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Items 1 to 33 of about 33
1. Batirel HF, Metintas M, Caglar HB, Yildizeli B, Lacin T, Bostanci K, Akgul AG, Evman S, Yuksel M: Trimodality treatment of malignant pleural mesothelioma. J Thorac Oncol; 2008 May;3(5):499-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trimodality treatment of malignant pleural mesothelioma.
  • INTRODUCTION: Multimodality treatment has achieved significant success in local control and treatment of early-stage malignant pleural mesothelioma patients.
  • METHODS: We have instituted a trimodality treatment protocol consisting of extrapleural pneumonectomy, adjuvant high-dose (54 Gy) hemithoracic irradiation, and platin-based chemotherapy in a multi-institutional setting.
  • Preoperative pulmonary function tests, echocardiogram, chest computed tomography, and magnetic resonance imaging scans were performed in all patients.
  • Seventeen had a history of environmental asbestos/erionite exposure.
  • Twelve patients completed all three treatments.
  • CONCLUSIONS: Trimodality treatment in malignant pleural mesothelioma seems to prolong survival in patients without lymph node metastasis.
  • [MeSH-major] Mesothelioma / therapy. Pleural Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Combined Modality Therapy. Feasibility Studies. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Pneumonectomy. Radiotherapy, Adjuvant. Survival Analysis. Treatment Outcome

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  • (PMID = 18449002.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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2. Nefedova Y, Cheng P, Alsina M, Dalton WS, Gabrilovich DI: Involvement of Notch-1 signaling in bone marrow stroma-mediated de novo drug resistance of myeloma and other malignant lymphoid cell lines. Blood; 2004 May 1;103(9):3503-10
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  • [Title] Involvement of Notch-1 signaling in bone marrow stroma-mediated de novo drug resistance of myeloma and other malignant lymphoid cell lines.
  • The bone marrow (BM) microenvironment plays a critical role in malignant cell growth, patient survival, and response to chemotherapy in hematologic malignancies.
  • However, mechanisms associated with this environmental influence remain unclear.
  • In this study, we investigated the role of Notch family proteins in myeloma and other malignant lymphoid cell line growth and response to chemotherapeutic drugs.
  • Overexpression of Notch-1 in Notch-1(-) U266 myeloma cells up-regulated p21 and resulted in protection from drug-induced apoptosis.
  • Thus, this is a first report demonstrating that Notch-1 signaling may be a primary mechanism mediating the BMS influence on hematologic malignant cell growth and survival.
  • [MeSH-major] Drug Resistance, Neoplasm. Multiple Myeloma / pathology. Receptors, Cell Surface / physiology. Stromal Cells / metabolism. Transcription Factors
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Bone Marrow Cells. Cell Communication. Cell Line, Tumor. Coculture Techniques. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / biosynthesis. Humans. Lymphoproliferative Disorders / pathology. Membrane Proteins / physiology. Receptor, Notch1. Receptors, Notch. Signal Transduction. Up-Regulation

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  • (PMID = 14670925.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Membrane Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Receptors, Cell Surface; 0 / Receptors, Notch; 0 / Transcription Factors
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3. Smida J, Baumhoer D, Rosemann M, Walch A, Bielack S, Poremba C, Remberger K, Korsching E, Scheurlen W, Dierkes C, Burdach S, Jundt G, Atkinson MJ, Nathrath M: Genomic alterations and allelic imbalances are strong prognostic predictors in osteosarcoma. Clin Cancer Res; 2010 Aug 15;16(16):4256-67
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • PURPOSE: Osteosarcoma, the most common primary malignant tumor of the bone, is characterized by complex karyotypes with numerous structural and numerical alterations.
  • Despite attempts to establish molecular prognostic markers at the time of diagnosis, the most accepted predictive factor remains the histologic evaluation of necrosis after neoadjuvant chemotherapy.
  • The present approach was carried out to search for genome-wide recurrent loss of heterozygosity and copy number variations that could have prognostic and therapeutic impact for osteosarcoma patients.
  • Numerical aberrations and allelic imbalances were correlated with the histologically assessed response to therapy and clinical follow-up.
  • CONCLUSIONS: Structural chromosomal alterations detected by single nucleotide polymorphism analysis provide a simple but robust parameter to anticipate response to chemotherapy.
  • The proposed chromosomal alteration staging system might therefore help to better predict the clinical course of osteosarcoma patients at the time of initial diagnosis and to adapt neoadjuvant treatment in patients resistant to the current protocols.
  • [MeSH-major] Bone Neoplasms / genetics. Drug Resistance, Neoplasm / genetics. Osteosarcoma / genetics
  • [MeSH-minor] Adolescent. Adult. Allelic Imbalance. Child. Child, Preschool. Female. Gene Dosage. Genome-Wide Association Study. Humans. Kaplan-Meier Estimate. Loss of Heterozygosity. Male. Middle Aged. Neoadjuvant Therapy. Oligonucleotide Array Sequence Analysis. Polymorphism, Single Nucleotide. Prognosis. Young Adult

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  • (PMID = 20610556.001).
  • [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
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4. Kossoy G, Anisimov VN, Ben-Hur H, Kossoy N, Zusman I: Effect of the synthetic pineal peptide epitalon on spontaneous carcinogenesis in female C3H/He mice. In Vivo; 2006 Mar-Apr;20(2):253-7
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • Epitalon was injected at a dose of 0.1 microg, 5 times a week.
  • Treatment with Epitalon decreased the number of tumor-bearing mice with malignant tumors and prevented the development of metastases.
  • Treatment with Epitalon slowed down the development of metastases from spontaneous tumors, and no metastases were found in the experimental mice.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Intraductal, Noninfiltrating / drug therapy. Mammary Neoplasms, Animal / drug therapy. Neoplasm Metastasis / drug therapy. Neoplasms / drug therapy. Oligopeptides / pharmacology
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Female. Lung Neoplasms / drug therapy. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mice. Mice, Inbred C3H

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  • (PMID = 16634527.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligopeptides; O65P17785G / alanyl-glutamyl-aspartyl-glycine
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5. Kelemen LE: The role of folate receptor alpha in cancer development, progression and treatment: cause, consequence or innocent bystander? Int J Cancer; 2006 Jul 15;119(2):243-50
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  • [Title] The role of folate receptor alpha in cancer development, progression and treatment: cause, consequence or innocent bystander?
  • Folate is a basic component of cell metabolism and DNA synthesis and repair, and rapidly dividing cancer cells have an increased requirement for folate to maintain DNA synthesis, an observation supported by the widespread use of antifolates in cancer chemotherapy.
  • FRalpha levels are high in specific malignant tumors of epithelial origin compared to normal cells, and are positively associated with tumor stage and grade, raising questions of its role in tumor etiology and progression.
  • Epidemiologic and clinical studies using human tumor specimens are lacking and increasingly needed to understand the role of environmental and genetic influences on FOLR1 expression in tumor etiology and progression.

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  • [Copyright] 2006 Wiley-Liss, Inc.
  • (PMID = 16453285.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R25 CA092049; United States / NCI NIH HHS / CA / R25 CA92049
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA, Neoplasm; 0 / FOLR1 protein, human; 0 / Folate Receptor 1; 0 / Folate Receptors, GPI-Anchored; 0 / Gonadal Steroid Hormones; 0 / Receptors, Cell Surface; 0 / Transcription Factors; 0LVT1QZ0BA / Homocysteine; 935E97BOY8 / Folic Acid
  • [Number-of-references] 115
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6. Jiang T, Chen N, Zhao F, Wang XJ, Kong B, Zheng W, Zhang DD: High levels of Nrf2 determine chemoresistance in type II endometrial cancer. Cancer Res; 2010 Jul 1;70(13):5486-96
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  • [Title] High levels of Nrf2 determine chemoresistance in type II endometrial cancer.
  • Type II endometrial cancer, which mainly presents as serous and clear cell types, has proved to be the most malignant and recurrent carcinoma among various female genital malignancies.
  • Activation of the Nrf2-mediated cellular defense response protects cells against the toxic and carcinogenic effects of environmental insults by upregulating an array of genes that detoxify reactive oxygen species and restore cellular redox homeostasis.
  • However, the cancer-promoting role of Nrf2 has recently been revealed.
  • Nrf2 is constitutively upregulated in several types of human cancer tissues and cancer cell lines.
  • Furthermore, inhibition of Nrf2 expression sensitizes cancer cells to chemotherapeutic drugs.
  • In this study, the constitutive level of Nrf2 was compared in different types of human endometrial tumors.
  • Silencing of Nrf2 rendered SPEC-2 cells more susceptible to chemotherapeutic drugs, whereas it had a limited effect on Ishikawa cells.
  • Inhibition of Nrf2 expression by overexpressing Keap1 sensitized SPEC-2 cells or SPEC-2-derived xenografts to chemotherapeutic treatments using both cell culture and severe combined immunodeficient mouse models.
  • Collectively, we provide a molecular basis for the use of Nrf2 inhibitors to increase the efficacy of chemotherapeutic drugs and to combat chemoresistance, the biggest obstacle in chemotherapy.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20530669.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA23074; United States / NCI NIH HHS / CA / P30 CA023074; United States / NIEHS NIH HHS / ES / ES015010-04; United States / NIEHS NIH HHS / ES / R01 ES015010-04; United States / NIEHS NIH HHS / ES / ES015010; United States / NIEHS NIH HHS / ES / R01 ES015010
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / KEAP1 protein, human; 0 / NF-E2-Related Factor 2; 0 / NFE2L2 protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS203767; NLM/ PMC2896449
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7. Burgos San Juan L: [Cholangiocarcinoma]. Rev Med Chil; 2008 Feb;136(2):240-8
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  • [Transliterated title] Colangiocarcinoma: Actualización, diagnóstico y terapia.
  • Cholangiocarcinoma is a malignant lesion of the bile duct epithelium.
  • Its etiology is unknown but there are predisposing conditions and environmental risk factors such as primary sclerosing cholangitis, Caroli's disease, bile duct malformations, industrial toxins and parasitic infections.
  • Hilar cholangiocarcinoma must be distinguished from other malignant or benign causes of biliary obstruction.
  • Cholangiocarcinoma of the distal common bile duct must be differentiated from other periampullary tumors and intrahepatic cholangiocarcinoma can be confused with a hepatocellular carcinoma.
  • The best treatment is the complete surgical excision with negative histological margins, although the resectability index is low.
  • The type and size of surgery depends on the location and extent of the tumor.
  • Chemotherapy is not effective.
  • [MeSH-minor] Humans. Neoplasm Staging / methods

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  • (PMID = 18483680.001).
  • [ISSN] 0034-9887
  • [Journal-full-title] Revista médica de Chile
  • [ISO-abbreviation] Rev Med Chil
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Chile
  • [Number-of-references] 43
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8. Rhines LD, Sampath P, DiMeco F, Lawson HC, Tyler BM, Hanes J, Olivi A, Brem H: Local immunotherapy with interleukin-2 delivered from biodegradable polymer microspheres combined with interstitial chemotherapy: a novel treatment for experimental malignant glioma. Neurosurgery; 2003 Apr;52(4):872-9; discussion 879-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Local immunotherapy with interleukin-2 delivered from biodegradable polymer microspheres combined with interstitial chemotherapy: a novel treatment for experimental malignant glioma.
  • CONCLUSION: By showing synergy of IL-2 and BCNU in an animal glioma model and using a reproducible synthetic delivery system for each agent (i.e., one that did not rely on genetically engineered cells or viruses), we hope that the combination of local immunotherapy and chemotherapy can take an important step closer to clinical application in patients with malignant brain tumors.
  • [MeSH-major] Brain Neoplasms / drug therapy. Carmustine / administration & dosage. Gliosarcoma / drug therapy. Interleukin-2 / administration & dosage. Parietal Lobe
  • [MeSH-minor] Animals. Biodegradation, Environmental. Biological Availability. Chondroitin Sulfates. Female. Gelatin. Injections, Intralesional. Microspheres. Neoplasm Transplantation. Polymers. Rats. Rats, Inbred F344. Stereotaxic Techniques. Tumor Cells, Cultured

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  • (PMID = 12657184.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01-CA 52857
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-2; 0 / Polymers; 9000-70-8 / Gelatin; 9007-28-7 / Chondroitin Sulfates; U68WG3173Y / Carmustine
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9. Kawano N, Tashiro M, Taguchi M, Kihara Y, Yoshikawa I, Syukuwa K, Yamasaki M, Kume K, Otsuki M: [Combined treatment with dacarbazine, nimustine, cisplatin, and tamoxifen plus interferon-beta in a patient with advanced anorectal malignant melanoma]. Nihon Shokakibyo Gakkai Zasshi; 2008 Nov;105(11):1627-33
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  • [Title] [Combined treatment with dacarbazine, nimustine, cisplatin, and tamoxifen plus interferon-beta in a patient with advanced anorectal malignant melanoma].
  • A 73-year-old man, who was diagnosed as having advanced anorectal malignant melanoma (Stage IV), was treated with combination chemotherapy using dacarbazine, nimustine, cisplatin, and tamoxifen plus interferon-beta.
  • After the first course of chemotherapy, rectal tumor was decreased in size with less anal pain and liver tumor was disappeared.
  • Twenty-four months after the first treatment, the patient is survived.
  • DAC-Tam IFN-beta therapy may improve the management of patients who have advanced MM of the anorectum.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Anus Neoplasms / drug therapy. Melanoma / drug therapy. Rectal Neoplasms / drug therapy
  • [MeSH-minor] Aged. Cisplatin / administration & dosage. Dacarbazine / administration & dosage. Humans. Interferon-beta / administration & dosage. Liver Neoplasms / secondary. Male. Neoplasm Staging. Nimustine / administration & dosage. Tamoxifen / administration & dosage. Treatment Outcome

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  • (PMID = 18987448.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen; 0S726V972K / Nimustine; 77238-31-4 / Interferon-beta; 7GR28W0FJI / Dacarbazine; Q20Q21Q62J / Cisplatin
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10. Stewart DJ, Edwards JG, Smythe WR, Waller DA, O'Byrne KJ: Malignant pleural mesothelioma--an update. Int J Occup Environ Health; 2004 Jan-Mar;10(1):26-39
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  • [Title] Malignant pleural mesothelioma--an update.
  • Exposure to asbestos is the most frequent, but not exclusive, cause of malignant mesothelioma.
  • Conventional treatments such as chemotherapy, surgery, and radiotherapy have had variable impacts, although chemotherapy is useful in palliation and can improve both survival and quality of life.
  • Multimodality treatments appear to be the most successful for management of potentially resectable disease.
  • With new treatments based on better understanding of the biology of the disease, there is cautious optimism for the future for patients with malignant pleural mesothelioma.
  • [MeSH-major] Mesothelioma / pathology. Mesothelioma / therapy. Pleural Neoplasms / pathology. Pleural Neoplasms / therapy
  • [MeSH-minor] Asbestos / toxicity. Combined Modality Therapy. Environmental Exposure / adverse effects. Environmental Pollutants / toxicity. Genetic Therapy / methods. Global Health. Humans. Immunotherapy / methods. Neoplasm Staging. Prognosis

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  • (PMID = 15070023.001).
  • [ISSN] 1077-3525
  • [Journal-full-title] International journal of occupational and environmental health
  • [ISO-abbreviation] Int J Occup Environ Health
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Environmental Pollutants; 1332-21-4 / Asbestos
  • [Number-of-references] 180
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11. Matsuura Y, Kitajima M, Hachisuga T, Tanimoto A, Okura N, Kihara I: Malignant mixed müllerian tumor with malignant neuroectodermal components (teratoid carcinosarcoma) of the ovary: Report of a case with clinicopathologic findings. J Obstet Gynaecol Res; 2010 Aug;36(4):907-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant mixed müllerian tumor with malignant neuroectodermal components (teratoid carcinosarcoma) of the ovary: Report of a case with clinicopathologic findings.
  • Malignant mixed müllerian tumor (MMMT) or carcinosarcoma of the female genital tract is a rare neoplasm.
  • Malignant ovarian tumor composed of müllerian epithelial tumor and malignant germ cell tumor is also rare, with most cases composed of endometrioid adenocarcinoma and yolk sac tumor.
  • Ovarian MMMT with malignant neuroectodermal components resembling immature teratoma is extremely rare.
  • Microscopic examination showed a heterogenous mixed tumor composed of malignant epithelial, malignant mesodermal and malignant neuroectodermal components.
  • In spite of aggressive combination chemotherapy and three times of laparotomy, the patient died of disease 3 years 10 months after the initial treatment.
  • Further cases need to be accumulated to make diagnosis and to determine a successful treatment modality.

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  • (PMID = 20666968.001).
  • [ISSN] 1447-0756
  • [Journal-full-title] The journal of obstetrics and gynaecology research
  • [ISO-abbreviation] J. Obstet. Gynaecol. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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12. Jennings MT, Iyengar S: The molecular genetics of therapeutic resistance in malignant astrocytomas. Am J Pharmacogenomics; 2001;1(2):93-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The molecular genetics of therapeutic resistance in malignant astrocytomas.
  • The adverse prognosis associated with malignant astrocytomas (MA) is due in part to the development of resistance by the tumor to chemo- and radiotherapy-induced cytotoxic damage.
  • The classic examples of drug resistance proteins, such as the p-glycoprotein/multidrug resistance protein 1, have been identified within MA biopsy specimens.
  • The interaction between the products of these genes and intratumoral environmental factors appears to involve a dynamic and prognostically adverse selection process.
  • It is from this perspective that the mechanism(s) of hypoxic-ischaemic selection for resistance and its therapeutic repercussions will be analyzed.
  • [MeSH-major] Astrocytoma / drug therapy. Astrocytoma / genetics. Cell Transformation, Neoplastic / genetics. Drug Resistance, Neoplasm / genetics

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  • (PMID = 12174677.001).
  • [ISSN] 1175-2203
  • [Journal-full-title] American journal of pharmacogenomics : genomics-related research in drug development and clinical practice
  • [ISO-abbreviation] Am J Pharmacogenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Number-of-references] 85
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13. Gulmez I, Kart L, Buyukoglan H, Er O, Balkanli S, Ozesmi M: Evaluation of malignant mesothelioma in central Anatolia: a study of 67 cases. Can Respir J; 2004 May-Jun;11(4):287-90
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  • [Title] Evaluation of malignant mesothelioma in central Anatolia: a study of 67 cases.
  • BACKGROUND: Malignant mesothelioma (MM) is a fatal neoplasm which frequently results from exposure to asbestos or erionite.
  • Their clinical and radiological features, as well as the therapy, were retrospectively evaluated.
  • Pleural effusion (92.4%) was the most common chest x-ray finding, whereas pleural effusion (60.8%), pleural nodules (34.7%) and pleural thickening (34.7%) were the most common computed tomography findings in pleural MM patients.
  • Exposures were environmental as opposed to occupational.
  • Thirty-five patients (52.2%) were administered chemotherapy, and follow-up data were available for 22 patients.
  • MM is a major public health problem in parts of Turkey and compulsory environmental control of fibrous mineral should be considered.
  • [MeSH-minor] Adult. Aged. Asbestos / adverse effects. Environmental Exposure. Female. Humans. Male. Middle Aged. Pleural Effusion / etiology. Tomography, X-Ray Computed. Turkey / epidemiology. Zeolites / adverse effects

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  • [CommentIn] Can Respir J. 2004 May-Jun;11(4):273-4 [15254607.001]
  • (PMID = 15254610.001).
  • [ISSN] 1198-2241
  • [Journal-full-title] Canadian respiratory journal
  • [ISO-abbreviation] Can. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 12510-42-8 / erionite; 1318-02-1 / Zeolites; 1332-21-4 / Asbestos
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14. Emri S, Akbulut H, Zorlu F, Dinçol D, Akay H, Güngen Y, Içli F: Prognostic significance of flow cytometric DNA analysis in patients with malignant pleural mesothelioma. Lung Cancer; 2001 Aug-Sep;33(2-3):109-14
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  • [Title] Prognostic significance of flow cytometric DNA analysis in patients with malignant pleural mesothelioma.
  • Malignant pleural mesothelioma (MPM) due to environmental exposure to asbestos and erionite is a relatively common cancer in Turkey.
  • In this study, we investigated the value of flow cytometric (FCM) DNA analysis and other prognostic factors such as age and etiologic factor in the patients with MPM, treated with surgery+/-combination chemotherapy+/-radiotherapy.
  • [MeSH-major] DNA, Neoplasm / analysis. Mesothelioma / genetics. Pleural Neoplasms / genetics


15. Zhu H, Zheng J, Xiao X, Zheng S, Dong K, Liu J, Wang Y: Environmental endocrine disruptors promote invasion and metastasis of SK-N-SH human neuroblastoma cells. Oncol Rep; 2010 Jan;23(1):129-39
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  • [Title] Environmental endocrine disruptors promote invasion and metastasis of SK-N-SH human neuroblastoma cells.
  • Neuroblastoma (NB) is the most common pediatric extracranial cancer.
  • Environmental endocrine disruptors (EED) are recently identified risk factors associated with various human diseases including malignant tumors.
  • SK-N-SH cells expressed estrogen receptor (ER)-beta, matrix metalloproteinases-2 (MMP-2), MMP-9 and tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) at readily detectable levels.
  • ER-dependent pathway and PI3K/Akt pathway are involved, which may become potential therapeutic targets for neuroblastoma treatment.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Neuroblastoma / drug therapy. Neuroblastoma / pathology
  • [MeSH-minor] Benzhydryl Compounds. Cell Line, Tumor. Diethylhexyl Phthalate / toxicity. Endocrine System / drug effects. Estradiol / toxicity. Estrogens, Non-Steroidal / toxicity. Humans. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 9 / biosynthesis. Neoplasm Invasiveness. Neoplasm Metastasis. Phenols / toxicity. Phosphatidylinositol 3-Kinases / metabolism. Plasticizers / toxicity. Tissue Inhibitor of Metalloproteinase-2 / biosynthesis

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  • (PMID = 19956873.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Benzhydryl Compounds; 0 / Estrogens, Non-Steroidal; 0 / Phenols; 0 / Plasticizers; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; 4TI98Z838E / Estradiol; C42K0PH13C / Diethylhexyl Phthalate; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; MLT3645I99 / bisphenol A
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16. Voelter-Mahlknecht S, Mahlknecht U, Letzel S, Fierlbeck G: Phase 2 trial of the continuous IV administration of interferon-beta in patients with disseminated malignant melanoma. Skinmed; 2006 Nov-Dec;5(6):271-6
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  • [Title] Phase 2 trial of the continuous IV administration of interferon-beta in patients with disseminated malignant melanoma.
  • OBJECTIVE: The assessment of treatment toxicity and antitumoral effectiveness of continuous IV administration of interferon-beta based on an overall evaluation of laboratory, radiographic, and clinical parameters observed during the trial.
  • METHODS: The authors treated patients with advanced malignant melanoma with continuous IV infusions of 1 x 10(6) IU interferon-beta daily ( approximately 0.6 x 10(6) IU interferon-beta/m2 daily).
  • Interferon side effects were not a reason for treatment discontinuation in any of the patients observed during this trial.
  • CONCLUSIONS: Continuous IV interferon-beta had no significant effect on overall patient outcome in a group of patients with advanced malignant melanoma.
  • To our knowledge, this is the first report on the continuous IV administration of interferon-beta in patients with advanced malignant melanoma.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Interferon-beta / administration & dosage. Melanoma / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Aged. Combined Modality Therapy. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Metastasis. Treatment Outcome

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  • (PMID = 17085993.001).
  • [ISSN] 1540-9740
  • [Journal-full-title] Skinmed
  • [ISO-abbreviation] Skinmed
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 77238-31-4 / Interferon-beta
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17. Yamate J, Kotera T, Kuwamura M, Kotani T: Potential osteogenic differentiation of cisplatin-resistant rat malignant fibrous histiocytoma-derived cell lines. Exp Toxicol Pathol; 2007 Apr;58(5):299-309
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  • [Title] Potential osteogenic differentiation of cisplatin-resistant rat malignant fibrous histiocytoma-derived cell lines.
  • Histological modulations in tumor cells treated with anti-cancer drugs have been reported.
  • The histogenesis of malignant fibrous histiocytoma (MFH) remains elusive.
  • MT-10 developed tumors of a storiform pattern, while MT-10R and MT-PR tumors comprise round or polygonal cells arranged in a compact sheet.
  • Cisplatin-resistant MFH cells had potential to differentiate into osteogenic tissues by producing osteogenic factors, suggesting that MFH histology may be altered under anti-cancer drug treatments.
  • Recently, cancer differentiation-based therapy, that could be induced by anti-cancer drugs, has been implied.
  • MT-10R and MT-PR become useful experimental systems for studies on cellular differentiation provoked by anti-cancer drugs.
  • [MeSH-major] Bone Morphogenetic Proteins / biosynthesis. Cell Differentiation / drug effects. Cisplatin / pharmacology. Drug Resistance, Neoplasm / drug effects. Histiocytoma, Malignant Fibrous / pathology. Osteoblasts / pathology
  • [MeSH-minor] Animals. Bone Morphogenetic Protein 1. Bone Morphogenetic Protein 6. Clone Cells. Enzyme-Linked Immunosorbent Assay. Immunohistochemistry. Metalloendopeptidases / biosynthesis. Neoplasm Transplantation. Osteopontin / biosynthesis. RNA, Messenger / biosynthesis. Rats. Rats, Inbred F344. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17267196.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bmp6 protein, rat; 0 / Bone Morphogenetic Protein 6; 0 / Bone Morphogenetic Proteins; 0 / RNA, Messenger; 106441-73-0 / Osteopontin; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.19 / Bmp1 protein, rat; EC 3.4.24.19 / Bone Morphogenetic Protein 1; Q20Q21Q62J / Cisplatin
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18. Olnes MJ, Erlich R: A review and update on cholangiocarcinoma. Oncology; 2004;66(3):167-79
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  • Cholangiocarcinoma is a malignant neoplasm arising from the biliary epithelium that was first described by Durand-Fardel in 1840.
  • Today, it continues to defy diagnosis and treatment.
  • There is marked geographic variability in the prevalence of this disease, due in large part to regional environmental risk factors.
  • Surgical resection remains the only curative treatment, and high priorities are improving diagnostic methods, and clinical staging for resection once the disease is suspected.
  • Chemotherapy, palliative stenting, and radiation are reserved for patients who are not resectable, those with recurrence after surgery, and those who decline surgical intervention.
  • Recent trials using combination systemic chemotherapy and neoadjuvant chemoradiation are promising, but require further study.
  • In this review we discuss epidemiology, etiologic factors, molecular pathogenesis, diagnosis, staging, and treatment of cholangiocarcinoma.
  • Particular focus is on recent studies into the cellular and molecular pathogenesis of the disease, recent chemotherapy trials, and newer methods of staging and screening for this devastating malignancy.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cholangitis, Sclerosing / complications. Diagnosis, Differential. Humans. Neoplasm Staging

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  • [Copyright] Copyright 2004 S. Karger AG, Basel
  • (PMID = 15218306.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 128
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19. Yang KM, Pyo JO, Kim GY, Yu R, Han IS, Ju SA, Kim WH, Kim BS: Capsaicin induces apoptosis by generating reactive oxygen species and disrupting mitochondrial transmembrane potential in human colon cancer cell lines. Cell Mol Biol Lett; 2009;14(3):497-510
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  • [Title] Capsaicin induces apoptosis by generating reactive oxygen species and disrupting mitochondrial transmembrane potential in human colon cancer cell lines.
  • Although genetic factors are a well-known cause of colorectal cancer, environmental factors contribute more to its development.
  • Despite advances in the fields of surgery, radiotherapy and chemotherapy, the cure rates for colon cancer have not substantially improved over the past few decades.
  • Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide), the principal pungent ingredient of hot chili pepper, has exhibited an anti-tumor effect in many cell types.
  • In this study, we investigated whether capsaicin induces apoptosis in colon cancer cell lines.
  • Treatment with capsaicin induced a dramatic increase in caspase 3 activity, as assessed by the cleavage of Ac-DEVD-AMC, a fluorogenic substrate.
  • In conclusion, our results clearly showed that capsaicin induced apoptosis in colon cancer cells.
  • Although the actual mechanisms of capsaicin-induced apoptosis remain uncertain, it may be a beneficial agent for colon cancer treatment and chemoprevention.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Capsaicin / pharmacology. Colonic Neoplasms / metabolism. Membrane Potential, Mitochondrial / drug effects. Mitochondria / drug effects. Reactive Oxygen Species / metabolism

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  • (PMID = 19381455.001).
  • [ISSN] 1689-1392
  • [Journal-full-title] Cellular & molecular biology letters
  • [ISO-abbreviation] Cell. Mol. Biol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Reactive Oxygen Species; EC 3.4.22.- / Caspase 3; S07O44R1ZM / Capsaicin
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20. Keely NO, Meegan MJ: Targeting tumors using estrogen receptor ligand conjugates. Curr Cancer Drug Targets; 2009 May;9(3):370-80
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  • When treating cancer, cytotoxic agents are intended to exert their effect on rapidly proliferating cancer cells.
  • However, often cancer chemotherapies lack specificity which can lead to toxicity and undesirable side affects.
  • Selective chemotherapies can be established by focusing on distinctive physiological, morphological and environmental differences between tumor and healthy tissue.
  • For example, agents targeting nuclear receptors over-expressed in tumors can hone in on malignant tissue and result in improved chemotherapeutic treatments.
  • In hormone-dependent cancers, such as certain breast cancers, a number of structurally varied estrogen receptor ligand conjugates have been investigated attempting to take advantage of the presence of over-expressed estrogen receptor.
  • Estrogen receptor ligand conjugates containing a variety of cytotoxic agents, photodynamic therapeutic agents and radioligands have been reported.
  • In this review, developments in these specific types of estrogen receptor targeting approaches are discussed which highlight the potential advantages of these conjugates in the discovery of more effective cancer chemotherapy agents.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasms / drug therapy. Receptors, Estrogen / metabolism
  • [MeSH-minor] Binding Sites. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Drug Design. Estradiol / analogs & derivatives. Estradiol / therapeutic use. Estrogen Receptor Modulators / metabolism. Estrogen Receptor Modulators / therapeutic use. Female. Humans. Ligands. Neoplasm Staging

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  • (PMID = 19442056.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Estrogen Receptor Modulators; 0 / Ligands; 0 / Receptors, Estrogen; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol
  • [Number-of-references] 85
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21. Szotkowski T, Rohon P, Zapletalova L, Sicova K, Hubacek J, Indrak K: Secondary acute myeloid leukemia - a single center experience. Neoplasma; 2010;57(2):170-8
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  • Secondary acute myeloid leukemia (sAML) may arise from the previous clonal disorder of hematopoiesis, usually from myelodysplastic syndrome (MDS) or from chronic myeloproliferative neoplasia (cMPN) or after exposure to a leukemogenic agent (previous chemotherapy or radiotherapy, some immunosuppressive drugs or environmental leukemogenic agents).
  • Over that period of time, a total 574 patients with AML were diagnosed.
  • Of those, 430 patients were diagnosed as having primary AML; in 86 patients, sAML transformed from myelodysplastic syndrome and 58 patients were followed or treated for various malignancies or were treated with potentially leukemogenic agents because of non-malignant disorders.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Neoplasm Recurrence, Local / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Adult. Aged. Chronic Disease. Female. Humans. Male. Middle Aged. Prognosis. Remission Induction. Retrospective Studies. Survival Rate. Treatment Outcome. Young Adult


22. Guha A, Mukherjee J: Advances in the biology of astrocytomas. Curr Opin Neurol; 2004 Dec;17(6):655-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE OF REVIEW: Conventional surgery, radio- and chemotherapy have failed to significantly improve the prognosis of patients with malignant astrocytomas--hence the need for understanding their molecular biology.
  • Harvesting this understanding to yield novel biological targeted therapies has approached the clinical doorstep.
  • Therapeutic efficacy will likely require combinatorial therapy involving biologicals and conventional therapies, with small incremental efficacy in selected sub-groups.
  • SUMMARY: Astrocytomas, like other cancers, are a result of several molecular alterations, some of which strongly correlate to their pathological grade.
  • However, molecular heterogeneity exists between astrocytomas of similar grades and likely between varying micro-environmental regions of a single tumor.
  • Characterization of the molecular signature of an astrocytoma and linking with the appropriate 'tailored' therapie(s) is the hope of the future.
  • [MeSH-minor] Animals. Apoptosis / genetics. Cell Transformation, Neoplastic / genetics. Growth Substances / genetics. Growth Substances / metabolism. Humans. Models, Biological. Neoplasm Invasiveness / genetics. Neovascularization, Pathologic / genetics. Signal Transduction / genetics

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  • (PMID = 15542973.001).
  • [ISSN] 1350-7540
  • [Journal-full-title] Current opinion in neurology
  • [ISO-abbreviation] Curr. Opin. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Growth Substances
  • [Number-of-references] 54
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23. Sullivan R, Graham CH: Chemosensitization of cancer by nitric oxide. Curr Pharm Des; 2008;14(11):1113-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemosensitization of cancer by nitric oxide.
  • Recent evidence from experimental and clinical studies links the development of intratumoral hypoxia and oxidative stress with malignant progression.
  • Cellular adaptation induced by these environmental stresses is also associated with the emergence of drug resistant populations.
  • Experimental data suggest that treatment of human cancer cells with nitric oxide (NO) and NO mimetic agents can effectively restore the sensitivity of resistant populations to the cytotoxic effects of chemotherapeutics both in vitro and in vivo.
  • Furthermore, preliminary results from Phase II clinical trials evaluating NO as an adjuvant to chemotherapy are promising.
  • However, the data suggest that chemosensitization is likely to involve NO-mediated activities associated with both prevention and inhibition of cellular drug resistance mechanisms.
  • Potential mechanisms contributing to the chemosensitizing activity of NO include vascular changes that promote increased blood delivery and tumor oxygenation, antioxidant effects and down-regulation of the glutathione detoxification/redox buffering system, inhibition of key transcription factors such as HIF-1 and NF-kappaB, as well as inhibition of drug efflux transporters and DNA repair enzymes.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Neoplasms / drug therapy. Nitric Oxide / pharmacology
  • [MeSH-minor] Animals. Clinical Trials as Topic. Drug Resistance, Neoplasm. Humans. Oxidative Stress / drug effects. Signal Transduction

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  • (PMID = 18473858.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 124
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24. Lin YM, Zhang GZ, Leng ZX, Lu ZX, Bu LS, Gao S, Yang SJ: Study on the bone marrow mesenchymal stem cells induced drug resistance in the U937 cells and its mechanism. Chin Med J (Engl); 2006 Jun 5;119(11):905-10
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  • [Title] Study on the bone marrow mesenchymal stem cells induced drug resistance in the U937 cells and its mechanism.
  • BACKGROUND: The hematopoietic microenvironment (HM) plays a critical role in malignant cell growth, patient survival, and response to chemotherapy in hematologic malignancies.
  • However, mechanisms associated with this environmental influence remain unclear.
  • In this study, we investigated the role of bone marrow derived mesenchymal stem cells (MSCs) in U937 cell line, to find out the relations between leukemia drug resistance and the MSCs.
  • Apoptosis and sensitivity of U937 to daunoblastina (DNR) were quantified by DNA ladder detection and trypan blue exclusion assays, respectively.
  • The gene expression profile chip technology was used to determine and analyze the changes in apoptosis-related gene expression after adherent culture and the expression of MDR1 mRNA was assessed by reverse transcriptional polymerase chain reaction (RT-PCR) at the same time.
  • U937 cell viability was enhanced and cell apoptosis was blocked during DNR treatment in adherent culture with MSCs.
  • Thirty-nine differently expressed genes were screened from the 487 apoptosis related genes in the adherent culture U937 cells.
  • CONCLUSIONS: MSCs play a role in modulating the proliferation of U937 cells and response of U937 cells to DNR, and Bcl-XL apoptosis-inhibiting gene may be most important in determining the sensitivity of leukemic cells to treatment, which is not related to MDR1.
  • [MeSH-major] Bone Marrow Cells / physiology. Drug Resistance, Neoplasm. Mesenchymal Stromal Cells / physiology. U937 Cells / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Cell Proliferation. Daunorubicin / pharmacology. Genes, MDR. Humans. Immunophenotyping

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  • (PMID = 16780769.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] ZS7284E0ZP / Daunorubicin
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25. Morandi E, Zingaretti C, Chiozzotto D, Severini C, Semeria A, Horn W, Vaccari M, Serra R, Silingardi P, Colacci A: A cDNA-microarray analysis of camptothecin resistance in glioblastoma cell lines. Cancer Lett; 2006 Jan 8;231(1):74-86
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  • Chemotherapy, as generally available, is of a limited value in curing malignant brain tumors (gliomas), which often develop resistance to drugs, becoming completely unresponsive to any standard therapeutic approach.
  • Camptothecins, a family of topoisomerase I inhibitor drugs, represent a new promising treatment strategy and are currently under evaluation for testing the clinical efficacy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Brain Neoplasms / pathology. Camptothecin / pharmacology. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Neoplastic / drug effects. Glioblastoma / pathology

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  • (PMID = 16356833.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; XT3Z54Z28A / Camptothecin
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26. Yasumoto K, Hanagiri T, Takenoyama M: Lung cancer-associated tumor antigens and the present status of immunotherapy against non-small-cell lung cancer. Gen Thorac Cardiovasc Surg; 2009 Sep;57(9):449-57
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  • [Title] Lung cancer-associated tumor antigens and the present status of immunotherapy against non-small-cell lung cancer.
  • Despite recent advances in surgery, irradiation, and chemotherapy, the prognosis of patients with lung cancer is still poor.
  • Therefore, the development and application of new therapeutic strategies are essential for improving the prognosis of this disease.
  • Immune responses and tumor-associated antigens against not only malignant melanoma but also lung cancer have been elucidated at the molecular level.
  • However, many clinical trials of cancer vaccination with defined tumor antigens have resulted in objective clinical responses in only a small number of patients.
  • Tumor escape mechanisms from host immune surveillance remain a major obstacle for cancer immunotherapy.
  • A better understanding of the immune escape mechanisms employed by tumor cells is necessary before we can develop a more effective immunotherapeutic approach to lung cancer.
  • We review recent studies regarding the identification of tumor antigens in lung cancer, tumor immune escape mechanisms, and clinical vaccine trials in lung cancer.
  • [MeSH-major] Antigens, Neoplasm / immunology. Cancer Vaccines. Carcinoma, Non-Small-Cell Lung / therapy. Immunotherapy / methods. Lung Neoplasms / therapy. Lymphocytes, Tumor-Infiltrating / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Clinical Trials as Topic. Humans. Treatment Outcome. Tumor Escape

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  • (PMID = 19756930.001).
  • [ISSN] 1863-6713
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines
  • [Number-of-references] 76
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27. Vasilevskaya I, O'Dwyer PJ: Role of Jun and Jun kinase in resistance of cancer cells to therapy. Drug Resist Updat; 2003 Jun;6(3):147-56
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  • [Title] Role of Jun and Jun kinase in resistance of cancer cells to therapy.
  • A series of kinases, the mitogen-activated protein (MAP) kinases, serves to regulate cellular responses to various environmental influences in metazoans.
  • The activation of one of these, the Jun kinase pathway, has been implicated in apoptotic responses to DNA damage, cell stress and cytotoxic drugs.
  • Under most circumstances in non-malignant cells it appears that c-Jun N-terminal kinase (JNK) activation is a pro-apoptotic event that results in turn in activation of pro-apoptotic members of Bcl-2 family and cytochrome c release from mitochondria.
  • In certain cell types, c-Jun overexpression is clearly a basis for resistance to DNA-damaging drugs, and resistance reversal has been observed using c-jun antisense.
  • This preliminary evidence suggests that c-jun may have a role in drug resistance, but additional work with patient tumor samples is required to validate the potential of the JNK pathway as a target.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. JNK Mitogen-Activated Protein Kinases. Mitogen-Activated Protein Kinase Kinases / biosynthesis. Neoplasms. Proto-Oncogene Proteins c-jun / biosynthesis
  • [MeSH-minor] Animals. Apoptosis / drug effects. DNA Damage. DNA, Neoplasm / drug effects. Humans. MAP Kinase Kinase 4. Tumor Cells, Cultured

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  • (PMID = 12860462.001).
  • [ISSN] 1368-7646
  • [Journal-full-title] Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
  • [ISO-abbreviation] Drug Resist. Updat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 49820
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / Proto-Oncogene Proteins c-jun; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
  • [Number-of-references] 86
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28. Chow KC, Lu MP, Wu MT: Expression of dihydrodiol dehydrogenase plays important roles in apoptosis- and drug-resistance of A431 squamous cell carcinoma. J Dermatol Sci; 2006 Mar;41(3):205-12
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  • [Title] Expression of dihydrodiol dehydrogenase plays important roles in apoptosis- and drug-resistance of A431 squamous cell carcinoma.
  • BACKGROUND: Dihydrodiol dehydrogenase (DDH) is a member of the aldo-keto reductases superfamily which may be involved in normal detoxification process of environmental mutagenic hazards like polycyclic aromatic hydrocarbons (PAH).
  • Previous clinical studies have demonstrated the over-expression of DDH in various types of cancers, including cutaneous squamous cell carcinoma (SCC), and its correlation with tumor progression and grave prognosis.
  • METHODS: DDH expression in SCC A431 cell line was examined by quantitative real-time PCR and immunoblotting.
  • RESULTS: DDH was found highly expressed by SCC A431 cells, which was barely detectable in other normal or malignant cutaneous cells, including keratinocytes, fibroblast, and basal cell carcinoma cell line.
  • RNAi Inhibition of DDH expression in A431 cells led to increased sensitivity to UVB-induced apoptosis and cytotoxicity of bleomycin treatment.
  • CONCLUSION: DDH may play important roles in tumor progression of SCC via induction of apoptosis- and drug-resistance.
  • [MeSH-major] Apoptosis. Carcinoma, Squamous Cell / drug therapy. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Oxidoreductases / biosynthesis
  • [MeSH-minor] Bleomycin / pharmacology. Caspase 3. Caspases / metabolism. Cell Line. Cell Line, Tumor. Disease Progression. Fibroblasts / metabolism. Humans. In Situ Nick-End Labeling. Keratinocytes / metabolism. Models, Statistical. Polycyclic Hydrocarbons, Aromatic / metabolism. Prognosis. RNA Interference. Skin Neoplasms / drug therapy. Skin Neoplasms / enzymology. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. Ultraviolet Rays. Up-Regulation

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  • (PMID = 16361083.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Polycyclic Hydrocarbons, Aromatic; 0 / Tetrazolium Salts; 0 / Thiazoles; 11056-06-7 / Bleomycin; 298-93-1 / thiazolyl blue; EC 1.- / Oxidoreductases; EC 1.3.1.20 / trans-1,2-dihydrobenzene-1,2-diol dehydrogenase; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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29. Jimeno A, Hidalgo M: Blockade of epidermal growth factor receptor (EGFR) activity. Crit Rev Oncol Hematol; 2005 Mar;53(3):179-92
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  • The rapidly expanding knowledge of the pathogenesis of cancer at the molecular level is providing new targets for drug discovery and development.
  • The key role that EGFR plays in the intracellular transduction of environmental variations and the maintenance of cellular homeostasis explains the dependence that many tumor types have on this pathway, and the pivotal role that it plays in the development of malignant features such as uncontrolled proliferation, augmented invasion, and the ability to escape apoptosis.
  • An enormous body of knowledge has been gathered in the past 20 years that has enabled the development of rationally designed EGFR-targeted therapies, and the results of their clinical evaluation are now becoming available.
  • The lack of positive results of some of these trials has highlighted the need for a robust preclinical knowledge in order to efficiently select patients for therapy, and have prompted the implementation of novel trial designs with rational endpoints.
  • [MeSH-major] Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Drug Design. Drug Resistance, Neoplasm. Humans. Treatment Outcome

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  • (PMID = 15718144.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 122
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30. Dasanu CA, Alexandrescu DT: Risk of additional cancers in untreated and treated hairy cell leukemia patients. Expert Opin Pharmacother; 2010 Jan;11(1):41-50
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  • [Title] Risk of additional cancers in untreated and treated hairy cell leukemia patients.
  • IMPORTANCE OF THE FIELD: One of the feared events encountered in hairy cell leukemia (HCL) survivors is the subsequent development of a malignant neoplasm.
  • The increased incidence of second cancers in HCL has been documented in large epidemiologic studies conducted in various locations on the globe.
  • AREAS COVERED IN THIS REVIEW: The authors explore the current clinico-epidemiologic evidence, as well as the immune alterations, that link HCL and its therapies to the development of second cancers.
  • WHAT THE READER WILL GAIN: Although HCL patients could develop both HCL and secondary malignancies because of a shared genetic predisposition, a common environmental carcinogen, or not yet identified infectious agents, multiple immune defects documented in HCL might play an important role in second carcinogenesis.
  • Furthermore, the 'gold standards' of HCL therapy - cladribine and pentostatin - are associated with profound and prolonged suppression of the CD4(+) T-lymphocyte counts, often in excess of 2 - 3 years.
  • And while there is no clear-cut evidence that pentostatin or interferon-alpha play an established role in generation of an excess of second cancers in HCL, the safety of cladribine, the preferred agent by a majority of clinicians worldwide, in this regard is a still largely unsettled issue.
  • TAKE-HOME MESSAGE: Therefore, it remains to be seen if the immune deficiencies induced by the HCL therapies and their consequences can be offset by the benefit conferred by controlling the leukemic process.
  • [MeSH-major] Cladribine / therapeutic use. Leukemia, Hairy Cell / drug therapy. Neoplasms, Second Primary / complications. Pentostatin / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Female. Humans. Incidence. Male. Neoplasm Recurrence, Local

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  • (PMID = 20001428.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 395575MZO7 / Pentostatin; 47M74X9YT5 / Cladribine
  • [Number-of-references] 54
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31. Rajput A, Koterba AP, Kreisberg JI, Foster JM, Willson JK, Brattain MG: A novel mechanism of resistance to epidermal growth factor receptor antagonism in vivo. Cancer Res; 2007 Jan 15;67(2):665-73
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  • Epidermal growth factor receptor (EGFR) is widely expressed in a number of solid tumors including colorectal cancers.
  • We have elucidated the role of constitutive EGFR signaling in malignant progression by stably transfecting colon cancer cells with a human transforming growth factor-alpha cDNA (a ligand for EGFR) under repressible control by tetracycline.
  • We show that constitutive expression of transforming growth factor-alpha and its subsequent constitutive activation of EGFR allows for cancer cell survival in response to environmental stress in vitro and in vivo as well.
  • This novel escape mechanism is a possible explanation of why anti-EGFR therapies have shown disappointing results in clinical trials.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Cell Growth Processes. Cell Line, Tumor. Colonic Neoplasms / drug therapy. Colonic Neoplasms / enzymology. Colonic Neoplasms / genetics. Drug Resistance, Neoplasm. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Immunohistochemistry. MAP Kinase Signaling System / drug effects. Mice. Mice, Inbred BALB C. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, ErbB-2 / metabolism. Signal Transduction. Transfection. Transforming Growth Factor alpha / antagonists & inhibitors. Transforming Growth Factor alpha / genetics. Transforming Growth Factor alpha / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 17234777.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / CA34432; United States / NCI NIH HHS / CA / CA54807
  • [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 / Morpholines; 0 / Transforming Growth Factor alpha; C78W1K5ASF / Canertinib; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; 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 / Extracellular Signal-Regulated MAP Kinases
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32. Gallardo-Williams MT, Chapin RE, King PE, Moser GJ, Goldsworthy TL, Morrison JP, Maronpot RR: Boron supplementation inhibits the growth and local expression of IGF-1 in human prostate adenocarcinoma (LNCaP) tumors in nude mice. Toxicol Pathol; 2004 Jan-Feb;32(1):73-8
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  • PSA is used as a well-established marker of prostate cancer.
  • The involvement of PSA in several early events leading to the development of malignant prostate tumors has made it a target for prevention and intervention.
  • Circulating IGF-1 levels were not different among groups, though expression of IGF-1 in the tumors was markedly reduced by boron treatment, which we have shown by immunohistochemistry.
  • [MeSH-major] Adenocarcinoma / drug therapy. Boric Acids / administration & dosage. Dietary Supplements. Enzyme Inhibitors / administration & dosage. Insulin-Like Growth Factor I / metabolism. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Cell Line, Tumor. Humans. Male. Mice. Mice, Nude. Neoplasm Transplantation. Prostate-Specific Antigen / antagonists & inhibitors. Transplantation, Heterologous. Xenograft Model Antitumor Assays


33. Harris RE: Cyclooxygenase-2 (cox-2) and the inflammogenesis of cancer. Subcell Biochem; 2007;42:93-126
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  • [Title] Cyclooxygenase-2 (cox-2) and the inflammogenesis of cancer.
  • Cohesive scientific evidence from molecular, animal, and human investigations supports the hypothesis that aberrant induction of COX-2 and up-regulation of the prostaglandin cascade play a significant role in carcinogenesis, and reciprocally, blockade of the process has strong potential for cancer prevention and therapy.
  • Supporting evidence includes the following: [1] expression of constitutive COX-2-catalyzed prostaglandin biosynthesis is induced by most cancer-causing agents including tobacco smoke and its components (polycylic aromatic amines, heterocyclic amines, nitrosamines), essential polyunsaturated fatty acids (unconjugated linoleic acid), mitogens, growth factors, proinflammatory cytokines, microbial agents, tumor promoters, and other epigenetic factors, [2] COX-2 expression is a characteristic feature of all premalignant neoplasms, [3] COX-2 expression is a characteristic feature of all malignant neoplasms, and expression intensifies with stage at detection and cancer progression and metastasis, [4] all essential features of carcinogenesis (mutagenesis, mitogenesis, angiogenesis, reduced apoptosis, metastasis, and immunosuppression) are linked to COX-2-driven prostaglandin (PGE-2) biosynthesis, [5] animal studies show that COX-2 up-regulation (in the absence of genetic mutations) is sufficient to stimulate the transformation of normal cells to invasive cancer and metastatic disease, [6] non-selective COX-2 inhibitors, such as aspirin and ibuprofen, reduce the risk of human cancer and precancerous lesions, and [7] selective COX-2 inhibitors, such as celecoxib, reduce the risk of human cancer and precancerous lesions at all anatomic sites thus far investigated.
  • Results confirming that COX-2 blockade is effective for both cancer prevention and therapy have been tempered by observations that some COX2 inhibitors pose a risk to the cardiovascular system, and more studies are needed in order to determine if certain of these drugs can be taken at dosages that prevent cancer without increasing cardiovascular risk.
  • It is emphasized that the "inflammogenesis model of cancer" is not mutually exclusive and may in fact be synergistic with the accumulation of somatic mutations in tumor suppressor genes and oncogenes or epigenetic factors in the development of cancer.
  • [MeSH-major] Cyclooxygenase 2 / biosynthesis. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Membrane Proteins / biosynthesis. Neoplasm Proteins / biosynthesis. Neoplasms / enzymology
  • [MeSH-minor] Animals. Carcinogens / toxicity. Cardiovascular Diseases / drug therapy. Cardiovascular Diseases / enzymology. Cardiovascular Diseases / genetics. Cyclooxygenase 2 Inhibitors / therapeutic use. Epigenesis, Genetic / drug effects. Humans. Inflammation / chemically induced. Inflammation / enzymology. Inflammation / genetics. Inflammation / prevention & control. Inflammation Mediators / metabolism. Up-Regulation / drug effects

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  • (PMID = 17612047.001).
  • [ISSN] 0306-0225
  • [Journal-full-title] Sub-cellular biochemistry
  • [ISO-abbreviation] Subcell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Cyclooxygenase 2 Inhibitors; 0 / Inflammation Mediators; 0 / Membrane Proteins; 0 / Neoplasm Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
  • [Number-of-references] 312
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