BACKGROUND: Molecular predictors for the effectiveness of adjuvant chemotherapy in colorectal cancer are of considerable clinical interest.
  • To this aim, we analyzed the serine threonine receptor-associated protein (STRAP), an inhibitor of TGF-beta signaling, with regard to prognosis and prediction of adjuvant 5-FU chemotherapy benefit.
  • METHODS: The gene copy status of STRAP was determined using quantitative real-time polymerase chain reaction in 166 colorectal tumor biopsies, which had been collected from a randomized multicenter trial of 5-fluorouracil (5-FU)/mitomycin C (MMC) adjuvant chemotherapy of the Swiss Group for Clinical Cancer Research (SAKK).
  • RESULTS: Amplification of STRAP was found in 22.8% of the tumors.
  • When left without adjuvant chemotherapy, patients bearing tumors with a STRAP amplification had a significantly better prognosis (hazard ratio for death: 0.26; P=.004).
  • Interestingly, these patients, when receiving adjuvant treatment, had a worse survival (hazard ratio for death: 3.48; P=.019) than without chemotherapy, whereas patients carrying tumors with diploidy or deletion of STRAP benefited from the treatment (hazard ratio for death: 0.44; P=.052).
  • This suggests the amplification of STRAP as a strong predictor of an unfavorable effect of 5-FU-based adjuvant chemotherapy.
  • CONCLUSION: If confirmed, the STRAP gene copy status might provide a parameter to decide about the use of 5-FU-based adjuvant chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Carrier Proteins / biosynthesis. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / genetics
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Chemotherapy, Adjuvant. Female. Fluorouracil / therapeutic use. Gene Dosage. Humans. Male. Middle Aged. Mitomycin / therapeutic use. Polymerase Chain Reaction. Prognosis

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  • (PMID = 15720808.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Strap protein; 50SG953SK6 / Mitomycin; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC1531685
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90. Gialeli Ch, Kletsas D, Mavroudis D, Kalofonos HP, Tzanakakis GN, Karamanos NK: Targeting epidermal growth factor receptor in solid tumors: critical evaluation of the biological importance of therapeutic monoclonal antibodies. Curr Med Chem; 2009;16(29):3797-804
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  • [Title] Targeting epidermal growth factor receptor in solid tumors: critical evaluation of the biological importance of therapeutic monoclonal antibodies.
  • Numerous cellular pathways have a significant impact in the growth and metastatic potential of tumors.
  • One of the most important issues in cancer, which attracted the attention of clinical oncologists, is the potential use of targeted therapies.
  • EGFR is, therefore, an appealing target for molecular-targeted cancer therapy as it is expressed in a variety of solid tumors (colorectal, breast, head and neck, etc.).
  • Multiple therapeutic strategies have been developed to target EGFR, including monoclonal antibodies (mAbs), tyrosine kinase inhibitors (TKIs), ligand-toxin conjugates, and antisense oligonucleotides.
  • This review highlights the cellular effects of EGFR blockade by mAbs and their relationship to therapeutic efficacy and biological significance.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Drug Delivery Systems. Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Cell Proliferation / drug effects. Cetuximab. Humans

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  • (PMID = 19747140.001).
  • [ISSN] 1875-533X
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / panitumumab; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
  • [Number-of-references] 80
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91. Bardelli A, Siena S: Molecular mechanisms of resistance to cetuximab and panitumumab in colorectal cancer. J Clin Oncol; 2010 Mar 1;28(7):1254-61
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  • [Title] Molecular mechanisms of resistance to cetuximab and panitumumab in colorectal cancer.
  • Personalized cancer medicine based on the genetic milieu of individual colorectal tumors has long been postulated, but until recently this concept was not supported by clinical evidence.
  • The advent of the epidermal growth factor receptor (EGFR) -targeted monoclonal antibodies cetuximab and panitumumab has paved the way to the individualized treatment of metastatic colorectal cancer (mCRC).
  • Here we discuss the evidence that mCRCs respond differently to EGFR-targeted agents and that the tumor-specific response has a genetic basis.
  • The role of oncogenic activation of EGFR downstream effectors such as KRAS, BRAF, PIK3CA, and PTEN on response to therapy is discussed.
  • We suggest that CRCs lacking oncogenic alterations in these four genes have the highest probability of response to anti-EGFR therapies and are defined as "quadruple negative."
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Biomarkers, Tumor / analysis. Cetuximab. Drug Resistance, Neoplasm. Humans. Mutation. PTEN Phosphohydrolase / physiology. Phosphatidylinositol 3-Kinases / physiology. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Signal Transduction. ras Proteins / genetics

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  • [CommentIn] J Clin Oncol. 2010 Mar 1;28(7):1181-9 [20100964.001]
  • (PMID = 20100961.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / panitumumab; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / ras Proteins; PQX0D8J21J / Cetuximab
  • [Number-of-references] 54
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92. Pezo RC, Gandhi SJ, Shirley LA, Pestell RG, Augenlicht LH, Singer RH: Single-cell transcription site activation predicts chemotherapy response in human colorectal tumors. Cancer Res; 2008 Jul 1;68(13):4977-82
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  • [Title] Single-cell transcription site activation predicts chemotherapy response in human colorectal tumors.
  • Candidate gene and pathway approaches, and unbiased gene expression profiling, have identified marker signatures predictive of tumor phenotypes, such as drug sensitivity and invasive or metastatic potential.
  • However, application of such information to evaluation of tumors in the clinic is limited by cell heterogeneity in the tumor.
  • We have developed a novel method of fluorescence in situ hybridization (FISH) that can detect transcriptional activation of individual genes at their site in single cells in the interphase nucleus.
  • A major obstacle in the treatment of colorectal cancer is relative insensitivity to the chemotherapeutic agent 5-Fluorouracil (5-FU).
  • Here, we have developed a sensitive approach to predict relative sensitivity of colorectal cancer cells to 5-FU, using FISH with probes targeted to nascent mRNAs to measure the number of individual cells with active transcription sites for a panel of candidate genes.
  • As proof of principle, we show that this transcriptional profile is predictive of response to 5-FU in a small number of patient colon tumor tissues.
  • This approach provides a novel ability to identify and characterize unique minor cell populations in the tumor that may exhibit relative resistance to chemotherapy.

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  • (PMID = 18593893.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075503; United States / NCI NIH HHS / CA / R33 CA083208-05A1; United States / NCI NIH HHS / CA / CA100926-04; United States / NCI NIH HHS / CA / P30CA56036; United States / NCI NIH HHS / CA / CA083208-06; United States / NCI NIH HHS / CA / R01CA75503; United States / NCI NIH HHS / CA / R33CA83208; United States / NCI NIH HHS / CA / R33 CA083208-06; United States / NCI NIH HHS / CA / R33 CA083208; United States / NCI NIH HHS / CA / CA083208-05A1; United States / NCI NIH HHS / CA / U54 CA100926-05; United States / NCI NIH HHS / CA / U54 CA100926-04; United States / NCI NIH HHS / CA / CA083208-07; United States / NIGMS NIH HHS / GM / T32GM07288; United States / NCI NIH HHS / CA / R33 CA083208-07; United States / NCI NIH HHS / CA / R01 CA070896; United States / NCI NIH HHS / CA / P30CA13330; United States / NCI NIH HHS / CA / U54CA100926; United States / NCI NIH HHS / CA / R01CA107382; United States / NCI NIH HHS / CA / U54 CA100926-03; United States / NCI NIH HHS / CA / CA100926-03; United States / NCI NIH HHS / CA / R01CA70896; United States / NCI NIH HHS / CA / R01CA86072; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NCI NIH HHS / CA / R01 CA086072; United States / NCI NIH HHS / CA / P30 CA013330; United States / NCI NIH HHS / CA / R01 CA107382; United States / NCI NIH HHS / CA / P30 CA056036; United States / NCI NIH HHS / CA / CA100926-05; United States / NCI NIH HHS / CA / U54 CA100926
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAK1 protein, human; 0 / Biomarkers, Pharmacological; 0 / Cation Transport Proteins; 0 / MORF4L2 protein, human; 0 / Transcription Factors; 0 / bcl-2 Homologous Antagonist-Killer Protein; EC 2.1.1.45 / Thymidylate Synthase; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.3.4 / Wilson disease protein; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ NIHMS296021; NLM/ PMC3107669
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93. Gel'fand EB, Karabak VI, Platova ES, Gel'fand BR: [A trial of using timentin (ticarcillin/clavulanate) in treating abdominal surgical infection]. Antibiot Khimioter; 2000;45(3):24-9