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1. Yang J, Du X, Lazar AJ, Pollock R, Hunt K, Chen K, Hao X, Trent J, Zhang W: Genetic aberrations of gastrointestinal stromal tumors. Cancer; 2008 Oct 1;113(7):1532-43
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  • [Title] Genetic aberrations of gastrointestinal stromal tumors.
  • Gastrointestinal stromal tumor (GIST) is the most common mesenchymal neoplasm in the gastrointestinal tract and is associated with mutations of the KIT or PDGFRA gene.
  • In addition, other genetic events are believed to be involved in GIST tumorigenesis.
  • GISTs in patients with neurofibromatosis type 1 appear to lack the KIT and PDGFRA mutations characteristic of GISTs and may have a different pathogenetic mechanism.
  • Gene mutations of KIT or PDGFRA are critical in GISTs, because the aberrant versions not only are correlated with the specific cell morphology, histologic phenotype, metastasis, and prognosis, but also are the targets of therapy with imatinib and other agents.
  • Furthermore, specific mutations in KIT and PDGFR appear to lead to differential drug sensitivity and may in the future guide selection of tyrosine kinase inhibitors.
  • A new paradigm of classification, integrating the standard clinical and pathological criteria with molecular aberrations, may permit personalized prognosis and treatment.

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  • (PMID = 18671247.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA109060; United States / NCI NIH HHS / CA / K23CA109060; United States / NCI NIH HHS / CA / R01 CA098570; United States / NCI NIH HHS / CA / CA098570-04; United States / NCI NIH HHS / CA / R01 CA098570-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 74
  • [Other-IDs] NLM/ NIHMS64614; NLM/ PMC2651090
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2. El-Zohairy M, Khalil el-SA, Fakhr I, El-Shahawy M, Gouda I: Gastrointestinal stromal tumor (GIST)'s surgical treatment, NCI experience. J Egypt Natl Canc Inst; 2005 Jun;17(2):56-66
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  • [Title] Gastrointestinal stromal tumor (GIST)'s surgical treatment, NCI experience.
  • PURPOSE: To review the clinical presentation, surgical management, and prognostic factors for gastrointestinal stromal tumors.
  • PATIENTS AND METHODS: A prospective study which was carried out between January 2002 and March 2004 on thirty-three patients with gastrointestinal stromal tumor (GIST) at the National Cancer Institute, Cairo University.
  • Clinical findings included gastrointestinal bleeding (42.4%), palpable mass (33.3%) and abdominal pain (24.3%).
  • The stomach was the most common site of origin of the disease (39.4%), followed by the colorectal region (24.2%).
  • Complete resection of all gross disease was accomplished in 26 patients (78.7%), among whom, multiple adjacent organ resection was required in 6 patients (22.2 %) and metastatic disease was identified in the liver in 3 patients at the time of exploratory surgery of these one could be resected.
  • None of the patients received adjuvant or palliative chemotherapy.
  • CONCLUSION: Surgical resection, including en bloc resection of locally advanced tumors, remains the only curative treatment.
  • [MeSH-major] Gastrointestinal Stromal Tumors / surgery

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  • (PMID = 16508676.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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3. Gunaratnam M, Swank S, Haider SM, Galesa K, Reszka AP, Beltran M, Cuenca F, Fletcher JA, Neidle S: Targeting human gastrointestinal stromal tumor cells with a quadruplex-binding small molecule. J Med Chem; 2009 Jun 25;52(12):3774-83

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting human gastrointestinal stromal tumor cells with a quadruplex-binding small molecule.
  • Most of human gastrointestinal stromal tumors (GIST) are driven by activating mutations in the proto-oncogene KIT, a tyrosine kinase receptor.
  • Clinical treatment with imatinib targets the kinase domain of KIT, but tumor regrowth occurs as a result of the development of resistant mutations in the kinase active site.
  • An alternative small-molecule approach to GIST therapy is described, in which the KIT gene is directly targeted, and thus, kinase resistance may be circumvented.
  • It is shown here that the compound is a potent inducer of growth arrest in a patient-derived GIST cell line at a concentration (approximately 1 microM) that also results in effective inhibition of telomerase activity and almost complete suppression of KIT mRNA and KIT protein expression.

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  • (PMID = 19469547.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA072791-03; United States / NCI NIH HHS / CA / P50 CA127003; United States / NCI NIH HHS / CA / R01 CA072791-03; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Imides; 0 / Naphthalenes; 0 / Phenanthrolines; 0 / RNA, Messenger; 22291-04-9 / naphthalenediimide; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ NIHMS212267; NLM/ PMC2900250
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4. Ochs MF, Rink L, Tarn C, Mburu S, Taguchi T, Eisenberg B, Godwin AK: Detection of treatment-induced changes in signaling pathways in gastrointestinal stromal tumors using transcriptomic data. Cancer Res; 2009 Dec 1;69(23):9125-32
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  • [Title] Detection of treatment-induced changes in signaling pathways in gastrointestinal stromal tumors using transcriptomic data.
  • Numerous therapeutics in use or under development target signaling proteins; however, off-target effects often limit assignment of positive clinical response to the intended target.
  • As direct measurements of signaling protein activity are not generally feasible during treatment, there is a need for more powerful methods to determine if therapeutics inhibit their targets and when off-target effects occur.
  • We applied DESIDE to deduce signaling activity in gastrointestinal stromal tumor cell lines treated with the targeted therapeutic imatinib mesylate (Gleevec).
  • Pursuing these findings, we have determined that imatinib-induced DNA damage is responsible for the increased activity of p53, identifying a novel off-target activity for this drug.
  • We then used DESIDE on data from resected, post-imatinib treatment tumor samples and identified a pattern in these tumors similar to that at late time points in the cell lines, and this pattern correlated with initial clinical response.
  • DESIDE infers the global reprogramming of signaling networks during treatment, permitting treatment modification that leverages ongoing drug development efforts, which is crucial for personalized medicine.

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  • (PMID = 19903850.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106588-01; United States / NCI NIH HHS / CA / R01 CA106588-05; United States / NLM NIH HHS / LM / LM009382; United States / NCI NIH HHS / CA / CA106588-04; United States / NCI NIH HHS / CA / R01 CA106588-02; United States / NCI NIH HHS / CA / CA009035; United States / NCI NIH HHS / CA / R01 CA106588-03; United States / NCI NIH HHS / CA / CA106588; United States / NLM NIH HHS / LM / R21 LM009382; United States / NCI NIH HHS / CA / T32 CA009035-28; United States / NCI NIH HHS / CA / CA21661; United States / NCI NIH HHS / CA / CA106588-03; United States / NCI NIH HHS / CA / CA106588-01; United States / NCI NIH HHS / CA / R01 CA106588; United States / NCI NIH HHS / CA / CA106588-02; United States / NLM NIH HHS / LM / LM009382-01A2; United States / NCI NIH HHS / CA / U10 CA021661; United States / NCI NIH HHS / CA / R01 CA106588-04; United States / NLM NIH HHS / LM / R21 LM009382-01A2; United States / NCI NIH HHS / CA / CA106588-05; United States / NCI NIH HHS / CA / CA009035-28; United States / NCI NIH HHS / CA / T32 CA009035
  • [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 / Benzamides; 0 / ELK1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / ets-Domain Protein Elk-1; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS149886; NLM/ PMC2789202
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5. Cohen MH, Cortazar P, Justice R, Pazdur R: Approval summary: imatinib mesylate in the adjuvant treatment of malignant gastrointestinal stromal tumors. Oncologist; 2010;15(3):300-7
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Approval summary: imatinib mesylate in the adjuvant treatment of malignant gastrointestinal stromal tumors.
  • Food and Drug Administration approved imatinib mesylate tablets for oral use (Gleevec(R); Novartis Pharmaceuticals Corporation, East Hanover, NJ) for the adjuvant treatment of adult patients following complete gross resection of Kit(+) (CD117(+)) gastrointestinal stromal tumor (GIST).
  • Eligible patients were > or =18 years of age with a histological diagnosis of GIST (Kit(+)), resected tumor size > or =3 cm, and a complete gross resection within 14-70 days prior to registration.
  • At that time, 100 RFS events were confirmed by a blinded central independent review.
  • Drug was discontinued for adverse reactions in 17% and 3% of the imatinib and placebo-treated patients, respectively.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gastrointestinal Stromal Tumors / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Aged. Benzamides. Chemotherapy, Adjuvant. Disease-Free Survival. Double-Blind Method. Drug Approval. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Treatment Outcome

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  • (PMID = 20200041.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC3227955
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6. Tzilves D, Gatopoulou A, Zervas K, Katodritou E, Patakiouta F, Tarpagos A, Katsos I: Development of multiple myeloma in a patient with gastrointestinal stromal tumor treated with imatinib mesylate: a case report. World J Gastroenterol; 2007 Apr 7;13(13):2011-3
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of multiple myeloma in a patient with gastrointestinal stromal tumor treated with imatinib mesylate: a case report.
  • Gastrointestinal stromal tumors (GISTs) are rare tumors, which represent approximately 1% of the neoplasms of the gastrointestinal tract.
  • Here we present a case of a 74-year old male with GIST, which was managed by surgical resection.
  • During treatment, the patient reported skeletal pain and plane X-rays revealed osteolytic bone lesions.
  • To the best of our knowledge, this is the first report of the co-existence of multiple myeloma (MM) with GIST.
  • [MeSH-major] Gastrointestinal Stromal Tumors. Multiple Myeloma. Neoplasms, Multiple Primary
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Benzamides. Humans. Imatinib Mesylate. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Male. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17461509.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC4146985
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7. Eisenberg BL, Harris J, Blanke CD, Demetri GD, Heinrich MC, Watson JC, Hoffman JP, Okuno S, Kane JM, von Mehren M: Phase II trial of neoadjuvant/adjuvant imatinib mesylate (IM) for advanced primary and metastatic/recurrent operable gastrointestinal stromal tumor (GIST): early results of RTOG 0132/ACRIN 6665. J Surg Oncol; 2009 Jan 1;99(1):42-7
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of neoadjuvant/adjuvant imatinib mesylate (IM) for advanced primary and metastatic/recurrent operable gastrointestinal stromal tumor (GIST): early results of RTOG 0132/ACRIN 6665.
  • BACKGROUND: Therapy for gastrointestinal stromal tumors (GIST) has changed significantly with the use of imatinib mesylate (IM).
  • Despite the success of this drug in metastatic GIST, disease progression remains a perplexing clinical issue suggesting the need for multimodality management.
  • There have been no prospective studies either evaluating the neoadjuvant use of IM in primary GIST or as a preoperative cytoreduction agent for metastatic GIST.
  • METHODS: RTOG 0132/ACRIN 6665 was a prospective phase II study evaluating safety and efficacy of neoadjuvant IM (600 mg/day) for patients with primary GIST or the preop use of IM in patients with operable metastatic GIST.
  • RESULTS: Sixty-three patients were entered (52 analyzable), 30 patients with primary GIST (Group A) and 22 with recurrent metastatic GIST (Group B).
  • CONCLUSION: This trial represents the first prospective report of preop IM in GIST.

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  • (PMID = 18942073.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106588-01; United States / NCI NIH HHS / CA / U10 CA32115; United States / NCI NIH HHS / CA / U10 CA21661; United States / NCI NIH HHS / CA / CA106588-01; United States / NCI NIH HHS / CA / R01 CA106588; United States / NCI NIH HHS / CA / U10 CA37422; United States / NCI NIH HHS / CA / U10 CA037422; United States / NCI NIH HHS / CA / U10 CA021661; United States / NCI NIH HHS / CA / U10 CA032115
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; 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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ NIHMS75514; NLM/ PMC2606912
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8. Sleijfer S, Seynaeve C, Wiemer E, Verweij J: Practical aspects of managing gastrointestinal stromal tumors. Clin Colorectal Cancer; 2006 Nov;6 Suppl 1:S18-23
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Practical aspects of managing gastrointestinal stromal tumors.
  • Gastrointestinal stromal tumors (GISTs) are rare tumors of the digestive tract.
  • Gastrointestinal stromal tumors are one of the first solid tumor types in which specific factors responsible for malignant behavior have been elucidated and for which drugs specifically targeting these factors form the mainstay of treatment in advanced-stage disease.
  • This review addresses several aspects of the current management of GIST as well as some novel developments.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gastrointestinal Stromal Tumors / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 17101064.001).
  • [ISSN] 1533-0028
  • [Journal-full-title] Clinical colorectal cancer
  • [ISO-abbreviation] Clin Colorectal Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 32
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9. Tarn C, Godwin AK: The molecular pathogenesis of gastrointestinal stromal tumors. Clin Colorectal Cancer; 2006 Nov;6 Suppl 1:S7-17
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The molecular pathogenesis of gastrointestinal stromal tumors.
  • Gastrointestinal stromal tumors (GISTs) are clinically diagnosed by positive immunohistochemical staining of KIT, a type III receptor tyrosine kinase.
  • Most GISTs contain gain-of-function, ie, oncogenic mutations in c-KIT or in platelet-derived growth factor receptor-alpha (PDGFR-alpha), which appears to be the major initiating event that drives the pathogenesis for GIST.
  • Furthermore, mutations in either of these genes appear to be required for tumor growth and progression.
  • This scenario can be thought of as "oncogenic addiction" and is one of the major reasons why some GISTs respond significantly to therapies that target these mutant receptors.
  • Moreover, GISTs that harbor different c-KIT or PDGFR-alpha mutations have different molecular signatures at the level of gene expression, which further contributes to the complexity of GIST biology and variable responses to treatment.
  • This article will discuss the molecular basis of pathogenesis and genetic and genomic alterations that contribute to GIST tumorigenesis and disease progression as well as the heterogeneity of this disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gastrointestinal Stromal Tumors / drug therapy. Gastrointestinal Stromal Tumors / genetics. Piperazines / pharmacology. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology. Receptors, Platelet-Derived Growth Factor / genetics
  • [MeSH-minor] Benzamides. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Neoplastic. Humans. Imatinib Mesylate. Mutation. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 17101067.001).
  • [ISSN] 1533-0028
  • [Journal-full-title] Clinical colorectal cancer
  • [ISO-abbreviation] Clin Colorectal Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA106588
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Number-of-references] 123
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10. Schirru A, Cavaliere D, Cosce U, Scarimbolo M, Griseri G, Caristo I, Bianchi M, Ingravaglieri E, Aiello D, Venturino E: [Surgical treatment of gastrointestinal stromal tumors: personal cases]. Tumori; 2003 Jul-Aug;89(4 Suppl):141-2
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical treatment of gastrointestinal stromal tumors: personal cases].
  • Surgical management of gastrointestinal stromal tumors: our experience.
  • Gastrointestinal stromal tumors (GIST) are rare neoplasm even if they are the most common mesenchimal malignancies of the gastrointestinal tract.
  • GIST have long been a source of confusion and controversy, in particular to define their pathological classification, preoperative diagnosis, management strategies, and prognosis.
  • A radical resection of the tumor is often possible and always recommended.
  • An effective adjuvant therapy treatment (STI571) have been found for advanced and metastatic GIST.
  • [MeSH-major] Gastrointestinal Neoplasms / surgery. Sarcoma / surgery
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzamides. Chemotherapy, Adjuvant. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / surgery. Disease-Free Survival. Enzyme Inhibitors / therapeutic use. Follow-Up Studies. Gastrectomy. Humans. Ileal Neoplasms / drug therapy. Ileal Neoplasms / surgery. Imatinib Mesylate. Jejunal Neoplasms / genetics. Jejunal Neoplasms / surgery. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Retroperitoneal Neoplasms / surgery. Retrospective Studies. Stomach Neoplasms / drug therapy. Stomach Neoplasms / surgery. Treatment Outcome

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  • (PMID = 12903574.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 0
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11. Eisenberg BL: Combining imatinib with surgery in gastrointestinal stromal tumors: rationale and ongoing trials. Clin Colorectal Cancer; 2006 Nov;6 Suppl 1:S24-9
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combining imatinib with surgery in gastrointestinal stromal tumors: rationale and ongoing trials.
  • Gastrointestinal stromal tumor (GIST) has become a well-recognized pathologic entity defined by expression of the KIT protein and often associated with gain of function mutations of the c-KIT oncogene.
  • Imatinib, a specific inhibitor of the aberrant KIT protein, is an approved, well-tolerated oral drug for the management of metastatic or inoperable GIST.
  • Traditional radical surgery resection for locally advanced, recurrent, or metastatic GIST is associated with a poor outcome.
  • The rationale for combining imatinib with surgery for GIST, either as an adjuvant agent in the situation of primary resection for patients at high risk or in the neoadjuvant setting for patients with locally advanced, recurrent, or metastatic disease, is compelling in the continuous effort to improve disease-free and overall survival.
  • Several clinical trials are addressing these issues as well as timing of surgery, assessment of drug response, and the addition of surgical resection in the situation of focal progressive disease on imatinib.
  • The results of these studies will be meaningful in future standard therapy consideration.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gastrointestinal Stromal Tumors / drug therapy. Gastrointestinal Stromal Tumors / surgery. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Clinical Trials as Topic. Combined Modality Therapy. Humans. Imatinib Mesylate. Neoadjuvant Therapy. Tomography, Emission-Computed. Tomography, X-Ray Computed

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  • (PMID = 17101065.001).
  • [ISSN] 1533-0028
  • [Journal-full-title] Clinical colorectal cancer
  • [ISO-abbreviation] Clin Colorectal Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 38
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12. Whisenant J, Bergsland E: Anti-angiogenic strategies in gastrointestinal malignancies. Curr Treat Options Oncol; 2005 Sep;6(5):411-21
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] Anti-angiogenic strategies in gastrointestinal malignancies.
  • Advances in our understanding of the mechanisms underlying tumor progression suggest that angiogenesis plays a key role in gastrointestinal malignancies.
  • Vascular endothelial growth factor (VEGF) has emerged as an important therapeutic target, and a variety of strategies to inhibit VEGF are under investigation.
  • The approval of bevacizumab for use in patients with previously untreated metastatic colorectal cancer was based on clinical data suggesting that VEGF is a valid therapeutic target in this disease.
  • As the data mature from ongoing trials, the role of angiogenesis inhibitors in the treatment of colon cancer and other gastrointestinal malignancies will be more clearly defined.
  • Additional information is needed to identify the diseases and stages most likely to benefit from anti-angiogenic agents and the optimal sequences and therapeutic combinations that should be studied.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Gastrointestinal Neoplasms / drug therapy
  • [MeSH-minor] Carcinoma, Hepatocellular / drug therapy. Colorectal Neoplasms / drug therapy. Esophageal Neoplasms / drug therapy. Gastrointestinal Stromal Tumors / drug therapy. Humans. Lymphatic Metastasis. Neoplasm Invasiveness. Neuroendocrine Tumors / drug therapy. Neuroendocrine Tumors / secondary. Pancreatic Neoplasms / drug therapy. Stomach Neoplasms / drug therapy

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  • (PMID = 16107244.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
  • [Number-of-references] 96
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13. Ohtsu A: The latest advances in chemotherapy for gastrointestinal cancers. Int J Clin Oncol; 2003 Aug;8(4):234-8
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  • [Title] The latest advances in chemotherapy for gastrointestinal cancers.
  • During the past decade, there has been much progress in various nonsurgical treatments for gastrointestinal malignancies.
  • Endoscopic mucosal resection (EMR) has been widely used as a standard treatment for early gastrointestinal cancers in Japan.
  • For esophageal cancer, definitive chemoradiotherapy with or without EMR has shown the possibility of results comparable with those of surgery in stage I-III disease and is being evaluated in Japan Clinical Oncology Group (JCOG) studies.
  • Definitive chemoradiotherapy with curative intent for locally advanced (T4/M1a) diseases has had a 5-year survival of 17%.
  • In gastric cancers, although no standard regimen has been established yet, recently developed new agents have achieved higher response rates than before.
  • There has been obvious progress in chemotherapy for colorectal cancer.
  • Newly developed agents such as irinotecan and oxaliplatin have provided significant survival prolongation for metastatic colorectal cancer in randomized trials.
  • In other gastrointestinal malignancies, nonsurgical treatments, including eradication of Helicobacter pylori, chemotherapy, and radiotherapy for primary gastric lymphoma are being evaluated in prospective studies.
  • A new molecular targeting agent, imatinib, has provided significant impact in the treatment of gastrointestinal stromal tumor.
  • To provide these advantages to patients, many more gastrointestinal oncologists are urgently needed in Japan.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gastrointestinal Neoplasms / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Helicobacter Infections / drug therapy. Helicobacter pylori. Humans

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  • (PMID = 12955579.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 16
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14. Lindebjerg J: [Immunohistochemical markers in colorectal cancer]. Ugeskr Laeger; 2005 Oct 31;167(44):4168-70
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  • [Title] [Immunohistochemical markers in colorectal cancer].
  • In colorectal cancer, immunohistochemical staining can routinely be used for tumour classification, screening for defective DNA mismatch repair and possibly identification of markers relevant to prediction of outcome of chemotherapy.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Colorectal Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenosine Triphosphatases / metabolism. Bacterial Proteins / metabolism. Base Pair Mismatch. Carcinoma / diagnosis. Carcinoma / drug therapy. Carcinoma / metabolism. Chemotherapy, Adjuvant. Colorectal Neoplasms, Hereditary Nonpolyposis / diagnosis. Colorectal Neoplasms, Hereditary Nonpolyposis / drug therapy. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA-Binding Proteins / metabolism. Gastrointestinal Stromal Tumors / diagnosis. Gastrointestinal Stromal Tumors / drug therapy. Gastrointestinal Stromal Tumors / metabolism. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Lymphoma / diagnosis. Lymphoma / drug therapy. Lymphoma / metabolism. MutS DNA Mismatch-Binding Protein

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  • (PMID = 16266569.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.3 / MutS DNA Mismatch-Binding Protein
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15. Lièvre A, Landi B, Mitry E, Taïeb J: [Antiangiogenic agents and gastrointestinal cancers]. Gastroenterol Clin Biol; 2008 May;32(5 Pt 1):504-20
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  • [Title] [Antiangiogenic agents and gastrointestinal cancers].
  • The role of angiogenesis in tumor development and the identification of VEGF as a key factor in this process have recently led to the development of anti-angiogenic agents in the treatment of cancer.
  • Other therapeutic strategies inhibiting angiogenesis are under investigation, targeting the VEGF pathway or other crucial steps of angiogenesis.
  • In digestive oncology, bevacizumab was the first anti-angiogenic agent to be registered in the fist-line treatment of metastatic colorectal cancer in which it was proved to be efficient in combination with a 5-fluorouracile (5FU)/acide folinique (AF) with or without irinotecan-based chemotherapy.
  • Sunitinib and sorafenib have more recently been shown to be active in gastrointestinal stromal tumors and advanced hepatocellular carcinoma, respectively.
  • Side effects associated with these anti-angiogenic agents are not those usually observed with conventional anticancer drugs and require a specific management.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Gastrointestinal Neoplasms / drug therapy

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  • (PMID = 18472378.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors
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16. Wiedmann MW, Caca K: Molecularly targeted therapy for gastrointestinal cancer. Curr Cancer Drug Targets; 2005 May;5(3):171-93
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  • [Title] Molecularly targeted therapy for gastrointestinal cancer.
  • Receptor and non-receptor tyrosine kinases (TKs) have emerged as clinically useful drug target molecules for treating gastrointestinal cancer.
  • Imatinib mesilate (STI-571, Gleevec(TM)), an inhibitior of bcr-abl TK, which was primarily designed to treat chronic myeloid leukemia is also an inhibitor of c-kit receptor TK, and is currently the drug of choice for the therapy of metastatic gastrointestinal stromal tumors (GISTs), which frequently express constitutively activated forms of the c-kit-receptor.
  • Gefitinib (ZD1839, Iressa(TM)) has been on trial for esophageal and colorectal cancer (CRC) and erlotinib (OSI-774, Tarceva(TM)) on trial for esophageal, colorectal, hepatocellular, and biliary carcinoma.
  • In addition, erlotinib has been evaluated in a Phase III study for the treatment of pancreatic cancer.
  • Cetuximab (IMC-C225, Erbitux(TM)), a monoclonal EGFR antibody, has been FDA approved for the therapy of irinotecan resistant colorectal cancer and has been tested for pancreatic cancer.
  • Vascular endothelial growth factor (VEGF) and its receptor (VEGFR) are critical regulators of tumor angiogenesis.
  • Bevacizumab (Avastin(TM)), a monoclonal antibody against VEGF, was efficient in two randomized clinical trials investigating the treatment of metastatic colorectal cancer.
  • It is also currently investigated for the therapy of pancreatic cancer in combination with gemcitabine.
  • Other promising new drugs currently under preclinical and clinical evaluation, are VEGFR2 inhibitor PTK787/ZK 222584, thalidomide, farnesyl transferase inhibitor R115777 (tipifarnib, Zarnestra(TM)), matrix metalloproteinase inhibitors, proteasome inhibitor bortezomib (Velcade(TM)), mammalian target of rapamycin (mTOR) inhibitors, cyclooxygenase-2 (COX-2) inhibitors, platelet derived growth factor receptor (PDGF-R) inhibitors, protein kinase C (PKC) inhibitors, mitogen-activated protein kinase kinase (MEK) 1/2 inhibitors, Rous sarcoma virus transforming oncogene (SRC) kinase inhibitors, histondeacetylase (HDAC) inhibitors, small hypoxia-inducible factor (HIF) inhibitors, aurora kinase inhibitors, hedgehog inhibitors, and TGF-beta signalling inhibitors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gastrointestinal Neoplasms / drug therapy
  • [MeSH-minor] Animals. Humans. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / drug effects. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, Epidermal Growth Factor / drug effects. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / metabolism. Vascular Endothelial Growth Factor A / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15892618.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 102
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17. Cao J, Tan MH, Yang P, Li WL, Xia J, Du H, Tang WB, Wang H, Chen XW, Xiao HQ: Effects of adjuvant chemotherapy on bone marrow mesenchymal stem cells of colorectal cancer patients. Cancer Lett; 2008 May 18;263(2):197-203
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  • [Title] Effects of adjuvant chemotherapy on bone marrow mesenchymal stem cells of colorectal cancer patients.
  • BACKGROUND: Chemotherapy damages the bone marrow and that is one of the most important problems in the treatment of malignancies, particularly colorectal cancer.
  • The aim of the present study was to assess the effects of surgical adjuvant chemotherapy for CRC patients on human MSCs using an in vitro culture system.
  • METHODS: The bone marrows of 43 CRC patients were harvested for separation and culture of MSC at pre- and post-chemotherapy.
  • RESULTS: In the CRC patients with chemotherapy, we have demonstrated that the CFU-F exhibit significantly decreased.
  • Most importantly, decreased CFU-F and the adhesive rate of BMSC were correlated significantly with decreased interleukins and stem-cell factor (IL-6, SCF and FLT-3L) expressions in the CRC patients after chemotherapy.
  • CONCLUSION: Our results suggest that MSCs of CRC patients can be damaged by chemotherapy.
  • [MeSH-major] Bone Marrow Cells / drug effects. Chemotherapy, Adjuvant / adverse effects. Colorectal Neoplasms / drug therapy. Mesenchymal Stromal Cells / drug effects
  • [MeSH-minor] Aged. Cell Adhesion / drug effects. Cell Proliferation / drug effects. Cell Shape. Cells, Cultured. Cytokines / analysis. Female. Humans. Male. Middle Aged. Tumor Stem Cell Assay


18. Gill S, Thomas RR, Goldberg RM: New targeted therapies in gastrointestinal cancers. Curr Treat Options Oncol; 2003 Oct;4(5):393-403
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  • [Title] New targeted therapies in gastrointestinal cancers.
  • Despite surgical, radiotherapeutic, and chemotherapeutic advances, a large proportion of gastrointestinal (GI) cancers remain incurable.
  • The crucial role of the epidermal growth factor receptor (EGFR) in tumor proliferation and the overexpression of EGFR in several GI cancers provides the rationale for targeting and interrupting this key signaling network.
  • Cyclooxygenase-2 inhibitors in colorectal cancer and STI571 in GI stromal tumors represent novel therapies of interest for these specific GI cancers.
  • Evidence suggests that novel agents can be administered alone or in combination with standard therapies with little additional toxicity.
  • The results of ongoing and future research efforts will clarify the optimal use and survival benefit of targeted therapies for patients with GI malignancies.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Gastrointestinal Neoplasms / therapy. Immunotherapy / methods. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / drug effects
  • [MeSH-minor] Adult. Aged. Drug Therapy, Combination. Erlotinib Hydrochloride. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Randomized Controlled Trials as Topic. Risk Assessment. Survival Analysis. Treatment Outcome

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  • (PMID = 12941199.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Quinazolines; 6A901E312A / panitumumab; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Number-of-references] 63
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19. Zhang JM, Liu MJ, Mizoi T, Shiiba K, Sasak I, Matsuno S: [Thymidine phosphorylase expressed in monocyte-macrophages enhanced anticancer effect of 5'-deoxy-5-fluorouridine on colorectal carcinoma cells]. Zhonghua Yi Xue Za Zhi; 2004 May 2;84(9):718-24
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  • [Title] [Thymidine phosphorylase expressed in monocyte-macrophages enhanced anticancer effect of 5'-deoxy-5-fluorouridine on colorectal carcinoma cells].
  • OBJECTIVE: To detect the thymidine phosphorylase (dThdPase) expression in colorectal carcinoma tissue, and clarify whether dThdPase expressed in macrophage-like cell lines, and monocytes from human peripheral blood can modulate the anticancer effect of 5'-deoxy-5-fluorouridine (5'-DFUR) on colorectal carcinoma cells.
  • METHODS: Forty specimens resected from 40 patients with colorectal carcinoma were immunohistochemically stained by the monoclonal antibodies 654-1 (anti-dThdPase) and PG-M1 (anti-macrophage marker CD68).
  • The dThdPase level were also measured by ELISA in 4 colorectal cancer cell lines, LS174T, Clone A, Colo320, MIP101, and 2 macrophage-like cell lines, THP-1, U937.
  • After estimated the drug sensitivities of each colorectal carcinoma cell both to 5'-DFUR and 5-Fu by MTT assay, THP-1, U937, or monocytes isolated from human blood were incubated in the medium containing 5-Fu or 5'-DFUR for 24 hours, respectively.
  • Using the serially diluted medium, MTT assay were also carried out on 4 colorectal carcinoma cell lines.
  • Each experiment was repeated six times and the means of IC50 value +/- standard errors (mean +/- S.E.M.) were calculated.
  • RESULTS: dThdPase activities was significantly increased (139.7 micro g x 5-Fu x h(-1) x ml(-1) +/- 61.5 micro g x 5-Fu x h(-1) x ml(-1)) in colorectal carcinoma tissues compared with adjacent normal tissues (42.2 micro g x 5-Fu x h(-1) x ml(-1) +/- 21.4 micro g x 5-Fu x h(-1) x ml(-1)), P < 0.001.
  • In immunohistochemical analysis, it was confirmed that most cells expressed dThdPase-positive cells were the stromal cells, especially macrophages, which surrounding cancer nests, or along the invasive margin of cancer.
  • The distribution patterns of dThdPase-positive stromal cells are similar to that of the CD68-positive cells.
  • The number of dThdPase positive cells was correlated with the number of macrophages in the cancerous tissues, r = 0.76.
  • The dThdPase protein were detected at the levels of 18.2 unit/mg in THP-1, 19.3 unit/mg in U937, and 0.5 unit/mg in LS174T, however, not detected in other 3 colorectal carcinoma cells.
  • The values of IC50 of 5'-DFUR on the 4 colorectal carcinoma cell lines were 11.5 approximately 84.8 times higher than those of 5-Fu (all P < 0.01).
  • CONCLUSION: 5'-DFUR cannot be converted into 5-Fu in colorectal carcinoma cells in vitro because no dThdPase is expressed in those cells.
  • [MeSH-major] Macrophages / drug effects. Monocytes / drug effects. Thymidine Phosphorylase / analysis
  • [MeSH-minor] Adenocarcinoma / chemistry. Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Antimetabolites, Antineoplastic / pharmacology. Cell Line, Tumor. Colorectal Neoplasms / chemistry. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / pathology. Enzyme-Linked Immunosorbent Assay. Floxuridine / pharmacology. Humans. Immunohistochemistry. U937 Cells

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  • (PMID = 15200906.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antimetabolites, Antineoplastic; 0 / CD68 antigen, human; 039LU44I5M / Floxuridine; EC 2.4.2.4 / Thymidine Phosphorylase; V1JK16Y2JP / doxifluridine
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20. 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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  • [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.
  • 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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21. Treska V, Liska V, Skalický T, Sutnar A, Smíd D, Narsanská A, Vachtová M, Tresková I, Brůha J, Vycítal O: [Liver metastases of other than colorectal origin]. Rozhl Chir; 2010 Mar;89(3):202-7
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  • [Title] [Liver metastases of other than colorectal origin].
  • AIM: Colorectal carcinoma is the commonest malignancy with liver metastases.
  • Liver metastases of so called non-colorectal carcinomas are significantly less common, and considering different biological character of these metastases, compared to colorectal ones, surgical management of some of these types is debatable, however, in some cases remains highly successful.
  • The aim of this study was to assess the authors' outcomes of surgical and termoablation therapy of non-colorectal liver metastases.
  • METHODS: The authors present their experience with surgical treatment in 68 patients - mean age of 58.2 y.o.a (33.1-77.5) with liver metastases of non-colorectal carcinomas- NKJM (the commonest types: breast carcinoma--32.4%, carcinoid--20.6%, renal carcinoma--13.3%, gynecological tumors--13.3%, gastrointestinal stromal tumor--4.4%, gastric carcinoma--4.4% ) during 2001-2008.
  • The mean time after primary surgery for carcinoma was 3.9 years (0-8.5 let).
  • Preoperative chemotherapeutical "downstaging" or portal vein embolization on the tumor side, in order to improve the NKJM resecability, was performed in 10 subjects (14.7%).
  • Postoperative adjuvant chemotherapy, combined with biological treatment in some patients, was administered to a total of 33 patients (48.5%).
  • RESULTS: One year after the procedure and RFA, a total of 88.6% of patients were surviving, at 3 years 72.5 % and at 5 years 36.9% of the subjects.
  • CONCLUSION: Liver resection and RFA have their definite place in multimodal treatment strategy in the management of non- colorectal carcinoma liver metastases (NKJM).
  • [MeSH-minor] Adult. Aged. Catheter Ablation. Colorectal Neoplasms / pathology. Female. Humans. Male. Middle Aged. Survival Rate

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  • (PMID = 20514918.001).
  • [ISSN] 0035-9351
  • [Journal-full-title] Rozhledy v chirurgii : měsíčník Československé chirurgické společnosti
  • [ISO-abbreviation] Rozhl Chir
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
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22. Ryan P, Nguyen VH, Gholoum S, Carpineta L, Abish S, Ahmed NN, Laberge JM, Riddell RH: Polypoid PEComa in the rectum of a 15-year-old girl: case report and review of PEComa in the gastrointestinal tract. Am J Surg Pathol; 2009 Mar;33(3):475-82

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  • [Title] Polypoid PEComa in the rectum of a 15-year-old girl: case report and review of PEComa in the gastrointestinal tract.
  • PEComa of the gastrointestinal tract, composed of perivascular epithelioid cells with myomelanocytic differentiation, is rare with previous literature limited to 16 case reports.
  • We report PEComa with lymph node involvement occurring in the rectum of a 15-year-old girl, treated by surgical resection and adjuvant chemotherapy.
  • We review the differential diagnosis of intestinal PEComa, which includes malignant melanoma, epithelioid gastrointestinal stromal tumors, clear cell sarcoma of soft parts, alveolar soft part sarcoma, leiomyosarcoma with HMB45 expression, and paraganglioma.
  • We discuss the determination of pathologic features indicative of malignancy in PEComa, which is complicated in the gastrointestinal tract due to the small number of cases, variability of pathologic features reported, and inconsistent reporting of outcome.
  • All 4 tumors reporting early recurrence or progression were greater than 5 cm in size and had areas of coagulative tumor necrosis.
  • We propose that a minimum dataset for gastrointestinal PEComa should include these features along with mitotic count, infiltrative border, and tumor stage analogous to that used in colorectal carcinoma.
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Diagnosis, Differential. Digestive System Surgical Procedures. Female. Humans. Immunohistochemistry. Microscopy, Electron, Transmission. Reverse Transcriptase Polymerase Chain Reaction. Tomography, X-Ray Computed

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  • (PMID = 19092636.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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23. Okita NT, Yamada Y, Takahari D, Hirashima Y, Matsubara J, Kato K, Hamaguchi T, Shirao K, Shimada Y, Taniguchi H, Shimoda T: Vascular endothelial growth factor receptor expression as a prognostic marker for survival in colorectal cancer. Jpn J Clin Oncol; 2009 Sep;39(9):595-600
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  • [Title] Vascular endothelial growth factor receptor expression as a prognostic marker for survival in colorectal cancer.
  • OBJECTIVE: Vascular endothelial growth factor (VEGF) and its receptors VEGF-R1, -R2 and -R3 play important roles in tumor angiogenesis and are associated with poor prognosis in several solid tumors.
  • Here, we investigated the associations between the expression of these receptors and the clinical outcomes of colorectal cancer (CRC) patients.
  • METHODS: An immunohistochemical approach was used to detect VEGF-R1, -R2 and -R3 expression in 91 CRC patients who underwent surgery and received chemotherapy at the National Cancer Center Hospital.
  • RESULTS: Immunoreactivity for VEGF-R2 and -R3 was localized in microvessels and that for VEGF-R1 in cancer cells and stromal microvessels.
  • VEGF-R1 staining in cancer cells (>10% staining) was found in 84 patients (92%) and in stromal vessels in 75 patients (82%).
  • VEGF-R2 staining in tumor vessels (>10% staining) was found in 84 patients (92%), whereas VEGF-R3 staining was found in 85 patients (93%).
  • Strong positive staining (>60% staining) of VEGF-R1 in tumor cells, and VEGF-R1, -R2 and -R3 in vessels was identified in 58 (64%), 33 (36%), 52 (57%) and 60 (66%) patients, respectively.
  • CONCLUSIONS: VEGF-R1, -R2 and -R3 were highly expressed in CRC cells and stromal vessels.
  • [MeSH-major] Colorectal Neoplasms / metabolism. Colorectal Neoplasms / mortality. Vascular Endothelial Growth Factor Receptor-1 / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism. Vascular Endothelial Growth Factor Receptor-3 / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / mortality. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Combinations. Female. Fluorouracil / administration & dosage. Humans. Immunoenzyme Techniques. Leucovorin / administration & dosage. Male. Middle Aged. Neoplasm Staging. Oxonic Acid / administration & dosage. Prognosis. Retrospective Studies. Survival Rate. Tegafur / administration & dosage. Uracil / administration & dosage

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  • (PMID = 19535387.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; 5VT6420TIG / Oxonic Acid; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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24. Caponigro F, Basile M, de Rosa V, Normanno N: New drugs in cancer therapy, National Tumor Institute, Naples, 17-18 June 2004. Anticancer Drugs; 2005 Feb;16(2):211-21
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  • [Title] New drugs in cancer therapy, National Tumor Institute, Naples, 17-18 June 2004.
  • An international meeting on 'New Drugs in Cancer Therapy' was held at the National Tumor Institute of Naples, on 17-18 June 2004.
  • The first session of the meeting focused on analogs of conventional anti-cancer drugs, such as taxanes, platinum compounds, anthracyclines and topoisomerase I inhibitors.
  • Data were also presented on BBR-3464, a trinucleate platinum analog which was developed on the grounds of greater potency, a more rapid rate of DNA binding and the ability to induce apoptosis regardless of the p53 status of the cell.
  • Pegylated-coated liposomal formulation doxorubicin (Caelyx) has shown efficacy in metastatic breast cancer and in advanced ovarian cancer; sabarubicin is a third-generation anthracycline with equal or superior potency to doxorubicin or idarubicin in a variety of human tumor cell lines of different histotypes.
  • The main mechanisms of resistance to topoisomerase I inhibitors were discussed; data on diflomotecan were reported, showing a narrow therapeutic index of the drug.
  • The second session of the meeting focused on the ErbB family as a target for anti-cancer therapy.
  • Recent evidence of a correlation between epidermal growth factor receptor (EGFR) mutations at exons 18-21 and clinical response of advanced non-small cell lung cancer to gefitinib therapy was commented on.
  • Cetuximab is reaching market registration in advanced colorectal cancer; in particular, due to the results of the BOND study.
  • The recently presented results of the Bonner study strongly support the activity of this drug in head and neck cancer.
  • Imatinib mesylate is probably the most outstanding example of an effective targeted therapy--its activity in gastrointestinal stromal tumors was so exciting that the drug reached the market without undergoing phase III evaluation.
  • Drugs may interfere with the angiogenic process via different mechanisms and there is a sound rationale for combining anti-angiogenic agents with chemotherapy or multiple anti-angiogenic strategies.
  • Several clinical studies of different phases with compounds belonging to this class have been carried out, either alone or in combination with chemotherapy; unfortunately, all of them have turned out to be negative.
  • Phase I/II clinical trials have shown low toxicity and evidence of anti-tumor activity; on the other hand, this compound has potential for synergism with radiotherapy, chemotherapy and biologicals.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Angiogenesis Inhibitors / therapeutic use. Benzamides. Clinical Trials as Topic. Drug Resistance, Neoplasm. Drugs, Investigational / pharmacology. Genes, erbB / drug effects. Imatinib Mesylate. Piperazines / pharmacology. Piperazines / therapeutic use. Pyrimidines / pharmacology. Pyrimidines / therapeutic use. Signal Transduction / drug effects


25. Heng DY, Kollmannsberger C: Sunitinib. Recent Results Cancer Res; 2010;184:71-82
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  • These attributes have proven to be efficacious in the treatment of metastatic renal cell carcinoma (RCC) and unresectable gastrointestinal stromal tumors (GIST).
  • Clinical trials are underway to determine the efficacy of sunitinib in other tumor types including metastatic breast, colorectal, and lung cancers.
  • This chapter will detail the preclinical data leading to the results of the pivotal phase III clinical trials that have led to the widespread use of sunitinib in metastatic RCC and advanced GIST.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Indoles / therapeutic use. Neoplasms / drug therapy. Pyrroles / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Renal Cell / drug therapy. Clinical Trials as Topic. Drug Interactions. Gastrointestinal Stromal Tumors / drug therapy. Humans. Kidney Neoplasms / drug therapy

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  • (PMID = 20072832.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib
  • [Number-of-references] 62
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26. Lièvre A, Laurent-Puig P: [Molecular biology in clinical cancer research: the example of digestive cancers]. Rev Epidemiol Sante Publique; 2005 Jun;53(3):267-82
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  • [Transliterated title] Apport de la biologie moléculaire dans la recherche clinique en cancérologie: exemple des cancers digestifs.
  • Recent progress in molecular biology allowed the identification of markers potentially usefull for patients management through the identification of these genetic alterations and a best understanding of chemotherapy molecular targets.
  • If almost all colorectal cancers (CRC) correspond to the same histopathological type (adenocarcinoma), molecular biology allowed the identification of two different molecular mechanisms of colorectal carcinogenesis: chromosomal instability characterized by recurrent allelic losses on chromosomes 17, 5, 18, 8 and 22 that contribute to the inactivation of tumor suppressor genes, and genetic instability characterized by the instability of microsatellite loci due to an alteration of DNA mismatch repair leading to the accumulation of mutations in genes involved in the control of cell cycle and apoptosis.
  • Indeed, microsatellite instability seems not only to be a good prognostic factor but also a molecular factor that can predict response to adjuvant 5-fluorouracil based chemotherapy.
  • Therapeutic clinical trials taking into account these molecular parameters are still going on.
  • DNA microarray-based gene expression profiling technology that allows the simultaneous analysis of thousand of tumor genes represents also an interesting approach in oncology with the recent identification of a "genetic signature" as a risk factor of tumor recurrence in stage II CRC, a setting in which the benefit of adjuvant chemotherapy remains on debate.
  • At last, a best understanding of chemotherapy molecular targets allowed the identification of genetic markers that can predict the response and/or the toxicity of anti-cancer drugs used in gastrointestinal cancers, which could be helpful in the future to propose for each patient a personalized treatment.
  • Mutations that can predict the response of new target therapies such as the inhibitors of the c-KIT tyrosine kinase activity in gastrointestinal stromal tumors have also been found and will allow the selection of patients who can have benefit from these new therapeutic drugs.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / genetics. Pharmacogenetics
  • [MeSH-minor] Alleles. Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / metabolism. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Phytogenic / metabolism. Antineoplastic Agents, Phytogenic / therapeutic use. Biomedical Research. Camptothecin / analogs & derivatives. Camptothecin / metabolism. Camptothecin / therapeutic use. Chromosomal Instability. Chromosomes, Human, 16-18 / genetics. Chromosomes, Human, 21-22 and Y / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 8 / genetics. Clinical Trials as Topic. Colorectal Neoplasms, Hereditary Nonpolyposis / genetics. DNA, Neoplasm / genetics. Fluorouracil / administration & dosage. Fluorouracil / metabolism. Fluorouracil / therapeutic use. Forecasting. Genes, Tumor Suppressor. Genetic Markers. Humans. Immunohistochemistry. Molecular Biology. Multivariate Analysis. Mutation. Neoplasm Recurrence, Local. Organoplatinum Compounds / metabolism. Organoplatinum Compounds / therapeutic use. Phenotype. Prognosis. Stomach Neoplasms / drug therapy

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  • (PMID = 16227914.001).
  • [ISSN] 0398-7620
  • [Journal-full-title] Revue d'épidémiologie et de santé publique
  • [ISO-abbreviation] Rev Epidemiol Sante Publique
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / DNA, Neoplasm; 0 / Genetic Markers; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 7673326042 / irinotecan; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
  • [Number-of-references] 72
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27. Verschraegen CF, Kumagai S, Davidson R, Feig B, Mansfield P, Lee SJ, Maclean DS, Hu W, Khokhar AR, Siddik ZH: Phase I clinical and pharmacological study of intraperitoneal cis-bis-neodecanoato( trans- R, R-1, 2-diaminocyclohexane)-platinum II entrapped in multilamellar liposome vesicles. J Cancer Res Clin Oncol; 2003 Oct;129(10):549-55
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  • [Title] Phase I clinical and pharmacological study of intraperitoneal cis-bis-neodecanoato( trans- R, R-1, 2-diaminocyclohexane)-platinum II entrapped in multilamellar liposome vesicles.
  • Laparoscopy was performed on the first two courses for evaluation, adhesiolysis, and chemotherapy administration.
  • Afterwards, chemotherapy was administered through a peritoneal catheter.
  • Diagnoses were: malignant mesothelioma (six patients), signet ring cell (three), colon adenocarcinoma, pseudomyxoma peritonei, gastrointestinal stromal tumor (two each), and ovarian carcinoma (one).
  • Pharmacokinetics studies indicated a rapid but low absorption of drug into the systemic circulation, with a prolonged retention of platinum in the plasma compartment.
  • Peritoneal L-NDDP exposure was 17 to 49-times greater than in the plasma compartment.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adult. Aged. Area Under Curve. Ascites / metabolism. Carcinoma, Signet Ring Cell / drug therapy. Carcinoma, Signet Ring Cell / metabolism. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Endometrial Stromal Tumors / drug therapy. Endometrial Stromal Tumors / metabolism. Female. Humans. Injections, Intraperitoneal. Liposomes. Male. Mesothelioma / drug therapy. Mesothelioma / metabolism. Middle Aged. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / metabolism. Peritoneum / diagnostic imaging. Peritoneum / metabolism. Radionuclide Imaging. Technetium. Tissue Distribution

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  • (PMID = 14513369.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Liposomes; 0 / Organoplatinum Compounds; 113427-19-3 / bis-neodecanoato-1,2-diaminocyclohexaneplatinum(II); 7440-26-8 / Technetium
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28. Boone SL, Jameson G, Von Hoff D, Lacouture ME: Blackberry-induced hand-foot skin reaction to sunitinib. Invest New Drugs; 2009 Aug;27(4):389-90

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  • Sunitinib is an orally administered small molecule that was approved by the US Food and Drug Administration in January 2006 as monotherapy for the treatment of patients with advanced renal cell carcinoma (RCC) and patients with gastrointestinal stromal tumor after disease progression on or intolerance to imatinib mesylate.
  • We describe a 48-year-old woman with a history of metastatic colorectal cancer treated with single-agent sunitinib who developed pain and tenderness in areas of friction secondary to Blackberry use, and was diagnosed with trauma-induced hand-foot skin reaction (HFSR) secondary to sunitinib therapy.
  • [MeSH-minor] Colorectal Neoplasms / drug therapy. Drug Eruptions / etiology. Female. Foot Dermatoses / etiology. Hand Dermatoses / etiology. Humans. Middle Aged

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  • [ErratumIn] Invest New Drugs. 2009 Aug;27(4):391
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  • (PMID = 18998055.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; V99T50803M / sunitinib
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29. Jain RK, Duda DG, Clark JW, Loeffler JS: Lessons from phase III clinical trials on anti-VEGF therapy for cancer. Nat Clin Pract Oncol; 2006 Jan;3(1):24-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lessons from phase III clinical trials on anti-VEGF therapy for cancer.
  • In one approach, the addition of bevacizumab, a VEGF-specific antibody, to standard chemotherapy improved overall survival in colorectal and lung cancer patients and progression-free survival in breast cancer patients.
  • In the second approach, multitargeted tyrosine kinase inhibitors that block VEGF receptor and other kinases in both endothelial and cancer cells, demonstrated survival benefit in gastrointestinal stromal tumor and renal-cell-carcinoma patients.
  • By contrast, adding bevacizumab to chemotherapy failed to increase survival in patients with previously treated and refractory metastatic breast cancer.
  • Furthermore, addition of vatalanib, a kinase inhibitor developed as a VEGF receptor-selective agent, to chemotherapy did not show a similar benefit in metastatic colorectal cancer patients.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Agents / therapeutic use. Clinical Trials, Phase III as Topic. Neoplasms / drug therapy. Neovascularization, Pathologic / drug therapy. Vascular Endothelial Growth Factors / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Bevacizumab. Biomarkers, Tumor. Humans. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 16407877.001).
  • [ISSN] 1743-4254
  • [Journal-full-title] Nature clinical practice. Oncology
  • [ISO-abbreviation] Nat Clin Pract Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factors; 2S9ZZM9Q9V / Bevacizumab; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 95
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30. Morabito A, De Maio E, Di Maio M, Normanno N, Perrone F: Tyrosine kinase inhibitors of vascular endothelial growth factor receptors in clinical trials: current status and future directions. Oncologist; 2006 Jul-Aug;11(7):753-64
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Angiogenesis plays a central role in the process of tumor growth and metastatic dissemination.
  • Agents directed either against VEGF or VEGF receptors (VEGFRs) have been developed.
  • Large randomized phase III trials have demonstrated the efficacy of sunitinib and sorafenib in the treatment of patients affected by gastrointestinal stromal tumors and renal cancer refractory to standard therapies, respectively.
  • Positive results also have been reported with the combination of ZD6474 and chemotherapy in previously treated non-small cell lung cancer patients.
  • For other agents, such as vatalanib, contrasting outcomes in metastatic colorectal cancer patients have been reported: the final results of these trials are expected in 2006.
  • [MeSH-major] Neoplasms / drug therapy. Piperidines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Clinical Trials as Topic. Humans. Protein-Tyrosine Kinases / antagonists & inhibitors. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16880234.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 96
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31. Chen EX, Siu LL: Development of molecular targeted anticancer agents: successes, failures and future directions. Curr Pharm Des; 2005;11(2):265-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent advances in molecular biology have identified numerous steps and proteins involved in malignant transformation as targets of anticancer therapy.
  • Successful developments of trastuzumab in treating breast cancer, imatinib in chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GISTs), and bevacizumab in colorectal cancer, have validated the concept of molecular targeting and raised expectations of patients and oncologists alike.
  • In this review, we will address several issues related to tumor biology and clinical trial design that might have contributed to these successes and failures, and discuss strategies to best optimize the development of these novel agents.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Delivery Systems / methods. Drug Delivery Systems / trends. Drug Design. Treatment Failure
  • [MeSH-minor] Cell Transformation, Neoplastic / drug effects. Clinical Trials as Topic / methods. Forecasting. Humans. Molecular Biology / methods. Molecular Biology / trends. Randomized Controlled Trials as Topic

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  • (PMID = 15638762.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 96
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32. Boehm S, Rothermundt C, Hess D, Joerger M: Antiangiogenic drugs in oncology: a focus on drug safety and the elderly - a mini-review. Gerontology; 2010;56(3):303-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiangiogenic drugs in oncology: a focus on drug safety and the elderly - a mini-review.
  • Angiogenesis is essential for normal tissue and even more so for solid malignancies.
  • At present, inhibition of tumor angiogenesis is a major focus of anticancer drug development.
  • Bevacizumab, a humanized antibody against VEGF, was the first antiangiogenic agent to be approved for advanced non-small cell lung cancer, breast cancer and colorectal cancer.
  • Sunitinib, a small molecule blocking intracellular VEGF, KIT, Flt3 and PDGF receptors, which regulate angiogenesis and cell growth, is approved for the treatment of advanced renal cell cancer (RCC) and malignant gastrointestinal stromal tumor.
  • Sorafenib, an oral multikinase inhibitor, is approved for the second-line treatment of advanced RCC and upfront treatment of advanced hepatocellular carcinoma.
  • More recently, cardiovascular toxicity has increasingly been recognized as a potential adverse event associated with sunitinib and sorafenib treatment.
  • The safety of antiangiogenic drugs is of special concern when taking these agents for longer-term adjuvant or maintenance treatment.
  • Furthermore, newer investigational antiangiogenic drugs are briefly reviewed.
  • [MeSH-major] Angiogenesis Inhibitors / adverse effects. Drugs, Investigational / adverse effects. Neoplasms / drug therapy

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  • [Copyright] 2009 S. Karger AG, Basel.
  • (PMID = 19940466.001).
  • [ISSN] 1423-0003
  • [Journal-full-title] Gerontology
  • [ISO-abbreviation] Gerontology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Drugs, Investigational
  • [Number-of-references] 40
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