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Items 1 to 39 of about 39
1. Igawa T, Nagafuji K, Ejima J, Nakasuga K, Ito H, Kaji Y, Miyamoto T, Harada M: Surgical resection of malignant lymphoma in the right atrium after systemic chemotherapy. Intern Med; 2003 Apr;42(4):336-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgical resection of malignant lymphoma in the right atrium after systemic chemotherapy.
  • A 74-year-old man was referred to us for evaluation of a tumor in the right atrium (RA).
  • Based on histological findings of subcutaneous tumors in the right abdominal wall, he was diagnosed as malignant lymphoma (ML), and treated with a THP-COP regimen.
  • Upon completion of first THO-COP therapy, TEE showed marked regression of the mass and division into 3 masses, one of which showed marked floating movement with a small stalk.
  • Resected tumors were necrotic tissues.
  • Serial imaging of cardiac tumor and surgical resection is desirable to decrease the possibility of embolic complication.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Heart Neoplasms / surgery. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Aged. Echocardiography, Transesophageal. Heart Atria. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 12729322.001).
  • [ISSN] 0918-2918
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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2. Hamada S, Ito K, Kanbara T, Yoshii T, Sato K, Sumitomo M, Kimura F, Asano T: [A case of malignant lymphoma mimicking a seminal vesicle tumor]. Hinyokika Kiyo; 2010 Jul;56(7):393-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [A case of malignant lymphoma mimicking a seminal vesicle tumor].
  • Abdominal computed tomography (CT) showed a mass 7 cm in diameter mimicking a seminal vesicle tumor and magnetic resonance imaging showed a heterogeneously enhanced mass with an unclear borderline to the rectum.
  • The differential diagnosis of the lesion included a tumor arising from a seminal vesicle, a local recurrence of rectal cancer, a rectal GIST, and a mesenchymal tumor.
  • Transrectal needle biopsy revealed non-Hodgkin's malignant lymphoma (diffuse large B cell lymphoma).
  • Chest and abdominal CT showed no specific findings except the lesion for the seminal vesicle lesion, but positron emission tomography showed accumulations in the gastrointestinal tract, pleura, and lymph nodes.
  • The patient was thus determined to have stage IV malignant lymphoma and was given two courses of combination chemotherapy including RCHOP.
  • The tumor responded to one course, but the patient died of neutropenic sepsis during the second course.
  • [MeSH-major] Genital Neoplasms, Male / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Seminal Vesicles

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  • (PMID = 20724815.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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3. Kanzawa T, Kondo Y, Ito H, Kondo S, Germano I: Induction of autophagic cell death in malignant glioma cells by arsenic trioxide. Cancer Res; 2003 May 1;63(9):2103-8
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  • [Title] Induction of autophagic cell death in malignant glioma cells by arsenic trioxide.
  • Laboratory data suggest that As(2)O(3) induces apoptosis or cell differentiation of hematopoietic or solid tumor cells.
  • In this study, we investigated the in vitro effect of As(2)O(3) on cell growth inhibition and cell death mechanisms in human glioma cells.
  • As(2)O(3) significantly inhibited the proliferation of all six of the glioma cell lines (U373, U87, U251, GB1, A-172, and T98G) tested in this study in a dose-dependent manner.
  • The IC(50) of As(2)O(3) for all of the tumor cell lines was <2 micro M.
  • Treatment with 2 micro M As(2)O(3) induced G(2)/M arrest in all of the glioma cell lines.
  • Autophagy (programmed cell death type II), but not apoptosis (programmed cell death type I), was detected by electron microscopy in U-373-MG cells treated with 2 micro M As(2)O(3).
  • Caspase inhibitors did not halt As(2)O(3)-induced cell death.
  • These findings suggest that As(2)O(3) at a clinically safe concentration may be an effective chemotherapeutic agent for malignant gliomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / pharmacology. Glioma / drug therapy. Macrolides. Oxides / pharmacology
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Anti-Bacterial Agents / pharmacology. Apoptosis / drug effects. Autophagy / drug effects. Caspase Inhibitors. Cell Division / drug effects. Cytoplasm / drug effects. Cytoplasm / metabolism. Drug Interactions. Enzyme Inhibitors / pharmacology. G2 Phase / drug effects. Humans. Mitosis / drug effects. Tumor Cells, Cultured

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  • (PMID = 12727826.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Macrolides; 0 / Oxides; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 88899-55-2 / bafilomycin A1; S7V92P67HO / arsenic trioxide
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4. Ito A, Fujioka M, Yoshida T, Wakamatsu K, Ito S, Yamashita T, Jimbow K, Honda H: 4-S-Cysteaminylphenol-loaded magnetite cationic liposomes for combination therapy of hyperthermia with chemotherapy against malignant melanoma. Cancer Sci; 2007 Mar;98(3):424-30
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  • [Title] 4-S-Cysteaminylphenol-loaded magnetite cationic liposomes for combination therapy of hyperthermia with chemotherapy against malignant melanoma.
  • Previously, in order to improve the adsorption of magnetite nanoparticles to target cell surfaces, and generate heat in an alternating magnetic field (AMF) for cancer hyperthermia, we produced hyperthermia using magnetite cationic liposomes (MCL) that have a positive charge at the liposomal surface.
  • In the present study, we constructed 4-S-CAP-loaded MCL (4-S-CAP/MCL), which act as a novel modality, combining melanoma-specific chemotherapy by 4-S-CAP with intracellular hyperthermia mediated by MCL.
  • Significantly higher therapeutic effects were observed in mice treated with the combination therapy mediated by 4-S-CAP/MCL plus AMF irradiation compared with mice treated with 4-S-CAP/MCL alone (without AMF) or mice treated with hyperthermia alone (MCL + AMF irradiation).
  • These results suggest that this novel therapeutic tool is applicable to the treatment of malignant melanoma.
  • [MeSH-major] Cysteamine / analogs & derivatives. Hyperthermia, Induced. Liposomes / metabolism. Melanoma, Experimental / therapy
  • [MeSH-minor] Animals. Cations. Combined Modality Therapy. Magnetics. Mice. Nanoparticles. Neoplasm Transplantation. Tumor Cells, Cultured

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  • (PMID = 17270032.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cations; 0 / Liposomes; 5UX2SD1KE2 / Cysteamine; 91281-34-4 / 4-S-cysteaminylphenol
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5. Takahashi T, Otani I, Okuda M, Inoue M, Ito K, Sakai M, Koie H, Yamaya Y, Watari T, Sato T, Kanayama K, Tokuriki M: Malignant transformation of T-cell large granular lymphocyte leukemia in a dog. J Vet Med Sci; 2007 Jun;69(6):677-81

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignant transformation of T-cell large granular lymphocyte leukemia in a dog.
  • Clonal rearrangement of the T-cell receptor gene was identified in the peripheral blood, and the dog was therefore diagnosed with LGL chronic leukemia.
  • The dog was subclinical without treatment until hospitalization on day 154, at which point the lymphocytes looked like lymphoblasts and the surface markers changed to CD3-8-.
  • This was regarded as malignant transformation from LGL chronic leukemia to the acute type.
  • Sequential chemotherapy was started, but the dog died on day 190.
  • Necropsy revealed tumor cell infiltration into the heart, skin, and brain.

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  • (PMID = 17611371.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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6. Nakamura Y, Matsumura A, Katsura H, Sakaguchi M, Ito N, Kitahara N, Ose N, Kitaichi M: Cisplatin-based chemotherapy followed by surgery for malignant nonseminomatous germ cell tumor of mediastinum: one institution's experience. Gen Thorac Cardiovasc Surg; 2009 Jul;57(7):363-8
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  • [Title] Cisplatin-based chemotherapy followed by surgery for malignant nonseminomatous germ cell tumor of mediastinum: one institution's experience.
  • OBJECTIVE: The objective of this study was to evaluate the efficacy and safety of cisplatin-based chemotherapy followed by surgery for patients with a malignant nonseminomatous germ cell tumor (NSGCT) of the mediastinum.
  • METHODS: Ten patients with malignant NSGCTs received cisplatin-based induction chemotherapy and then underwent surgery.
  • RESULTS: A partial response to induction chemotherapy was noted in eight patients and no response in two.
  • The induction chemotherapy was tolerated well by all the patients.
  • Each patient underwent complete surgical resection of the residual tumor following chemotherapy.
  • A yolk sac tumor was detected in one patient and malignant teratoma along with a yolk sac tumor in one patient postoperatively.
  • CONCLUSION: Postchemotherapy surgical resection of the residual tumor plays an integral role in the management of patients with NSGCT.
  • The presence of viable tumor cells in the resected specimens is associated with poor survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Mediastinal Neoplasms / drug therapy. Neoadjuvant Therapy. Neoplasms, Germ Cell and Embryonal / drug therapy
  • [MeSH-minor] Bleomycin / administration & dosage. Bleomycin / therapeutic use. Cisplatin / administration & dosage. Cisplatin / therapeutic use. Combined Modality Therapy. Etoposide / administration & dosage. Etoposide / therapeutic use. Humans. Male. Neoplasm, Residual. Prognosis. Survival Analysis

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  • [Cites] J Clin Oncol. 2001 Feb 1;19(3):682-8 [11157018.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):594-603 [9053482.001]
  • [Cites] Urol Clin North Am. 1987 May;14(2):389-98 [2437682.001]
  • [Cites] Ann Thorac Surg. 2008 Feb;85(2):379-84 [18222229.001]
  • [Cites] Ann Thorac Surg. 2008 Feb;85(2):371-8 [18222228.001]
  • [Cites] Surg Today. 1994;24(2):137-41 [8054792.001]
  • [Cites] J Thorac Cardiovasc Surg. 1999 Oct;118(4):692-700 [10504636.001]
  • [Cites] Cancer. 1951 Mar;4(2):265-76 [14821919.001]
  • [Cites] Ann Thorac Surg. 1987 Dec;44(6):578-82 [2446572.001]
  • [Cites] Cancer. 1993 Sep 15;72(6):1894-901 [7689921.001]
  • [Cites] Cancer. 1991 Mar 1;67(5):1305-10 [1703917.001]
  • [Cites] Cancer. 1975 Sep;36(3):1162-8 [1237349.001]
  • [Cites] Jpn J Clin Oncol. 2004 Jul;34(7):386-92 [15342665.001]
  • [Cites] Ann Thorac Surg. 1982 Apr;33(4):333-9 [7073378.001]
  • [Cites] Br J Urol. 1964 Jun;36:SUPPL:1-11 [14184707.001]
  • [Cites] Cancer. 1991 Apr 15;67(8):2049-57 [1848473.001]
  • [Cites] Cancer. 2003 Jan 15;97(2):367-76 [12518361.001]
  • (PMID = 19597926.001).
  • [ISSN] 1863-6705
  • [Journal-full-title] General thoracic and cardiovascular surgery
  • [ISO-abbreviation] Gen Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin; BEP protocol
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7. Igawa S, Watanabe R, Ito I, Murakami H, Takahashi T, Nakamura Y, Tsuya A, Kaira K, Naito T, Endo M, Yamamoto N, Kameya T: Comparison of chemotherapy for unresectable pulmonary high-grade non-small cell neuroendocrine carcinoma and small-cell lung cancer. Lung Cancer; 2010 Jun;68(3):438-45
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  • [Title] Comparison of chemotherapy for unresectable pulmonary high-grade non-small cell neuroendocrine carcinoma and small-cell lung cancer.
  • BACKGROUND: Pulmonary large cell neuroendocrine carcinoma (LCNEC) shares several features with small cell lung carcinoma (SCLC).
  • While the diagnosis of LCNEC by biopsy specimens is challenging, a definitive diagnosis of this highly malignant tumor is critical in unresectable cases to determine the optimal therapeutic strategy.
  • The objective of this study was to assess the efficacy of chemotherapy for unresectable high-grade non-small cell neuroendocrine carcinoma (HNSCNEC) called by us, which likely includes most LCNECs except for combined types, and to compare the efficacy of chemotherapy for HNSCNEC, with that for extended disease SCLC (ED-SCLC).
  • We simultaneously evaluated the clinical response to the chemotherapy and survival time of the 14 HNSCNEC and 77 ED-SCLC patients.
  • RESULTS: The chemotherapy regimens in the 14 patients with unresectable HNSCNEC were platinum-based combination regimens or irinotecan or vinorelbine or docetaxel alone.
  • The chemotherapy regimens in the 77 patients with ED-SCLC were platinum-based combination regimens.
  • We assessed an objective response rate, a one-year survival rate, and median survival time as 50% (7/14), 34% and 10 months, respectively, in the 14 HNSCNEC patients, and as 53% (41/77), 48% and 12.3 months, respectively, in the 77 ED-SCLC patients.
  • CONCLUSION: The clinical efficacy of chemotherapy for unresectable HNSCNECs, including most LCNECs, is comparable to that for ED-SCLC.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Neuroendocrine Tumors / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Camptothecin / administration & dosage. Camptothecin / adverse effects. Camptothecin / analogs & derivatives. Disease Progression. Drug Therapy, Combination. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Platinum Compounds / administration & dosage. Platinum Compounds / adverse effects. Survival Analysis. Taxoids / administration & dosage. Taxoids / adverse effects. Vinblastine / administration & dosage. Vinblastine / adverse effects. Vinblastine / analogs & derivatives

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  • [Copyright] Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19699548.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Platinum Compounds; 0 / Taxoids; 15H5577CQD / docetaxel; 5V9KLZ54CY / Vinblastine; 7673326042 / irinotecan; Q6C979R91Y / vinorelbine; XT3Z54Z28A / Camptothecin
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8. Kondo H, Takino H, Akino K, Yamasaki H, Yamaguchi Y, Ito M, Eguchi K: Octreotide treatment suppresses malignant somatotrophic pituitary tumor cell growth in rats. Oncol Rep; 2000 Sep-Oct;7(5):965-9
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  • [Title] Octreotide treatment suppresses malignant somatotrophic pituitary tumor cell growth in rats.
  • We have recently established an in vitro cell line (metastatic mGH3) derived from lymph node metastases of the rat pituitary somatotroph.
  • Here we examined the in vivo effects of octreotide, a somatostatin analog, against malignant pituitary tumors.
  • Four rats were treated with octreotide three times daily while another group of four rats were treated with saline only.
  • After 6 weeks of treatment, histopathological and immunohistological analyses were performed.
  • The tumor weights of rats treated with octreotide were significantly lighter than those of untreated rats.
  • All rats implanted mGH3, but not administered treatment, developed inguinal lymph node metastases, whereas none of those implanted mGH3 and treated with octreotide developed such metastases.
  • The proportion of PCNA-stained tumor cells was higher in tumors of untreated rats than in those of octreotide-treated rats.
  • However, the proportion of apoptotic cells in the tumor was not different between treated and untreated rats.
  • Our results suggest that octreotide might be potentially effective for invasive and malignant human pituitary tumors by regulating the tumor cell cycle.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Growth Hormone / blood. Octreotide / pharmacology. Pituitary Neoplasms / drug therapy
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Division / drug effects. Female. Immunohistochemistry. Neoplasm Transplantation. Rats. Rats, Inbred WF. Tumor Cells, Cultured

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  • (PMID = 10948323.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GREECE
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9002-72-6 / Growth Hormone; RWM8CCW8GP / Octreotide
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9. Suzuki-Uematsu S, Shiraishi K, Ito T, Adachi N, Inage Y, Taeda Y, Ueki H, Ohtani H: Malignant phyllodes tumor composed almost exclusively of a fibrosarcomatous component: a case report and review of malignant phyllodes tumors with metastases. Breast Cancer; 2010 Jul;17(3):218-24
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  • [Title] Malignant phyllodes tumor composed almost exclusively of a fibrosarcomatous component: a case report and review of malignant phyllodes tumors with metastases.
  • Here we present a case of malignant phyllodes tumor which was composed almost exclusively of a fibrosarcomatous component.
  • A 52-year-old Japanese female noted a rapid increase of her right breast tumor.
  • The tumor, 10 x 10 cm in the largest dimension, had somewhat of a pushing margin, and showed a flesh-like appearance with marked necrosis.
  • Microscopically, the tumor showed proliferation of atypical ovoid- or spindle-shaped cells in a myxoid matrix.
  • Multiple sectioning revealed that the tumor had only focal occurrence of elongated tubular structures, and the occurrence of a small component of benign phyllodes tumor, leading to the aforementioned final diagnosis.
  • Spindle cell carcinoma was excluded on the basis of the HE findings and the lack of immunoreactivity for cytokeratin when using a broad spectrum antibody mixture.
  • Although the patient received adjuvant chemotherapy, no responsiveness was obtained.
  • We reviewed 15 malignant phyllodes tumors with metastases reported in Japan.
  • The estimated 2.2-year survival rate following detection of metastasis was 11%, thus confirming the aggressiveness of the disease.
  • [MeSH-major] Breast Neoplasms / pathology. Fibrosarcoma / pathology. Lung Neoplasms / secondary. Phyllodes Tumor / secondary
  • [MeSH-minor] Female. Humans. Mastectomy, Simple. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 19350353.001).
  • [ISSN] 1880-4233
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
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10. Ito H, Aoki H, Kühnel F, Kondo Y, Kubicka S, Wirth T, Iwado E, Iwamaru A, Fujiwara K, Hess KR, Lang FF, Sawaya R, Kondo S: Autophagic cell death of malignant glioma cells induced by a conditionally replicating adenovirus. J Natl Cancer Inst; 2006 May 3;98(9):625-36
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  • [Title] Autophagic cell death of malignant glioma cells induced by a conditionally replicating adenovirus.
  • BACKGROUND: Conditionally replicating adenoviruses (CRAds) can be engineered to replicate selectively in cancer cells and cause cancer-specific cell lysis; thus they are considered a promising cancer therapy.
  • METHODS: To elucidate the mechanisms by which CRAds induce cancer-specific cell death, we infected normal human fibroblasts (MRC5, telomerase negative), human malignant glioma (U373-MG and U87-MG), human cervical cancer (HeLa), and human prostate cancer (PC3) cells (all telomerase positive) with CRAds regulated by the human telomerase reverse transcriptase promoter (hTERT-Ad) or control nonreplicating adenoviruses (Ad-GFP).
  • Nonapoptotic autophagy was assessed in Ad-GFP- and hTERT-Ad-infected cells by examining cell morphology, the development of acidic vesicular organelles, and the conversion of microtubule-associated protein 1 light chain 3 from the cytoplasmic form to the autophagosome membrane form; signaling via mammalian target of rapamycin (mTOR), an autophagy-associated molecule, was monitored by western blot analysis.
  • RESULTS: hTERT-Ad induced tumor-specific autophagic cell death in tumor cells and in subcutaneous gliomas. hTERT-Ad-induced autophagy was associated with hTERT-Ad infection kinetics.
  • The mTOR signaling pathway was suppressed in tumor cells and in subcutaneous gliomas treated with hTERT-Ad compared with GFP-Ad or no treatment as shown by reduced phosphorylation of mTOR's downstream target p70S6 kinase (p70S6K).
  • hTERT-Ad treatment of mice (n = 7) slowed growth of subcutaneous gliomas (mean tumor volume = 39 mm3, 95% confidence interval [CI] = 23 to 54 mm3) compared with GFP-Ad treatment (n = 7) (mean tumor volume = 200 mm3, 95% CI = 149 to 251 mm3) at day 7 (volume difference = 161 mm3, 95% CI = 126 to 197 mm3; P < .001).
  • Mice carrying intracranial tumors that were treated with three intratumoral injections of hTERT-Ad survived longer (53 days) than after treatment with GFP-Ad (29 days) (seven mice per group, difference = 24 days, 95% CI = 20 to 28 days; P < .001).
  • CONCLUSIONS: hTERT-Ad may kill telomerase-positive cancer cells by inducing autophagic cell death.
  • [MeSH-major] Adenoviridae. Antineoplastic Agents / pharmacology. Autophagy / drug effects. Brain Neoplasms / drug therapy. DNA-Binding Proteins / pharmacology. Glioma / drug therapy. Telomerase / pharmacology
  • [MeSH-minor] Animals. Blotting, Western. Cell Cycle. Cell Line, Tumor. Female. Fibroblasts. HeLa Cells. Humans. Injections, Intralesional. Mice. Mice, Nude. Uterine Cervical Neoplasms / drug therapy. Uterine Cervical Neoplasms / pathology

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  • [ErratumIn] J Natl Cancer Inst. 2006 Jun 7;98(11):796
  • (PMID = 16670388.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-088936; United States / NCI NIH HHS / CA / CA-108558; United States / NCI NIH HHS / CA / CA-16672
  • [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 / DNA-Binding Proteins; EC 2.7.7.49 / Telomerase
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11. Yamashita K, Nakazato H, Ito K, Ougolkov A, Takahashi Y, Mai M, Minamoto T: Effect of adjuvant immunochemotherapy with PSK for colon cancer patients showing oncogenic β-catenin activation in primary tumor. J Clin Oncol; 2004 Jul 15;22(14_suppl):3650

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  • [Title] Effect of adjuvant immunochemotherapy with PSK for colon cancer patients showing oncogenic β-catenin activation in primary tumor.
  • : 3650 Background & Aim: β-catenin translocated into cell nucleus functions as an oncogene transactivating a number of oncogenes.
  • + PSK 3000mg/day; p.o.) or chemotherapy (5-Fu 200mg/day; p.o.) alone after curative resection of the cancer.
  • METHODS: Subjecting 202 colon cancer patients, we determined the patterns of β-catenin activation in primary tumors and correlated data with survival of patients undergoing different protocols of adjuvant therapies.
  • RESULTS: In 53% of patients, we found two distinct patterns of β-catenin activation on the basis of its nuclear accumulation (NA) in tumor cells: diffuse NA (NAd) in 89 cases (44%) and selective NA at tumor invasion front (NAinv) in 18 (9%).
  • While NAinv pattern was significantly correlated with advanced Dukes' stage, resulting in extremely unfavorable clinical outcome, no significant difference in survival was observed between the two groups of the patients underwent different therapy protocols.
  • In patients with NAd pattern of β-catenin activation, immunochemotherapy significantly improved 5-year cancer death- (5yCDS) and over all (5yOAS) survival rates in comparison with those with chemotherapy alone (n=55) (Table).
  • Multivariate analysis determined Dukes' tumor stage and administrating PSK as independent prognosis factors in these patients.
  • CONCLUSION: Our results indicates that of different patterns of β-catenin activation that determine malignant potential of tumors, the presence of NAd pattern could identify patients with colon cancer better responding to the immunotherapy with PSK.

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  • (PMID = 28014589.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Kanzawa T, Germano IM, Komata T, Ito H, Kondo Y, Kondo S: Role of autophagy in temozolomide-induced cytotoxicity for malignant glioma cells. Cell Death Differ; 2004 Apr;11(4):448-57
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  • [Title] Role of autophagy in temozolomide-induced cytotoxicity for malignant glioma cells.
  • To date, however, little is known about the role of autophagy in cancer therapy.
  • In this study, we present that temozolomide (TMZ), a new alkylating agent, inhibited the viability of malignant glioma cells in a dose-dependent manner and induced G2/M arrest.
  • At a clinically achievable dose (100 microM), TMZ induced autophagy, but not apoptosis in malignant glioma cells.
  • After the treatment with TMZ, microtubule-associated protein light-chain 3 (LC3), a mammalian homologue of Apg8p/Aut7p essential for amino-acid starvation-induced autophagy in yeast, was recruited on autophagosome membranes.
  • On the other hand, bafilomycin A1, a specific inhibitor of vacuolar type H(+)-ATPase, that prevents autophagy at a late stage by inhibiting fusion between autophagosomes and lysosomes, sensitized tumor cells to TMZ by inducing apoptosis through activation of caspase-3 with mitochondrial and lysosomal membrane permeabilization, while LC3 localization pattern stayed the same.
  • These results indicate that TMZ induces autophagy in malignant glioma cells.
  • Application of an autophagy inhibitor that works after the association of LC3 with autophagosome membrane, such as bafilomycin A1, is expected to enhance the cytotoxicity of TMZ for malignant gliomas.
  • [MeSH-major] Adenine / analogs & derivatives. Antineoplastic Agents, Alkylating / pharmacology. Autophagy / physiology. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Glioma / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. Macrolides / pharmacology. Microtubule-Associated Proteins / metabolism. Organelles / metabolism

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  • (PMID = 14713959.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1RO1 CA88936
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Macrolides; 0 / Microtubule-Associated Proteins; 0 / light chain 3, human; 5142-23-4 / 3-methyladenine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 88899-55-2 / bafilomycin A1; JAC85A2161 / Adenine
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13. Hamaguchi N, Hamada H, Miyoshi S, Irifune K, Ito R, Miyazaki T, Higaki J: In vitro and in vivo therapeutic efficacy of the PPAR-γ agonist troglitazone in combination with cisplatin against malignant pleural mesothelioma cell growth. Cancer Sci; 2010 Sep;101(9):1955-64
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  • [Title] In vitro and in vivo therapeutic efficacy of the PPAR-γ agonist troglitazone in combination with cisplatin against malignant pleural mesothelioma cell growth.
  • Malignant pleural mesothelioma (MPM), an aggressive and refractory tumor type, is increasing in frequency throughout the world.
  • Peroxisome proliferator activated receptor-γ (PPAR-γ) agonists have anticancer activity against several cancer cell lines in vitro and in vivo.
  • However, there have been no reports that PPAR-γ agonists induce growth inhibition of MPM cell lines.
  • In this study, we investigated the inhibitory effect of a PPAR-γ agonist in combination with an anticancer agent on MPM cell growth in vitro and in vivo.
  • We examined the therapeutic efficacy of the PPAR-γ agonist troglitazone (TGZ) in combination with cisplatin against a human MPM cell line, both in vitro and orthotopically inoculated into severe combined immunodeficient (SCID) mice.
  • Troglitazone (TGZ) alone inhibited MPM cell growth in vitro in a dose-dependent manner via induction of G1 cell cycle arrest and apoptosis.
  • The combination of TGZ and cisplatin showed an additive inhibitory effect on MPM cell growth compared to treatment with either individual drug.
  • Treatment with 500 mg/kg or 1000 mg/kg TGZ effectively inhibited the production of thoracic tumors and pleural effusion in EHMES-10 cell-bearing SCID mice.
  • Moreover, treatment with 500 mg/kg TGZ in combination with 3 mg/kg cisplatin more effectively prolonged survival compared to treatment with either individual drug.
  • These results suggest that TGZ in combination with cisplatin may become a novel therapy for MPM.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Proliferation / drug effects. Mesothelioma / drug therapy. Pleural Neoplasms / drug therapy. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Chromans / administration & dosage. Chromans / pharmacology. Cisplatin / administration & dosage. Cisplatin / pharmacology. Dose-Response Relationship, Drug. Drug Synergism. Flow Cytometry. G1 Phase / drug effects. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Mice. Mice, SCID. PPAR gamma / agonists. PPAR gamma / metabolism. Thiazolidinediones / administration & dosage. Thiazolidinediones / pharmacology

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  • [Copyright] © 2010 Japanese Cancer Association.
  • (PMID = 20608936.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chromans; 0 / Ki-67 Antigen; 0 / PPAR gamma; 0 / Thiazolidinediones; I66ZZ0ZN0E / troglitazone; Q20Q21Q62J / Cisplatin
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14. Kawaguchi K, Murakami H, Taniguchi T, Fujii M, Kawata S, Fukui T, Kondo Y, Osada H, Usami N, Yokoi K, Ueda Y, Yatabe Y, Ito M, Horio Y, Hida T, Sekido Y: Combined inhibition of MET and EGFR suppresses proliferation of malignant mesothelioma cells. Carcinogenesis; 2009 Jul;30(7):1097-105
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  • [Title] Combined inhibition of MET and EGFR suppresses proliferation of malignant mesothelioma cells.
  • Malignant pleural mesothelioma (MPM) is an aggressive neoplasm associated with asbestos exposure.
  • To determine whether the lack of response of MET inhibitors was due to cooperation with other RTKs, we determined activation status of MET and other RTKs, including epidermal growth factor receptor (EGFR) family of 20 MPM cell lines, and tested whether dual RTK inhibition is an effective therapeutic strategy.
  • We detected MET upregulation and phosphorylation (thus indicating activation) in 14 (70%) and 13 (65%) cell lines, but treatment with MET-specific inhibitors showed weak or modest effect of suppression in most of the cell lines.
  • Combination of MET and EGFR inhibitors triggered stronger inhibition on cell proliferation and invasion of MPM cells than that of each in vitro.
  • These results indicated that coactivation of RTKs was essential in mesothelioma cell proliferation and/or survival, thus suggesting that simultaneous inhibition of RTKs may be a more effective strategy for the development of molecular target therapy for MPM.
  • [MeSH-major] Cell Proliferation / drug effects. Mesothelioma / metabolism. Pleural Neoplasms / metabolism. Proto-Oncogene Proteins c-met / metabolism. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Neoplasm Invasiveness. Phosphorylation. Receptor, ErbB-2 / antagonists & inhibitors. Receptor, ErbB-2 / metabolism. Receptor, Platelet-Derived Growth Factor beta / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor beta / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology. Up-Regulation


15. Sakuma M, Otsuki T, Yoshinaga K, Utsunomiya H, Nagase S, Takano T, Niikura H, Ito K, Otomo K, Tase T, Watanabe Y, Yaegashi N: Malignant transformation arising from mature cystic teratoma of the ovary: a retrospective study of 20 cases. Int J Gynecol Cancer; 2010 Jul;20(5):766-71
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  • [Title] Malignant transformation arising from mature cystic teratoma of the ovary: a retrospective study of 20 cases.
  • OBJECTIVES: Mature cystic teratoma (MCT) of the ovary rarely undergoes malignant transformation (MT).
  • Malignant transformation carries a significantly worse prognosis than epithelial ovarian cancer, regardless of whether postoperative chemotherapy or radiotherapy is applied.
  • The rarity of this tumor has posed a significant challenge to developing standardized postoperative management protocols.
  • The aim of this study was to review our experience with MT and to describe our current treatment practices.
  • Fifteen patients had squamous cell carcinoma (SCC), and 5 patients had other histological subtypes.
  • Eleven patients received adjuvant treatment: 8 were treated with chemotherapy, 2 with concurrent chemoradiation therapy, and 1 with radiation therapy.
  • Platinum-based chemotherapy was the first-line regimen.
  • Significant correlations between overall survival and age, stage, and residual tumor were presented (P = 0.044, P = 0.0107, P < 0.0001, respectively).
  • Four patients, however, were treated with adjuvant chemotherapy or concurrent chemoradiation therapy and survived more than 1 year.
  • Two cases of SCC treated with combination platinum/taxane chemotherapy temporarily responded.
  • In the other 2 cases of SCC, concurrent chemoradiation therapy with nedaplatin also resulted in tumor regression.
  • Adjuvant treatment has not been standardized, although our experience supports the use of combination platinum/taxane chemotherapy.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Ovarian Neoplasms / pathology. Teratoma / pathology
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic. Female. Humans. Middle Aged. Prognosis. Retrospective Studies

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  • (PMID = 20973266.001).
  • [ISSN] 1525-1438
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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16. Kanzawa T, Germano IM, Kondo Y, Ito H, Kyo S, Kondo S: Inhibition of telomerase activity in malignant glioma cells correlates with their sensitivity to temozolomide. Br J Cancer; 2003 Sep 1;89(5):922-9
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  • [Title] Inhibition of telomerase activity in malignant glioma cells correlates with their sensitivity to temozolomide.
  • Temozolomide (TMZ, 3,4-dihydro-3-methyl-4-oxoimidazo [5,1-d]-as-tetrazine-8-carboxamide) is a new alkylating agent with promising antitumour efficacy for malignant gliomas.
  • However, it is unknown if TMZ sensitivity of malignant glioma cells correlates with telomerase.
  • In this study, using malignant glioma cells with low levels of AGT (U373-MG and U87-MG) and high levels of AGT (T98G), we investigated the association among AGT, telomerase, and TMZ sensitivity.
  • U373-MG and U87-MG cells were sensitive to TMZ (IC(50) for a 2-day treatment=100 microM), while T98G cells were resistant to TMZ (IC(50) for a 2-day treatment >500 microM).
  • Treatment with TMZ (100 microM) suppressed telomerase activity in U373-MG and U87-MG cells in a time-dependent manner, but not in T98G cells.
  • These findings suggest that response of malignant glioma cells to TMZ can be monitored by reduction in telomerase activity.
  • Therefore, quantification of telomerase activity during or after treatment with TMZ may be a useful marker to detect treatment efficacy.

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  • [Cites] J Clin Oncol. 1999 Sep;17(9):2762-71 [10561351.001]
  • [Cites] Biochemistry. 1994 Aug 9;33(31):9045-51 [8049205.001]
  • [Cites] Anticancer Res. 2000 Mar-Apr;20(2A):661-7 [10810337.001]
  • [Cites] Clin Cancer Res. 2000 Jul;6(7):2585-97 [10914698.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4461-7 [10969793.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6531-6 [11103824.001]
  • [Cites] Gene Ther. 2000 Dec;7(24):2071-9 [11223987.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):3053-61 [11306487.001]
  • [Cites] J Cell Physiol. 2001 Aug;188(2):143-60 [11424081.001]
  • [Cites] Cancer Res. 2001 Aug 1;61(15):5796-802 [11479218.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):711-9 [11485929.001]
  • [Cites] J Clin Invest. 2001 Nov;108(10):1541-7 [11714746.001]
  • [Cites] Oncogene. 2002 Feb 28;21(10):1485-92 [11896576.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2388-99 [11981013.001]
  • [Cites] J Biol Chem. 2002 Aug 2;277(31):27748-56 [12019268.001]
  • [Cites] Mol Pharmacol. 2003 Jan;63(1):192-202 [12488552.001]
  • [Cites] Science. 1985 Nov 1;230(4725):511-7 [2996137.001]
  • [Cites] Cell. 1987 Dec 24;51(6):1079-90 [3319186.001]
  • [Cites] Genome. 1989;31(2):553-60 [2698831.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5368-72 [2164681.001]
  • [Cites] Science. 1994 Dec 23;266(5193):2011-5 [7605428.001]
  • [Cites] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412.001]
  • [Cites] Ann Oncol. 1995 Apr;6(4):389-93 [7619755.001]
  • [Cites] Science. 1995 Sep 1;269(5228):1236-41 [7544491.001]
  • [Cites] Oncogene. 1995 Sep 7;11(5):893-8 [7675448.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1994;59:307-15 [7587082.001]
  • [Cites] J Biol Chem. 1996 Jun 7;271(23):13916-24 [8662860.001]
  • [Cites] Br J Cancer. 1996 Oct;74(7):1030-6 [8855970.001]
  • [Cites] Curr Opin Oncol. 1996 Jan;8(1):66-71 [8868103.001]
  • [Cites] Science. 1997 Feb 14;275(5302):973-7 [9020079.001]
  • [Cites] Cell. 1997 Mar 21;88(6):875-84 [9118230.001]
  • [Cites] Science. 1997 Aug 15;277(5328):955-9 [9252327.001]
  • [Cites] Cell. 1997 Aug 22;90(4):785-95 [9288757.001]
  • [Cites] Cancer Res. 1998 May 15;58(10):2117-25 [9605755.001]
  • [Cites] Oncogene. 1998 Apr 30;16(17):2243-8 [9619833.001]
  • [Cites] FASEB J. 1998 Jul;12(10):801-11 [9657520.001]
  • [Cites] Mol Pharmacol. 1998 Aug;54(2):334-41 [9687575.001]
  • [Cites] Clin Cancer Res. 1997 Apr;3(4):579-85 [9815723.001]
  • [Cites] Cancer Res. 1999 Feb 1;59(3):551-7 [9973199.001]
  • [Cites] Cancer Res. 1999 Feb 15;59(4):826-30 [10029071.001]
  • [Cites] FASEB J. 1999 Jun;13(9):1047-54 [10336887.001]
  • [Cites] Gene. 1999 Sep 17;237(2):281-302 [10521653.001]
  • [Cites] EMBO J. 1992 Oct;11(10):3663-71 [1356762.001]
  • [Cites] Eur J Cancer. 1993;29A(7):940-2 [8499146.001]
  • [Cites] Br J Cancer. 1993 Jun;67(6):1299-302 [8512814.001]
  • [Cites] Cancer Res. 1994 Jul 15;54(14):3793-9 [8033099.001]
  • [Cites] Nucleic Acids Res. 2000 Feb 1;28(3):669-77 [10637317.001]
  • (PMID = 12942127.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088936; United States / NCI NIH HHS / CA / 1R01 CA88936
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / RNA, Messenger; 0 / Transcription Factors; 19916-73-5 / O(6)-benzylguanine; 5Z93L87A1R / Guanine; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2394478
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17. Maeda S, Kagami Y, Ogura M, Taji H, Suzuki R, Kondo E, Asakura S, Takeuchi T, Miura K, Ando M, Nakamura S, Ito T, Kinoshita T, Ueda R, Morishima Y: CD34+-selected autologous peripheral blood stem cell transplantation conditioned with total body irradiation for malignant lymphoma: increased risk of infectious complications. Int J Hematol; 2001 Aug;74(2):214-21
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  • [Title] CD34+-selected autologous peripheral blood stem cell transplantation conditioned with total body irradiation for malignant lymphoma: increased risk of infectious complications.
  • Although high-dose chemotherapy with autologous peripheral blood stem cell transplantation (autoPBSCT) has been shown or confirmed to be an effective treatment for high-risk and relapsed non-Hodgkin's lymphoma (NHL), relapse after autoPBSCT remains a serious problem.
  • In a clinical trial to overcome relapse, we adopted a treatment plan in which PBSCs purified in vitro to CD34+ cells to deplete tumor cells (CD34+ autoPBSCT), total body irradiation (TBI) of 1200 cGy, and melphalan, 180 mg/m2, were used as a preconditioning regimen.
  • After day 30 posttransplantation, 6 of 10 patients treated with the TBI regimen developed 11 infectious complications in total, compared with only 1 of 8 patients treated with the non-TBI regimen and 4 of 19 patients given unselected autoPBSCT.
  • [MeSH-major] Antigens, CD34. Hematopoietic Stem Cell Transplantation / methods. Infection / etiology. Lymphoma / therapy. Transplantation Conditioning / methods. Whole-Body Irradiation / adverse effects
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Combined Modality Therapy / methods. Female. Humans. Male. Middle Aged. Risk Factors. Transplantation, Autologous / adverse effects. Transplantation, Autologous / methods. Transplantation, Autologous / standards. Treatment Outcome

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  • [Cites] Br J Haematol. 1997 Jun;97(4):881-8 [9217192.001]
  • [Cites] Bone Marrow Transplant. 1997 Nov;20(10 ):827-34 [9404922.001]
  • [Cites] J Clin Oncol. 1992 Jun;10(6):936-41 [1588372.001]
  • [Cites] Br J Haematol. 1998 Feb;100(2):348-50 [9488625.001]
  • [Cites] J Clin Oncol. 1992 Nov;10(11):1712-22 [1403054.001]
  • [Cites] Bone Marrow Transplant. 1996 May;17(5):715-21 [8733687.001]
  • [Cites] N Engl J Med. 1995 Dec 7;333(23):1540-5 [7477169.001]
  • [Cites] Bone Marrow Transplant. 1995 Sep;16(3):413-25 [8535315.001]
  • [Cites] Blood. 1995 Jul 1;86(1):390-7 [7540888.001]
  • [Cites] Bone Marrow Transplant. 1999 Jun;23(12):1309-15 [10414921.001]
  • [Cites] Bone Marrow Transplant. 1993 Nov;12(5):469-75 [7905331.001]
  • [Cites] Transplantation. 1994 May 27;57(10):1465-73 [7910987.001]
  • [Cites] Blood. 1999 Dec 15;94(12):4029-35 [10590046.001]
  • [Cites] N Engl J Med. 1997 May 1;336(18):1290-7 [9113932.001]
  • [Cites] Am J Pathol. 1987 Nov;129(2):242-56 [3314529.001]
  • [Cites] J Clin Oncol. 1990 Apr;8(4):648-56 [2313334.001]
  • [Cites] J Clin Oncol. 1996 Jan;14(1):214-9 [8558200.001]
  • [Cites] N Engl J Med. 1991 Nov 28;325(22):1525-33 [1944436.001]
  • [Cites] N Engl J Med. 1987 Jun 11;316(24):1493-8 [3295541.001]
  • [Cites] J Clin Oncol. 1994 Jan;12(1):28-36 [7505806.001]
  • [Cites] Br J Haematol. 1999 Feb;104(2):382-91 [10050723.001]
  • [Cites] Bone Marrow Transplant. 1992 Apr;9(4):285-91 [1376185.001]
  • [Cites] Bone Marrow Transplant. 1998 Aug;22(3):307-9 [9720750.001]
  • [Cites] Int J Hematol. 1999 Oct;70(3):193-9 [10561914.001]
  • [Cites] Bone Marrow Transplant. 1999 Jul;24(2):153-61 [10455343.001]
  • [Cites] Blood. 1998 Dec 1;92(11):4464-71 [9834254.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;40 Suppl:S51-7 [9272135.001]
  • [Cites] Blood. 1999 Nov 15;94(10):3325-33 [10552941.001]
  • [Cites] N Engl J Med. 1995 Jan 19;332(3):143-9 [7800006.001]
  • [Cites] Blood. 1997 Jul 15;90(2):850-7 [9226186.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1858-68 [10068658.001]
  • [Cites] J Clin Oncol. 1990 Apr;8(4):638-47 [2313333.001]
  • [Cites] Transplantation. 1980;29(1):61-6 [6989042.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1421-6 [7520769.001]
  • [Cites] Blood. 1999 Jan 15;93(2):467-80 [9885208.001]
  • [Cites] Am J Pathol. 1986 Mar;122(3):531-40 [3513603.001]
  • [Cites] Bone Marrow Transplant. 1991 Oct;8(4):245-51 [1756321.001]
  • (PMID = 11594525.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34
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18. Dewan MZ, Terashima K, Taruishi M, Hasegawa H, Ito M, Tanaka Y, Mori N, Sata T, Koyanagi Y, Maeda M, Kubuki Y, Okayama A, Fujii M, Yamamoto N: Rapid tumor formation of human T-cell leukemia virus type 1-infected cell lines in novel NOD-SCID/gammac(null) mice: suppression by an inhibitor against NF-kappaB. J Virol; 2003 May;77(9):5286-94
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  • [Title] Rapid tumor formation of human T-cell leukemia virus type 1-infected cell lines in novel NOD-SCID/gammac(null) mice: suppression by an inhibitor against NF-kappaB.
  • We established a novel experimental model for human T-cell leukemia virus type 1 (HTLV-1)-induced tumor using NOD-SCID/gammac(null) (NOG) mice.
  • This model is very useful for investigating the mechanism of tumorigenesis and malignant cell growth of adult T-cell leukemia (ATL)/lymphoma, which still remains unclear.
  • Nine HTLV-1-infected cell lines were inoculated subcutaneously in the postauricular region of NOG mice.
  • As early as 2 to 3 weeks after inoculation, seven cell lines produced a visible tumor while two transformed cell lines failed to do so.
  • Five of seven lines produced a progressively growing large tumor with leukemic infiltration of the cells in various organs that eventually killed the animals.
  • Leukemic cell lines formed soft tumors, whereas some transformed cell lines developed into hemorrhagic hard tumors in NOG mice.
  • One of the leukemic cell lines, ED-40515(-), was unable to produce visible tumors in NOD-SCID mice with a common gamma-chain after 2 weeks.
  • In vivo NF-kappaB DNA binding activity of the ED-40515(-) cell line was higher and the NF-kappaB components were changed compared to cells in vitro.
  • Bay 11-7082, a specific and effective NF-kappaB inhibitor, prevented tumor growth at the sites of the primary region and leukemic infiltration in various organs of NOG mice.
  • This in vivo model of ATL could provide a novel system for use in clarifying the mechanism of growth of HTLV-1-infected cells as well as for the development of new drugs against ATL.
  • [MeSH-major] Cell Line, Transformed / transplantation. Disease Models, Animal. Human T-lymphotropic virus 1 / pathogenicity. Leukemia, T-Cell. Lymphoma. Nitriles. Organic Chemicals. Sulfones
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Graft Survival. HTLV-I Infections / complications. Humans. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Mice. Mice, Inbred NOD. Mice, SCID. NF-kappa B / antagonists & inhibitors. Neoplasm Transplantation / pathology. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / etiology. Neoplasms, Experimental / pathology

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  • [Cites] Science. 1989 Dec 22;246(4937):1597-600 [2595371.001]
  • [Cites] Blood. 1995 Sep 15;86(6):2350-7 [7662981.001]
  • [Cites] Cell. 1990 Sep 7;62(5):1007-18 [2203531.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1053-63 [1850779.001]
  • [Cites] Mol Cell Biol. 2000 May;20(10):3377-86 [10779327.001]
  • [Cites] Invest New Drugs. 2000 May;18(2):109-21 [10857991.001]
  • [Cites] Blood. 2000 Oct 1;96(7):2537-42 [11001908.001]
  • [Cites] Rinsho Byori. 1996 Jan;44(1):19-23 [8691635.001]
  • [Cites] Annu Rev Immunol. 1996;14:649-83 [8717528.001]
  • [Cites] J Biol Chem. 1997 Aug 22;272(34):21096-103 [9261113.001]
  • [Cites] Int J Hematol. 1997 Oct;66(3):257-78 [9401272.001]
  • [Cites] Br J Haematol. 1998 Nov;103(2):335-42 [9827902.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] Clin Cancer Res. 1999 Sep;5(9):2638-45 [10499643.001]
  • [Cites] Hum Pathol. 2000 Dec;31(12):1482-90 [11150373.001]
  • [Cites] J Clin Invest. 2001 Jan;107(2):143-51 [11160127.001]
  • [Cites] Immunity. 2001 Apr;14(4):357-68 [11336681.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1083-6 [11861386.001]
  • [Cites] J Biol Chem. 2002 May 10;277(19):16639-47 [11872748.001]
  • [Cites] Leuk Res. 2002 Jun;26(6):561-7 [12007504.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1828-34 [12176906.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3175-82 [12384415.001]
  • [Cites] J Immunol. 1981 Apr;126(4):1393-7 [6970774.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Nature. 1983 Feb 10;301(5900):527-30 [6823332.001]
  • [Cites] J Clin Invest. 1984 Jun;73(6):1711-8 [6327770.001]
  • [Cites] Science. 1984 Jul 27;225(4660):381-5 [6330891.001]
  • [Cites] J Exp Med. 1985 Jan 1;161(1):40-52 [2981954.001]
  • [Cites] J Immunol. 1985 Jun;134(6):3798-801 [3989296.001]
  • [Cites] Science. 1985 Aug 16;229(4714):675-9 [2992082.001]
  • [Cites] J Clin Invest. 1985 Aug;76(2):446-53 [2993359.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Nat Immun Cell Growth Regul. 1986;5(4):169-99 [2430177.001]
  • [Cites] Cell. 1987 Jan 30;48(2):343-50 [3026643.001]
  • [Cites] Cell. 1987 Apr 10;49(1):47-56 [3030566.001]
  • [Cites] Science. 1988 Sep 23;241(4873):1632-9 [2971269.001]
  • [Cites] Science. 1988 Sep 23;241(4873):1652-5 [2843985.001]
  • [Cites] J Exp Med. 1991 Jul 1;174(1):139-49 [1711560.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):5989-92 [2068075.001]
  • [Cites] Adv Immunol. 1991;50:303-25 [1950798.001]
  • [Cites] Blood. 1991 Dec 1;78(11):2973-81 [1835412.001]
  • [Cites] Blood. 1992 Apr 15;79(8):2089-98 [1562735.001]
  • [Cites] Jpn J Cancer Res. 1992 Apr;83(4):320-3 [1506264.001]
  • [Cites] Blood. 1991 Nov 15;78(10):2650-65 [1824259.001]
  • [Cites] Science. 1992 Dec 11;258(5089):1792-5 [1299224.001]
  • [Cites] J Virol. 1995 Feb;69(2):1328-33 [7815516.001]
  • [Cites] Immunity. 1995 Mar;2(3):223-38 [7697543.001]
  • [Cites] J Immunol. 1990 Feb 1;144(3):796-803 [2136898.001]
  • (PMID = 12692230.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-(4-methylphenylsulfonyl)-2-propenenitrile; 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Nitriles; 0 / Organic Chemicals; 0 / Sulfones
  • [Other-IDs] NLM/ PMC153944
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19. Lee CM, Tanaka T, Murai T, Kondo M, Kimura J, Su W, Kitagawa T, Ito T, Matsuda H, Miyasaka M: Novel chondroitin sulfate-binding cationic liposomes loaded with cisplatin efficiently suppress the local growth and liver metastasis of tumor cells in vivo. Cancer Res; 2002 Aug 1;62(15):4282-8
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  • [Title] Novel chondroitin sulfate-binding cationic liposomes loaded with cisplatin efficiently suppress the local growth and liver metastasis of tumor cells in vivo.
  • An increased level of chondroitin sulfate (CS) expression on the cell surface is often associated with malignant transformation and the progression of tumor cells.
  • In this study, CSs expressed on highly metastatic tumor cells were used as a target for the selective delivery of anticancer drugs by polyethylene glycol (PEG)-coated liposomes that contained a new cationic lipid 3,5-dipentadecycloxybenzamidine hydrochloride (TRX-20).
  • In vitro, TRX-20 liposomes, but not plain PEG liposomes, avidly bound to and were readily internalized by highly metastatic tumor cells such as LM8G5 and ACHN cells, which express large amounts of CS on the cell surface.
  • When TRX-20 liposomes were loaded with cisplatin, they effectively killed the CS-expressing tumor cells in vitro, whereas cisplatin-PEG liposomes lacking TRX-20 were totally ineffective.
  • LM8G5 tumors. Therapeutic experiments in mice bearing a s.c.
  • LM8G5 tumor revealed that cisplatin-loaded TRX-20 liposomes were significantly more effective in reducing the local tumor growth than cisplatin-loaded plain PEG liposomes or free cisplatin.
  • Furthermore, the cisplatin-loaded TRX-20 liposomes markedly suppressed metastatic spreading of LM8G5 tumor cells to the liver, significantly increasing the survival time of the tumor-bearing mice.
  • These results demonstrate that the CS-targeted delivery of anticancer drugs by novel cationic liposomes represents a potentially useful strategy to prevent the local growth and metastasis, particularly to the liver, of tumor cells that have enhanced expression of CS.
  • [MeSH-major] Chondroitin Sulfates / metabolism. Cisplatin / administration & dosage. Liver Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Animals. Cations / metabolism. Cell Division / drug effects. Female. Humans. Liposomes. Mice. Mice, Inbred C3H. Mice, Inbred ICR. Mice, Nude. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12154030.001).
  • [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 / Cations; 0 / Liposomes; 9007-28-7 / Chondroitin Sulfates; Q20Q21Q62J / Cisplatin
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20. Shang D, Liu Y, Ito N, Kamoto T, Ogawa O: Defective Jak-Stat activation in renal cell carcinoma is associated with interferon-alpha resistance. Cancer Sci; 2007 Aug;98(8):1259-64
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  • [Title] Defective Jak-Stat activation in renal cell carcinoma is associated with interferon-alpha resistance.
  • Chemotherapy is ineffective against metastatic renal cell carcinoma (RCC).
  • Interferon (IFN)-alpha has become the most common agent used in clinical therapy to overcome this malignant tumor, although a satisfactory response has not been achieved and the mechanism of resistance of RCC to IFN-alpha remains unclear.
  • Six RCC cell lines and three types of IFN-alpha were used, and the expression, activation and effects of transfection of possible proteins or factors reported to be involved in IFN-alpha signaling were examined to clarify the mechanism of resistance.
  • These results suggest that restoring the expression of Jak or Stat1 might strikingly increase the susceptibility of RCC to IFN-alpha and may be a new strategy for improving the response of RCC to IFN-alpha treatment.
  • The Jak-Stat pathway should therefore be an appropriate target for the treatment of RCC.
  • [MeSH-major] Carcinoma, Renal Cell / drug therapy. Drug Resistance, Neoplasm. Interferon-alpha / pharmacology. Janus Kinase 1 / metabolism. Kidney Neoplasms / drug therapy. STAT1 Transcription Factor / metabolism
  • [MeSH-minor] Cell Line, Tumor. Enzyme Activation. Humans. Phosphorylation. Receptor, Interferon alpha-beta / metabolism. Signal Transduction. TYK2 Kinase / metabolism. Transfection

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  • (PMID = 17573897.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 156986-95-7 / Receptor, Interferon alpha-beta; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / TYK2 Kinase
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21. Ito T, Akao Y, Yi H, Ohguchi K, Matsumoto K, Tanaka T, Iinuma M, Nozawa Y: Antitumor effect of resveratrol oligomers against human cancer cell lines and the molecular mechanism of apoptosis induced by vaticanol C. Carcinogenesis; 2003 Sep;24(9):1489-97
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  • [Title] Antitumor effect of resveratrol oligomers against human cancer cell lines and the molecular mechanism of apoptosis induced by vaticanol C.
  • Twenty resveratrol (3,5,4'-trihydroxystilbene) (Res) derivatives, which were isolated from stem bark of Vatica rassak (Dipterocarpaceae), were evaluated for in vitro cytotoxicity against a panel of human tumor cell lines.
  • Vaticanol C (Vat C) as a major component induced a considerable cytotoxicity in all cell lines tested and exhibited growth suppression in colon cancer cell lines at low dose.
  • Vat C caused two cell lines (SW480 and HL60) to induce cell death at four to seven times lower concentrations, compared with Res.
  • The growth suppression by Vat C was found to be due to apoptosis, which was assessed by morphological findings (nuclear condensation and fragmentation) and DNA ladder formation in the colon cancer cell lines.
  • Furthermore, the mitochondrial membrane potential of apoptotic SW480 cells after 12 h treatment with Vat C was significantly lost, and concurrently the cytochrome c release and activation of caspase-9 were also detected by western blot analysis.
  • Over-expression of Bcl-2 protein in SW480 cells significantly prevented the cell death induced by Vat C.
  • Taken together, the findings presented here indicate that Vat C induced marked apoptosis in malignant cells mainly by affecting mitochondrial membrane potential.
  • [MeSH-minor] Apoptosis / drug effects. Caspases / biosynthesis. Cell Division / drug effects. Colonic Neoplasms / drug therapy. Enzyme Activation. Humans. Membrane Potentials / drug effects. Mitochondria / drug effects. Tumor Cells, Cultured

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  • (PMID = 12844481.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Stilbenes; 0 / vaticanol C; EC 3.4.22.- / Caspases; Q369O8926L / resveratrol
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22. Duxbury MS, Ito H, Zinner MJ, Ashley SW, Whang EE: siRNA directed against c-Src enhances pancreatic adenocarcinoma cell gemcitabine chemosensitivity. J Am Coll Surg; 2004 Jun;198(6):953-9
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  • [Title] siRNA directed against c-Src enhances pancreatic adenocarcinoma cell gemcitabine chemosensitivity.
  • BACKGROUND: The c-Src tyrosine kinase is a determinant of malignant cellular behavior in a variety of human cancers.
  • STUDY DESIGN: PANC1, MIAPaCa2, BxPC3, and Capan2 pancreatic adenocarcinoma cell lines were studied.
  • RESULTS: Src expression and kinase activity in cell lines were directly correlated with gemcitabine chemoresistance. c-Src-specific siRNA suppressed c-Src expression and kinase activity. c-Src-specific siRNA increased gemcitabine-induced, caspase-mediated apoptosis.
  • CONCLUSIONS: c-Src is a determinant of pancreatic adenocarcinoma chemoresistance and represents a potential target for therapeutic intervention.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / pharmacology. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Pancreatic Neoplasms / drug therapy. RNA, Small Interfering / pharmacology. src-Family Kinases / physiology
  • [MeSH-minor] Apoptosis. Blotting, Western. Drug Resistance, Neoplasm. Humans. Tumor Cells, Cultured

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  • (PMID = 15194078.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / RNA, Small Interfering; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.10.2 / src-Family Kinases
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23. Saito S, Nojiri H, Satoh M, Ito A, Ohyama C, Orikasa S: Inverse relationship of expression between GM3 and globo-series ganglioside in human renal cell carcinoma. Tohoku J Exp Med; 2000 Apr;190(4):271-8
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  • [Title] Inverse relationship of expression between GM3 and globo-series ganglioside in human renal cell carcinoma.
  • Renal cell carcinoma (RCC) is highly metastatic.
  • However, the mechanism of metastasis remains largely unknown, and there is no effective therapy for metastasis.
  • To get a clue to a new method of therapy for RCC, we investigated whether the similar changes occur in RCC cells expressing globo-series ganglioside.
  • Growth suppression and an increase of GM3 simultaneous with a decrease of monosialosyl galactosyl globoside, a member of globo-series gangliosides, were observed in human RCC cell line ACHN following brefeldin A treatment.
  • The resultant change of the ganglioside profile is inversely related to the ganglioside pattern associated with the malignant potential of RCC and almost coincided with that representative of RCC cases showing favorable prognoses.
  • It is suggested that the inverse relationship of expression between GM3 and globo-series ganglioside is reflected on the degree of malignancy of RCC, and may be useful as one of the indicators for exploiting treatment methods of RCC.
  • [MeSH-major] Carcinoma, Renal Cell / metabolism. G(M3) Ganglioside / metabolism. Gangliosides / metabolism. Globosides / metabolism. Kidney Neoplasms / metabolism
  • [MeSH-minor] Brefeldin A / pharmacology. Cell Division / drug effects. Humans. Prognosis. Protein Synthesis Inhibitors / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / pathology

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  • (PMID = 10877509.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / G(M3) Ganglioside; 0 / Gangliosides; 0 / Globosides; 0 / Protein Synthesis Inhibitors; 20350-15-6 / Brefeldin A
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24. Yoshiba S, Ito D, Nagumo T, Shirota T, Hatori M, Shintani S: Hypoxia induces resistance to 5-fluorouracil in oral cancer cells via G(1) phase cell cycle arrest. Oral Oncol; 2009 Feb;45(2):109-15
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  • [Title] Hypoxia induces resistance to 5-fluorouracil in oral cancer cells via G(1) phase cell cycle arrest.
  • Malignant tumors are exposed to various levels of hypoxic condition in vivo.
  • It has been known that tumor cells under hypoxia are resistant to chemotherapies.
  • To clarify the mechanism of the hypoxia-induced chemoresistance, we evaluated the effects of hypoxia on the resistance of oral squamous cell carcinoma (OSCC) cell lines to 5-fluorouracil (5-FU).
  • Growth of HS cells were inhibited by hypoxia and introduced to G(1) arrest in cell cycle.
  • 5-FU effect on HS cell viability was markedly reduced in hypoxic condition without an induction of chemoresistant related protein, P-glycoprotein.
  • However, proliferation, cell cycle, and 5-FU sensitivity of HR cells were not affected by hypoxia.
  • Hypoxia-inducible factor (HIF)-1alpha was induced by hypoxia in all OSCC cell lines, but diminished in HS cells within 48h.
  • From these findings, we concluded that HS OSCC cells acquire 5-FU resistance under hypoxia by G(1)/S transition through an upregulation of cell cycle inhibitors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Squamous Cell / drug therapy. Cell Hypoxia / physiology. Drug Resistance, Neoplasm / physiology. Fluorouracil / pharmacology. Mouth Neoplasms / drug therapy
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Proliferation / drug effects. Cyclin D / metabolism. G1 Phase / drug effects. G1 Phase / physiology. Humans. Transcription Factors / metabolism

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  • (PMID = 18710819.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin D; 0 / Transcription Factors; U3P01618RT / Fluorouracil
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25. Ohno S, Nishi T, Kojima Y, Haraoka J, Ito H, Mizuguchi J: Combined stimulation with interferon alpha and retinoic acid synergistically inhibits proliferation of the glioblastoma cell line GB12. Neurol Res; 2002 Oct;24(7):697-704
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  • [Title] Combined stimulation with interferon alpha and retinoic acid synergistically inhibits proliferation of the glioblastoma cell line GB12.
  • Since malignant glioma displays moderate resistance to conventional therapy, a new treatment modality is needed to improve the outcome of patients with these tumors.
  • In this study, we examined whether combination stimulation with interferon alpha (IFN-alpha) and retinoic acid (RA) affected proliferation of the glioblastoma cell line GB 12 in vitro.
  • Stimulation with IFN-alpha alone inhibited the GB 12 cell proliferation in a dose/time-dependent fashion, as assessed by WST-1 assay and uptake of 3H-thymidine, while RA limited it only slightly.
  • These findings suggest that the IFN-alpha/RA combination would synergistically affect glioblastoma cell growth, probably through apoptosis induction as well as a decreased cellular DNA synthesis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Brain Neoplasms / drug therapy. Cell Division / drug effects. Glioblastoma / drug therapy. Interferon-alpha / administration & dosage. Tretinoin / administration & dosage
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Dose-Response Relationship, Drug. Humans. Proto-Oncogene Proteins / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reaction Time / drug effects. Reaction Time / physiology. Thymidine / metabolism. Tritium. Tumor Cells, Cultured. bcl-2-Associated X Protein

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  • (PMID = 12392208.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / Interferon-alpha; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 10028-17-8 / Tritium; 5688UTC01R / Tretinoin; VC2W18DGKR / Thymidine
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26. Arakawa Y, Mizunuma N, Aiba K, Ito Y, Takahashi S, Irie T, Watanabe J, Tada K, Okudaira T, Seki M, Yamaguchi T, Muto T, Hatake K: [Pancreatic islet cell carcinoma with multiple hepatic metastases successfully treated with a streptozocin/5-FU regimen--a case report]. Gan To Kagaku Ryoho; 2002 Dec;29(13):2561-4
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  • [Title] [Pancreatic islet cell carcinoma with multiple hepatic metastases successfully treated with a streptozocin/5-FU regimen--a case report].
  • CT scans revealed a pancreatic head tumor along with multiple liver tumors.
  • The pancreatic head tumor had spread to the duodenum.
  • Following tumor biopsy with gastrointestinal fiberscopy, we diagnosed a pancreatic malignant islet cell tumor with multiple liver metastases.
  • Since there was no clinical evidence of recognized endocrinopathy, we diagnosed "nonfunctioning" tumor.
  • However, neither the pancreatic head tumor nor the metastatic liver tumors changed in size.
  • After this treatment, the enlarged metastatic liver tumors were reduced in size, with marked improvement in liver enzyme.
  • Only grade 1 nausea and alopecia were observed during the treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Islet Cell / drug therapy. Carcinoma, Islet Cell / secondary. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Drug Administration Schedule. Female. Fluorouracil / administration & dosage. Humans. Middle Aged. Streptozocin / administration & dosage

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  • (PMID = 12506483.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 5W494URQ81 / Streptozocin; U3P01618RT / Fluorouracil
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27. Hasegawa S, Ito H, Kojima Y, Nakayama H, Wada N, Inui K, Imoto K, Rino Y, Takanashi Y: [A case of thymic cancer with pericardial tamponade as initial manifestation]. Gan To Kagaku Ryoho; 2006 Jan;33(1):79-82
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  • The effusion was serous fluid, not bloody, and no malignant cells were found.
  • The patient underwent a tumor resection, and the final pathological diagnosis was squamous cell carcinoma of the thymus.
  • In a review of 14 cases of thymic tumor with pericardial tamponade as initial manifestations in the Japanese literature,there were only three cases of thymic cancer.
  • The prognosis was reported to be extremely poor.Some reports showed the effectiveness of chemotherapy and irradiation therapy.
  • We should keep looking for the best treatment for this disease.
  • [MeSH-major] Carcinoma, Squamous Cell / complications. Cardiac Tamponade / etiology. Thymus Neoplasms / complications
  • [MeSH-minor] Aged. Bone Neoplasms / secondary. Combined Modality Therapy. Female. Humans. Liver Neoplasms / secondary. Pericardial Effusion / etiology

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  • (PMID = 16410702.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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28. Nakamura K, Ito Y, Kawano Y, Kurozumi K, Kobune M, Tsuda H, Bizen A, Honmou O, Niitsu Y, Hamada H: Antitumor effect of genetically engineered mesenchymal stem cells in a rat glioma model. Gene Ther; 2004 Jul;11(14):1155-64
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  • The prognosis of patients with malignant glioma is extremely poor, despite the extensive surgical treatment that they receive and recent improvements in adjuvant radio- and chemotherapy.
  • In the present study, we propose the use of gene-modified mesenchymal stem cells (MSCs) as a new tool for gene therapy of malignant brain neoplasms.
  • Primary MSCs isolated from Fischer 344 rats possessed excellent migratory ability and exerted inhibitory effects on the proliferation of 9L glioma cell in vitro.
  • MSCs implanted directly into the tumor localized mainly at the border between the 9L tumor cells and normal brain parenchyma, and also infiltrated into the tumor bed.
  • Intratumoral injection of MSCs caused significant inhibition of 9L tumor growth and increased the survival of 9L glioma-bearing rats.
  • Gene-modification of MSCs by infection with an adenoviral vector encoding human interleukin-2 (IL-2) clearly augmented the antitumor effect and further prolonged the survival of tumor-bearing rats.
  • Thus, gene therapy employing MSCs as a targeting vehicle would be promising as a new therapeutic approach for refractory brain tumor.
  • [MeSH-major] Adenoviridae / genetics. Brain Neoplasms / therapy. Genetic Therapy / methods. Genetic Vectors / administration & dosage. Glioma / therapy. Interleukin-2 / genetics. Stem Cell Transplantation

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  • (PMID = 15141157.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-2
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29. Shimizu A, Yamane M, Ito H, Araki S, Yoshida T, Suzuki M: [Clinicopathological study of salivary duct carcinoma]. Nihon Jibiinkoka Gakkai Kaiho; 2002 Jun;105(6):727-31
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  • It is a rare but highly malignant tumor.
  • Two had chemotherapy, but showed no effect.
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Humans. Immunohistochemistry. Male. Middle Aged. Prognathism. Proliferating Cell Nuclear Antigen / analysis. Salivary Ducts / pathology. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 12138700.001).
  • [ISSN] 0030-6622
  • [Journal-full-title] Nihon Jibiinkoka Gakkai kaiho
  • [ISO-abbreviation] Nippon Jibiinkoka Gakkai Kaiho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proliferating Cell Nuclear Antigen; 0 / Tumor Suppressor Protein p53
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30. Fujita Y, Kojima K, Ohhashi R, Hamada N, Nozawa Y, Kitamoto A, Sato A, Kondo S, Kojima T, Deguchi T, Ito M: MiR-148a attenuates paclitaxel resistance of hormone-refractory, drug-resistant prostate cancer PC3 cells by regulating MSK1 expression. J Biol Chem; 2010 Jun 18;285(25):19076-84
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  • [Title] MiR-148a attenuates paclitaxel resistance of hormone-refractory, drug-resistant prostate cancer PC3 cells by regulating MSK1 expression.
  • MicroRNAs are involved in cancer pathogenesis and act as tumor suppressors or oncogenes.
  • It has been recently reported that miR-148a expression is down-regulated in several types of cancer.
  • Transfection with miR-148a precursor inhibited cell growth, and cell migration and invasion, and increased the sensitivity to anti-cancer drug paclitaxel in PC3 cells.
  • Suppression of MSK1 expression by siRNA, however, showed little or no effects on malignant phenotypes of PC3 cells.
  • In PC3PR cells, a paclitaxel-resistant cell line established from PC3 cells, miR-148a inhibited cell growth, and cell migration and invasion, and also attenuated the resistance to paclitaxel.
  • Furthermore, MSK1 knockdown reduced paclitaxel-resistance of PC3PR cells, indicating that miR-148a attenuates paclitaxel-resistance of hormone-refractory, drug-resistant PC3PR cells in part by regulating MSK1 expression.
  • Our findings suggest that miR-148a plays multiple roles as a tumor suppressor and can be a promising therapeutic target for hormone-refractory prostate cancer especially for drug-resistant prostate cancer.
  • [MeSH-major] Drug Resistance, Neoplasm. MicroRNAs / chemistry. Paclitaxel / pharmacology. Prostatic Neoplasms / drug therapy. Ribosomal Protein S6 Kinases, 90-kDa / metabolism
  • [MeSH-minor] Animals. Base Sequence. Cell Line, Tumor. Epithelial Cells / cytology. Hormones / metabolism. Humans. Male. Molecular Sequence Data. Neoplasm Invasiveness. Ribosomal Protein S6 Kinases / metabolism. Sequence Homology, Amino Acid

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  • [Cites] Curr Pharm Des. 2009;15(4):456-62 [19199973.001]
  • [Cites] Mol Cell Biochem. 2009 Feb;322(1-2):103-12 [19002563.001]
  • [Cites] Sci China C Life Sci. 2009 Mar;52(3):224-31 [19294347.001]
  • [Cites] Pancreatology. 2009;9(1-2):66-72 [19077456.001]
  • [Cites] Curr Cancer Drug Targets. 2009 Jun;9(4):572-94 [19519323.001]
  • [Cites] Annu Rev Med. 2009;60:167-79 [19630570.001]
  • [Cites] Hepatology. 2009 Aug;50(2):630-7 [19585622.001]
  • [Cites] J Biol Chem. 2001 Aug 31;276(35):33213-9 [11441012.001]
  • [Cites] Cancer Res. 2002 Jan 1;62(1):75-8 [11782362.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(8):2871-81 [11909979.001]
  • [Cites] J Biol Chem. 2002 Dec 27;277(52):50550-6 [12414794.001]
  • [Cites] Oncogene. 2003 Feb 6;22(5):746-55 [12569367.001]
  • [Cites] EMBO J. 2003 Mar 17;22(6):1313-24 [12628924.001]
  • [Cites] EMBO J. 2003 Jun 2;22(11):2788-97 [12773393.001]
  • [Cites] BMC Mol Biol. 2003 May 26;4:6 [12769834.001]
  • [Cites] Sci STKE. 2003 Aug 12;2003(195):PE33 [12915720.001]
  • [Cites] EMBO J. 1998 Aug 3;17(15):4426-41 [9687510.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3108-16 [15833840.001]
  • [Cites] Br J Cancer. 2006 Jan 30;94(2):179-83 [16404435.001]
  • [Cites] J Biol Chem. 2006 May 5;281(18):12521-5 [16517600.001]
  • [Cites] J Invest Dermatol. 2006 Aug;126(8):1784-91 [16543895.001]
  • [Cites] Oncogene. 2006 Jul 27;25(32):4449-57 [16532028.001]
  • [Cites] Mol Cancer. 2006;5:24 [16784538.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] J Immunol. 2006 Dec 1;177(11):7950-8 [17114467.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6130-5 [17616669.001]
  • [Cites] J Pathol. 2008 Jan;214(1):17-24 [17948228.001]
  • [Cites] Nat Rev Genet. 2008 Feb;9(2):102-14 [18197166.001]
  • [Cites] Oncogene. 2008 Mar 13;27(12):1788-93 [17891175.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2538-47 [18381464.001]
  • [Cites] J Biol Chem. 2008 Apr 11;283(15):9674-80 [18268015.001]
  • [Cites] RNA. 2008 May;14(5):872-7 [18367714.001]
  • [Cites] J Cell Biochem. 2008 Jun 1;104(3):785-94 [18172855.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13556-61 [18768788.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Dec 5;377(1):114-9 [18834855.001]
  • [Cites] J Cell Mol Med. 2008 Sep-Oct;12(5A):1456-65 [18624768.001]
  • [Cites] Int J Oncol. 2009 Feb;34(2):537-42 [19148490.001]
  • [Cites] Cancer Gene Ther. 2009 Mar;16(3):206-16 [18949015.001]
  • (PMID = 20406806.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones; 0 / MicroRNAs; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 90-kDa; EC 2.7.11.1 / mitogen and stress-activated protein kinase 1; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC2885186
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31. Min Y, Adachi Y, Yamamoto H, Ito H, Itoh F, Lee CT, Nadaf S, Carbone DP, Imai K: Genetic blockade of the insulin-like growth factor-I receptor: a promising strategy for human pancreatic cancer. Cancer Res; 2003 Oct 1;63(19):6432-41
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  • Pancreatic cancer is one of the most lethal malignant tumors.
  • We have shown previously successful therapy in colorectal and lung cancer xenograft models using recombinant adenoviruses expressing dominant negative IGF-I receptors.
  • In this study, we sought to better dissect the mechanism of action of this virus and determine whether IGF-Ir targeted adenoviruses represent potentially effective therapeutics for human pancreatic cancer cells.
  • We assessed the effect of IGF-Ir/dn on signaling blockade, growth, stress response, chemotherapy, radiation-induced apoptosis, and in vivo therapeutic efficacy in xenografts.
  • IGF-Ir/dn expression increased radiation and chemotherapy-induced apoptosis, and the combination therapy of IGF-Ir/dn with chemotherapy was very effective against tumors in mice.
  • In an i.p. model, IGF-Ir/dn therapy reduced dissemination and prolonged survival times.
  • The antitumor activity of IGF-Ir/dn is mediated through inhibition of Akt-1 and enhances the efficacy of chemotherapy.
  • Adenovirus-IGF-Ir/482st may be a useful anticancer therapeutic for pancreatic cancer.
  • [MeSH-major] Genetic Therapy / methods. Pancreatic Neoplasms / therapy. Peptide Fragments / genetics. Proto-Oncogene Proteins. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, IGF Type 1 / genetics
  • [MeSH-minor] Adenoviruses, Human / genetics. Animals. Antimetabolites, Antineoplastic / pharmacology. Cell Division / physiology. Cell Line, Tumor. Combined Modality Therapy. DNA, Complementary / genetics. Female. Fluorouracil / pharmacology. Humans. Mice. Mice, Inbred BALB C. Protein-Serine-Threonine Kinases / physiology. Proto-Oncogene Proteins c-akt. Signal Transduction / physiology. Xenograft Model Antitumor Assays

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  • (PMID = 14559833.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / DNA, Complementary; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; U3P01618RT / Fluorouracil
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32. Ito A, Saito H, Mitobe K, Minamiya Y, Takahashi N, Maruyama K, Motoyama S, Katayose Y, Ogawa J: Inhibition of heat shock protein 90 sensitizes melanoma cells to thermosensitive ferromagnetic particle-mediated hyperthermia with low Curie temperature. Cancer Sci; 2009 Mar;100(3):558-64
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  • Heat shock protein (Hsp) 90 is a key regulator of a variety of oncogene products and cell-signaling molecules, and the therapeutic benefit of its inhibition in combination with radiation or chemotherapy has been investigated.
  • In addition, hyperthermia has been used for many years to treat various malignant tumors.
  • FMP were then injected into the resultant tumors, and the mice were divided into four groups: group I, no treatment (control); group II, one hyperthermia treatment; group III, GA alone; and group IV, GA with hyperthermia.
  • When exposed to a magnetic field, the temperature of tissues containing FMP increased and stabilized at the Tc.
  • In group IV, complete regression of tumors was observed in five of nine mice (56%), whereas no tumor regression was seen in groups I-III.
  • Thus, the combination of FMP-mediated, self-regulating hyperthermia with Hsp90 inhibition has important implications for the treatment of cancer.
  • [MeSH-major] Ferric Compounds / therapeutic use. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Hyperthermia, Induced / methods. Melanoma, Experimental / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / administration & dosage. Benzoquinones / administration & dosage. Blotting, Western. Cell Line, Tumor. Combined Modality Therapy. Female. In Situ Nick-End Labeling. Lactams, Macrocyclic / administration & dosage. Mice. Mice, Inbred C57BL. Proto-Oncogene Proteins c-akt / metabolism

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  • (PMID = 19154416.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Benzoquinones; 0 / Ferric Compounds; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 1317-54-0 / ferrite; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; Z3K3VJ16KU / geldanamycin
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33. Fujimura T, Nakagawa S, Ohtani T, Ito Y, Aiba S: Inhibitory effect of the polyinosinic-polycytidylic acid/cationic liposome on the progression of murine B16F10 melanoma. Eur J Immunol; 2006 Dec;36(12):3371-80
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  • The local administration of PIC has been demonstrated to be effective in anti-tumor immunotherapy.
  • However, the effects of PIC delivered cross the cell membrane have not yet been examined.
  • To address this issue, we used a complex of PIC and cationic liposome (PIC liposome) and examined its anti-tumor effects in vitro and in vivo.
  • This treatment induced tyrosinase-related protein-2 (TRP-2)-tetramer(+) CD8(+) cells in the lymph nodes.
  • As the mechanism for its anti-tumor immune response, we showed that the intradermal injection of PIC liposome induced the maturation of dendritic cells (DC).
  • Moreover, the intratumoral injection of immature DC after treatment with PIC liposome significantly increased the number of TRP-2-specific IFN-gamma-producing cells in the lymph nodes as well as spleen, which resulted in an augmentation of the anti-tumor immune response.
  • These studies demonstrate the potential of peritumoral injection of PIC liposome as immunotherapy for malignant melanoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Growth Inhibitors / therapeutic use. Melanoma, Experimental / drug therapy. Poly I-C / therapeutic use
  • [MeSH-minor] Animals. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. Cations. Cell Line, Tumor. Cells, Cultured. Disease Progression. Female. Humans. Injections, Intralesional. Interferon Inducers / administration & dosage. Interferon Inducers / therapeutic use. Interferon-gamma / biosynthesis. Liposomes. Mice. Mice, Inbred C57BL

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  • (PMID = 17109465.001).
  • [ISSN] 0014-2980
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cations; 0 / Growth Inhibitors; 0 / Interferon Inducers; 0 / Liposomes; 24939-03-5 / Poly I-C; 82115-62-6 / Interferon-gamma
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34. Ito S, Natsume A, Shimato S, Ohno M, Kato T, Chansakul P, Wakabayashi T, Kim SU: Human neural stem cells transduced with IFN-beta and cytosine deaminase genes intensify bystander effect in experimental glioma. Cancer Gene Ther; 2010 May;17(5):299-306
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  • Previously, we have shown that the genetically modified human neural stem cells (NSCs) show remarkable migratory and tumor-tropic capability to track down brain tumor cells and deliver therapeutic agents with significant therapeutic benefit.
  • In our pilot clinical trial in glioma, the IFN-beta gene has shown potent antitumor activity in patients with malignant glioma.
  • Furthermore, the same gene therapy regimen prolonged survival periods significantly in the experimental animals.
  • The results of the present study indicate that the multimodal NSC-based treatment strategy might have therapeutic potential against gliomas.
  • [MeSH-major] Cytosine Deaminase / physiology. Genetic Therapy / methods. Glioma / drug therapy. Glioma / therapy. Interferon-beta / physiology
  • [MeSH-minor] Animals. Bystander Effect. Cell Line, Tumor. Disease Models, Animal. Female. Flucytosine / therapeutic use. Humans. Mice. Mice, Nude

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  • (PMID = 19893595.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 77238-31-4 / Interferon-beta; D83282DT06 / Flucytosine; EC 3.5.4.1 / Cytosine Deaminase
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35. Terui Y, Sakurai T, Mishima Y, Mishima Y, Sugimura N, Sasaoka C, Kojima K, Yokoyama M, Mizunuma N, Takahashi S, Ito Y, Hatake K: Blockade of bulky lymphoma-associated CD55 expression by RNA interference overcomes resistance to complement-dependent cytotoxicity with rituximab. Cancer Sci; 2006 Jan;97(1):72-9
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  • Recently, anti-CD20 (rituximab) and anti-Her2/neu (trastuzumab) antibodies have been developed and applied to the treatment of malignant lymphoma and breast cancer, respectively.
  • However, bulky lymphoma is known to be resistant to rituximab therapy, and this needs to be overcome.
  • Susceptibility to CDC with rituximab was decreased in a tumor size-dependent manner (r=-0.895, P<0.0001), but not in a CD20-dependent manner (r=-0.076, P=0.6807) using clinical samples.
  • A decrease in susceptibility to CDC with rituximab was statistically dependent on CD55 expression (r=-0.927, P<0.0001) and the relationship between tumor size and CD55 expression showed a significant positive correlation (r=0.921, P<0.0001) using clinical samples.
  • Introduction of this siRNA decreased CD55 expression in the breast cancer cell line SK-BR3 and in CD20-positive cells of patients with recurrent lymphoma; resistance to CDC was also inhibited.
  • This observation gives us a novel strategy to suppress bulky disease-related resistance to monoclonal antibody treatment.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD55 / metabolism. Complement System Proteins / drug effects. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Lymphoma / genetics. Lymphoma / pathology
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Cell Line, Tumor. Humans. RNA Interference. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Rituximab

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  • [Copyright] (Cancer Sci 2006; 97: 72-79).
  • (PMID = 16367924.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD55; 0 / RNA, Small Interfering; 4F4X42SYQ6 / Rituximab; 9007-36-7 / Complement System Proteins
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36. Tsunoo H, Komura S, Ohishi N, Akiyama S, Kasai Y, Ito K, Nakao A, Yagi K: Effects of interferon-beta in combination with 5-fluorouracil on the growth of esophageal cancer cells in vitro. Anticancer Res; 2001 Sep-Oct;21(5):3301-6
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  • The possible antiproliferative potency of human recombinant interferon-beta (hIFN-beta) towards ten human esophageal cancer cell lines was examined in comparison with the activity of the factor towards human malignant melanoma cell lines.
  • The cell growth of esophageal cancer cell lines was inhibited by hIFN-beta in a dose- and time- dependent manner.
  • The 50% inhibitory concentrations (IC50) of hIFN-beta on nine cell lines out of ten ranged between 23 to 332 IU/ml of culture medium.
  • The remaining cell line, T.Tn, was less sensitive to the interferon (IC50, 611 IU/ml).
  • Under the same culture conditions, the melanoma cell lines tested differed markedly in their sensitivity to hIFN-beta.
  • All these data suggest that combination therapy with hIFN-beta and the anticancer drug 5-FU would be beneficial for the treatment of carcinoma of the esophagus.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma, Squamous Cell / drug therapy. Esophageal Neoplasms / drug therapy. Interferon-gamma / pharmacology
  • [MeSH-minor] Cell Division / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Drug Synergism. Fluorouracil / administration & dosage. Growth Inhibitors / administration & dosage. Growth Inhibitors / pharmacology. Humans. Recombinant Proteins. Tumor Cells, Cultured

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  • (PMID = 11848487.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Growth Inhibitors; 0 / Recombinant Proteins; 82115-62-6 / Interferon-gamma; U3P01618RT / Fluorouracil
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37. Mori H, Ohno Y, Yoshikawa T, Ito F, Endo J, Funaguchi N, Minatoguchi S: [Sarcoidosis-lymphoma syndrome with vertebral bone destruction]. Nihon Kokyuki Gakkai Zasshi; 2009 Nov;47(11):1057-62
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  • Histopathologic examination of lumbar vertebral tumor obtained by CT-guided biopsy revealed non-caseating epithelioid granuloma with CD 68 (+), AE1/AE3 (-), and no malignant cells.
  • Flow cytometry of tumor cells obtained from the gastric ulcer floor showed CD 5 (+), CD 20 (+), K chain monoclonality and we diagnosed B-cell non Hodgkin's lymphoma.
  • She was treated by eight cycles of CHOP plus rituximab chemotherapy and achieved complete response.
  • Sarcoidosis had been diagnosed for two and half years before lymphoma developed.

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  • (PMID = 19994605.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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38. Abraham JM, Cheng Y, Hamilton JP, Paun B, Jin Z, Agarwal R, Kan T, David S, Olaru A, Yang J, Ito T, Selaru FM, Mori Y, Meltzer SJ: Generation of small 32P-labeled peptides as a potential approach to colorectal cancer therapy. PLoS One; 2008 Jun 25;3(6):e2508
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Generation of small 32P-labeled peptides as a potential approach to colorectal cancer therapy.
  • Cancers have been revealed to be extremely heterogenous in terms of the frequency and types of mutations present in cells from different malignant tumors.
  • Thus, it is likely that uniform clinical treatment is not optimal for all patients, and that the development of individualized therapeutic regimens may be beneficial.
  • We describe the generation of multiple, unique small peptides nine to thirty-four amino acids in length which, when labeled with the radioisotope (32)P, bind with vastly differing efficiencies to cell lines derived from different colon adenocarcinomas.
  • In addition, the most effective of these peptides permanently transfers the (32)P radioisotope to colorectal cancer cellular proteins within two hours at a rate that is more than 150 times higher than in cell lines derived from other cancers or from the normal tissues tested.
  • Currently, the only two FDA-approved radioimmunotherapeutic agents in use both employ antibodies directed against the B cell marker CD20 for the treatment of non-Hodgkin's lymphoma.
  • By using the method described herein, large numbers of different (32)P-labeled peptides can be readily produced and assayed against a broad spectrum of cancer types.
  • This report proposes the development and use of (32)P-labeled peptides as potential individualized peptide-binding therapies for the treatment of colon adenocarcinoma patients.

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  • [Cites] Curr Drug Targets. 2006 Oct;7(10):1301-11 [17073592.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 2):741s-746s [17255303.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1374-82 [17309914.001]
  • [Cites] Protein Pept Lett. 2007;14(3):273-9 [17346233.001]
  • [Cites] J Clin Oncol. 2007 May 1;25(13):1658-64 [17470858.001]
  • [Cites] Expert Opin Biol Ther. 2007 May;7(5):739-49 [17477810.001]
  • [Cites] Anticancer Agents Med Chem. 2007 May;7(3):335-43 [17504159.001]
  • [Cites] Cancer Res. 2007 Dec 15;67(24):11896-905 [18089820.001]
  • [Cites] Science. 2007 Nov 16;318(5853):1108-13 [17932254.001]
  • [Cites] PLoS One. 2007;2(10):e964 [17912343.001]
  • [Cites] N Engl J Med. 2001 Mar 15;344(11):783-92 [11248153.001]
  • [Cites] J Clin Oncol. 2000 Sep;18(17):3135-43 [10963642.001]
  • [Cites] Crit Rev Oncol Hematol. 2001 Jul-Aug;39(1-2):181-94 [11418315.001]
  • [Cites] Biopolymers. 2002;66(3):184-99 [12385037.001]
  • [Cites] Curr Opin Mol Ther. 2003 Feb;5(1):44-51 [12669470.001]
  • [Cites] Med Res Rev. 2004 May;24(3):357-97 [14994368.001]
  • [Cites] Oncologist. 2004;9(2):160-72 [15047920.001]
  • [Cites] Mol Cancer Ther. 2005 May;4(5):806-13 [15897245.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4637-8 [16000553.001]
  • [Cites] Nat Biotechnol. 2005 Sep;23(9):1137-46 [16151407.001]
  • [Cites] N Engl J Med. 2005 Oct 20;353(16):1673-84 [16236738.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):7811-9 [16258083.001]
  • [Cites] J Nucl Med. 2006 Feb;47(2):196-9 [16455623.001]
  • [Cites] Eur J Cancer. 2006 May;42(8):994-1003 [16564689.001]
  • [Cites] AAPS J. 2006;8(3):E532-51 [17025272.001]
  • [Cites] Science. 2006 Oct 13;314(5797):268-74 [16959974.001]
  • (PMID = 18575578.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA001808-05; United States / NCI NIH HHS / CA / R21 CA106763; United States / NCI NIH HHS / CA / 2R01CA077057-09; United States / NCI NIH HHS / CA / 7R21/R33CA106763; United States / NCI NIH HHS / CA / 2R01CA095323-14; United States / NCI NIH HHS / CA / R01 CA077057; United States / NCI NIH HHS / CA / R01 CA095323; United States / NCI NIH HHS / CA / R01 CA001808; United States / NIDDK NIH HHS / DK / T32 DK067872
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptides; 0 / Phosphorus Radioisotopes
  • [Other-IDs] NLM/ PMC2423481
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39. Yukitake J, Otake H, Inoue S, Wakamatsu K, Olivares C, Solano F, Hasegawa K, Ito S: Synthesis and selective in vitro anti-melanoma effect of enantiomeric alpha-methyl- and alpha-ethyl-4-S-cysteaminylphenol. Melanoma Res; 2003 Dec;13(6):603-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Melanogenesis provides a unique target for the development of antitumour agents specific for malignant melanoma.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Cysteamine / analogs & derivatives. Cysteamine / therapeutic use. Melanoma / drug therapy
  • [MeSH-minor] 3T3 Cells. Acetylcysteine / metabolism. Animals. Cell Line, Tumor. Glutathione / metabolism. Inhibitory Concentration 50. Kinetics. Magnetic Resonance Spectroscopy. Melanoma, Experimental. Mice. Models, Chemical. Monophenol Monooxygenase / antagonists & inhibitors. Monophenol Monooxygenase / metabolism. Phenols / chemistry. Stereoisomerism. Time Factors. Tyrosine / metabolism

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  • (PMID = 14646624.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phenols; 0 / methyl-4-S-cysteaminylphenol; 42HK56048U / Tyrosine; 5UX2SD1KE2 / Cysteamine; 91281-34-4 / 4-S-cysteaminylphenol; EC 1.14.18.1 / Monophenol Monooxygenase; GAN16C9B8O / Glutathione; WYQ7N0BPYC / Acetylcysteine
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