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1. Zhang S, Lovejoy KS, Shima JE, Lagpacan LL, Shu Y, Lapuk A, Chen Y, Komori T, Gray JW, Chen X, Lippard SJ, Giacomini KM: Organic cation transporters are determinants of oxaliplatin cytotoxicity. Cancer Res; 2006 Sep 1;66(17):8847-57
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  • Although the platinum-based anticancer drugs cisplatin, carboplatin, and oxaliplatin have similar DNA-binding properties, only oxaliplatin is active against colorectal tumors.
  • The mechanisms for this tumor specificity of platinum-based compounds are poorly understood but could be related to differences in uptake.
  • The cytotoxicity of oxaliplatin was greater than that of cisplatin in six colon cancer cell lines [mean +/- SE of IC(50) in the six cell lines, 3.9 +/- 1.4 micromol/L (oxaliplatin) versus 11 +/- 2.0 micromol/L (cisplatin)] but was reduced by an OCT inhibitor, cimetidine, to a level similar to, or even lower than that of, cisplatin (29 +/- 11 micromol/L for oxaliplatin versus 19 +/- 4.3 micromol/L for cisplatin).
  • They also strongly suggest that expression of OCTs in tumors should be investigated as markers for selecting specific platinum-based therapies in individual patients.
  • The development of new anticancer drugs, specifically targeted to OCTs, represents a novel strategy for targeted drug therapy.

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  • (PMID = 16951202.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 34992; United States / NCI NIH HHS / CA / R37 CA034992; United States / NCI NIH HHS / CA / U54 CA112970-02; United States / NIGMS NIH HHS / GM / GM61390; United States / NCI NIH HHS / CA / U54 CA112970; United States / NIGMS NIH HHS / GM / U01 GM061390; United States / NIGMS NIH HHS / GM / R01 GM036780; United States / NIGMS NIH HHS / GM / U19 GM061390; United States / NCI NIH HHS / CA / R01 CA034992; United States / NIGMS NIH HHS / GM / GM36780; United States / NCI NIH HHS / CA / CA112970-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Adducts; 0 / Octamer Transcription Factor-1; 0 / Organic Cation Transport Proteins; 0 / Organoplatinum Compounds; 0 / POU2F1 protein, human; 0 / Pyridines; 0 / SLC22A2 protein, human; 0 / oxiplatin; 49DFR088MY / Platinum; 63231-63-0 / RNA; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS123190; NLM/ PMC2775093
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2. 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
University of Turin Instituional Repository AperTO. Full Text from .

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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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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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4. 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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5. 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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6. 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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7. D'Andrea MR, Gasparini G: The future of anti-EGFR therapy. Int J Biol Markers; 2007 S4 - Jan-Mar;22(4):88-93
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  • [Title] The future of anti-EGFR therapy.
  • A critical review of the anti-EGFR therapeutic strategies is also outlined.
  • The chimeric anti- EGFR monoclonal antibody cetuximab has been approved for EGFR-expressing colorectal tumors in patients who progress after irinotecan-based chemotherapy in combination with irinotecan and in squamous cell head and neck carcinomas for patients with locally advanced disease in combination with radiation therapy or after failure of platinum-based chemotherapy in recurrent or metastatic disease (FDA).
  • Cetuximab has the potential to provide an improvement of clinical outcome also in other indications and tumor types, particularly when used as first-line therapy combined with standard chemotherapy for metastatic disease or in the adjuvant setting.
  • (ii) the development of standardized predictive biomarkers as surrogates for early monitoring of drug efficacy; and (iii) adequate study design, statistical analysis and proper end points of efficacy to be applied in future prospective trials.

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  • (PMID = 28207119.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Paradisi A, Mehlen P: Netrin-1, a missing link between chronic inflammation and tumor progression. Cell Cycle; 2010 Apr 1;9(7):1253-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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9. 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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10. 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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11. Tono T, Ukei T, Masutani S, Shibata K, Ohzato H, Hasuike Y, Monden T: Management of hepatic arterial infusion port following prophylactic regional chemotherapy in patients who have undergone curative resection of colorectal liver metastases. Surg Today; 2003;33(9):679-83
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  • [Title] Management of hepatic arterial infusion port following prophylactic regional chemotherapy in patients who have undergone curative resection of colorectal liver metastases.
  • PURPOSE: Although hepatic arterial infusion (HAI) is widely performed as a prophylactic chemotherapy for patients who have undergone a curative resection of a metastatic liver tumor from colorectal cancer, the optimal management of implantable ports and catheters after the cessation of such adjuvant therapy remains to be elucidated.
  • METHODS: The survival and recurrence rate of 30 patients who received adjuvant regional chemotherapy following a hepatectomy were examined.
  • RESULTS: With a median follow-up period of 38.1 months, local recurrence in the residual liver was observed in only 5 patients (17%), and the 3-year hepatic disease-free survival was as high as 82%.
  • Furthermore, a second course of regional chemotherapy was carried out in only one patient, while a repeat hepatectomy was performed instead of chemotherapy in the other patients with hepatic recurrence.
  • CONCLUSIONS: Because HAI remarkably reduced the degree of relapse in the residual liver, there is no benefit in maintaining the port after discontinuing the chemotherapy.
  • Heparin administration via the same port after a cessation of the prophylactic HAI chemotherapy is not justified, and it is desirable to remove the implanted catheter when possible.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Colorectal Neoplasms / pathology. Infusion Pumps, Implantable. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Liver Neoplasms / surgery
  • [MeSH-minor] Anticoagulants / administration & dosage. Catheterization / instrumentation. Chemotherapy, Adjuvant. Disease-Free Survival. Female. Heparin / administration & dosage. Hepatectomy. Hepatic Artery. Humans. Infusions, Intra-Arterial / instrumentation. Male. Middle Aged. Neoplasm Recurrence, Local

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  • (PMID = 12928845.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anticoagulants; 9005-49-6 / Heparin
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12. Casado E, Folprecht G, Paz-Ares L, Rojo F, Köhne CH, Cortes-Funes H, Vauthier JM, Zacharchuk C, Baselga J, Tabernero J: A phase I/IIA pharmacokinetic (PK) and serial skin and tumor pharmacodynamic (PD) study of the EGFR irreversible tyrosine kinase inhibitor EKB-569 in combination with 5-fluorouracil (5FU), leucovorin (LV) and irinotecan (CPT-11) (FOLFIRI regimen) in patients (pts) with advanced colorectal cancer (ACC). J Clin Oncol; 2004 Jul 15;22(14_suppl):3543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I/IIA pharmacokinetic (PK) and serial skin and tumor pharmacodynamic (PD) study of the EGFR irreversible tyrosine kinase inhibitor EKB-569 in combination with 5-fluorouracil (5FU), leucovorin (LV) and irinotecan (CPT-11) (FOLFIRI regimen) in patients (pts) with advanced colorectal cancer (ACC).
  • : 3543 Background: In preclinical models, EKB-569 has shown growth inhibition of EGFR-expressing colorectal tumor cell lines with at least additive inhibition when combined with chemotherapy.
  • METHODS: We have conducted a phase I/IIA study with EKB-569 used in combination with the FOLFIRI regimen as first-line treatment in pts with ACC.
  • The objectives were to determine its safety, MTD, PK profile, antitumor activity and correlation with EGFR-signalling pathways in skin and tumors before and after treatment.
  • Oral EKB-569 was given daily starting on day 3 of cycle 1 (28 days per cycle) with IV infusion of FOLFIRI on days 1-2 and 15-16 (CPT-11 180 mg/m<sup>2</sup> 90 min, simultaneously with LV 400 mg/m<sup>2</sup> 120 min, followed by 5FU 400 mg/m<sup>2</sup> bolus and 2400 mg/m<sup>2</sup> 46-h continuous infusion).
  • Pts were enrolled to receive 10, 25, 50 or 75 mg EKB-569 (3-6 pts per cohort).
  • EKB-569 treatment resulted in complete inhibition of pEGFR and significant inhibition of pMAPK in both skin samples (11 pts) and tumor samples (3 pts) with no change in pAKT activity.

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  • (PMID = 28016564.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Morris E, Thomas J, Forman D, Quirke P, Cottier B, Poston GJ: The need for a revised staging system of metastatic (M) colorectal cancer (CRC): Evidence from a national perspective on survival following surgically treated (HPX) liver metastases. J Clin Oncol; 2009 May 20;27(15_suppl):4099

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The need for a revised staging system of metastatic (M) colorectal cancer (CRC): Evidence from a national perspective on survival following surgically treated (HPX) liver metastases.
  • : 4099 Background: AJCC V.6 (2002) places all patients with MCRC beyond the lymph node basin of the primary tumor in a homogenous Stage 4.
  • Patients with inoperable hepatic MCRC can be made operable with curative intent with chemotherapy yet remaining in Stage 4.
  • All care episodes in the 3 years following initial colorectal surgery were examined to determine the frequency of subsequent HPX.
  • Survival was calculated from the date of resection of each patient's primary colorectal tumor.
  • 1,483 (2.2%) subsequently underwent HPX <3 years of their colorectal operation.
  • Crude 5-year survival of patients who underwent HPX was 41.6% (95%CI 39.0-44.1%) from time of initial colectomy.

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  • (PMID = 27960750.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Rice SD, Ervin PR, Brower SL: Use of an in vitro chemoresponse assay to define a subset of colorectal carcinomas responsive to cetuximab. J Clin Oncol; 2009 May 20;27(15_suppl):e15127

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  • [Title] Use of an in vitro chemoresponse assay to define a subset of colorectal carcinomas responsive to cetuximab.
  • Thus, a singular approach to drug mechanism likely would not capture the true effects of cetuximab.
  • Cetuximab is FDA-approved to treat head and neck cancer and colorectal carcinomas and is being evaluated for use in non-small cell lung and endometrial cancer.
  • The current study describes an in vitro chemoresponse assay to predict response of primary cultures of human colorectal tumor specimens to cetuximab.
  • METHODS: The chemoresponse assay (ChemoFx) was developed using four different immortalized carcinoma cell lines (NCI-H292, NCI-H522, NCI-H1666, Calu3).
  • The chemoresponse assay was also performed on 54 first passage primary cultures of human colorectal tumor specimens.
  • Cell lines and specimens were treated with a 10 dose concentration range of cetuximab for 72 hours, stained with a nuclear dye, and remaining post-treatment live cells were counted.
  • RESULTS: Two of the examined cell lines showed response to cetuximab treatment; EC50 values for NCI-H292 and NCI-H1666 were 825nM and 13nM, respectively.
  • Dose-response curves of the 54 primary colorectal cultures revealed that 8% of the cultures tested were responsive to cetuximab, 22% had an intermediate response, and 70% were deemed non-responsive.
  • These results are consistent with a reported clinical response rate of 11% for cetuximab in colorectal carcinoma patients.
  • This could increase the efficacy of the current chemotherapy decision-making process for oncologists and their patients.

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  • (PMID = 27960835.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Tomita N, Fukunaga M, Okamura S, Ohzato H, Takatsuka Y, Shirane M, Yasuno H, Mori K, Fujii M, Matsuura N: The induction of apoptosis in colorectal cancers by preoperative administration of 5'-deoxy-5-fluorouridine (5'-DFUR) and its prediction from gene expression profile analysis using DNA microarray. J Clin Oncol; 2004 Jul 15;22(14_suppl):3710

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The induction of apoptosis in colorectal cancers by preoperative administration of 5'-deoxy-5-fluorouridine (5'-DFUR) and its prediction from gene expression profile analysis using DNA microarray.
  • : 3710 Background: In the respect of individualized chemotherapy for the patients with the sensitivity for fluoropyrimidines, we analyzed the induction of apoptosis in the tumors of colorectal cancer patients by preoperative administration of 5'-DFUR, which is an intermediate metabolite of capecitabine and has been widely used in Japan, and also investigated the possibility of the prediction of apoptosis induction by microarray-based analysis in the preoperative biopsy specimens.
  • METHODS: 48 preoperative colorectal cancer patients were enrolled in the study, and the first 24 patients were randomized into two groups, 5'-DFUR administration group and a group without administration.
  • After the operation, resected colorectal cancer specimens were also processed in the same manner.
  • The induction of apoptosis in tumor tissue was evaluated by immunohistochemical staining using anti-single-strand (ss) DNA antibody.
  • CONCLUSIONS: The induction of apoptosis in tumor tissues by preoperative administration of 5'-DFUR was confirmed in colorectal cancer patients.

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  • (PMID = 28013665.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Cantwell MJ, Spears CP, Robbins JM: Antitumor activity of combination 5,10-methylenetetrahydrofolate, 5-fluorouracil, and anti-vascular endothelial growth factor against human colorectal HT-29 tumors in nude mice. J Clin Oncol; 2004 Jul 15;22(14_suppl):3768

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of combination 5,10-methylenetetrahydrofolate, 5-fluorouracil, and anti-vascular endothelial growth factor against human colorectal HT-29 tumors in nude mice.
  • : 3768 Background: Folinic acid (leucovorin) has been used as the standard combination therapy as a modulator of 5-fluorouracil (5-FU) for cancer treatment.
  • In contrast, CoFactor supplies 5,10-methylenetetrahydrofolate directly and has demonstrated enhancement of the antitumor effects of 5-FU in Phase I/II human clinical trials for colorectal and breast cancer.
  • To determine if the antitumor activity of CoFactor/5-FU could be enhanced further, we examined its use in combination with a recombinant antibody specific for vascular endothelial growth factor (αVEGF), an inhibitor of angiogenesis, against human colorectal HT-29 tumors in nude mice.
  • When tumors reached 0.1 to 0.3 cm<sup>3</sup> in volume, mice were treated with various combinations of 5-FU, CoFactor, leucovorin, and αVEGF administered by intraperitoneal injection.
  • All drugs were dosed daily (0.6 mg/mouse/drug) for five consecutive days with the exception of αVEGF, dosed once (100 μg/mouse) on day 1.
  • Tumor volumes were calculated every 2 to 3 days.
  • RESULTS: One month following treatment, we observed smaller mean tumor volumes in mice treated with combination CoFactor/αVEGF/5-FU (0.48 cm<sup>3</sup> ± 0.1, n=8, mean ± SEM) than mice treated with either 5-FU alone (0.75 cm<sup>3</sup> ± 0.1), CoFactor/FU (0.52 cm<sup>3</sup> ± 0.08), or leucovorin/5-FU (0.71 cm<sup>3</sup> ± 0.09).
  • CONCLUSIONS: This study suggests combination CoFactor/αVEGF/5-FU treatment might have utility as a colorectal tumor therapy with greater antitumor activity than standard 5-FU therapies.

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  • (PMID = 28014143.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Rosell R, Daniel C, Ramlau R, Szczesna A, Constenla M, Mennecier B, Pfeifer W, Mueser M, Montaner I, Gatzemeier U: Randomized phase II study of cetuximab in combination with cisplatin (C) and vinorelbine (V) vs. CV alone in the first-line treatment of patients (pts) with epidermal growth factor receptor (EGFR)-expressing advanced non-small-cell lung cancer (NSCLC). J Clin Oncol; 2004 Jul 15;22(14_suppl):7012

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized phase II study of cetuximab in combination with cisplatin (C) and vinorelbine (V) vs. CV alone in the first-line treatment of patients (pts) with epidermal growth factor receptor (EGFR)-expressing advanced non-small-cell lung cancer (NSCLC).
  • : 7012 Background: NSCLC is a tumor with high EGFR-expression in the majority of cases.
  • Since there is still a need for improvement in the outcome of patients with NSCLC, we evaluated the addition of cetuximab (Erbitux), an IgG1 monoclonal antibody targeting the EGFR, to CV, a standard chemotherapy in NSCLC, in first-line treatment of patients with NSCLC.
  • Combinations of cetuximab and chemotherapy have shown to be effective and safe in several EGFR-expressing tumors such as colorectal cancer and head and neck cancer.
  • METHODS: Neither of the patients had received prior chemotherapy.
  • All patients were treated with C 80 mg/m<sup>2</sup> d1 and V 25 mg/m<sup>2</sup> d1 and 8, q3 and were randomized to either receive additional cetuximab 400 mg/m<sup>2</sup> week 1 and 250 mg/m<sup>2</sup> weekly thereafter (arm A) or no additional treatment (arm B).
  • RESULTS: 101/112 (90%) of pts screened had EGFR-expressing tumors.
  • The following patient/tumor characteristics were similar in both treatment arms: median age of 58 y (34-75), median KPS of 90, 92% of patients had stage IV NSCLC, 42% had adenocarcinoma and 42% had squamous cell carcinoma.

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  • (PMID = 28016270.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Villanueva A, Dotor E, Cuatrecasas M, Pareja L, Martinez M, Navarro M, Moreno V, Peinado MA, Capella G, Germa JR: Comprehensive thymidylate synthase genotyping in adjuvant therapy of CRC. J Clin Oncol; 2004 Jul 15;22(14_suppl):3588

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comprehensive thymidylate synthase genotyping in adjuvant therapy of CRC.
  • : 3588 Background: Adjuvant chemotherapy treatment, mainly based in the inhibition of thymidylate synthase (TS) enzyme with 5-FU (5-fluorouracil) is offered to all Dukes C and indications for Dukes B2 cases are being evaluated.
  • METHODS: 213 patients resected of stage II-IV colorectal tumors [63 Dukes B2, 121 Dukes C and 29 Dukes D] were treated with 5-FU plus levamisole or leucovorin as a standard treatment.
  • TS polymorphisms [TSER, the G/C polymorphism based in the second repeat of the 3R allele of TSER, and TS 1494del6], point mutations and allelic imbalances were analyzed in 128 of the 213 cases after tumor cell enrichment.
  • RESULTS: 174 tumors (81.7.
  • Allelic imbalances were present in 35% of all informative tumors.
  • No point mutations were detected in the 128 tumors analyzed.
  • CONCLUSIONS: A 6-bp deletion in the 3'-untranslated region of the TS and high TS protein expression are effective in predicting outcome of adjuvant chemotherapy in patients with resected CRC.
  • TS allelic imbalances are a frequent event in human colorectal tumorigenesis of unknown significance.

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  • (PMID = 28016323.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Syed SK, Beeram M, Takimoto CH, Jakubowitz J, Kimura M, Ducharme M, Gadgeel S, De Jager R, Rowinsky E, Lorusso P: Phase I and Pharmacokinetics (PK) of DJ-927, an oral taxane, in patients (Pts) with advanced cancers. J Clin Oncol; 2004 Jul 15;22(14_suppl):2028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2028 Background: DJ-927, a novel semi-synthetic taxane and a poor substrate of P-glycoprotein (Pgp), is orally bioavailable and possesses potent anti-tumor activity against Pgp expressing human cancers.
  • Pts were stratified based on prior therapy into minimally (MP) and heavily (HP) pretreated cohorts.
  • Primary tumors are colorectal [15], breast [4], pancreas [5], renal cell [3], soft tissue sarcoma [3] and others [10].
  • Minimal drug-related toxicities were observed at doses 5 days duration [7] and grade 3 thrombocytopenia [4] were the predominant hematological toxicities observed at 40 and 35 mg/m<sup>2</sup> doses.
  • Disease stabilization for >3 months was noted in 8 pts.
  • CONCLUSIONS: DJ-927 generates predictable systemic drug exposures and has been well tolerated when orally administered.

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  • (PMID = 28015577.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Des Guetz G, Uzzan B, Nicolas P, Chouahnia K, Perret G, Zelek L, Morere J: Does microsatellite instability predict the effect of adjuvant chemotherapy in stage III colorectal cancer? A meta-analysis. J Clin Oncol; 2009 May 20;27(15_suppl):4121

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does microsatellite instability predict the effect of adjuvant chemotherapy in stage III colorectal cancer? A meta-analysis.
  • : 4121 Background: Microsatellite instability (MSI) is a prognostic factor in colorectal cancer.
  • Whether it predicts the effect of adjuvant chemotherapy (CT) on overall survival (OS) and relapse-free survival (RFS) is controversial.
  • METHODS: Studies were identified by an electronic search using online PubMed, with simultaneous keywords (colorectal neoplasm, microsatellite instability, chemotherapy, prognosis).
  • MSI-H status did not predict response to CT compared with no treatment.

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  • (PMID = 27961250.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Er O, Inanc M, Dikilitas M, Ozkan M, Karaca H, Saraymen R, Elmali F: VEGF, EGF, HGF, and PDGF levels during chemotherapy in patients with metastatic colorectal cancer. J Clin Oncol; 2009 May 20;27(15_suppl):4057

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] VEGF, EGF, HGF, and PDGF levels during chemotherapy in patients with metastatic colorectal cancer.
  • : 4057 Background: Colon cancer is the third most common type of cancer in USA.
  • Angiogenesis is necessary for the growth and metastasis of tumors in colorectal cancer (CRC).
  • Increased angiogenesis in the primary tumor has been associated with poor prognosis and relapse of the disease.
  • The aim of the present study was to measure plasma levels of the angiogenic factors in metastatic CRC patients before and after chemotherapy and to correlate with prognosis, in order to estimate the possible predictive value of angiogenic factor levels.
  • METHODS: Thirty-eight patients with metastatic CRC were recruited to the study and blood samples were taken to measure VEGF, EGF, HGF and PDGF before chemotherapy.
  • Angiogenic factors were measured after third cycle of chemotherapy.
  • RESULTS: Eighteen patients (47.3%) achieved partial response (PR), 10 (26.3%) stable disease (SD), and 10 (26.3%) progressive disease (PD).
  • VEGF, EGF, HGF and PDGF levels at baseline and after three cycles of chemotherapy are summarized in table .
  • After 3 cycles of XELOX therapy VEGF, EGF, HGF and PDGF levels significantly decreased respectively, (p<0.0001, p=0.011, p=0.049, p<0.0001), in PR group.
  • Serum HGF levels significantly increased (p<0.046) after 3 cycles of chemotherapy, however, VEGF, EGF, and PDGF levels were not significantly different in patients with PD.

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  • (PMID = 27961585.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Vilar Sanchez E, Chow A, Raskin L, Iniesta MD, Mukherjee B, Gruber SB: Preclinical testing of the PARP inhibitor ABT-888 in microsatellite instable colorectal cancer. J Clin Oncol; 2009 May 20;27(15_suppl):11028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preclinical testing of the PARP inhibitor ABT-888 in microsatellite instable colorectal cancer.
  • : 11028 Background: Microsatellite instability (MSI) represents approximately 15% of colorectal cancer (CRC) cases.
  • ABT-888 shows a preferential activity on those MSI cell lines harboring mutations in both MRE11 and RAD50 genes compared to MSS cell lines (wild-type for both genes).
  • Flow cytometry analyses show a G1 arrest following to the treatment with ABT-888 that is higher in MSI cell lines with mutations in MRE11 and RAD50 compared to MSS cell lines.
  • MSI colorectal tumors deficient in DSB repair show a higher sensitivity to PARP inhibition.
  • Further clinical investigation of ABT-888 as a single agent or in combination with other chemotherapy drugs inducing DSB is warranted in MSI CRC with mutations in MRE11 and RAD50.

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  • (PMID = 27963963.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Van Damme N, Demetter P, De Bock W, De Hemptinne B, Praet M, Peeters M, Hepatobiliary Study Group: Limited influences of chemotherapy on healthy and metastatic liver parenchyma from colorectal cancer. J Clin Oncol; 2004 Jul 15;22(14_suppl):3640

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Limited influences of chemotherapy on healthy and metastatic liver parenchyma from colorectal cancer.
  • : 3640 Background: Liver metastasis often occurs in patients who undergo surgical removal of the primary colorectal tumor.
  • The adhesion molecules, E-cadherin/catenin complex, are closely involved in the development and growth of metastatic tumors.
  • Today, no data are available on the effect of chemotherapy on liver parenchyma.
  • METHODS: Thirty-nine patients (27 males and 12 females, with a mean age of 60.3 years) who underwent liver resection for hepatic metastasis from colorectal cancer were included in the study.
  • Tissue samples taken from the tumor and surrounding liver parenchyma were immunohistochemically stained for E-cadherin, α -, β -, and γ -catenin, VEGF and p53.
  • The patients were divided in two groups: those (n=15) who had no chemotherpay for at least 6 months before the liver resections and those (n=24) who were treated with chemotherapy before liver resections.
  • RESULTS: In the non-involved liver parenchyma no differences could be observed for E-cadherin/catenin complex, VEGF and p53 between patients receiving or not receiving chemotherapy.
  • In the metastatic liver parenchyma, VEGF expression was more pronounced in patients receiving chemotherapy in comparison with patients receiving no chemotherapy (p=0.048).
  • There were no differences for the E-cadherin/catenin complex.
  • A limited influence of chemotherapy was noticed on metastatic liver parenchyma.

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  • (PMID = 28014597.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Uchida K, Hayashi K, Danenberg KD, Schneider S, Kuramochi H, Takasaki K, Danenberg PV: Intratumoral COX-2 gene expression is a predictive factor for colorectal cancer response to chemotherapy with S-1 as well as a prognostic factor for survival of patients after S-1 chemotherapy. J Clin Oncol; 2004 Jul 15;22(14_suppl):3642

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intratumoral COX-2 gene expression is a predictive factor for colorectal cancer response to chemotherapy with S-1 as well as a prognostic factor for survival of patients after S-1 chemotherapy.
  • : 3642 Background:Cyclooxygenase-2 (COX-2) has an important role in tumor development.
  • Although a number of studies have found high expression of COX-2 to be an unfavorable prognostic factor, the influence of COX-2 expression levels on tumor response to chemotherapy has been relatively little studied.
  • The purpose of this study was to discover if there is a relationship between COX-2 gene expression and chemosensitivity of tumors in clinical treatment of colorectal tumors with the fluoropyrimidine based therapy S-1.
  • PATIENTS & METHODS: Forty pts with advanced (stage IV) CRC were treated with S-1 twice daily (BSA=1.5m2, 60mg/day ) for 28 days followed by a 2-week period rest .
  • mRNA was isolated from paraffin-embedded pretreatment primary tumor specimens, and relative expression levels of each COX-2/b-actin were measured using a quantitative reverse transcription polymerase chain reaction (RT-PCR) (Taqman") system.
  • COX-2 gene expression was significantly lower in the responding tumors compared to the non-responders respectively (P= 0.016, Mann-Whitney U test).
  • CONCLUSIONS: Intratumoral COX-2 gene expression is a predictive factor for response to chemotherapy with S-1 as well as a prognostic factor for survival of patients after S-1 chemotherapy.
  • These results suggest that combination therapy of S-1 and COX-2 inhibitors may provide more effective treatment for patients with CRC than S-1 alone, whereas measurement of COX-2 status may identify patients with a lower probability of response and unfavorable prognosis.

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  • (PMID = 28014592.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Funahashi K, Miki T, Koike J, Washizawa N, Shibata Y, Matsumoto H, Tokuyama T, Ryu M, Shiokawa H, Goto T, Teramoto T: [A case of metastatic liver tumor of colorectal cancer responding to low-dose CPT-11 chemotherapy]. Gan To Kagaku Ryoho; 2003 Mar;30(3):419-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of metastatic liver tumor of colorectal cancer responding to low-dose CPT-11 chemotherapy].
  • We report a case in which low-dose CPT-11 chemotherapy was effective for metastatic liver tumor of sigmoid colon cancer.
  • A 49-year-old male with metastatic liver tumor, who had undergone sigmoidectomy with D2 lymphadenectomy, was treated by low-dose CPT-11 chemotherapy (CPT-11 30 mg/m2 x 3 days, every 2 weeks).
  • After 7 courses of this chemotherapy, CT and ultrasound examinations showed a reduction of tumor size in the liver.
  • This chemotherapy also showed no high grade toxicities.
  • Therefore, low-dose CPT-11 chemotherapy seems to be effective for metastatic colorectal cancer, and safe in view of toxicities.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Phytogenic / administration & dosage. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Colorectal Neoplasms / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Male. Middle Aged

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  • (PMID = 12669404.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 7673326042 / irinotecan; XT3Z54Z28A / Camptothecin
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26. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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27. Mild G, Bachmann F, Boulay JL, Glatz K, Laffer U, Lowy A, Metzger U, Reuter J, Terracciano L, Herrmann R, Rochlitz C: DCR3 locus is a predictive marker for 5-fluorouracil-based adjuvant chemotherapy in colorectal cancer. Int J Cancer; 2002 Nov 20;102(3):254-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DCR3 locus is a predictive marker for 5-fluorouracil-based adjuvant chemotherapy in colorectal cancer.
  • Adjuvant chemotherapy reduces the incidence of distant metastasis and increases survival of patients with colorectal cancer.
  • However, predictive markers are needed to define subsets of patients with stage II and III disease that may benefit from adjuvant treatment.
  • A secreted member of the TNF receptor superfamily, the decoy receptor 3 (DcR3), was reported to be amplified in colorectal cancer as a negative regulator of Fas-mediated apoptosis.
  • We analyzed DcR3 gene copy number and protein expression in a large series of tumors from a randomized multicenter trial of 5-fluorouracil/mitomycin C (FU/MMC) adjuvant chemotherapy of the Swiss Group for Clinical Cancer Research (SAKK 40/81), using real-time quantitative PCR and immunohistochemistry on tumor microarrays.
  • Results of gene status and protein expression of DcR3 were correlated with disease-free and overall survival of patients.
  • We observed amplification of the DcR3 gene in 185/294 (63%) and overexpression of the DcR3 protein in 163/223 (73%) of colorectal tumors.
  • However, adjuvant chemotherapy was significantly more beneficial in patients with normal DcR3 gene copy number than in patients with amplification (DFS: HR 2.84, 95% CI 1.16-6.98, p = 0.02; OS: HR 3.15, 95% CI 1.19-8.32, p = 0.02), whereas DcR3 protein overexpression did not influence the effect of adjuvant chemotherapy (DFS: HR 1.02, 95% CI 0.65-1.60, p = 0.95; OS: HR 0.95, 95% CI 0.61-1.49, p = 0.83).
  • We conclude that amplification of the 20q13 locus is a predictive marker for adjuvant chemotherapy in colorectal cancer.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / genetics. Fluorouracil / therapeutic use. Membrane Glycoproteins / genetics. Receptors, Cell Surface / genetics
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Apoptosis. Biomarkers, Tumor. Chromosomes, Human, Pair 20. Disease-Free Survival. Humans. Immunohistochemistry. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction. Receptors, Tumor Necrosis Factor. Receptors, Tumor Necrosis Factor, Member 6b. Time Factors

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12397645.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human; U3P01618RT / Fluorouracil
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28. Takanashi K, Takahashi M, Miyanishi K, Hayashi T, Takada K, Oku T, Ishiwatari H, Kogawa T, Takayama T, Kato J, Niitsu Y: [A case of metastatic liver tumor from colorectal carcinoma--continued arterial infusion chemotherapy through a microcatheter located in replaced right hepatic artery]. Gan To Kagaku Ryoho; 2004 Sep;31(9):1415-7
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  • [Title] [A case of metastatic liver tumor from colorectal carcinoma--continued arterial infusion chemotherapy through a microcatheter located in replaced right hepatic artery].
  • The patient was a 78-year-old male with a history of colon cancer.
  • After surgical resection of colon cancer, he suffered a multiple liver metastasis.
  • We treated him by arterial infusion chemotherapy with the catheter edge embedded at the common hepatic artery.
  • After changing the treatment to systemic intravenous chemotherapy, the metastatic lesions began to enlarge.
  • Then, we somehow were able to put a microcatheter into the replaced right hepatic artery (rRHA), and could restart arterial infusion chemotherapy.
  • We continued this procedure for over a year without any complication.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Camptothecin / analogs & derivatives. Colonic Neoplasms / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary
  • [MeSH-minor] Aged. Catheters, Indwelling. Combined Modality Therapy. Drug Administration Schedule. Fluorouracil / administration & dosage. Hepatic Artery. Humans. Infusions, Intra-Arterial / methods. Leucovorin / administration & dosage. Male

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  • (PMID = 15446568.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 7673326042 / irinotecan; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
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29. 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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30. Poultsides GA, Servais EL, Saltz LB, Patil S, Kemeny NE, Guillem JG, Weiser M, Temple LK, Wong WD, Paty PB: Outcome of primary tumor in patients with synchronous stage IV colorectal cancer receiving combination chemotherapy without surgery as initial treatment. J Clin Oncol; 2009 Jul 10;27(20):3379-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of primary tumor in patients with synchronous stage IV colorectal cancer receiving combination chemotherapy without surgery as initial treatment.
  • PURPOSE: The purpose of this study was to describe the frequency of interventions necessary to palliate the intact primary tumor in patients who present with synchronous, stage IV colorectal cancer (CRC) and who receive up-front modern combination chemotherapy without prophylactic surgery.
  • PATIENTS AND METHODS: By using a prospective institutional database, we identified 233 consecutive patients from 2000 through 2006 with synchronous metastatic CRC and an unresected primary tumor who received oxaliplatin- or irinotecan-based, triple-drug chemotherapy (infusional fluorouracil, leucovorin, and oxaliplatin; bolus fluorouracil, leucovorin, and irinotecan; or fluorouracil, leucovorin, and irinotecan) with or without bevacizumab as their initial treatment.
  • The incidence of subsequent use of surgery, radiotherapy, and/or endoluminal stenting to manage primary tumor complications was recorded.
  • RESULTS: Of 233 patients, 217 (93%) never required surgical palliation of their primary tumor.
  • Sixteen patients (7%) required emergent surgery for primary tumor obstruction or perforation, 10 patients (4%) required nonoperative intervention (ie, stent or radiotherapy), and 213 (89%) never required any direct symptomatic management for their intact primary tumor.
  • Of those 213 patients, 47 patients (20%) ultimately underwent elective colon resection at the time of metastasectomy, and eight patients (3%) underwent this resection during laparotomy for hepatic artery infusion pump placement.
  • Use of bevacizumab, location of the primary tumor in the rectum, and metastatic disease burden were not associated with increased intervention rate.
  • CONCLUSION: Most patients with synchronous, stage IV CRC who receive up-front modern combination chemotherapy never require palliative surgery for their intact primary tumor.
  • These data support the use of chemotherapy, without routine prophylactic resection, as the appropriate standard practice for patients with neither obstructed nor hemorrhaging primary colorectal tumors in the setting of metastatic disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / drug therapy. Palliative Care / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cohort Studies. Databases, Factual. Humans. Middle Aged. Neoplasm Staging. Survival Analysis. Treatment Outcome

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  • [Cites] Ann Surg Oncol. 1999 Oct-Nov;6(7):651-7 [10560850.001]
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  • (PMID = 19487380.001).
  • [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
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3646319
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31. Dietmaier W, Bettstetter M, Wild PJ, Woenckhaus M, Rümmele P, Hartmann A, Dechant S, Blaszyk H, Pauer A, Klinkhammer-Schalke M, Hofstädter F: Nuclear Maspin expression is associated with response to adjuvant 5-fluorouracil based chemotherapy in patients with stage III colon cancer. Int J Cancer; 2006 May 1;118(9):2247-54
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  • [Title] Nuclear Maspin expression is associated with response to adjuvant 5-fluorouracil based chemotherapy in patients with stage III colon cancer.
  • Maspin, a member of the Serpin protease inhibitor family, is overexpressed in poorly differentiated colorectal tumors and more frequently found in tumors with microsatellite instability.
  • Immunohistochemical nuclear Maspin staining is predominantly seen in tumor cells at the invasion front of such cancers, suggesting that this molecule is associated with local tumor cell infiltration and aggressiveness.
  • In a retrospective study, we studied nuclear Maspin expression as a potential prognostic tool in a total of 172 primary stage III colon cancers by immunohistochemistry.
  • Of those 172 patients, 76 were treated by surgery only, and 96 patients received additional adjuvant 5-fluorouracil (5-FU) based chemotherapy.
  • However, patients with primary tumors expressing Maspin in the nucleus showed a significant treatment benefit from 5-FU chemotherapy (hazard ratio 0.384; 95% CI, 0.188-0.784; p = 0.009) compared to adjuvantly treated patients whose tumors did not express this molecule.
  • Nuclear Maspin expression is highly predictive of 5-FU chemotherapy response in patients with advanced stage colon cancer.
  • Patients with negative immunohistochemical Maspin expression do not benefit from 5-FU treatment and may be candidates for an alternative (non-5-FU based) adjuvant therapy regime.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Colonic Neoplasms / drug therapy. Colonic Neoplasms / genetics. Fluorouracil / therapeutic use. Serpins / biosynthesis
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Cell Nucleus. Chemotherapy, Adjuvant. Female. Gene Expression Profiling. Genes, Tumor Suppressor. Humans. Immunohistochemistry. Male. Predictive Value of Tests. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16331619.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / SERPIN-B5; 0 / Serpins; U3P01618RT / Fluorouracil
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32. Yamagishi S, Shimada H, Ishikawa T, Fujii S, Tanaka K, Masui H, Yamaguchi S, Ichikawa Y, Togo S, Ike H: Expression of dihydropyrimidine dehydrogenase, thymidylate synthase, p53 and p21 in metastatic liver tumor from colorectal cancer after 5-fluorouracil-based chemotherapy. Anticancer Res; 2005 Mar-Apr;25(2B):1237-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of dihydropyrimidine dehydrogenase, thymidylate synthase, p53 and p21 in metastatic liver tumor from colorectal cancer after 5-fluorouracil-based chemotherapy.
  • However, little data is available on the expression patterns of these genes after chemotherapy.
  • PATIENTS AND METHODS: We investigated the expression of four genes, DPD, TS, p53 and p21, in the metastatic liver lesions obtained from colorectal cancer patients who had been treated with hepatic arterial infusions of 5-fluorouracil(5-FU)-based chemotherapy.
  • RESULTS: Expression of DPD, TS and p53 in the metastatic liver lesions was significantly higher in the chemotherapy-response group than in the no response group.
  • In the response group, viable cancer cell nests were seen in confined spaces surrounded by fibrous tissue.
  • CONCLUSION: An analysis of genes involved in 5-FU sensitivity revealed that surviving tumor cells exhibited resistance characteristics, indicating that the chemotherapy regimen should be altered, even in partially responding cases, unless the response is pathologically complete.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Dihydrouracil Dehydrogenase (NADP) / metabolism. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Oncogene Protein p21(ras) / metabolism. Thymidylate Synthase / metabolism. Tumor Suppressor Protein p53 / metabolism


33. 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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34. Zubariev MH, Fetsych TH, Konoval'ov OO, Koval'ov KO, Iarema RR, Revura AP: [Resection of the liver combined with chemotherapy for the optimization of treatment in patients with metastatic colorectal cancer]. Klin Khir; 2010 Jul;(7):5-11
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  • [Title] [Resection of the liver combined with chemotherapy for the optimization of treatment in patients with metastatic colorectal cancer].
  • Anatomic hepatic resection is considered now a "gold standard" in the treatment of patients, suffering metastatic colorectal cancer (CRR) because it secures 23-35% survival solely and 35-58% in combination with chemotherapy.
  • The immediate results of cornbined treatment and its impact on survival of patients, suffering CRR with hepatic metastases, were studied up.
  • In Lvivskiy Oncological Centre and Zaporizhskiy Oncological Dispensary in 2000-2009 yrs there was conducted combined treatment of 60 patients, suffering metastatic CRR.
  • Combined treatment consisted of the large bowel tumor extirpation, hepatic resection and adjuvant chemotherapy (ACT).
  • Median of overall survival in patients after combined treatment conduction had constituted 24.1 mo.


35. Duffy A, Shia J, Klimstra D, Temple L, O'Reilly EM: Collision tumor of the large bowel in the context of advanced pregnancy and ulcerative colitis. Clin Colorectal Cancer; 2008 Nov;7(6):402-5
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  • [Title] Collision tumor of the large bowel in the context of advanced pregnancy and ulcerative colitis.
  • Investigation revealed a collision-type primary tumor of the large bowel, containing adenocarcinoma and neuroendocrine elements.
  • Platinum-based chemotherapy resulted in a divergent pathologic response as assessed after colectomy.
  • The diagnosis and classification of mixed endocrine-exocrine tumors of the colon are discussed, along with treatment considerations.
  • [MeSH-major] Colitis, Ulcerative / complications. Colonic Neoplasms / diagnosis. Colonic Neoplasms / therapy. Pregnancy Complications, Neoplastic / diagnosis. Pregnancy Complications, Neoplastic / therapy
  • [MeSH-minor] Adult. Biopsy. Colonoscopy. Combined Modality Therapy. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging. Pregnancy. Pregnancy Outcome. Tomography, Emission-Computed. Tomography, X-Ray Computed


36. Becerra CR, Frenkel EP, Ashfaq R, Gaynor RB: Increased toxicity and lack of efficacy of Rofecoxib in combination with chemotherapy for treatment of metastatic colorectal cancer: A phase II study. Int J Cancer; 2003 Jul 20;105(6):868-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased toxicity and lack of efficacy of Rofecoxib in combination with chemotherapy for treatment of metastatic colorectal cancer: A phase II study.
  • Preclinical and clinical models have demonstrated that cyclooxygenase-2 (COX-2) is overexpressed in primary and metastatic colorectal tumors.
  • In preclinical models, there appears to be additive or synergistic effects when combining 5-Fluorouracil (5-FU) with nonsteroidal anti-inflammatory agents (NSAIDs) for the treatment of colorectal neoplasms.
  • This data raised the question as to whether adding a COX-2 inhibitor to 5-FU-based regimens would increase the response rates with an acceptable toxicity profile in patients with metastatic colon cancer.
  • In the current study, patients with metastatic colorectal cancer, who were either untreated or previously treated (more than 1 year ago) with adjuvant 5-FU and Leucovorin (LV) received 5-FU and LV (Mayo regimen) in addition to Rofecoxib.
  • Tumor samples from all patients exhibited evidence of moderate COX-2 over-expression.
  • 4 patients entered on the study developed upper gastrointestinal bleeding (grade III).
  • There were no partial or complete responses in the first 10 patients entered on the study so the study was terminated (probability of success < 0.3 with type 1 error of 0.05 and power of 0.8).
  • Future studies will need to consider the added gastrointestinal toxicity of Rofecoxib when combined with chemotherapy for the treatment of patients with colorectal cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / drug therapy. Cyclooxygenase Inhibitors / adverse effects. Cyclooxygenase Inhibitors / therapeutic use. Lactones / adverse effects. Lactones / therapeutic use
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Female. Fluorouracil / administration & dosage. Humans. Isoenzymes / analysis. Isoenzymes / antagonists & inhibitors. Leucovorin / administration & dosage. Male. Membrane Proteins. Middle Aged. Neoplasm Metastasis. Prostaglandin-Endoperoxide Synthases / analysis. Sulfones

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • [CommentIn] Int J Cancer. 2004 Jun 10;110(2):309; author reply 310 [15069699.001]
  • (PMID = 12767075.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Lactones; 0 / Membrane Proteins; 0 / Sulfones; 0QTW8Z7MCR / rofecoxib; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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37. Muratore A, Zorzi D, Bouzari H, Amisano M, Massucco P, Sperti E, Capussotti L: Asymptomatic colorectal cancer with un-resectable liver metastases: immediate colorectal resection or up-front systemic chemotherapy? Ann Surg Oncol; 2007 Feb;14(2):766-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Asymptomatic colorectal cancer with un-resectable liver metastases: immediate colorectal resection or up-front systemic chemotherapy?
  • BACKGROUND: About 20% of patients with colorectal cancer have synchronous un-resectable liver metastases.
  • Resection of colorectal cancer in patients with moderate-severe symptoms is mandatory before starting chemotherapy.
  • Surgical treatment of asymptomatic colorectal cancers is still a matter of discussion.
  • METHODS: From January 2000 to December 2004, we prospectively collected data on 35 consecutive patients who were treated straightaway by chemotherapy without primary tumor resection.
  • All patients underwent FOLFOX6 as first-line chemotherapy.
  • The aim of the study was to evaluate the rate of surgical complications related to un-resected colorectal tumor.
  • RESULTS: The mean interval between diagnosis and start of chemotherapy was 23.1 days (95% CI: 17.3-28.8).
  • Fifteen of the 35 patients (42.9%) were down-staged to surgery; the mean interval between chemotherapy start and colon-rectum cancer resection was 6.5 months (95% CI: 5.5-7.5).
  • None of them developed complications related to the primary tumor during chemotherapy.
  • Of the other 20 patients who did not undergo any curative surgery, 16 received a second line chemotherapy and 10 a third line: six patients are alive and without intestinal symptoms (mean follow up 22.5 months, 95% CI: 11.2-33.9).
  • Only one patient (2.8%) developed clinical signs of intestinal occlusion 5.6 months from the start of chemotherapy and required urgent colostomy.
  • CONCLUSIONS: The rate of complications related to the non-resected colorectal tumor is very low using oxaliplatin as first line chemotherapy.
  • Non-operative management of asymptomatic colorectal cancers with un-resectable liver metastases is a safe approach.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colectomy. Colorectal Neoplasms / therapy. Hepatectomy. Liver Neoplasms / therapy
  • [MeSH-minor] Combined Modality Therapy. Disease Progression. Fluorouracil / therapeutic use. Humans. Leucovorin / therapeutic use. Neoplasm Staging. Organoplatinum Compounds / therapeutic use. Postoperative Complications. Prospective Studies. Time Factors


38. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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39. Ichikawa W, Uetake H, Shirota Y, Yamada H, Nishi N, Nihei Z, Sugihara K, Hirayama R: Combination of dihydropyrimidine dehydrogenase and thymidylate synthase gene expressions in primary tumors as predictive parameters for the efficacy of fluoropyrimidine-based chemotherapy for metastatic colorectal cancer. Clin Cancer Res; 2003 Feb;9(2):786-91
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  • [Title] Combination of dihydropyrimidine dehydrogenase and thymidylate synthase gene expressions in primary tumors as predictive parameters for the efficacy of fluoropyrimidine-based chemotherapy for metastatic colorectal cancer.
  • Dihydropyrimidine dehydrogenase (DPD) and thymidylate synthase (TS) gene expressions in metastatic colorectal cancer have been reported to be predictive parameters for the efficacy of fluoropyrimidine-based chemotherapy.
  • In this study, we investigated the association between both DPD and TS expressions in primary colorectal tumor and the antitumor effect in patients with metastatic colorectal cancer when treated with a fluoropyrimidine-based protocol.
  • DPD and TS expressions were measured by reverse transcription-PCR in surgically resected materials of primary colorectal tumors from 37 patients who went on to receive oral treatment of uracil and tegafur and leucovorin for either synchronous or metachronous metastatic diseases.
  • Median values of DPD mRNA expressions were 0.30 and 0.65 for responding tumors and nonresponding ones, respectively, with a statistical significance (P < 0.0001).
  • No responding tumor had a DPD mRNA expression >/= 0.5.
  • A total of 19 tumors had low DPD mRNA expressions of <0.5, and 63% of them showed response.
  • There was no responding tumor with both high DPD and high TS (TS mRNA expression >/= 1.0).
  • However, the response rate was 75% in tumors with both low DPD and low TS.
  • The median survival time was 16.3 months in patients with both low DPD and low TS versus 8.4 months in patients with high DPD or high TS mRNA expression.
  • In conclusion, the combination of DPD and TS mRNA expressions in the primary tumor might be useful as predictive parameters for the efficacy of fluoropyrimidine-based chemotherapy for metastatic colorectal cancer.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Colonic Neoplasms / genetics. Gene Expression Regulation, Neoplastic / genetics. Oxidoreductases / genetics. Rectal Neoplasms / genetics. Thymidylate Synthase / genetics
  • [MeSH-minor] Adult. Aged. Dihydrouracil Dehydrogenase (NADP). Female. Gene Expression Regulation, Enzymologic / genetics. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Predictive Value of Tests. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Time Factors

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  • (PMID = 12576451.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / RNA, Messenger; EC 1.- / Oxidoreductases; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.1.1.45 / Thymidylate Synthase
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40. Nishimura G, Terada I, Kobayashi T, Ninomiya I, Kitagawa H, Fushida S, Fujimura T, Kayahara M, Shimizu K, Ohta T, Miwa K: Thymidine phosphorylase and dihydropyrimidine dehydrogenase levels in primary colorectal cancer show a relationship to clinical effects of 5'-deoxy-5-fluorouridine as adjuvant chemotherapy. Oncol Rep; 2002 May-Jun;9(3):479-82
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  • [Title] Thymidine phosphorylase and dihydropyrimidine dehydrogenase levels in primary colorectal cancer show a relationship to clinical effects of 5'-deoxy-5-fluorouridine as adjuvant chemotherapy.
  • We investigated TP and DPD levels in tumor tissue to assess their clinical significance as indicators for selecting colorectal cancer patients for 5'-DFUR adjuvant chemotherapy.
  • A total of 88 colorectal cancer patients were classified into Dukes' B and C groups and treated for 2 years with oral 5'-DFUR (800 mg/body/day).
  • During the follow-up period, 20 of the 88 patients developed a recurrence.
  • All the patients were examined retrospectively for primary tumor TP and DPD levels and clinical response to 5'-DFUR.
  • Results showed that: a) median levels of TP and DPD in the primary tumor, measured by enzyme-linked immunosorbent assay (ELISA), were, respectively, 43.6 and 32.3 U/mg protein.
  • Primary tumor TP levels of the 20 patients who had a recurrence were lower than those of the 68 patients with no recurrence (p=0.07);.
  • b) although there were no significant differences in clinicopathologic features between high and low median TP level groups, disease-free survival was better in the high TP than in the low TP group (89% vs. 64%, at year 4); and c) of patients classified into 4 groups such as high TP/DPD, high TP but low DPD, low TP but high DPD, and low TP/DPD, patients with high TP but low DPD had the best disease-free survival, whereas the low TP but high DPD group had the worst survival.
  • These results suggest that TP and DPD levels in primary colorectal tumors may be a useful indicator for selecting patients likely to respond to 5'-DFUR adjuvant chemotherapy and probably capecitabine, a prodrug of 5'-DFUR.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Chemotherapy, Adjuvant. Colorectal Neoplasms / enzymology. Deoxycytidine / analogs & derivatives. Floxuridine / therapeutic use. Oxidoreductases / biosynthesis. Thymidine Phosphorylase / biosynthesis
  • [MeSH-minor] Capecitabine. Dihydrouracil Dehydrogenase (NADP). Disease-Free Survival. Enzyme-Linked Immunosorbent Assay. Fluorouracil / analogs & derivatives. Humans. Recurrence. Time Factors

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  • (PMID = 11956613.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 039LU44I5M / Floxuridine; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; EC 1.- / Oxidoreductases; EC 1.3.1.2 / Dihydrouracil Dehydrogenase (NADP); EC 2.4.2.4 / Thymidine Phosphorylase; U3P01618RT / Fluorouracil; V1JK16Y2JP / doxifluridine
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41. 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


42. 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

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  • (PMID = 16573174.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Number-of-references] 50
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43. Shahrzad S, Lacombe K, Adamcic U, Minhas K, Coomber BL: Sodium dichloroacetate (DCA) reduces apoptosis in colorectal tumor hypoxia. Cancer Lett; 2010 Nov 1;297(1):75-83
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  • [Title] Sodium dichloroacetate (DCA) reduces apoptosis in colorectal tumor hypoxia.
  • We examined the effect of hypoxia on apoptosis of human colorectal cancer (CRC) cells in vitro and in vivo.
  • DCA treatment caused significant apoptosis under normoxia in SW480 and Caco-2 cells, but these cells displayed decreased apoptosis when treated with DCA combined with hypoxia, possibly through HIF-1alpha dependent pathways.
  • DCA treatment also induced significantly increased growth of SW480 tumor xenografts, and a decrease in TUNEL positive nuclei in hypoxic but not normoxic regions of treated tumors.
  • Thus DCA is cytoprotective to some CRC cells under hypoxic conditions, highlighting the need for further investigation before DCA can be used as a reliable apoptosis-inducing agent in cancer therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Colorectal Neoplasms / drug therapy. Dichloroacetic Acid / pharmacology. Oxygen / metabolism
  • [MeSH-minor] Animals. Caco-2 Cells. Caspase 3 / metabolism. Cell Hypoxia. Cytoprotection. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Mice. Necrosis. Proto-Oncogene Proteins c-akt / metabolism. Time Factors. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • [Copyright] 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20537792.001).
  • [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 / Antineoplastic Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 9LSH52S3LQ / Dichloroacetic Acid; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; S88TT14065 / Oxygen
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44. 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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45. Scartozzi M, Mandolesi A, Giampieri R, Pierantoni C, Loupakis F, Zaniboni A, Galizia E, Giustini L, Silva RR, Bisonni R, Berardi R, Biagetti S, Menzo S, Falcone A, Bearzi I, Cascinu S: Insulin-like growth factor 1 expression correlates with clinical outcome in K-RAS wild type colorectal cancer patients treated with cetuximab and irinotecan. Int J Cancer; 2010 Oct 15;127(8):1941-7
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  • [Title] Insulin-like growth factor 1 expression correlates with clinical outcome in K-RAS wild type colorectal cancer patients treated with cetuximab and irinotecan.
  • Seventy to 40% of K-RAS wild type colorectal tumors does not seem to benefit from treatment with antiepidermal growth factor receptor (anti-EGFR) monoclonal antibodies.
  • Recent data suggested that in presence of IGF-1 system, altered activation colorectal cancer cells may escape anti-EGFR mediated cell death.
  • The interaction between IGF-1 expression and K-RAS mutational analysis was tested to verify the ability of IGF-1 to identify a subgroup of patients more likely to benefit from EGFR-targeted antibodies treatment.
  • IGF-1 expression and K-RAS mutational status was assessed in advanced colorectal cancer patients receiving irinotecan/cetuximab.
  • In IGF-1 negative and IGF-1 positive tumors, we observed progressive disease in 9 (30%) and 55 (67%) patients, respectively (p = 0.001).
  • Median progression-free survival was 7.5 mo in patients showing IGF-1 negative tumors and 3 mo for IGF-1 expressing tumors (p = 0.002).
  • Among K-RAS wild type patients, IGF-1 negative and positive tumors showed a partial response to cetuximab-irinotecan in 13 (65%) and 11 (22%) cases, respectively (p = 0.002).
  • Median progression-free survival in IGF-1 negative tumors was 10 mo and 3.2 mo in IGF-1 positive colorectal cancers (p = 0.02).
  • IGF-1 proved to be a possible predictive factor for resistance to anti-EGFR monoclonal antibodies in K-RAS wild type colorectal cancer.
  • Combined IGF-1 and K-RAS analysis may represent an effective strategy for a better selection of responding colorectal cancer patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / drug therapy. Insulin-Like Growth Factor I / metabolism. Mutation / genetics. Proto-Oncogene Proteins / genetics. ras Proteins / genetics

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  • (PMID = 20099280.001).
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 67763-96-6 / Insulin-Like Growth Factor I; 7673326042 / irinotecan; EC 3.6.5.2 / ras Proteins; PQX0D8J21J / Cetuximab; XT3Z54Z28A / Camptothecin
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46. Kim JC, Shin ES, Kim CW, Roh SA, Cho DH, Na YS, Kim TW, Kim MB, Hyun YL, Ro S, Kim SY, Kim YS: In vitro evaluation of histone deacetylase inhibitors as combination agents for colorectal cancer. Anticancer Res; 2009 Aug;29(8):3027-34
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  • [Title] In vitro evaluation of histone deacetylase inhibitors as combination agents for colorectal cancer.
  • BACKGROUND: Our primary aim was to evaluate the additive efficacy of histone deacetylase inhibitors (HDACIs) in established treatment regimens for colorectal cancer in concurrence with identifying the clinicopathological markers significantly associated with tumor responsiveness.
  • PATIENTS AND METHODS: The chemosensitivities of 125 colorectal carcinomas to established regimens [FLOX (5-FU + leucovorin + oxaliplatin) and FLIRI (5-FU + leucovorin + irinotecan)], two biologically targeted drugs (avastin and erbitux), and two hydroxamic acid derivatives (vorinostat, SAHA(R), and a novel candidate, CG2) were comparatively evaluated using an in vitro tumor response assay.
  • RESULTS: The response rates of tumors (inhibition rate > or =30%) were significantly greater for FLOX and combinations (55.2-68%) compared to FLIRI and combinations (44-63.2%) (p=0.001 to 0.048), except in the case of the CG2 combination.
  • The additive effects of HDACIs on the respective established regimens were considerably greater for non-responsive tumors (64.3-80%) than responsive tumors (32.7-45%) (p< or =0.0001 to 0.008).
  • A number of biological parameters, including less advanced tumors and p53 overexpression, were significantly associated with additive chemosensitivity to HDACIs in combination with FLOX and FLIRI in multivariate analyses (p< or =0.001 to 0.023).
  • Expanding tumor growth, diffuse cytoplasmic carcinoembryonic antigen (CEA) expression and synchronous adenoma were associated with combination regimens with targeted drugs (p=0.013 to 0.032).
  • CONCLUSION: Our findings show additive chemoresponsiveness of colorectal tumors to HDAC inhibitors in combination with established regimens.
  • The significant parameters associated with combination regimens of targeted drugs and HDACIs may be applied as effective chemosensitive markers in future clinical trials.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma, Mucinous / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / drug therapy. Enzyme Inhibitors / therapeutic use. Histone Deacetylase Inhibitors
  • [MeSH-minor] Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Drug Therapy, Combination. Female. Humans. In Vitro Techniques. Male. Middle Aged. Neoplasm Staging. Prognosis. Prospective Studies. Treatment Outcome


47. 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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48. Daniel CR, Bostick RM, Flanders WD, Long Q, Fedirko V, Sidelnikov E, Seabrook ME: TGF-alpha expression as a potential biomarker of risk within the normal-appearing colorectal mucosa of patients with and without incident sporadic adenoma. Cancer Epidemiol Biomarkers Prev; 2009 Jan;18(1):65-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TGF-alpha expression as a potential biomarker of risk within the normal-appearing colorectal mucosa of patients with and without incident sporadic adenoma.
  • BACKGROUND: Transforming growth factor-alpha (TGF-alpha), a stimulatory growth factor and member of the epidermal growth factor family, is a mediator of oncogenesis and malignant progression in colorectal carcinogenesis.
  • Limited evidence suggests its utility as a growth-related biomarker of risk for colorectal cancer.
  • METHODS: We measured expression of TGF-alpha in biopsies of normal-appearing colorectal mucosa using automated immunohistochemistry and quantitative image analysis in a subsample of 29 cases and 31 controls from a colonoscopy-based case-control study (n = 203) of biomarkers of risk for incident sporadic colorectal adenoma.
  • RESULTS: TGF-alpha expression in the rectum was 51% higher in cases compared with controls (P = 0.05) and statistically significantly associated with accepted risk factors for colorectal neoplasms (36% lower among nonsteroidal anti-inflammatory drug users, 49% lower among women using hormone replacement therapy, 79% higher among persons with a family history of colorectal cancer).
  • CONCLUSIONS: TGF-alpha expression in the normal-appearing rectal mucosa shows promise as an early, potentially modifiable biomarker of risk for colorectal cancer.

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  • (PMID = 19124482.001).
  • [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 / CA115230-02; United States / NCI NIH HHS / CA / R03 CA115230; United States / NCI NIH HHS / CA / R03 CA115230-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor alpha
  • [Other-IDs] NLM/ NIHMS253319; NLM/ PMC2995992
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49. Linsalata M, Russo F: Nutritional factors and polyamine metabolism in colorectal cancer. Nutrition; 2008 Apr;24(4):382-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nutritional factors and polyamine metabolism in colorectal cancer.
  • Colorectal cancers are a significant cause of mortality in Western societies.
  • The progression of the disease from normal epithelium to the acquisition of the malignant phenotype is accompanied by several biochemical and genetic alterations.
  • Compelling experimental and epidemiologic evidences indicate that diet and nutrition are key factors in modulating colon cancer onset and progression.
  • Therefore, identifying dietary constituents with antitumor activity and investigating their mechanisms of action may lead to significant advances in the prevention of these neoplasms.
  • Moreover, it seems that the potential protection against colorectal cancers of some nutritional factors could be associated with modifications in cellular proliferation and growth.
  • The naturally occurring polyamines, spermine, spermidine, and putrescine, play a key role in hyperproliferation and cell migration and are involved in almost all steps of colorectal tumorigenesis.
  • Consequently, polyamine metabolism can be considered an attractive target for cancer chemoprevention and chemotherapy.
  • This review summarizes the findings on the possible mechanisms of action of some nutritional components such as flavonoids, polyphenols, and probiotics in colorectal cancers, focusing attention on polyamine metabolism as a possible target.
  • Acquiring more data on this aspect could represent an innovative and interesting approach for new therapeutic and chemopreventive strategies in the management of patients with colorectal neoplasms.
  • [MeSH-major] Cell Division / drug effects. Cell Transformation, Neoplastic / drug effects. Colorectal Neoplasms / metabolism. Polyamines / metabolism. Polyamines / pharmacology
  • [MeSH-minor] Diet. Disease Progression. Humans. Intestinal Mucosa / metabolism. Nutritional Physiological Phenomena. Nutritional Status. Risk Factors

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  • (PMID = 18262757.001).
  • [ISSN] 0899-9007
  • [Journal-full-title] Nutrition (Burbank, Los Angeles County, Calif.)
  • [ISO-abbreviation] Nutrition
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Polyamines
  • [Number-of-references] 88
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50. Jin XF, Tong JL, Ran ZH: [Selective cyclooxygenase-2 inhibitors for the prevention of colorectal adenomas: a meta-analysis]. Zhonghua Yi Xue Za Zhi; 2007 Jul 24;87(28):1958-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Selective cyclooxygenase-2 inhibitors for the prevention of colorectal adenomas: a meta-analysis].
  • OBJECTIVE: To determine the validity and safety of selective cyclooxygenase (COX)-2 inhibitors for the prevention of colorectal adenomas.
  • Compared with placebo, selective COX-2 inhibitors lowered the detection rates of both adenomas and advanced adenomas (RR: 0.70, 95% CI: 0.55 - 0.88, P = 0.0003 and RR: 0.69, 95% CI: 0.53 - 0.89, P = 0.005).
  • CONCLUSION: Selective COX-2 inhibitors can induce sufficient regression of colorectal adenomatous polyps and thus be used for chemoprevention of colorectal neoplasms.
  • [MeSH-major] Adenoma / drug therapy. Colorectal Neoplasms / drug therapy. Cyclooxygenase 2 Inhibitors / therapeutic use

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  • (PMID = 17923032.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Meta-Analysis
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors
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51. Durrant LG, Harding SJ, Green NH, Buckberry LD, Parsons T: A new anticancer glycolipid monoclonal antibody, SC104, which directly induces tumor cell apoptosis. Cancer Res; 2006 Jun 1;66(11):5901-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new anticancer glycolipid monoclonal antibody, SC104, which directly induces tumor cell apoptosis.
  • A novel monoclonal antibody was raised by immunization of mice with colorectal tumor cell lines.
  • The fusion was screened by immunohistochemistry for binding to primary colorectal tumors.
  • Subsequent analysis on primary disaggregated colorectal tumors show that the antibody recognizes a cell surface antigen expressed by the majority of colorectal tumors.
  • Binding to a frozen panel of tumor and normal tissue sections revealed that the antigen was also strongly expressed on esophageal, gastric, and endometrial tumors.
  • Its normal tissue distribution was largely restricted to moderate staining of large intestine.
  • Surprisingly, SC104 antibody directly induces tumor cell death without the need for immune effector cells or complement.
  • Caspase activation can be detected following SC104 treatment of colorectal cells, and cotreatment with caspase inhibitors has been shown to inhibit cell death.
  • Furthermore, SC104 antibody shows additive killing with complement and 5-fluorouracil/leucovorin in vivo, suggesting a new therapeutic approach for this class of antibodies.
  • [MeSH-major] Adenocarcinoma / therapy. Antibodies, Monoclonal / pharmacology. Apoptosis / drug effects. Colorectal Neoplasms / therapy. Glycolipids / immunology
  • [MeSH-minor] Animals. Carbohydrate Sequence. Cell Line, Tumor. Humans. Immunoglobulin G / immunology. Immunoglobulin G / pharmacology. Mice. Mice, Inbred BALB C. Mice, Nude. Molecular Sequence Data

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  • (PMID = 16740730.001).
  • [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 / Antibodies, Monoclonal; 0 / Glycolipids; 0 / Immunoglobulin G
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52. Kwon YE, Kim KH: Octahedral Pt(IV) complex K101 induces apoptosis via ERK1/2 activation and the p53 pathway in human colon cancer cells. Anticancer Drugs; 2006 Jun;17(5):553-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Octahedral Pt(IV) complex K101 induces apoptosis via ERK1/2 activation and the p53 pathway in human colon cancer cells.
  • Recently, the synthesized octahedral Pt(IV) compound trans,cis-Pt(acetato)2Cl2(1,4-butanediamine), K101, showed potent anti-tumor activity in vitro and in vivo.
  • For the further investigation of K101-induced anti-cancer activity, we tested cytotoxicity against various cancer cell lines and performed the histoculture drug response assay (HDRA) against human colorectal tumor tissues in vitro.
  • We investigated the signaling pathway of K101-induced apoptosis via expression of p53 and ERK1/2 in the human colon cell line HCT116.
  • Among several cancer cell lines, K101 showed greater potency than cisplatin in colon cancer cell lines.
  • In the HDRA, K101 showed 80.0-91.4% efficacy rates compared with 48.6% for cisplatin against colorectal cancer patient tissues.
  • In the signaling pathway, the expression of p53 and phospho-ERK1/2 was increased in a time-dependent manner by treatment with K101 in the HCT116 cells.
  • The octahedral Pt(IV) complex K101 could be an attractive candidate as a chemotherapeutic agent against colon cancer.
  • ERK1/2 activation and the p53 pathway may play significant functions in mediating K101-induced apoptosis in human colon cancer cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Colonic Neoplasms / drug therapy. Organoplatinum Compounds / pharmacology. Signal Transduction / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Butadienes / pharmacology. Cell Line, Tumor. Enzyme Activation / drug effects. Humans. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / metabolism. Nitriles / pharmacology. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16702812.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Butadienes; 0 / K101 compound; 0 / Nitriles; 0 / Organoplatinum Compounds; 0 / Tumor Suppressor Protein p53; 0 / U 0126; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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53. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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54. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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55. Kawasaki Y, Jigami T, Furukawa S, Sagara M, Echizen K, Shibata Y, Sato R, Akiyama T: The adenomatous polyposis coli-associated guanine nucleotide exchange factor Asef is involved in angiogenesis. J Biol Chem; 2010 Jan 8;285(2):1199-207
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

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  • Mutation of the tumor suppressor adenomatous polyposis coli (APC) is a key early event in the development of most colorectal tumors.
  • APC promotes degradation of beta-catenin and thereby negatively regulates Wnt signaling, whereas mutated APCs present in colorectal tumor cells are defective in this activity.
  • Truncated mutant APCs constitutively activate Asef and induce aberrant migration of colorectal tumor cells.
  • Furthermore, we show that the growth as well as vascularity of subcutaneously implanted tumors are markedly impaired in Asef(-/-) mice compared with wild-type mice.
  • Thus, Asef plays a critical role in tumor angiogenesis and may be a promising target for cancer chemotherapy.
  • [MeSH-major] Adenomatous Polyposis Coli Protein / metabolism. Cell Movement. Colorectal Neoplasms / mortality. Endothelial Cells / metabolism. Guanine Nucleotide Exchange Factors / metabolism. Neovascularization, Pathologic / metabolism

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  • (PMID = 19897489.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Guanine Nucleotide Exchange Factors; 0 / Rho Guanine Nucleotide Exchange Factors; 0 / Vascular Endothelial Growth Factor A; 0 / Wnt Proteins; 0 / beta Catenin; 0 / vascular endothelial growth factor A, mouse; 103107-01-3 / Fibroblast Growth Factor 2; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Other-IDs] NLM/ PMC2801248
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56. 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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57. Procacciante F, Caciolo F, Diamantini G, Flati D, Pitasi F, Abilaliaj V, Covotta A, Banelli E, Di Seri M, Citone G: [Integrated multidisciplinary treatment of colorectal neoplasms]. Chir Ital; 2009 Jan-Feb;61(1):1-10
Hazardous Substances Data Bank. LEUCOVORIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Integrated multidisciplinary treatment of colorectal neoplasms].
  • [Transliterated title] Trattamento multidisciplinare integrato delle neoplasie colo-rettali.
  • In this retrospective study, the modality and advantages of the multidisciplinary diagnostic work-up and therapy regarding colorectal neoplasm were analysed.
  • Over the period 2004-2008, 63 patients underwent multidisciplinary treatment for colorectal cancer.
  • Exeresis was supplemented by adjuvant chemotherapy in those cases beyond IIA stage; all cases of extraperitoneal rectal and anal canal neoplasms plus one case of carcinoma of the transverse colon, initially inoperable, underwent neoadjuvant radiotherapy plus chemotherapy.
  • The treatment was initiated approximately 3 weeks after the diagnosis.
  • Fifty-four percent of patients with colonic and upper rectal neoplasms were given adjuvant chemotherapy, starting around 4 weeks after surgery.
  • Exeresis was performed in those patients with extraperitoneal rectal and anal canal neoplasms (12.7%) about 6-8 weeks after they had completed neoadjuvant therapy.
  • At the end of the treatment, 76% of the overall total numbers of patients were in good condition (follow-up 4-50 months).
  • The remaining 24% suffered recurrences about 13 months after the treatment for colonic and upper rectal neoplasm, and 8 1/2 months after treatment for extraperitoneal rectal/anal canal neoplasms.
  • Seventy-five percent of the recurring cases underwent treatment again, with 50% success; the others are still undergoing treatment.
  • The best therapeutic results were obtained by programmed integration of the various diagnostic-therapeutic steps according to an algorithm which we elaborated to evaluate all types of neoplasm at any stage of illness.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / radiotherapy. Colorectal Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Colectomy. Combined Modality Therapy. Female. Fluorouracil / therapeutic use. Follow-Up Studies. Humans. Laparoscopy. Laparotomy. Leucovorin / therapeutic use. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Organoplatinum Compounds / therapeutic use. Positron-Emission Tomography. Postoperative Complications. Radiography, Abdominal. Radiotherapy Dosage. Radiotherapy, Adjuvant. Time Factors. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19391334.001).
  • [ISSN] 0009-4773
  • [Journal-full-title] Chirurgia italiana
  • [ISO-abbreviation] Chir Ital
  • [Language] ita
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
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58. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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59. 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
Hazardous Substances Data Bank. LEUCOVORIN .

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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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60. Spina CS, Ton L, Yao M, Maehr H, Wolfe MM, Uskokovic M, Adorini L, Holick MF: Selective vitamin D receptor modulators and their effects on colorectal tumor growth. J Steroid Biochem Mol Biol; 2007 Mar;103(3-5):757-62
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective vitamin D receptor modulators and their effects on colorectal tumor growth.
  • It is well documented that 1,25(OH)(2)D(3) also has anti-tumor effects on a number of cancers and cancer cell lines including breast, colorectal, gastric, liver, ovarian, prostate, and non-melanoma skin cancers.
  • Included in the anti-tumor activities of 1,25(OH)(2)D(3) are its ability to cause antiproliferation, prodifferentation and decrease angiogenesis.
  • Furthermore, through regulation of the plaminogen activator (PA) system and a class of proteolytic enzymes called matrix metalloproteinases (MMPs), 1,25(OH)(2)D(3) reduces the invasive spread of tumor cells.
  • Because of the calcemic limitations of using 1,25(OH)(2)D(3) as a therapy, we have tested the effects of a novel Gemini vitamin D analogue, Deuterated Gemini (DG), on mouse colorectal cancer.
  • We demonstrated that DG is more potent in reducing tumor volume and mass, compared to control and 1,25(OH)(2)D(3).
  • DG significantly prevented (100% reduction, p<0.05) the invasive spread of colorectal tumor cells into the surrounding muscle, and had no effect on serum calcium levels.
  • Thus, DG acts as a selective vitamin D receptor modulator (SVDRM) by enhancing select anti-tumor characteristic 1,25(OH)(2)D(3) activities, without inducing hypercalcemia.
  • Thus, DG shows promise in the development of colorectal cancer therapies.
  • [MeSH-major] Calcitriol / therapeutic use. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Receptors, Calcitriol / metabolism
  • [MeSH-minor] Animals. Calcium / blood. Cell Line, Tumor. Cell Proliferation. Disease Progression. Male. Mice. Mice, Inbred BALB C. Muscle Neoplasms / pathology. Muscle Neoplasms / secretion. Neoplasm Invasiveness

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  • (PMID = 17368190.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Calcitriol; FXC9231JVH / Calcitriol; SY7Q814VUP / Calcium
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61. 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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62. Cunningham MP, Thomas H, Fan Z, Modjtahedi H: Responses of human colorectal tumor cells to treatment with the anti-epidermal growth factor receptor monoclonal antibody ICR62 used alone and in combination with the EGFR tyrosine kinase inhibitor gefitinib. Cancer Res; 2006 Aug 1;66(15):7708-15
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  • [Title] Responses of human colorectal tumor cells to treatment with the anti-epidermal growth factor receptor monoclonal antibody ICR62 used alone and in combination with the EGFR tyrosine kinase inhibitor gefitinib.
  • The anti-epidermal growth factor receptor (EGFR) monoclonal antibody cetuximab has been approved for the treatment of patients with metastatic colorectal cancer.
  • However, there is currently no reliable marker for response to therapy with the EGFR inhibitors.
  • In this study, we investigated the sensitivity of 10 human colorectal tumor cell lines (DiFi, CCL218, CCL221, CCL225, CCL227, CCL228, CCL231, CCL235, CCL244, and HCT-116) to treatment with our anti-EGFR monoclonal antibody, ICR62, and/or the EGFR tyrosine kinase inhibitor, gefitinib.
  • Of the cells examined, only DiFi contained high levels of constitutively active EGFR and were highly sensitive to treatment with both ICR62 (IC(50) = 0.52 nmol/L) and gefitinib (IC(50) = 27.5 nmol/L).
  • In contrast, the growth of other tumor cell lines, which contained low levels of the EGFR, HER-2, and pAkt but comparable or even higher basal levels of phosphorylated mitogen-activated protein kinase (pMAPK), were relatively resistant to treatment with both inhibitors.
  • However, treatment with a combination of ICR62 and gefitinib neither sensitized colorectal tumor cells that were insensitive to treatment with the single agent nor enhanced the growth-inhibitory effect of the single agent in DiFi cells.
  • These results indicate that basal levels of pMAPK and pAkt are not good indicators of response to the EGFR inhibitors in colorectal cancer cells and dual targeting of the EGFR by a combination of ICR62 and gefitinib is not superior to treatment with a single agent.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Colorectal Neoplasms / therapy. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / immunology
  • [MeSH-minor] Cell Growth Processes / drug effects. Cell Line, Tumor. Humans. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. Receptor, ErbB-2 / biosynthesis

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  • (PMID = 16885373.001).
  • [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 / Antibodies, Monoclonal; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; S65743JHBS / gefitinib
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63. González-Moreno S: Peritoneal Surface Oncology: A progress report. Eur J Surg Oncol; 2006 Aug;32(6):593-6
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  • The topics covered included diagnostic pathology, technology of hyperthermic peritoneal perfusion, quantitative prognostic indicators, accreditation of treatment programs, ovarian cancer, gastric cancer, peritoneal mesothelioma, appendiceal mucinous tumors, colorectal cancer, morbidity and mortality, and were presented by 25 invited speakers.
  • (1) cytoreductive surgery combined with perioperative intraperitoneal chemotherapy is unquestionably considered the standard of care for mucinous appendiceal tumors with peritoneal spread at the present time;.
  • (2) there is a need for standardization in the nomenclature used in this field and as a first step "HIPEC" was chosen as the recommended acronym to be used to refer to hyperthermic intraperitoneal chemotherapy in the future;.
  • (3) close international collaboration is needed to advance in the standardization of prognostic indicators, technology for HIPEC, accreditation of peritoneal surface malignancy treatment programs, anesthesia management and pathology, and ad hoc working groups were assembled for some of these issues.
  • Future directions for clinical research in this field, especially in carcinomatosis of colorectal origin were identified and extensively discussed.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / surgery. Medical Oncology. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / surgery. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / surgery. Stomach Neoplasms / drug therapy. Stomach Neoplasms / surgery
  • [MeSH-minor] Combined Modality Therapy. Congresses as Topic. Female. Humans. Hyperthermia, Induced. Male. Prognosis. Spain. Terminology as Topic

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  • (PMID = 16603332.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Congresses
  • [Publication-country] England
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64. 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


65. Seeliger H, Guba M, Koehl GE, Doenecke A, Steinbauer M, Bruns CJ, Wagner C, Frank E, Jauch KW, Geissler EK: Blockage of 2-deoxy-D-ribose-induced angiogenesis with rapamycin counteracts a thymidine phosphorylase-based escape mechanism available for colon cancer under 5-fluorouracil therapy. Clin Cancer Res; 2004 Mar 1;10(5):1843-52
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  • [Title] Blockage of 2-deoxy-D-ribose-induced angiogenesis with rapamycin counteracts a thymidine phosphorylase-based escape mechanism available for colon cancer under 5-fluorouracil therapy.
  • PURPOSE: Colorectal neoplasms remain a leading cause of cancer-related deaths.
  • A recognized weakness of conventional 5-fluorouracil (5-FU) therapy relates to expression of the intracellular enzyme, thymidine phosphorylase (TP).
  • Although TP promotes 5-FU cytotoxicity, TP-derived 2-deoxy-D-ribose (dRib) counterproductively stimulates tumor angiogenesis.
  • Here, the newly discovered antiangiogenic drug rapamycin was combined with 5-FU to counteract the potential escape mechanism of dRib-induced angiogenesis.
  • EXPERIMENTAL DESIGN: Orthotopic tumor growth was assessed in rapamycin and 5-FU-treated BALB/c mice with TP-expressing CT-26 colon adenocarcinoma cells.
  • RESULTS: Rapamycin treatment of mice bearing orthotopic tumors inhibited tumor growth more than did 5-FU, and mice treated with both drugs typically developed no tumors.
  • In the liver metastasis assay, combination therapy blocked metastatic expansion of solitary tumor cells.
  • Interestingly, complex drug activities were suggested by tumor-cell proliferation being more sensitive to 5-FU than to rapamycin in vitro, but more sensitive to rapamycin in vivo.
  • CONCLUSIONS: Inhibition of dRib-induced angiogenesis with rapamycin counteracts a potential TP-based escape mechanism for colorectal cancer under 5-FU therapy, introducing a novel, clinically feasible, combination treatment option for this common neoplasm.
  • [MeSH-major] Adenocarcinoma / drug therapy. Colonic Neoplasms / drug therapy. Deoxyribose / pharmacology. Fluorouracil / therapeutic use. Neovascularization, Pathologic / prevention & control. Sirolimus / pharmacology. Thymidine Phosphorylase / metabolism
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / therapeutic use. Aorta, Thoracic / physiology. Disease Models, Animal. Immunosuppressive Agents. Liver Neoplasms / prevention & control. Liver Neoplasms / secondary. Male. Mice. Mice, Inbred BALB C. Mice, SCID. Muscle, Smooth, Vascular / physiology. Rats. Rats, Inbred ACI

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  • (PMID = 15014039.001).
  • [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 / Immunosuppressive Agents; 533-67-5 / Deoxyribose; EC 2.4.2.4 / Thymidine Phosphorylase; U3P01618RT / Fluorouracil; W36ZG6FT64 / Sirolimus
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66. 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


67. 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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68. Oñate-Ocaña LF, Herrera-Goepfert R, Aiello-Crocifoglio V, Mondragón-Sánchez R, Ruiz-Molina JM: [Multiorgan resection in T4 colonic adenocarcinoma. Report of a case]. Rev Gastroenterol Mex; 2000 Jan-Mar;65(1):26-9
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  • [Transliterated title] Resección multiorgánica en adenocarcinoma de colon T4. Informe de un caso.
  • BACKGROUND: Colorectal cancer is the second among gastrointestinal malignancies in Mexico Locally advanced disease or metastatic lesions are frequently found.
  • To resect or not such a tumor is a difficult decision.
  • OBJECTIVE: To report a case of colon cancer with multivisceral invasion resected and to review the published information.
  • CLINICAL MATERIAL: A 43 year-old Mexican male with rectal bleeding and weight loss with a tumor located in transverse colon with direct invasion to stomach.
  • En-bloc radical-extended right colectomy, total gastrectomy, distal pancreatectomy, splenectomy and left adrenalectomy was performed.
  • Adjuvant chemotherapy was used.
  • CONCLUSION: An aggressive multiorganic resection in T4 colorectal tumors is justified in selected cases.
  • [MeSH-major] Adenocarcinoma / surgery. Colonic Neoplasms / surgery
  • [MeSH-minor] Adrenalectomy. Adult. Antimetabolites, Antineoplastic / therapeutic use. Colectomy. Fluorouracil / therapeutic use. Gastrectomy. Humans. Leucovorin / administration & dosage. Leucovorin / therapeutic use. Lymph Node Excision. Male. Neoplasm Invasiveness. Neoplasm Staging. Pancreas / pathology. Pancreas / surgery. Pancreatectomy. Remission Induction. Spleen / pathology. Spleen / surgery. Splenectomy. Stomach / pathology. Stomach / surgery

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  • (PMID = 11464588.001).
  • [ISSN] 0375-0906
  • [Journal-full-title] Revista de gastroenterología de México
  • [ISO-abbreviation] Rev Gastroenterol Mex
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
  • [Number-of-references] 8
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69. 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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70. Li JQ, Wang SL, Xu F, Liu ZY, Li R: Therapeutic effectiveness of slow-release PLGA-oxaliplatin microsphere on human colorectal tumor-bearing mice. Anticancer Drugs; 2010 Jul;21(6):600-8
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  • [Title] Therapeutic effectiveness of slow-release PLGA-oxaliplatin microsphere on human colorectal tumor-bearing mice.
  • The aim was to develop a slow-release poly-lactic-coglycolic acid (PLGA)-oxaliplatin microsphere and to assess the therapeutic effectiveness and safety of this preparation on colorectal tumor in vivo.
  • The PLGA-oxaliplatin microsphere was prepared based on a spray-drying method, and the drug loading and in-vitro oxaliplatin release profile were carried out using high performance liquid chromatography.
  • The inhibiting effect on tumor growth was examined using in-vivo subcutaneously inoculated colorectal tumor models of nude mice.
  • The size of the microsphere was less than 100 microm, drug loading was 18-22% and drug release time lasted as long as 30 days.
  • PLGA-oxaliplatin microspheres significantly restrained tumor growth and this effect correlated with decreased expression of proliferating cell nuclear antigen and increased expression of terminal deoxynucleotidyltransferase dUTP nick end labeling in tumor cells.
  • The PLGA-oxaliplatin microsphere developed here was suitable for regional use; it appears safe and effective in controlling the tumor growth.
  • This preparation shows promise in reducing local recurrence of colorectal cancer after resection, but needs further investigation.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Colorectal Neoplasms / drug therapy. Lactic Acid / chemistry. Organoplatinum Compounds / administration & dosage. Polyglycolic Acid / chemistry
  • [MeSH-minor] Animals. Cell Line, Tumor. Delayed-Action Preparations. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Microspheres. Treatment Outcome

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  • (PMID = 20527722.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Delayed-Action Preparations; 0 / Organoplatinum Compounds; 0 / polylactic acid-polyglycolic acid copolymer; 04ZR38536J / oxaliplatin; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid
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71. Monzon FA, Ogino S, Hammond ME, Halling KC, Bloom KJ, Nikiforova MN: The role of KRAS mutation testing in the management of patients with metastatic colorectal cancer. Arch Pathol Lab Med; 2009 Oct;133(10):1600-6
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  • [Title] The role of KRAS mutation testing in the management of patients with metastatic colorectal cancer.
  • CONTEXT: KRAS mutations can be detected in approximately 30% to 40% of all patients with colorectal cancer.
  • Several recent studies have shown that patients with KRAS mutations in codons 12 or 13 in metastatic tumors do not benefit from anti-epidermal growth factor receptor therapy with cetuximab or panitumumab.
  • OBJECTIVE: To review the literature on the role of KRAS mutation testing for management of patients with metastatic colorectal cancer and to discuss testing strategies.
  • CONCLUSIONS: Multiple methods for detecting KRAS mutations in colorectal tumors are available, and all methods in current clinical use appear to have adequate clinical sensitivity for predicting a lack of response to cetuximab and panitumumab.
  • Pathologist expertise is essential to quality KRAS testing and to determining effective treatment for patients with metastatic colorectal cancer.
  • [MeSH-major] Adenocarcinoma / genetics. Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / genetics. Mutation. Proto-Oncogene Proteins / genetics. ras Proteins / genetics
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Cetuximab. DNA Mutational Analysis. DNA, Neoplasm / analysis. Humans. Randomized Controlled Trials as Topic. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / drug effects. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects

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  • (PMID = 19792050.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / panitumumab; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins; PQX0D8J21J / Cetuximab
  • [Number-of-references] 44
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72. Baynes RD, Gansert J: KRAS mutational status as a predictor of epidermal growth factor receptor inhibitor efficacy in colorectal cancer. Am J Ther; 2009 Nov-Dec;16(6):554-61
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  • [Title] KRAS mutational status as a predictor of epidermal growth factor receptor inhibitor efficacy in colorectal cancer.
  • Inhibitors of the epidermal growth factor receptor (EGFR) have demonstrated promising potential in the treatment of advanced colorectal cancer.
  • However, a proportion of patients do not respond to therapy with EGFR inhibitors, and therefore, there has been interest in identifying those patients most likely to benefit from therapy with these agents.
  • Although there is still some debate regarding the prognostic importance of KRAS mutations in patients with metastatic colorectal cancer, several recent phase 2 and 3 studies have identified the presence of mutations at codons 12 and 13 of KRAS as predictors of poor response to the anti-EGFR monoclonal antibodies panitumumab and cetuximab.
  • Patients with wild-type KRAS were found to have significantly better progression-free survival, overall survival, and/or objective response rate compared with patients harboring KRAS mutations.
  • As a result, there has been growing interest in the development of KRAS mutational status as a biomarker for predicting patient response to EGFR-targeted therapy.
  • Screening colorectal tumors for the absence of KRAS mutations may help identify patients most likely to benefit from anti-EGFR therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / antagonists & inhibitors. ras Proteins / genetics
  • [MeSH-minor] Antibodies, Monoclonal / pharmacokinetics. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Cetuximab. Disease-Free Survival. Genetic Testing. Humans. Mutation. Pharmacogenetics. Treatment Outcome

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  • [CommentIn] Am J Ther. 2009 Nov-Dec;16(6):477-9 [19829092.001]
  • (PMID = 19352138.001).
  • [ISSN] 1536-3686
  • [Journal-full-title] American journal of therapeutics
  • [ISO-abbreviation] Am J Ther
  • [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 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / panitumumab; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins; PQX0D8J21J / Cetuximab
  • [Number-of-references] 59
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73. Gade TP, Buchanan IM, Motley MW, Mazaheri Y, Spees WM, Koutcher JA: Imaging intratumoral convection: pressure-dependent enhancement in chemotherapeutic delivery to solid tumors. Clin Cancer Res; 2009 Jan 1;15(1):247-55
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  • [Title] Imaging intratumoral convection: pressure-dependent enhancement in chemotherapeutic delivery to solid tumors.
  • PURPOSE: Low-molecular weight (LMW) chemotherapeutics are believed to reach tumors through diffusion across capillary beds as well as membrane transporters.
  • Unexpectedly, the delivery of these agents seems to be augmented by reductions in tumor interstitial fluid pressure, an effect typically associated with high-molecular weight molecules that reach tumors principally through convection.
  • We investigated the hypothesis that improved intratumoral convection can alter tumor metabolism and enhance the delivery of a LMW chemotherapeutic agent to solid tumors.
  • EXPERIMENTAL DESIGN: For this purpose, we applied 31P/19F magnetic resonance spectroscopy (MRS) and magnetic resonance spectroscopic imaging (MRSI) to examine the influence of type I collagenase on tumor bioenergetics and the delivery of 5-fluorouracil (5FU) to HT29 human colorectal tumors grown s.c. in mice.
  • RESULTS: Collagenase effected a 34% reduction in tumor interstitial fluid pressure with an attendant disintegration of intratumoral collagen.
  • Neither mice-administered collagenase nor controls receiving PBS showed changes in (31)phosphorus MRS-measured tumor bioenergetics; however, a time-dependent increase in the content of extracellular inorganic phosphate (Pi(e)) was observed in tumors of collagenase-treated animals. (31)Phosphorus MRSI showed that this increase underscored a more homogeneous distribution of Pi(e) in tumors of experimental mice. (19)Fluorine MRS showed that these changes were associated with a 50% increase in 5FU uptake in tumors of experimental versus control animals; however, this increase resulted in an increase in 5FU catabolites rather than fluoronucleotide intermediates that are required for subsequent cytotoxicity.
  • CONCLUSIONS: These data indicate that the modulation of convective flow within tumors can improve the delivery of (LMW) chemotherapeutics and show the potential role for noninvasive imaging of this process in vivo.

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  • (PMID = 19118052.001).
  • [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 / U24 CA083084; United States / NCI NIH HHS / CA / P50 CA086438; United States / NCI NIH HHS / CA / P50CA115675-01; United States / NCI NIH HHS / CA / P30CA08748; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / P50CA86438; United States / NCI NIH HHS / CA / P01 CA115675; United States / NCI NIH HHS / CA / R24CA83084; United States / NCI NIH HHS / CA / R24 CA083084
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phosphates; EC 3.4.24.- / Collagenases; EC 3.4.24.- / collagenase 1; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ NIHMS453201; NLM/ PMC4217124
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74. Fukuda M, Kusama K, Sakashita H: Cimetidine inhibits salivary gland tumor cell adhesion to neural cells and induces apoptosis by blocking NCAM expression. BMC Cancer; 2008;8:376
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  • [Title] Cimetidine inhibits salivary gland tumor cell adhesion to neural cells and induces apoptosis by blocking NCAM expression.
  • BACKGROUND: Cimetidine, a histamine type-2 receptor antagonist, has been reported to inhibit the growth of glandular tumors such as colorectal cancer, however the mechanism of action underlying this effect is unknown.
  • Adenoid cystic carcinoma is well known as a malignant salivary gland tumor which preferentially invades neural tissues.
  • We demonstrated previously that human salivary gland tumor (HSG) cells spontaneously express neural cell adhesion molecule (NCAM), that HSG cell proliferation may be controlled via a homophilic (NCAM-NCAM) binding mechanism and that NCAM may be associated with perineural invasion by malignant salivary gland tumors.
  • Here, we investigated the effects of cimetidine on growth and perineural/neural invasion of salivary gland tumor cells.
  • RESULTS: We have demonstrated for the first time that cimetidine can block the adhesion of HSG cells to neural cell monolayers and that it can also induce significant apoptosis in the tumor mass in a nude mouse model.
  • CONCLUSION: These findings suggest that growth and perineural/neural invasion of salivary gland tumors can be blocked by administration of cimetidine via induction of apoptosis and in which NCAM plays a role.
  • [MeSH-major] Cell Adhesion / drug effects. Cimetidine / pharmacology. Histamine H2 Antagonists / pharmacology. Neoplasm Invasiveness / physiopathology. Neural Cell Adhesion Molecules / metabolism. Salivary Gland Neoplasms / drug therapy. Salivary Gland Neoplasms / physiopathology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Dose-Response Relationship, Drug. Down-Regulation. Gene Expression / drug effects. Humans. Mice. Mice, Nude. NF-kappa B / drug effects. Neurons / pathology. Tumor Cells, Cultured

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  • (PMID = 19091137.001).
  • [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 / Histamine H2 Antagonists; 0 / NF-kappa B; 0 / Neural Cell Adhesion Molecules; 80061L1WGD / Cimetidine
  • [Other-IDs] NLM/ PMC2635382
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75. Schlemmer M, Kuehl M, Schalhorn A, Rauch J, Jauch KW, Hentrich M: Tissue levels of reduced folates in patients with colorectal carcinoma after infusion of folinic acid at various dose levels. Clin Cancer Res; 2008 Dec 1;14(23):7930-4
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  • [Title] Tissue levels of reduced folates in patients with colorectal carcinoma after infusion of folinic acid at various dose levels.
  • PURPOSE: In patients with colorectal cancer (CRC), modulation of 5-fluorouracil (5-FU) by folinic acid (FA) improves response rate and overall survival compared with 5-FU alone.
  • We investigated reduced folate pools in various tissues from patients with CRC without and after prior administration of FA.
  • EXPERIMENTAL DESIGN: A total of 186 specimens (normal colorectal mucosa, primary colorectal tumor, normal liver, and liver metastases) from 86 consecutive patients with CRC were obtained and investigated for levels of reduced folates.
  • Tissue lysates were analyzed for reduced folate levels by means of the tritium release assay.
  • In primary tumor, only 200 and 500 mg/m2 FA resulted in a significant increase of reduced folates with highest values measured after 500 mg/m2 FA.
  • CONCLUSIONS: From a pharmacologic point of view, high-dose FA should be recommended for optimal modulation of 5-FU in patients with mCRC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Leucovorin / administration & dosage. Tetrahydrofolates / analysis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Fluorouracil / administration & dosage. Humans

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  • (PMID = 19047124.001).
  • [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 / Antineoplastic Agents; 0 / Tetrahydrofolates; 29347-89-5 / 5,6,7,8-tetrahydrofolic acid; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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76. 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
MedlinePlus Health Information. consumer health - Colorectal Cancer.

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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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77. Lopes EC, Valls E, Figueroa ME, Mazur A, Meng FG, Chiosis G, Laird PW, Schreiber-Agus N, Greally JM, Prokhortchouk E, Melnick A: Kaiso contributes to DNA methylation-dependent silencing of tumor suppressor genes in colon cancer cell lines. Cancer Res; 2008 Sep 15;68(18):7258-63
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  • [Title] Kaiso contributes to DNA methylation-dependent silencing of tumor suppressor genes in colon cancer cell lines.
  • Aberrant CpG methylation of tumor suppressor gene regulatory elements is associated with transcriptional silencing and contributes to malignant transformation of different tissues.
  • The Kaiso protein is a transcriptional repressor expressed in human and murine colorectal tumors that can bind to methylated clusters of CpG dinucleotides.
  • We show here that Kaiso represses methylated tumor suppressor genes and can bind in a methylation-dependent manner to the CDKN2A in human colon cancer cell lines.
  • The contribution of Kaiso to epigenetic silencing was underlined by the fact that Kaiso depletion induced tumor suppressor gene expression without affecting DNA methylation levels.
  • As a consequence, colon cancer cells became susceptible to cell cycle arrest and cell death mediated by chemotherapy.
  • The data suggest that Kaiso is a methylation-dependent "opportunistic" oncogene that silences tumor suppressor genes when they become hypermethylated.
  • Because Kaiso inactivation sensitized colon cancer cell lines to chemotherapy, it is possible that therapeutic targeting of Kaiso could improve the efficacy of current treatment regimens.
  • [MeSH-major] Colonic Neoplasms / genetics. DNA Methylation. Gene Silencing. Genes, Tumor Suppressor. Transcription Factors / metabolism
  • [MeSH-minor] Cell Cycle / physiology. Cell Death / physiology. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Genes, p16. HCT116 Cells. Humans. Promoter Regions, Genetic. Protein Binding. RNA, Small Interfering / genetics. Transfection

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  • (PMID = 18794111.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075090; United States / NCI NIH HHS / CA / R01 CA118699
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / ZNF-kaiso protein, human
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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. Baumhoer D, Armbrust T, Ramadori G: Nonsurgical treatment of the primary tumor in four consecutive cases of metastasized colorectal carcinoma. Endoscopy; 2005 Dec;37(12):1232-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonsurgical treatment of the primary tumor in four consecutive cases of metastasized colorectal carcinoma.
  • BACKGROUND AND STUDY AIMS: Surgical resection of the primary tumor is standard treatment in stage IV colorectal cancer, but palliative surgery is associated with high morbidity and mortality and with uncertain benefit.
  • The wisdom of surgical resection of asymptomatic or oligosymptomatic primary tumors is therefore questionable.
  • By studying a small series of such patients, we aimed to assess whether endoscopic techniques can offer an effective alternative form of nonsurgical palliative treatment for the prevention of local complications caused by a primary colorectal tumor.
  • PATIENTS AND METHODS: We treated four consecutive patients who had stage IV colorectal cancer by endoscopic tumor debulking, either using a standard polypectomy snare technique alone or by argon plasma coagulation ablation followed by snare debulking of the primary tumor.
  • RESULTS: Palliation was achieved in all patients, demonstrated by regression of the primary tumor and absence of symptoms related to the colonic tumor during the observation period of up to 24 months.
  • No procedure-associated complications were observed and it was possible to commence systemic chemotherapy immediately after the endoscopic treatment in all four patients.
  • CONCLUSIONS: We believe that surgical resection of the primary tumor is not appropriate in all patients with stage IV colorectal cancer, and that this form of treatment should be reserved for patients with signs of complete obstruction in whom local ablative procedures are not possible.
  • Simple endoscopic techniques for treatment of the primary tumor, in conjunction with systemic chemotherapy, may be the most suitable form of management for patients with stage IV colorectal tumors.
  • [MeSH-major] Adenocarcinoma / secondary. Adenocarcinoma / therapy. Colonoscopy / methods. Colorectal Neoplasms / therapy. Intestinal Obstruction / therapy. Liver Neoplasms / secondary. Palliative Care / methods
  • [MeSH-minor] Aged. Aged, 80 and over. Biopsy, Needle. Humans. Immunohistochemistry. Male. Neoplasm Staging. Prognosis. Risk Assessment. Survival Rate. Tomography, X-Ray Computed. Treatment Outcome


80. Balin-Gauthier D, Delord JP, Rochaix P, Mallard V, Thomas F, Hennebelle I, Bugat R, Canal P, Allal C: In vivo and in vitro antitumor activity of oxaliplatin in combination with cetuximab in human colorectal tumor cell lines expressing different level of EGFR. Cancer Chemother Pharmacol; 2006 Jun;57(6):709-18
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  • [Title] In vivo and in vitro antitumor activity of oxaliplatin in combination with cetuximab in human colorectal tumor cell lines expressing different level of EGFR.
  • This study aimed to assess the effect of cetuximab (C225, Erbitux, a chimeric anti-epidermal growth factor receptor (EGFR) monoclonal antibody) in combination with oxaliplatin in vitro and in vivo on four colon cancer cell lines (HCT-8; HT-29, SW620, HCT-116) expressing different levels of EGFR.
  • In vivo, the combination of cetuximab plus oxaliplatin significantly inhibited tumor growth of HCT-8 and HT-29 (tumor delay or Td = 21.6+/-2.9 and 18.0+/-2.9 days respectively, synergistic effect) compared to either oxaliplatin (Td=12.6+/-2.3 and 14.4+/-3.2 days respectively) or cetuximab (Td=13.4+/-2.9 and 14.5+/-2.4 days, respectively) alone in xenograft models.
  • The observed responses are strictly dependent on the cell type, and are not correlated with the level of EGFR expression but related to the basal level of phospho-EGFR.
  • This study provides promising preclinical results for a possible clinical investigation of the combination of oxaliplatin plus cetuximab in chemorefractory colorectal tumors.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Cetuximab. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Drug Synergism. Female. Humans. Mice. Mice, Nude. Organoplatinum Compounds / administration & dosage. Phosphorylation. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

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  • (PMID = 16320055.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
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81. Ellis LM: Angiogenesis and its role in colorectal tumor and metastasis formation. Semin Oncol; 2004 Dec;31(6 Suppl 17):3-9
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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82. 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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83. 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
Hazardous Substances Data Bank. RESVERATROL .

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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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84. Attoub S, Rivat C, Rodrigues S, Van Bocxlaer S, Bedin M, Bruyneel E, Louvet C, Kornprobst M, André T, Mareel M, Mester J, Gespach C: The c-kit tyrosine kinase inhibitor STI571 for colorectal cancer therapy. Cancer Res; 2002 Sep 1;62(17):4879-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The c-kit tyrosine kinase inhibitor STI571 for colorectal cancer therapy.
  • The c-kit tyrosine kinase inhibitor STI571 exhibits a substantial therapeutic activity in patients with chronic myeloid leukemia and gastrointestinal stromal tumors respectively associated with constitutive activation of the BCR-ABL and c-kit tyrosine kinases.
  • Human colorectal tumors also express the c-kit proto-oncogene.
  • The present study focuses on the anticancer activity of STI571 in human colorectal tumor cells in vitro and in vivo.
  • The c-kit receptor was identified as a M(r) 145,000 immunoreactive band in human colon cancer cells HT29, HCT8/S11, and HCT116.
  • Cellular invasion induced by 10 ng/ml stem cell factor (EC(50) = 3 ng/ml) in HT29 cells was blocked by 1 micro M STI571 (IC(50) = 56 nM) and pharmacological inhibitors of several oncogenic signaling pathways, namely, phosphatidylinositol 3-kinase (LY294002), Rho GTPases (Clostridium botulinum exoenzyme C3 transferase), and Rho-kinase (Y27632).
  • These cellular effects were associated with a decrease in tumor growth.
  • These encouraging results warrant further preclinical investigations and clinical trials on the use of the c-kit inhibitor STI571 as a chemotherapeutic agent in colon cancer prevention and in treatment of advanced colorectal cancers associated with liver metastases.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Colorectal Neoplasms / drug therapy. Enzyme Inhibitors / pharmacology. Piperazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / drug effects. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Benzamides. Cell Division / drug effects. Chick Embryo. Endothelium, Vascular / drug effects. Endothelium, Vascular / growth & development. Humans. Imatinib Mesylate. Mice. Mice, Nude. Neoplasm Invasiveness. Neovascularization, Physiologic / drug effects. Stem Cell Factor / antagonists & inhibitors. Stem Cell Factor / pharmacology. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12208734.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 0 / Stem Cell Factor; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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85. 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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86. Agard C, Ligeza C, Dupas B, Izembart A, El Kouri C, Moullier P, Ferry N: Immune-dependent distant bystander effect after adenovirus-mediated suicide gene transfer in a rat model of liver colorectal metastasis. Cancer Gene Ther; 2001 Feb;8(2):128-36
Hazardous Substances Data Bank. GANCICLOVIR .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immune-dependent distant bystander effect after adenovirus-mediated suicide gene transfer in a rat model of liver colorectal metastasis.
  • Gene transfer of the herpes simplex virus thymidine kinase (HSV-tk) gene sensitizes tumor cells to the toxic effect of ganciclovir (GCV).
  • A distant bystander effect, which involves anatomically separated tumors, has been reported in vivo.
  • Our aim was to evaluate and characterize such distant effect in a rat model of colorectal tumors implanted in the liver using adenovirus to carry the HSV-tk gene.
  • Two colorectal tumors were implanted in two distinct liver lobes of the liver.
  • One of the tumor was transduced with an adenoviral vector containing HSV-tk gene.
  • The volumes of the tumors were monitored after GCV treatment.
  • After GCV administration, the nontransduced distant tumor regressed partially or completely in the experimental group.
  • HSV-tk/GCV-induced immune response against tumors was evidenced by an adoptive transfer assay (Winn assay) and the distant bystander effect was blunted after CD8+ lymphocytes depletion.
  • [MeSH-major] Adenoviridae / genetics. Antiviral Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Ganciclovir / therapeutic use. Gene Transfer Techniques. Genetic Therapy / methods. Herpesvirus 1, Human / enzymology. Liver Neoplasms / drug therapy. Thymidine Kinase / genetics

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  • (PMID = 11263528.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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87. McCourt M, Wang JH, Sookhai S, Redmond HP: Taurolidine inhibits tumor cell growth in vitro and in vivo. Ann Surg Oncol; 2000 Oct;7(9):685-91
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  • [Title] Taurolidine inhibits tumor cell growth in vitro and in vivo.
  • We hypothesized that Taurolidine may inhibit tumor cell growth, both in an in vitro and in vivo setting.
  • Our aim was to examine the effect of Taurolidine on the growth of a rat metastatic colorectal tumor cell line (DHD/K12/TRb) in vitro and in vivo.
  • Group A (control) underwent laparotomy and instillation of DHD/K12/TRb tumor cells intraperitoneally followed by phosphate buffered saline (PBS).
  • Animals were killed after 24 days and tumor burden assessed by counting the number of tumor nodules in the peritoneal cavity.
  • RESULTS: Incubation of the tumor cells with Taurolidine resulted in a 4-fold decrease in proliferation rates (25+/-4% vs. 100+/-28% for controls) and a 4-fold increase in cell necrosis as demonstrated by the increase in LDH release (403+/-28% vs. 100+/-26% for controls), at a Taurolidine concentration of 25 microg/ml.
  • In the in vivo study, local Taurolidine administration resulted in significant decreases in tumor burden (3+/-1 nodules in Group B animals vs. 649+/-101 nodules in Group A animals).
  • CONCLUSIONS: Taurolidine inhibits the growth of a rat metastatic colorectal tumor cell line in vitro and in vivo and thus may have potential in the prevention of peritoneal metastases.
  • [MeSH-major] Adenocarcinoma / drug therapy. Anti-Infective Agents, Local / pharmacology. Colorectal Neoplasms / drug therapy. Peritoneal Neoplasms / drug therapy. Taurine / analogs & derivatives. Taurine / pharmacology. Thiadiazines / pharmacology
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Division / drug effects. Cell Survival / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Flow Cytometry. Fluorescent Antibody Technique. Male. Random Allocation. Rats. Rats, Inbred Strains. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects

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  • (PMID = 11034247.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anti-Infective Agents, Local; 0 / Thiadiazines; 1EQV5MLY3D / Taurine; 8OBZ1M4V3V / taurolidine
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88. 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
Hazardous Substances Data Bank. FAMOTIDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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89. Siena S, Sartore-Bianchi A, Di Nicolantonio F, Balfour J, Bardelli A: Biomarkers predicting clinical outcome of epidermal growth factor receptor-targeted therapy in metastatic colorectal cancer. J Natl Cancer Inst; 2009 Oct 07;101(19):1308-24
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  • [Title] Biomarkers predicting clinical outcome of epidermal growth factor receptor-targeted therapy in metastatic colorectal cancer.
  • The monoclonal antibodies panitumumab and cetuximab that target the epidermal growth factor receptor (EGFR) have expanded the range of treatment options for metastatic colorectal cancer.
  • Initial evaluation of these agents as monotherapy in patients with EGFR-expressing chemotherapy-refractory tumors yielded response rates of approximately 10%.
  • The realization that detection of positive EGFR expression by immunostaining does not reliably predict clinical outcome of EGFR-targeted treatment has led to an intense search for alternative predictive biomarkers.
  • Oncogenic activation of signaling pathways downstream of the EGFR, such as mutation of KRAS, BRAF, or PIK3CA oncogenes, or inactivation of the PTEN tumor suppressor gene is central to the progression of colorectal cancer.
  • Tumor KRAS mutations, which may be present in 35%-45% of patients with colorectal cancer, have emerged as an important predictive marker of resistance to panitumumab or cetuximab treatment.
  • In addition, among colorectal tumors carrying wild-type KRAS, mutation of BRAF or PIK3CA or loss of PTEN expression may be associated with resistance to EGFR-targeted monoclonal antibody treatment, although these additional biomarkers require further validation before incorporation into clinical practice.
  • Additional knowledge of the molecular basis for sensitivity or resistance to EGFR-targeted monoclonal antibodies will allow the development of new treatment algorithms to identify patients who are most likely to respond to treatment and could also provide rationale for combining therapies to overcome primary resistance.
  • The use of KRAS mutations as a selection biomarker for anti-EGFR monoclonal antibody (eg, panitumumab or cetuximab) treatment is the first major step toward individualized treatment for patients with metastatic colorectal cancer.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / drug therapy. Mutation. Proto-Oncogene Proteins / drug effects. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Cetuximab. Disease-Free Survival. Gene Expression Regulation, Neoplastic / drug effects. Humans. Neoplasm Staging. Odds Ratio. PTEN Phosphohydrolase / drug effects. PTEN Phosphohydrolase / genetics. Phosphatidylinositol 3-Kinases / drug effects. Phosphatidylinositol 3-Kinases / genetics. Predictive Value of Tests. Proto-Oncogene Proteins B-raf / drug effects. Proto-Oncogene Proteins B-raf / genetics. Proto-Oncogene Proteins p21(ras) / drug effects. Proto-Oncogene Proteins p21(ras) / genetics. Randomized Controlled Trials as Topic. Research Design

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  • [CommentIn] J Natl Cancer Inst. 2010 Apr 21;102(8):573; author reply 573-5 [20305131.001]
  • (PMID = 19738166.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [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 / Proto-Oncogene Proteins; 6A901E312A / 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 / Proto-Oncogene Proteins B-raf; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); PQX0D8J21J / Cetuximab
  • [Number-of-references] 140
  • [Other-IDs] NLM/ PMC2758310
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90. Niyazi M, Marini P, Daniel PT, Humphreys R, Jendrossek V, Belka C: Efficacy of a triple treatment with irradiation, agonistic TRAIL receptor antibodies and EGFR blockade. Strahlenther Onkol; 2009 Jan;185(1):8-18
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  • [Title] Efficacy of a triple treatment with irradiation, agonistic TRAIL receptor antibodies and EGFR blockade.
  • BACKGROUND AND PURPOSE: : Since the efficacy of a single targeted agent in combination with ionizing radiation is limited by putative treatment resistances, a rationally designed triple treatment consisting of an agonistic antibody targeting either TRAIL-R1 (mapatumumab) or TRAIL-R2 (lexatumumab), radiation and an epidermal growth factor receptor-(EGFR-)inhibiting antibody (cetuximab) was tested.
  • MATERIAL AND METHODS: : Induction of apoptosis after triple treatment was determined in Colo205, HCT116 and FaDu cells by Hoechst 33342 stain.
  • A knockout variant of HCT116 was used to examine Bax dependence of the triple treatment.
  • Clonogenic assays were performed to examine the effect on clonogenic survival of tumor cells.
  • RESULTS: : A synergistic effect of radiation, cetuximab and agonistic TRAIL-R antibodies was demonstrated in cell lines derived from colorectal tumors or head-and-neck cancers.
  • CONCLUSION: : These data suggest that rationally designed multimodal therapy approaches integrating radiation with more than one targeted agent will open new perspectives in radiation oncology.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Apoptosis / drug effects. Apoptosis / radiation effects. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / radiotherapy. Radiotherapy, Conformal / methods
  • [MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Cell Line, Tumor. Cetuximab. Chemotherapy, Adjuvant. Humans. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptors, TNF-Related Apoptosis-Inducing Ligand / antagonists & inhibitors. Treatment Outcome

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  • (PMID = 19224142.001).
  • [ISSN] 1439-099X
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / lexatumumab; 0 / mapatumumab; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
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91. 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


92. Dai GJ, Jin HY, Ding YJ, Xia JG, Liu XF, Liu F, Tan XZ, Geng JX: [Anticancer effects of tea polyphenols on colorectal cancer with microsatellite instability in nude mice]. Zhong Xi Yi Jie He Xue Bao; 2008 Dec;6(12):1263-6
MedlinePlus Health Information. consumer health - Colorectal Cancer.

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  • [Title] [Anticancer effects of tea polyphenols on colorectal cancer with microsatellite instability in nude mice].
  • OBJECTIVE: To study the anticancer effects of tea polyphenols on colorectal cancer with microsatellite instability (MSI) in nude mice and to explore its mechanism.
  • Tumor fragments collected from the subcutaneous tumor of hMSH2-absence colon carcinoma Lovo cell line were surgically implanted onto the submucosa of the caecum during colostomy to establish the model.
  • The inhibition rates of tumors were calculated, and microsatellite instability (MSI) and the alteration of transforming growth factor-beta1 (TGF-beta1), TGF-beta2 and insulin-like growth factor (IGF) were detected by Genescan method at different times after the injection.
  • RESULTS: The tumor volumes of the three groups began to decrease at the 1st week and decreased most greatly from 2 to 3 weeks after treatment, and then the tumors tended to increase.
  • The study found that tea polyphenols could inhibit the tumor growth.
  • The tumor inhibition rates in the three treated groups were significantly higher than those in untreated group 1, 2, 3 and 4 weeks after treatment (P<0.01).
  • Detection of MSI showed that the colorectal tumor in the untreated group presented with four MSI signs, including BAT-25, D2S123, D5S346 and D17S250, and TGF-beta1, TGF-beta2, IGF expressions.
  • CONCLUSION: Tea polyphenols can inhibit the mismatch-repair-gene deficient colorectal cancer in nude mice by down-regulating the microsatellite instability.
  • [MeSH-major] Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / genetics. Microsatellite Instability. Polyphenols / therapeutic use. Tea / chemistry

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  • (PMID = 19063841.001).
  • [ISSN] 1672-1977
  • [Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
  • [ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Polyphenols; 0 / Somatomedins; 0 / Tea; 0 / Transforming Growth Factor beta1; 0 / Transforming Growth Factor beta2
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93. Sauter A, Triller J, Schmidt F, Kickuth R: Treatment of superior vena cava (SVC) syndrome and inferior vena cava (IVC) thrombosis in a patient with colorectal cancer: combination of SVC stenting and IVC filter placement to palliate symptoms and pave the way for port implantation. Cardiovasc Intervent Radiol; 2008 Jul;31 Suppl 2:S144-8
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  • [Title] Treatment of superior vena cava (SVC) syndrome and inferior vena cava (IVC) thrombosis in a patient with colorectal cancer: combination of SVC stenting and IVC filter placement to palliate symptoms and pave the way for port implantation.
  • We report the case of a 61-year-old female suffering from an extended colorectal tumor who became affected by both of the mentioned complications.
  • Due to thrombus formation within the right vena jugularis interna, thrombosis of the inferior vena cava, and superior vena cava syndrome, a combined interventional procedure via a left jugular access with stenting of the superior vena cava and filter placement into the inferior vena cava was performed As a consequence, relief of the patient's symptoms, prevention of pulmonary embolism, and paving of the way for further venous chemotherapy were achieved.
  • [MeSH-major] Colorectal Neoplasms / complications. Stents. Superior Vena Cava Syndrome / therapy. Vena Cava Filters. Vena Cava, Inferior. Venous Thrombosis / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheterization, Peripheral. Contrast Media. Female. Fluorouracil / therapeutic use. Humans. Jugular Veins. Leucovorin / therapeutic use. Middle Aged. Organoplatinum Compounds / therapeutic use. Palliative Care. Radiography, Interventional. Tomography, X-Ray Computed. Ultrasonography, Interventional


94. Rad FH, Le Buanec H, Paturance S, Larcier P, Genne P, Ryffel B, Bensussan A, Bizzini B, Gallo RC, Zagury D, Uzan G: VEGF kinoid vaccine, a therapeutic approach against tumor angiogenesis and metastases. Proc Natl Acad Sci U S A; 2007 Feb 20;104(8):2837-42
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  • [Title] VEGF kinoid vaccine, a therapeutic approach against tumor angiogenesis and metastases.
  • Tumor growth depends on blood supply, requiring the development of new vessels, and vascular endothelial growth factor (VEGF) plays a central role in neoangiogenic processes.
  • For this reason, VEGF represents a target for the development of new therapeutic antiangiogenic molecules.
  • Clinical trials using anti-VEGF mAbs such as bevacizumab have validated the efficacy of this therapeutic approach but have also revealed adverse effects.
  • In mVEGF kinoid-immunized BALB/c mice challenged with syngeneic CT26 colorectal tumor cells, the number and size of lung metastases were significantly decreased.
  • In human (h)VEGF kinoid-immunized BALB/c mice, high levels of serum Abs to hVEGF were present, and purified IgG from these mice decreased by > or =50% the tumor growth of human A673 rhabdomyosarcoma cells and HT29 colon carcinoma xenografted in Swiss nude and NOD/SCID mice, respectively.
  • Tumor cell growth inhibition was similar to that observed in mice receiving therapeutic doses of bevacizumab.
  • These experiments suggest that a therapeutic vaccine containing VEGF kinoid may represent a strategy for safely combating VEGF-dependent neovascularization and metastases occurring in malignant tumors.
  • [MeSH-major] Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Neoplasms / blood supply. Neoplasms / drug therapy. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / prevention & control. Vascular Endothelial Growth Factor A / immunology
  • [MeSH-minor] Animals. Antibodies / isolation & purification. Antibody Formation / immunology. Cell Line, Tumor. Colorectal Neoplasms / pathology. Female. HT29 Cells. Humans. Immune Sera. Immunization. Lung Neoplasms / secondary. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Metastasis. Paclitaxel / therapeutic use. Rhabdomyosarcoma / pathology. Xenograft Model Antitumor Assays

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  • (PMID = 17301234.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Cancer Vaccines; 0 / Immune Sera; 0 / Vascular Endothelial Growth Factor A; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC1797624
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95. Iwama T, Akasu T, Utsunomiya J, Muto T: Does a selective cyclooxygenase-2 inhibitor (tiracoxib) induce clinically sufficient suppression of adenomas in patients with familial adenomatous polyposis? A randomized double-blind placebo-controlled clinical trial. Int J Clin Oncol; 2006 Apr;11(2):133-9
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  • BACKGROUND: There have been few placebo-controlled randomized double-blind studies of the clinical effects of selective cyclooxygenase-2 (COX-2) inhibitors on the regression of colorectal tumors.
  • This study was designed to examine the regressive effect of a selective COX-2 inhibitor, tiracoxib (JTE-522), on colorectal polyps in patients with familial adenomatous polyposis (FAP), and its safety.
  • Prior to and at the end of the medication period, endoscopy was performed.
  • Any adverse events that appeared in at least four persons were taken into consideration and compared between the JTE-522 treatment groups and the placebo group.
  • There were no differences between the placebo group and the two treatment groups in the change in polyp size.
  • CONCLUSION: Our findings, in keeping with other reports on COX-2 inhibitors, indicated that the inhibition of a COX-2 with a moderate dose of a selective COX-2 inhibitor did not induce clinically sufficient regression of adenomas in patients with FAP in a limited (6-month) medication period.
  • [MeSH-major] Adenomatous Polyposis Coli / drug therapy. Colonic Polyps / drug therapy. Cyclooxygenase 2 Inhibitors / therapeutic use. Organic Chemicals / therapeutic use
  • [MeSH-minor] Adult. Disease Progression. Dose-Response Relationship, Drug. Double-Blind Method. Female. Humans. Male

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  • (PMID = 16622748.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Organic Chemicals; 0 / tiracoxib
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96. Kankesan J, Laconi E, Medline A, Thiessen JJ, Ling V, Rao PM, Rajalakshmi S, Sarma DS: PSC 833, an inhibitor of P-glycoprotein inhibits 1,2-dimethylhydrazine-induced colorectal carcinogenesis in male Fischer F344 rats. Anticancer Res; 2006 Mar-Apr;26(2A):995-9
Hazardous Substances Data Bank. 1,2-DIMETHYLHYDRAZINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PSC 833, an inhibitor of P-glycoprotein inhibits 1,2-dimethylhydrazine-induced colorectal carcinogenesis in male Fischer F344 rats.
  • In order to explore the therapeutic value of Pgp as a target for chemotherapy, we studied the effect of PSC 833 (PSC), a potent inhibitor of Pgp, on 1,2-dimethylhydrazine (1,2-DMH)-initiated colorectal carcinogenesis in rats.
  • RESULTS: PSC significantly inhibited colorectal tumor multiplicity by 53% and tumor burden by 74%.
  • PSC-mediated inhibition was evident in tumors as small as 2 mm in diameter and remained effective throughout the course of tumor growth.
  • Histological assessment showed that PSC significantly inhibited tumor progression to colorectal adenocarcinoma by 63%.
  • CONCLUSION: Collectively, this study indicates that PSC inhibited experimental colorectal carcinogenesis initiated with 1,2-DMH in rats.
  • [MeSH-major] 1,2-Dimethylhydrazine / antagonists & inhibitors. Adenocarcinoma / prevention & control. Colorectal Neoplasms / prevention & control. Cyclosporins / pharmacology. P-Glycoprotein / antagonists & inhibitors
  • [MeSH-minor] Animals. Body Weight / drug effects. Eating / drug effects. Male. Rats. Rats, Inbred F344

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  • (PMID = 16619498.001).
  • [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 / Cyclosporins; 0 / P-Glycoprotein; 121584-18-7 / valspodar; IX068S9745 / 1,2-Dimethylhydrazine
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97. Lubbe WJ, Zhou ZY, Fu W, Zuzga D, Schulz S, Fridman R, Muschel RJ, Waldman SA, Pitari GM: Tumor epithelial cell matrix metalloproteinase 9 is a target for antimetastatic therapy in colorectal cancer. Clin Cancer Res; 2006 Mar 15;12(6):1876-82
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor epithelial cell matrix metalloproteinase 9 is a target for antimetastatic therapy in colorectal cancer.
  • BACKGROUND: The current paradigm suggests that matrix metalloproteinase 9 (MMP-9) expressed by stromal cells is a therapeutic target in human colorectal tumors which presumably regulates metastatic disease progression.
  • Conversely, whereas cancer cells within those tumors may induce stromal cells to produce MMP-9 and may be targets for MMP-9 activity, they are not the source of MMP-9 underlying metastasis.
  • METHODS: MMP-9 expression in matched colorectal tumors and normal adjacent mucosa from patients and human colon cancer cell lines was examined by real-time reverse transcription-PCR, laser capture microdissection, immunoelectron microscopy, and immunoblot analysis.
  • The role of colon cancer cell MMP-9 in processes underlying metastasis was explored in vitro by examining degradation of extracellular matrix components by gelatin zymography and formation of locomotory organelles by cell spreading analysis and in vivo by quantifying hematogenous tumor cell seeding of mouse lungs.
  • RESULTS: Primary colorectal tumors overexpress MMP-9 compared with matched normal adjacent mucosa.
  • In contrast to the current paradigm, MMP-9 is expressed equally by cancer and stromal cells within human colon tumors.
  • Moreover, this MMP-9 critically regulates hematogenous seeding of mouse lungs by human colon cancer cells in vivo.
  • CONCLUSIONS: These observations reveal that MMP-9 produced by human colon cancer, rather than stromal, cells is central to processes underlying metastasis.
  • They underscore the previously unrecognized potential of specifically targeting tumor cell MMP-9 in interventional strategies to reduce mortality from metastatic colorectal cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Colorectal Neoplasms / drug therapy. Matrix Metalloproteinase 9 / genetics. Neoplasm Metastasis / prevention & control
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Caco-2 Cells. Cell Line, Tumor. Epithelial Cells / enzymology. Epithelial Cells / pathology. Epithelial Cells / ultrastructure. Female. Gene Expression / genetics. Humans. Immunoblotting. Male. Matrix Metalloproteinase Inhibitors. Mice. Mice, Nude. Microscopy, Immunoelectron. Middle Aged. Neoplasms, Experimental / enzymology. Neoplasms, Experimental / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16551873.001).
  • [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 / 5T32 CA09662; United States / NCI NIH HHS / CA / CA75123; United States / NCI NIH HHS / CA / CA79663; United States / NCI NIH HHS / CA / CA95026; United States / NCI NIH HHS / CA / R01 CA61986
  • [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 / Antineoplastic Agents; 0 / Matrix Metalloproteinase Inhibitors; 0 / RNA, Messenger; EC 3.4.24.35 / Matrix Metalloproteinase 9
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98. Ohdaira T, Nagai H, Shoji M: Intraoperative localization of colorectal tumors in the early stages using a magnetic marking clip detector system (MMCDS). Surg Endosc; 2003 May;17(5):692-5
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  • [Title] Intraoperative localization of colorectal tumors in the early stages using a magnetic marking clip detector system (MMCDS).
  • BACKGROUND: In the laparoscopic surgical treatment of early stage colorectal carcinomas, intraoperative tumor site identification is often difficult.
  • We developed a novel marking method using a magnetic marking clip and a modified magnetometer system.
  • METHODS: We applied magnetic marking clips at the tumor site during preoperative colonoscopy and identified the clip site with a magnetic marking clip detector system (MMCDS) of our design.
  • RESULTS: In a basic ex vivo study, magnetic bodies of more than 300 mT magnetic force were easily detected with a 100% detection ratio.
  • The mean length between the detected site and clip along the longitudinal bowel axis was 14.1 mm (SD 5.6).
  • The mean detection time was 2.4 min (SD 0.2).
  • CONCLUSION: MMCDS accurately identifies tumor sites.
  • This method may be useful for tumor site identification during laparoscopic colectomy.
  • [MeSH-major] Colorectal Neoplasms / surgery. Intraoperative Period / methods. Magnetics / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Body Mass Index. Colonoscopes. Colonoscopy / methods. Double-Blind Method. Female. Humans. Laparoscopes. Laparoscopy / methods. Male. Middle Aged. Neoplasm Staging. Surgical Instruments / trends

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  • (PMID = 12618945.001).
  • [ISSN] 1432-2218
  • [Journal-full-title] Surgical endoscopy
  • [ISO-abbreviation] Surg Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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99. Matter MJ, Gygi C, Gillet M, Gebhard S, Bouzourene H: Malacoplakia simulating organ invasion in a rectosigmoid adenocarcinoma: report of a case. Dis Colon Rectum; 2001 Sep;44(9):1371-5
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  • Malacoplakia is a histiocytic inflammatory response that may be associated with colorectal tumors.
  • We report the case of a 65-year-old male taking steroids for a severe pulmonary disease.
  • He presented with a rectosigmoid tumor that seemed to infiltrate the urinary bladder and the sacrum on the preoperative CT scan and echography and at laparotomy.
  • The pathologic analysis showed a pT3pN0 adenocarcinoma with an extensive malacoplakia infiltrating the bladder and the pericolic and perirectal tissues.
  • Our observation confirms the association of malacoplakia, colorectal carcinoma, and steroid treatment.
  • [MeSH-major] Adenocarcinoma / pathology. Colorectal Neoplasms / pathology. Malacoplakia / pathology. Urinary Bladder Neoplasms / secondary
  • [MeSH-minor] Abdominal Pain / etiology. Aged. Diagnosis, Differential. False Positive Reactions. Humans. Inflammation. Lung Diseases / drug therapy. Male. Neoplasm Invasiveness. Neoplasm Staging. Steroids / therapeutic use

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  • (PMID = 11584219.001).
  • [ISSN] 0012-3706
  • [Journal-full-title] Diseases of the colon and rectum
  • [ISO-abbreviation] Dis. Colon Rectum
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Steroids
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100. Carlson HE, Zarrabi MH, Lyubsky SL: Lack of association between hyperprolactinemia and colon carcinoma. Cancer Invest; 2000;18(2):130-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of association between hyperprolactinemia and colon carcinoma.
  • Two recent studies reported that many patients with colorectal carcinoma have elevated serum prolactin (PRL) concentrations and have suggested ectopic PRL secretion as the cause.
  • In the present study, serum PRL was minimally elevated in 16 of 116 colon cancer patients and 2 of 25 control subjects; medications or chemotherapy appeared to be responsible for the PRL elevations in 11 of 16 cancer patients.
  • Serum PRL was not correlated with either plasma carcinoembryonic antigen or disease stage.
  • None of 19 colorectal tumors was positive for PRL staining by immunohistochemistry.
  • Thus, we could not confirm previous reports of frequent hyperprolactinemia in patients with colorectal cancer; factors such as medications, anxiety, pain, and nausea may have raised serum PRL in these earlier studies.
  • Serum PRL is not a useful marker for colon carcinoma, at least in patients in the United States.
  • [MeSH-major] Colonic Neoplasms / metabolism. Prolactin / metabolism

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  • (PMID = 10705875.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 9002-62-4 / Prolactin
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