[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 36 of about 36
1. Karavasilis V, Seddon BM, Ashley S, Al-Muderis O, Fisher C, Judson I: Significant clinical benefit of first-line palliative chemotherapy in advanced soft-tissue sarcoma: retrospective analysis and identification of prognostic factors in 488 patients. Cancer; 2008 Apr 1;112(7):1585-91
MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significant clinical benefit of first-line palliative chemotherapy in advanced soft-tissue sarcoma: retrospective analysis and identification of prognostic factors in 488 patients.
  • BACKGROUND: The efficacy of palliative chemotherapy was investigated in a large group of patients with advanced soft-tissue sarcomas (STS) treated on routine palliative protocols.
  • METHODS: Patients with STS who had first-line chemotherapy for advanced and/or metastatic disease between 1991 and 2005 were identified from the Royal Marsden Hospital's sarcoma database.
  • Patients with Ewing sarcoma, rhabdomyosarcoma, desmoplastic small round cell tumor, and gastrointestinal stromal tumors were excluded from the study.
  • The median age was 49 years and the majority (83%) received chemotherapy for metastatic disease.
  • The most common histologic subtypes were leiomyosarcoma (35%) synovial sarcoma (13%), liposarcoma (10%), and malignant fibrous histiocytoma (10%).
  • In all, 61% received single-agent chemotherapy, usually doxorubicin.
  • In multivariate analysis, age <40 years, liposarcoma, and synovial histology were found to be positive, and bone involvement to be negative, independent prognostic factors.
  • Patients treated with combination chemotherapy experienced longer OS than those treated with a single agent.
  • CONCLUSIONS: Palliative chemotherapy may be beneficial in approximately half of patients with advanced STS.
  • [MeSH-major] Sarcoma / drug therapy. Soft Tissue Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols. Bone Neoplasms / drug therapy. Bone Neoplasms / secondary. Chemotherapy, Adjuvant. Female. Follow-Up Studies. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Middle Aged. Neoplasm Staging. Palliative Care. Prognosis. Prospective Studies. Retrospective Studies. Survival Rate

  • Genetic Alliance. consumer health - Soft tissue sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18278813.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


2. Mittal R, Al Awadi S, Sahar O, Behbehani AM: Ewing's sarcoma as second malignant neoplasm after retinoblastoma: a case report. Med Princ Pract; 2008;17(1):84-5
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ewing's sarcoma as second malignant neoplasm after retinoblastoma: a case report.
  • OBJECTIVES: To report a case of a child with the hereditary form of unilateral retinoblastoma (RB), who developed Ewing's sarcoma of the right fibula 3 years after the enucleation of the right eye.
  • He was fully investigated and found to have locally advanced RB with bone marrow involvement (Reese-Ellsworth stage IVA).
  • The patient received chemotherapy and diode laser thermotherapy in Kuwait and the UK.
  • After 3 years, he was investigated for a small swelling in his right lower leg.
  • He was treated with chemotherapy, surgery (complete excision of the fibula) and high-dose chemotherapy followed by autologous stem cell transplantation.
  • The child is now nearly 2 years after completing the treatment and is disease free.
  • CONCLUSIONS: This case confirms the increased risk of a second malignant neoplasm (SMN) in children with hereditary RB.
  • These children need a very close follow-up for the early diagnosis of SMNs or even subsequent malignancies.
  • [MeSH-major] Bone Neoplasms / diagnosis. Fibula. Neoplasms, Second Primary / diagnosis. Retinal Neoplasms / diagnosis. Retinoblastoma / diagnosis. Sarcoma, Ewing / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child, Preschool. Diagnosis, Differential. Eye Enucleation. Humans. Infant. Male. Stem Cell Transplantation. Treatment Outcome

  • Genetic Alliance. consumer health - Ewing's Sarcoma.
  • Genetic Alliance. consumer health - Retinoblastoma.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 S. Karger AG, Basel.
  • (PMID = 18059108.001).
  • [ISSN] 1423-0151
  • [Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre
  • [ISO-abbreviation] Med Princ Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


3. Gopinath SC, Wadhwa R, Kumar PK: Expression of noncoding vault RNA in human malignant cells and its importance in mitoxantrone resistance. Mol Cancer Res; 2010 Nov;8(11):1536-46
SciCrunch. BioNumbers: The Database of Useful Biological Numbers: Data: Value observation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of noncoding vault RNA in human malignant cells and its importance in mitoxantrone resistance.
  • Several noncoding RNAs do vital cellular functions, including gene regulation and cell differentiation.
  • In the present study, we show that human glioblastoma-, leukemia-, and osteocarcinoma-derived cell lines overexpress vRNA and exhibit higher resistance toward mitoxantrone.
  • These results suggest a role of vRNA in mitoxantrone resistance in malignant cells and justify further studies on the importance and application of noncoding RNAs in cancer chemotherapeutics.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Base Sequence. Bone Neoplasms / drug therapy. Bone Neoplasms / genetics. Cell Line, Tumor. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Glioblastoma / drug therapy. Glioblastoma / genetics. Humans. Leukemia / drug therapy. Leukemia / genetics. Molecular Sequence Data. Osteosarcoma / drug therapy. Osteosarcoma / genetics. RNA Interference. RNA, Small Interfering / genetics. U937 Cells

  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • (PMID = 20881010.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Small Interfering; 0 / RNA, Untranslated; 0 / Vault Ribonucleoprotein Particles; BZ114NVM5P / Mitoxantrone
  •  go-up   go-down


Advertisement
4. Wu Z, Ma JY, Yang JJ, Zhao YF, Zhang SF: Primary small cell carcinoma of esophagus: report of 9 cases and review of literature. World J Gastroenterol; 2004 Dec 15;10(24):3680-2
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary small cell carcinoma of esophagus: report of 9 cases and review of literature.
  • AIM: To analyze the clinical manifestations, pathological features and treatment of primary small cell carcinoma (SCC) of the esophagus and to review the literature on this entity.
  • METHODS: The records of 9 patients with primary esophageal small cell carcinoma were examined and the demographic data, presenting symptoms, methods of tumor diagnosis, and types of treatment given, response to treatment, pathologic findings, and clinical outcome were reviewed.
  • Three of the nine resected specimens showed foci of squamous cell carcinoma in situ.
  • They received adjuvant systemic chemotherapy and local radiation therapy after discharge.
  • During follow-up, three patients developed multiple liver, brain, lung and bone metastases and died between 5 and 18 mo after the diagnosis.
  • Three patients developed widespread metastasis disease and died between 18 and 37 mo after the diagnosis.
  • CONCLUSION: Primary small cell carcinoma of the esophagus is a rare but very malignant tumor.
  • Radical resection combined with chemotherapy and radiotherapy is helpful in limited stage cases.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Esophageal Neoplasms / pathology
  • [MeSH-minor] Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging

  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15534932.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 18
  • [Other-IDs] NLM/ PMC4612018
  •  go-up   go-down


5. Zou J, Gan M, Mao N, Zhu X, Shi Q, Yang H: Sensitization of osteosarcoma cell line SaOS-2 to chemotherapy by downregulating survivin. Arch Med Res; 2010 Apr;41(3):162-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sensitization of osteosarcoma cell line SaOS-2 to chemotherapy by downregulating survivin.
  • BACKGROUND AND AIMS: Osteosarcoma is the most frequent malignant bone tumor with a peak incidence in the second and third decades of life.
  • Here we investigated the anti-cancer effects of downregulating survivin by shRNA vector pSUPER-sh in combination with chemotherapeutic drugs on human osteosarcoma cells.
  • The effects of pSUPER-sh and chemotherapeutic drugs on osteosarcoma cell lines Saos-2 and U2OS by cell viability assay and its underlying mechanisms were analyzed by flow cytometry and caspase-3 activity assay.
  • RESULTS: Downregulated survivin could significantly induce apoptosis of osteosarcoma cell lines Saos-2 and U2OS.
  • CONCLUSIONS: Downregulated survivin by pSUPER-sh could markedly induce apoptosis of osteosarcoma cells lines and pSUPER-sh may be a promising adjuvant in osteosarcoma chemotherapy.
  • [MeSH-major] Bone Neoplasms / genetics. Bone Neoplasms / therapy. Microtubule-Associated Proteins / antagonists & inhibitors. Microtubule-Associated Proteins / genetics. Osteosarcoma / genetics. Osteosarcoma / therapy
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Base Sequence. Caspase 3 / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cisplatin / pharmacology. Combined Modality Therapy. Down-Regulation / drug effects. Doxorubicin / pharmacology. Drug Resistance, Neoplasm / genetics. Etoposide / pharmacology. Genetic Therapy. Humans. Inhibitor of Apoptosis Proteins. Membrane Potential, Mitochondrial / drug effects. RNA, Small Interfering / genetics

  • Genetic Alliance. consumer health - Osteosarcoma.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 IMSS. All rights reserved.
  • (PMID = 20682173.001).
  • [ISSN] 1873-5487
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Small Interfering; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


6. Zent CS, LaPlant BR, Johnston PB, Call TG, Habermann TM, Micallef IN, Witzig TE: The treatment of recurrent/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) with everolimus results in clinical responses and mobilization of CLL cells into the circulation. Cancer; 2010 May 1;116(9):2201-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The treatment of recurrent/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) with everolimus results in clinical responses and mobilization of CLL cells into the circulation.
  • BACKGROUND: Patients with recurrent/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) often have chemotherapy-resistant disease, resulting in poor prognosis.
  • RESULTS: Four of 22 patients with CLL (18%; 95% confidence interval, 5%-40%) achieved a partial remission to therapy.
  • CONCLUSIONS: Everolimus has modest antitumor activity against CLL and can mobilize malignant cells from nodal masses into the peripheral circulation in a subset of CLL patients.
  • Because CLL cells in lymphatic tissue and bone marrow can be more resistant to therapy than circulating CLL cells, the ability of everolimus to mobilize CLL cells into the circulation could be used in combination therapeutic regimens.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2010 American Cancer Society.
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] J Clin Invest. 2005 Mar;115(3):755-64 [15711642.001]
  • [Cites] Cancer. 2001 Sep 1;92(5):1325-30 [11571749.001]
  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] N Engl J Med. 2002 Aug 8;347(6):452-3 [12167696.001]
  • [Cites] Blood. 2003 Jan 1;101(1):278-85 [12393642.001]
  • [Cites] Cancer. 2004 Feb 15;100(4):657-66 [14770419.001]
  • [Cites] Blood. 2004 May 1;103(9):3278-81 [14726385.001]
  • [Cites] Br J Haematol. 1996 Apr;93(1):151-3 [8611450.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Leuk Lymphoma. 2005 Jan;46(1):11-9 [15621776.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4079-88 [15767648.001]
  • [Cites] J Clin Oncol. 2005 Aug 10;23(23):5347-56 [15983389.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:292-8 [16304394.001]
  • [Cites] Br J Cancer. 2006 Oct 23;95(8):955-60 [16953237.001]
  • [Cites] Blood. 2007 Jan 15;109(2):405-11 [17008537.001]
  • [Cites] Leuk Res. 2007 Jul;31(7):899-906 [17241660.001]
  • [Cites] Br J Haematol. 2007 Nov;139(4):600-4 [17979945.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):508-14 [18543327.001]
  • [Cites] J Intern Med. 2008 Dec;264(6):549-62 [19017179.001]
  • [Cites] Leuk Lymphoma. 2008 Dec;49(12):2235-6 [19052968.001]
  • [Cites] Leuk Lymphoma. 2008 Dec;49(12):2333-43 [19052982.001]
  • [Cites] Ann Hematol. 2009 Mar;88(3):221-7 [18704419.001]
  • [Cites] Oncogene. 2000 Dec 27;19(56):6680-6 [11426655.001]
  • (PMID = 20166206.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097274-04; United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / CA97274; United States / NCI NIH HHS / CA / P50 CA097274-04
  • [Publication-type] Clinical Trial, Phase II; 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; 9HW64Q8G6G / Everolimus; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS189697; NLM/ PMC2861142
  •  go-up   go-down


7. Thongprasert S, Cheewakriangkrai R, Napapan S: Docetaxel as second-line chemotherapy for advanced non-small cell lung cancer. J Med Assoc Thai; 2002 Dec;85(12):1296-300
Hazardous Substances Data Bank. TAXOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Docetaxel as second-line chemotherapy for advanced non-small cell lung cancer.
  • The purpose of this study was to evaluate the efficacy and safety of docetaxel as second-line chemotherapy for advanced non-small cell lung cancer (NSCLC).
  • Of 28 evaluable cases, 18 were adenocarcinoma, 3 squamous cell, 3 large cell and 4 undifferentiated carcinoma.
  • Five cases (19.2%) had liver metastases, 3 (11.5%) brain metastases, 6 (23%) bone metastases, and 17 (65.3%) metastatic nodules in the lung.
  • Besides chemotherapy, seven cases had received prior thoracic irradiation and two whole brain irradiation.
  • Two cases had prior surgery for malignant pleural effusion and one had thoracotomy for the resection of the primary tumor.
  • The time from the last dose of chemotherapy to the start of this study was less than 6 months in 20 cases, 6-12 months in 9, 12-24 months in 3 and more than 24 months in 2 cases.
  • One patient with initial small cell lung cancer had developed NSCLC before entering this study.
  • The median survival time was 23.8 weeks.
  • Docetaxel should be considered as second line chemotherapy in advanced NSCLC when primary chemotherapy including cisplatin and/or paclitaxel had failed.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Paclitaxel / administration & dosage. Paclitaxel / analogs & derivatives. Palliative Care / methods. Taxoids
  • [MeSH-minor] Adult. Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Staging. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Palliative Care.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12678167.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


8. Shor AC, Keschman EA, Lee FY, Muro-Cacho C, Letson GD, Trent JC, Pledger WJ, Jove R: Dasatinib inhibits migration and invasion in diverse human sarcoma cell lines and induces apoptosis in bone sarcoma cells dependent on SRC kinase for survival. Cancer Res; 2007 Mar 15;67(6):2800-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib inhibits migration and invasion in diverse human sarcoma cell lines and induces apoptosis in bone sarcoma cells dependent on SRC kinase for survival.
  • Sarcomas are rare malignant mesenchymal tumors for which there are limited treatment options.
  • One potential molecular target for sarcoma treatment is the Src tyrosine kinase.
  • Dasatinib (BMS-354825), a small-molecule inhibitor of Src kinase activity, is a promising cancer therapeutic agent with p.o. bioavailability.
  • Dasatinib exhibits antitumor effects in cultured human cell lines derived from epithelial tumors, including prostate and lung carcinomas.
  • Based on our previous findings of Src activation in human sarcomas, we evaluated the effects of dasatinib in 12 cultured human sarcoma cell lines derived from bone and soft tissue sarcomas.
  • Dasatinib inhibited Src kinase activity at nanomolar concentrations in these sarcoma cell lines.
  • This inhibition of Src signaling was accompanied by blockade of cell migration and invasion.
  • Moreover, apoptosis was induced in the osteosarcoma and Ewing's subset of bone sarcomas at nanomolar concentrations of dasatinib.
  • Inhibition of Src protein expression by small interfering RNA also induced apoptosis, indicating that these bone sarcoma cell lines are dependent on Src activity for survival.
  • These results show that dasatinib inhibits migration and invasion of diverse sarcoma cell types and selectively blocks the survival of bone sarcoma cells.
  • Therefore, dasatinib may provide therapeutic benefit by preventing the growth and metastasis of sarcomas in patients.
  • [MeSH-major] Apoptosis / drug effects. Bone Neoplasms / drug therapy. Cell Movement / drug effects. Osteosarcoma / drug therapy. Pyrimidines / pharmacology. Thiazoles / pharmacology. src-Family Kinases / antagonists & inhibitors. src-Family Kinases / metabolism
  • [MeSH-minor] Cell Line, Tumor. Dasatinib. Enzyme Activation. Humans. Neoplasm Invasiveness. Protein Kinase Inhibitors / pharmacology. Rhabdomyosarcoma / drug therapy. Rhabdomyosarcoma / enzymology. Rhabdomyosarcoma / pathology. Sarcoma, Ewing / drug therapy. Sarcoma, Ewing / enzymology. Sarcoma, Ewing / pathology. Signal Transduction / drug effects

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17363602.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA55652; United States / NCI NIH HHS / CA / CA67360; United States / NCI NIH HHS / CA / CA93544
  • [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 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
  •  go-up   go-down


9. Chiappori A, Simon G, Williams C, Haura E, Rocha-Lima C, Wagner H, Bepler G, Antonia S: Phase II study of first-line sequential chemotherapy with gemcitabine-carboplatin followed by docetaxel in patients with advanced non-small cell lung cancer. Oncology; 2005;68(4-6):382-90
Hazardous Substances Data Bank. CARBOPLATIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of first-line sequential chemotherapy with gemcitabine-carboplatin followed by docetaxel in patients with advanced non-small cell lung cancer.
  • RATIONALE: Despite the use of novel chemotherapeutic agents, patients with advanced non-small cell lung cancer (NSCLC) continue to show a poor survival.
  • OBJECTIVES: To assess the safety and efficacy of a novel sequential and putatively non-cross-resistant chemotherapy regimen.
  • METHODS: Eligibility included: stages IV and IIIB (malignant pleural effusion), performance status 0-1, and adequate renal, hepatic and bone marrow function.
  • Treatment consisted of gemcitabine, 1,000 mg/m2, on days 1 and 8, and carboplatin, AUC = 5, on day 1 every 4 weeks (2-4 cycles) followed by docetaxel, 75 mg/m2, on day 1 every 3 weeks (4 cycles).
  • Median survival time and progression-free survival were 6.7 and 4.9 months, respectively, with a 1-year survival of 37.5%.
  • Our results are comparable to those achieved with other similar regimens and do not represent a significant improvement in the treatment of advanced NSCLC.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Carboplatin / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Humans. Male. Middle Aged. Neoplasm Staging. Survival Rate. Taxoids / administration & dosage. Treatment Outcome

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16020967.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Taxoids; 0W860991D6 / Deoxycytidine; 15H5577CQD / docetaxel; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
  • [Number-of-references] 37
  •  go-up   go-down


10. Koschmieder S, Fauth F, Kriener S, Hoelzer D, Seipelt G: Effective treatment of simultaneous small cell lung cancer and B-cell lymphoma. Leuk Lymphoma; 2002 Mar;43(3):645-7
Genetic Alliance. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective treatment of simultaneous small cell lung cancer and B-cell lymphoma.
  • Malignant lymphomas have been reported previously to coincide with adenocarcinomas of the stomach and, rarely, the kidney, breast, colon, liver, or lung.
  • Here, we describe the first case to our knowledge of a malignant lymphoma and an extensive disease small cell cancer of the lung.
  • A B-cell non-Hodgkin's lymphoma (NHL) was diagnosed from biopsies of the stomach and liver.
  • Further staging revealed a dense infiltration of the bone marrow by both a small cell lung cancer and a malignant lymphoma.
  • Both tumors responded well to chemotherapy.
  • This unique case report demonstrates that the simultaneous occurrence of small cell lung cancers and malignant lymphomas is extremely rare and may effectively be treated with chemotherapy.
  • [MeSH-major] Carcinoma, Small Cell / complications. Lymphoma, B-Cell / complications
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Bone Marrow / pathology. Humans. Liver / pathology. Male. Middle Aged. Neoplasm Invasiveness. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12002773.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


11. Eschmann SM, Friedel G, Paulsen F, Budach W, Harer-Mouline C, Dohmen BM, Bares R: FDG PET for staging of advanced non-small cell lung cancer prior to neoadjuvant radio-chemotherapy. Eur J Nucl Med Mol Imaging; 2002 Jun;29(6):804-8
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FDG PET for staging of advanced non-small cell lung cancer prior to neoadjuvant radio-chemotherapy.
  • The aim of this study was to evaluate positron emission tomography (PET) with fluorine-18 fluorodeoxyglucose (FDG) for the staging of non-small cell lung cancer (NSCLC) before combined neoadjuvant, i.e. preoperative, radio-chemotherapy (RCT).
  • The results of PET were compared with those obtained by mediastinoscopy, computed tomography (CT), bone scan and abdominal ultrasonography.
  • PET proved to be highly accurate for the detection of lymph node metastases (sensitivity 96%, specificity 73%, positive predictive value 88%, negative predictive value 89%, accuracy 88%) as well as distant metastases (in 25/101 patients, all previously unknown).
  • PET findings changed further treatment in 29/101 patients (29%).
  • One patient was free of metastases and therefore was operated on without pre-treatment.
  • Two patients did not receive any further treatment because a malignant tumour could be excluded after PET.
  • FDG PET is the most accurate non-invasive diagnostic procedure for the staging of advanced NSCLC.
  • Therefore use of FDG PET is highly recommended in order to select patients for neoadjuvant or other stage-dependent treatment modalities.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / radionuclide imaging. Carcinoma, Non-Small-Cell Lung / therapy. Lung Neoplasms / radionuclide imaging. Lung Neoplasms / therapy. Neoplasm Staging / methods
  • [MeSH-minor] Adult. Aged. Female. Fluorodeoxyglucose F18 / pharmacokinetics. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoadjuvant Therapy. Radiopharmaceuticals / pharmacokinetics

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12029555.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
  •  go-up   go-down


12. Yoshida A, Edgar MA, Garcia J, Meyers PA, Morris CD, Panicek DM: Primary desmoplastic small round cell tumor of the femur. Skeletal Radiol; 2008 Sep;37(9):857-62
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary desmoplastic small round cell tumor of the femur.
  • Desmoplastic small round cell tumor (DSRCT) is a rare malignant neoplasm typically involving the abdominal cavity of a young male.
  • Despite chemotherapy and complete tumor excision, the patient developed progressive lung and bone metastases and died 3 years after initial presentation.
  • This is the second reported case of primary DSRCT of bone with genetic confirmation.
  • [MeSH-major] Diagnostic Imaging. Femoral Neoplasms / diagnosis. Sarcoma, Small Cell / diagnosis
  • [MeSH-minor] Biopsy. Child. Diagnosis, Differential. Fatal Outcome. Female. Humans. Lung Neoplasms / secondary. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Desmoplastic Small Round Cell Tumor.
  • MedlinePlus Health Information. consumer health - Diagnostic Imaging.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1998 Sep;16(9):3028-36 [9738572.001]
  • [Cites] Hum Pathol. 2000 May;31(5):532-8 [10836292.001]
  • [Cites] Am J Surg Pathol. 2002 Jul;26(7):823-35 [12131150.001]
  • [Cites] Am J Surg Pathol. 1999 Nov;23(11):1408-13 [10555010.001]
  • [Cites] Am J Surg Pathol. 2007 Mar;31(3):454-9 [17325488.001]
  • [Cites] Pediatr Pathol. 1989;9(2):177-83 [2473463.001]
  • [Cites] Am J Surg Pathol. 1999 Feb;23 (2):159-65 [9989842.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Jan 15;156(2):167-71 [15642398.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):2837-40 [8187063.001]
  • [Cites] Am J Surg Pathol. 1991 Jun;15(6):499-513 [1709557.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3423-30 [12972518.001]
  • (PMID = 18470511.001).
  • [ISSN] 0364-2348
  • [Journal-full-title] Skeletal radiology
  • [ISO-abbreviation] Skeletal Radiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


13. He H, Cheng L, Weiss LM, Chu PG: Clinical outcome of incidental pelvic node malignant B-cell lymphomas discovered at the time of radical prostatectomy. Leuk Lymphoma; 2007 Oct;48(10):1976-80
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical outcome of incidental pelvic node malignant B-cell lymphomas discovered at the time of radical prostatectomy.
  • Incidental pelvic node malignant B-cell lymphomas diagnosed at the time of radical prostatectomy are rare.
  • Of 13 cases, 9 were chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), 3 marginal zone B-cell lymphoma (MZL) and 1 mantle cell lymphoma (MCL).
  • All 13 patients did not receive radiation or chemotherapy; and five of 13 cases showed hematologic evidence of lymphoma progression between 1 and 5 months after radical prostatectomy.
  • After progression, the mantle cell lymphoma patient received aggressive chemotherapy and had systemic dissemination.
  • In conclusion, most incidental pelvic node lymphomas (8/13) showed no evidence of systemic dissemination to peripheral blood or bone marrow after a mean 42.8 weeks of follow-up despite the fact that no additional treatment was given.
  • Strong consideration should be given to withholding further treatment in patients diagnosed with pelvic low-grade B-cell lymphoma at the time of radical prostatectomy until disease progression occurs.
  • [MeSH-major] Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / therapy. Neoplasms, Second Primary / therapy. Prostatic Neoplasms / surgery. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Disease-Free Survival. Follow-Up Studies. Humans. Male. Middle Aged. Models, Biological. Neoplasm Metastasis. Prognosis. Prostatectomy. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17917966.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


14. Kim HJ, Kim YJ, Seo MD, Yi HG, Lee SH, Lee SM, Kim DW, Yang SC, Lee CT, Lee JS, Kim YW, Heo DS: Patterns of palliative procedures and clinical outcomes in patients with advanced non-small cell lung cancer. Lung Cancer; 2009 Aug;65(2):242-6
MedlinePlus Health Information. consumer health - Palliative Care.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of palliative procedures and clinical outcomes in patients with advanced non-small cell lung cancer.
  • BACKGROUND: Despite recent progress in palliative chemotherapy for advanced non-small cell lung cancer (NSCLC), the prognosis is still poor.
  • Aside from multiple lines of chemotherapy, many patients need palliative procedures due to disease-related events.
  • METHODS: We evaluated 162 patients who were diagnosed with stage IIIB (with malignant effusion) or IV NSCLC at Seoul National University Hospital in 2005.
  • Forty-nine patients (30%) needed a palliative procedure at the time of diagnosis, and 59 patients (36%) required palliative procedure later during the course of their treatment.
  • The events requiring palliative procedures were thoracic events (malignant effusion or severe pneumonia requiring intensive care unit care not related to treatment) in 32 (30%), CNS events (brain metastasis or leptomeningeal metastasis) in 37 (34%), skeletal events (bone metastasis requiring radiation, spinal cord compression, hypercalcemia) in 29 (27%), and other events in 10 (9%).
  • The patients who had events at the time of diagnosis showed comparable overall survival to the patients without events at the time of diagnosis (14.6 months vs. 13.3 months, p=0.65).
  • The patients with later events during their course of treatment had a short median survival after the event requiring palliative procedures (median 2.7 months, 95% CI 2.19-3.21).
  • CONCLUSION: A considerable proportion of patients with advanced NSCLC receive palliative procedures apart from chemotherapy.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / complications. Carcinoma, Non-Small-Cell Lung / therapy. Lung Neoplasms / complications. Lung Neoplasms / therapy. Palliative Care / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Staging

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19147252.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  •  go-up   go-down


15. López-Martin A, Ballestín C, Garcia-Carbonero R, Castaño A, Lopez-Ríos F, López-Encuentra A, Sánchez-Cespedes M, Castellano D, Bartolomé A, Cortés-Funes H, Paz-Ares L: Prognostic value of KIT expression in small cell lung cancer. Lung Cancer; 2007 Jun;56(3):405-13
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of KIT expression in small cell lung cancer.
  • BACKGROUND: Small cell lung cancer (SCLC) is a very aggressive disease, with poor survival rates despite standard treatment with combination chemotherapy with or without radiotherapy.
  • Further insights into the molecular biology of this malignant tumour are needed to improve the therapeutic approaches and outcome.
  • RESULTS: KIT expression was observed in 149 of 204 tumour tissues (73%).
  • KIT expression was associated with advanced disease and with decreased incidence of bone metastases.
  • No significant differences were observed for time to disease progression (TTP) (9.1% versus 6.2% at 3 years, p=0.6) or overall survival (OS) (10.7% versus 6.9% at 3 years, p=0.37) among patients with KIT positive versus negative tumours, respectively.
  • Multivariate analysis showed that sex, tumour stage, albumin levels and response to therapy were the only independent predictors for survival.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Carcinoma, Small Cell / metabolism. Lung Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Severity of Illness Index

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17420067.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down


16. Hartmann TN, Burger M, Burger JA: The role of adhesion molecules and chemokine receptor CXCR4 (CD184) in small cell lung cancer. J Biol Regul Homeost Agents; 2004 Apr-Jun;18(2):126-30
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of adhesion molecules and chemokine receptor CXCR4 (CD184) in small cell lung cancer.
  • Small-cell lung cancer (SCLC) is a particularly aggressive form of lung cancer.
  • Responsible for this highly malignant phenotype is an early and widespread metastasis with a high propensity of SCLC cells for bone marrow involvement and the ability to develop resistance against chemotherapeutic agents.
  • Tumor cell migration and metastasis share many similarities with leukocyte trafficking, which is critically regulated by chemokines and adhesion molecules.
  • These adhesive interactions result in an increased resistance of SCLC cells to chemotherapy.
  • As such, inhibitors of the CXCR4/CXCL12 axis and/or integrin activation may increase the chemosensitivity of SCLC cells and lead to new therapeutic avenues for patients with SCLC.
  • [MeSH-major] Carcinoma, Small Cell / physiopathology. Cell Adhesion Molecules / physiology. Lung Neoplasms / physiopathology. Receptors, CXCR4 / physiology
  • [MeSH-minor] Cell Adhesion / physiology. Cell Movement / physiology. Chemokine CXCL12. Chemokines, CXC / physiology. Cytoskeleton / physiology. Drug Resistance, Neoplasm. Humans. Neoplasm Metastasis / physiopathology. Signal Transduction / physiology

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15471215.001).
  • [ISSN] 0393-974X
  • [Journal-full-title] Journal of biological regulators and homeostatic agents
  • [ISO-abbreviation] J. Biol. Regul. Homeost. Agents
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Cell Adhesion Molecules; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Receptors, CXCR4
  • [Number-of-references] 41
  •  go-up   go-down


17. Montillo M, Schinkoethe T, Elter T: Eradication of minimal residual disease with alemtuzumab in B-cell chronic lymphocytic leukemia (B-CLL) patients: the need for a standard method of detection and the potential impact of bone marrow clearance on disease outcome. Cancer Invest; 2005;23(6):488-96
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Eradication of minimal residual disease with alemtuzumab in B-cell chronic lymphocytic leukemia (B-CLL) patients: the need for a standard method of detection and the potential impact of bone marrow clearance on disease outcome.
  • The introduction of new therapeutic agents, such as fludarabine phosphate (Fludara) and alemtuzumab (MabCampath, Campath), has made it possible to treat B-cell chronic lymphocytic leukemia (B-CLL) more effectively, compared with alkylating agents.
  • However, although an increasing number of patients are able to achieve complete remission (CR), relapse is almost inevitable, because of the re-emergence of the malignant clone from small numbers of residual malignant cells.
  • This phenomenon has introduced a need for a more sensitive assessment of low-level disease which, in turn, has encouraged the development of therapies aimed at the eradication of all residual disease in CR patients.
  • Alemtuzumab is the foundation of many eradication-based treatment approaches because of its ability to achieve clinical remissions and to successfully purge minimal residual disease (MRD) from both blood and bone marrow in B-CLL patients.
  • This article describes and compares polymerase chain reaction (PCR) and flow cytometric methodologies for the assessment of MRD, and presents data demonstrating that alemtuzumab can eliminate residual malignant cells from blood and bone marrow (whether assessed by PCR or flow cytometry) at the highest levels of sensitivity currently available.
  • The ability to clear MRD from bone marrow in patients achieving clinical CR using alemtuzumab is a significant step forward in the treatment of B-CLL, and supports treatment strategies in which alemtuzumab is used in combination with other agents.
  • Purging of MRD from both blood and bone marrow also enables patients to proceed to autologous hematopoietic stem cell transplantation, a strategy that is able to achieve long-term remission.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Neoplasm, Residual / diagnosis. Neoplasm, Residual / drug therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16203656.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 55
  •  go-up   go-down


18. Edinger M, Cao YA, Verneris MR, Bachmann MH, Contag CH, Negrin RS: Revealing lymphoma growth and the efficacy of immune cell therapies using in vivo bioluminescence imaging. Blood; 2003 Jan 15;101(2):640-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Revealing lymphoma growth and the efficacy of immune cell therapies using in vivo bioluminescence imaging.
  • Cancer therapeutics have achieved success in the treatment of a variety of malignancies, however, relapse of disease from small numbers of persistent tumor cells remains a major obstacle.
  • Advancement of treatment regimens that effectively control minimal residual disease and prevent relapse would be greatly accelerated if sensitive and noninvasive assays were used to quantitatively assess tumor burden in animal models of minimal residual disease that are predictive of the human response.
  • In vivo bioluminescence imaging (BLI) is an assay for the detection of small numbers of cells noninvasively and enables the quantification of tumor growth within internal organs.
  • Fusion genes that encode bioluminescent and fluorescent reporter proteins effectively couple the powerful in vivo capabilities of BLI with the subset-discriminating capabilities of fluorescence-activated cell sorting.
  • We labeled 2 murine lymphoma cell lines with dual function reporter genes and monitored radiation and chemotherapy as well as immune-based strategies that employ the tumorcidal activity of ex vivo-expanded CD8(+) natural killer (NK)-T cells.
  • Using BLI we were able to visualize the entire course of malignant disease including engraftment, expansion, metastasis, response to therapy, and unique patterns of relapse.
  • These studies reveal the efficacy of immune cell therapies and the tempo of NK-T cell trafficking in vivo.
  • The complex cellular processes in bone marrow transplantation and antitumor immunotherapy, previously inaccessible to investigation, can now be revealed in real time in living animals.
  • [MeSH-major] Diagnostic Imaging / methods. Immunotherapy, Adoptive / methods. Lymphoma / pathology. Lymphoma / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Division / drug effects. Cell Division / genetics. Cell Division / radiation effects. Female. Genes, Reporter. Killer Cells, Lymphokine-Activated / metabolism. Killer Cells, Lymphokine-Activated / transplantation. Luminescent Measurements. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasm Metastasis / diagnosis. Neoplasm Metastasis / pathology. Radiotherapy. Transduction, Genetic

  • MedlinePlus Health Information. consumer health - Diagnostic Imaging.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12393519.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL04505-01; United States / NCI NIH HHS / CA / P01 CA49605; United States / NCI NIH HHS / CA / P20 CA86312; United States / NCI NIH HHS / CA / R01 CA80006; United States / NCI NIH HHS / CA / R24 CA92862; United States / NCI NIH HHS / CA / R33 CA88303
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


19. He Y, Zhang J, Zheng J, Du W, Xiao H, Liu W, Li X, Chen X, Yang L, Huang S: The insulin-like growth factor-1 receptor kinase inhibitor, NVP-ADW742, suppresses survival and resistance to chemotherapy in acute myeloid leukemia cells. Oncol Res; 2010;19(1):35-43
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The insulin-like growth factor-1 receptor kinase inhibitor, NVP-ADW742, suppresses survival and resistance to chemotherapy in acute myeloid leukemia cells.
  • Deregulation of insulin-like growth factor-1 receptor (IGF-1R) is closely associated with malignant transformation and tumor cell survival in various cancers.
  • We found that IGF-1R expression level in leukemia cells positively correlated with the percentage of blast in bone marrow from de novo acute myeloid leukemia (AML) patients.
  • Moreover, we showed that NVP-ADW742, a novel small weight molecular inhibitor of IGF-IR, could induce apoptosis in both HL-60 cell line and primary AML blasts.
  • However, no significant alteration of cell cycle was observed in HL-60 cells.
  • Finally, we demonstrated that NVP-ADW742 could synergize with Ara-C to induce the kill in a subset of drug-resistant AML specimens.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. Pyrroles / pharmacology. Receptor, IGF Type 1 / antagonists & inhibitors
  • [MeSH-minor] Apoptosis / drug effects. Cytarabine / pharmacology. Drug Resistance, Neoplasm. HL-60 Cells. Humans. Signal Transduction

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21141739.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NVP ADW742; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Pyrroles; 04079A1RDZ / Cytarabine; EC 2.7.10.1 / Receptor, IGF Type 1
  •  go-up   go-down


20. Burdach S, van Kaick B, Laws HJ, Ahrens S, Haase R, Körholz D, Pape H, Dunst J, Kahn T, Willers R, Engel B, Dirksen U, Kramm C, Nürnberger W, Heyll A, Ladenstein R, Gadner H, Jürgens H, Go el U: Allogeneic and autologous stem-cell transplantation in advanced Ewing tumors. An update after long-term follow-up from two centers of the European Intergroup study EICESS. Stem-Cell Transplant Programs at Düsseldorf University Medical Center, Germany and St. Anna Kinderspital, Vienna, Austria. Ann Oncol; 2000 Nov;11(11):1451-62
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic and autologous stem-cell transplantation in advanced Ewing tumors. An update after long-term follow-up from two centers of the European Intergroup study EICESS. Stem-Cell Transplant Programs at Düsseldorf University Medical Center, Germany and St. Anna Kinderspital, Vienna, Austria.
  • BACKGROUND: An update of results from the High Risk Protocol of the Meta-EICESS Study, conducted at the Pediatric Stem-Cell Transplant Centers of Düsseldorf and Vienna.
  • In order to evaluate a possible therapeutic benefit after allogeneic SCT in patients with advanced Ewing tumors (AET), we compared outcome after autologous and allogeneic stem-cell transplantation (SCT).
  • All patients underwent remission induction chemotherapy and local treatment before myeloablative therapy.
  • We analyzed the following risk factors, that could possibly influence the event-free survival (EFS): number of involved bones, degree of remission at time of SCT, type of graft, indication for SCT, bone marrow infiltration, bone with concomitant lung disease, age at time of diagnosis, pelvic involvement, involved compartment radiation, histopathological diagnosis.
  • Eighteen of thirty-six patients suffered relapse or died of disease, nine of thirty-six died of treatment related toxicity (DOC).
  • Age > or = 17 years at initial diagnosis (P < 0.005) significantly deteriorated outcome.
  • According to the type of graft, EFS was 0.25 +/- 0.08 after autologous and 0.20 +/- 0.13 after allogeneic SCT.
  • CONCLUSIONS: Because of the rather short observation period. secondary malignant neoplasms (SMN) may complicate the future clinical course of some of our patients who are currently viewed as event-free survivors.
  • The patient group was to small to analyze for a possible graft-versus-tumor effect.

  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11142486.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interleukin-2
  • [Number-of-references] 56
  •  go-up   go-down


21. Sebastian M, Passlick B, Friccius-Quecke H, Jäger M, Lindhofer H, Kanniess F, Wiewrodt R, Thiel E, Buhl R, Schmittel A: Treatment of non-small cell lung cancer patients with the trifunctional monoclonal antibody catumaxomab (anti-EpCAM x anti-CD3): a phase I study. Cancer Immunol Immunother; 2007 Oct;56(10):1637-44
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of non-small cell lung cancer patients with the trifunctional monoclonal antibody catumaxomab (anti-EpCAM x anti-CD3): a phase I study.
  • PURPOSE: Catumaxomab is a trifunctional monoclonal antibody with binding sites directed to human EpCAM and the human T cell antigen CD3 (anti-EpCAM x anti-CD3).
  • Catumaxomab demonstrated efficacy when administered intraperitoneally in patients with EpCAM positive malignant ascites from ovarian cancer in terms of tumor cell killing and reduction of ascites generation.
  • As EpCAM is also overexpressed in NSCLC, the present study was conducted in order to evaluate safety and tolerability of intravenous treatment with catumaxomab.
  • PATIENTS AND METHODS: UICC stage IB-IV NSCLC patients were eligible, if they had at least one prior therapy.
  • Other inclusion criteria were: age 18-75 years, adequate bone marrow function and AST or gamma-GT<or=2.5 ULN.
  • CONCLUSIONS: Five micrograms of catumaxomab with a pre-medication of 40 mg dexamethasone and antihistamines can be recommended as first dose for i.v. therapy consisting of multiple catumaxomab infusions for patients with NSCLC.
  • [MeSH-major] Antibodies, Bispecific / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Antigens, CD3 / immunology. Antigens, Neoplasm / immunology. Cell Adhesion Molecules / immunology. Disease Progression. Female. Humans. Male. Mice. Middle Aged. Rats


22. Wang HT, Lo YS, Huang JK: Primary lymphoma of the penis. J Chin Med Assoc; 2003 Jun;66(6):379-81
MedlinePlus Health Information. consumer health - Lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary penile lymphoma is a rare neoplasm.
  • Pathologic examination of needle biopsy showed diffuse, small and T-cell type malignant lymphoma.
  • Whole-body computed tomography scan and bone marrow aspiration revealed no evidence of distant metastasis.
  • We treated this patient with chemotherapy alone and achieved complete remission 2 months later.
  • There was absence of tumor recurrence 20 months after treatment.
  • [MeSH-major] Lymphoma / drug therapy. Penile Neoplasms / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12889509.001).
  • [ISSN] 1726-4901
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
  •  go-up   go-down


23. Paterson AH: Bisphosphonates: biological response modifiers in breast cancer. Clin Breast Cancer; 2002 Aug;3(3):206-16; discussion 217-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bone recurrence constitutes one third of initial sites of relapse and one half of distant sites of relapse at 10 years from diagnosis of breast cancer.
  • Bone pain, fracture (including vertebral fracture resulting from increased bone resorption following chemotherapy-induced menopause), and hypercalcemia are components of skeletal morbidity.
  • The pathophysiology of malignant osteopathy occurs because of the secretion of substances (such as parathyroid hormone-related peptide), by the malignant cell, which stimulate osteoclast function; this in turn feeds further growth, which causes a vicious cycle.
  • Interruption of this cycle by bisphosphonates may inhibit the growth of malignant cells.
  • Bisphosphonates are drugs that inhibit bone turnover by decreasing bone resorption.
  • Bisphosphonates have different molecular mechanisms of action: Nitrogen-containing bisphosphonates (eg, pamidronate and alendronate) inhibit the mevalonate-signaling pathway while the non-nitrogen-containing drugs (eg, clodronate) incorporate into adenosine triphosphate analogues.
  • There is in vitro evidence that these drugs also possess anticancer properties.
  • In hypercalcemia patients, treatment with pamidronate and zoledronate produce prompt and efficient normocalcemia.
  • Intravenous pamidronate and zoledronate, oral clodronate, and ibandronate reduce skeletal complications in patients with bone metastases; I.V. pamidronate and clodronate are useful for bone pain relief.
  • Three adjuvant bisphosphonate trials are discussed herein: 2 small open-label studies giving conflicting results and a large placebo-controlled trial of oral clodronate.
  • This latter trial shows a reduction in the incidence of skeletal metastases (while the patients are on therapy) and an improved survival at 5 years.
  • [MeSH-major] Bone Neoplasms / drug therapy. Breast Neoplasms / pathology. Diphosphonates / therapeutic use. Hypercalcemia / drug therapy. Neoplasm Recurrence, Local / drug therapy

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12196279.001).
  • [ISSN] 1526-8209
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphosphonates
  • [Number-of-references] 82
  •  go-up   go-down


24. Steinbach D, Gillet JP, Sauerbrey A, Gruhn B, Dawczynski K, Bertholet V, de Longueville F, Zintl F, Remacle J, Efferth T: ABCA3 as a possible cause of drug resistance in childhood acute myeloid leukemia. Clin Cancer Res; 2006 Jul 15;12(14 Pt 1):4357-63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABCA3 as a possible cause of drug resistance in childhood acute myeloid leukemia.
  • BACKGROUND: A major issue in the treatment of acute myeloid leukemia (AML) is resistance to chemotherapeutic drugs.
  • Multidrug resistance can be caused by ATP-binding cassette (ABC) transporters that function as drug efflux pumps.
  • The majority of these proteins have not yet been examined in malignant diseases.
  • EXPERIMENTAL DESIGN: A newly developed microarray for the simultaneous quantification of 38 ABC transporter genes and Taqman real-time PCR was used to analyze the expression of ABC transporters in pediatric AML and healthy bone marrow.
  • Small interfering RNA was used to verify the role of ABCA3 in drug resistance.
  • RESULTS: Using the microarray, we identified four new ABC transporters, which were overexpressed in many AML samples compared with healthy bone marrow: ABCA2, ABCA3, ABCB2, and ABCC10.
  • The overexpression of these four genes was verified by real-time PCR in 42 samples from children with AML and 18 samples of healthy bone marrow.
  • The median expression of ABCA3 was three times higher in 21 patients who had failed to achieve remission after the first course of chemotherapy than in a well-matched group of 21 patients who had achieved remission at this stage (P = 0.023).
  • Incubation of cell lines with a number of different cytostatic drugs induced an up-regulation of ABCA3.
  • Down-regulation of ABCA3 by small interfering RNA sensitized cells to doxorubicin.
  • CONCLUSION: Our results show that ABCA2, ABCA3, ABCB2, and ABCC10 are overexpressed in childhood AML compared with healthy bone marrow.
  • ABCA3 is the most likely transporter to cause drug resistance.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Cells / metabolism. Child. Child, Preschool. Cluster Analysis. Drug Resistance, Multiple. Female. Humans. Jurkat Cells. Male. Oligonucleotide Array Sequence Analysis. RNA, Small Interfering / metabolism

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Childhood.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16857811.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCA3 protein, human; 0 / ATP-Binding Cassette Transporters; 0 / RNA, Small Interfering
  •  go-up   go-down


25. Nakazato T, Suzuki K, Mihara A, Sanada Y, Yoshida S, Kakimoto T: [Intravascular large B-cell lymphoma with pontine involvement successfully treated with R-hyper-CVAD/R-MTX-Ara-C regimen]. Rinsho Ketsueki; 2010 Feb;51(2):148-52
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Intravascular large B-cell lymphoma with pontine involvement successfully treated with R-hyper-CVAD/R-MTX-Ara-C regimen].
  • Malignant lymphoma was suspected, but histological diagnosis was difficult because superficial lymph nodes could not be palpated.
  • Histological examination of the bone marrow biopsy specimen demonstrated the proliferation of large atypical lymphoid cells positive for CD20 and CD79a in the small capillaries, leading to the diagnosis of intravascular large B-cell lymphoma (IVLBCL).
  • We chose R-hyper-CVAD/R-MTX-Ara-C alternating therapy with MTX intrathecal injection because CNS involvement in IVLBCL was highly suspected, and she responded well.
  • R-hyper-CVAD/R-MTX-Ara-C alternating therapy was effective in an IVLBCL patient with CNS involvement.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Stem Neoplasms / drug therapy. Brain Stem Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Vascular Neoplasms / drug therapy
  • [MeSH-minor] Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Female. Humans. Methotrexate / administration & dosage. Middle Aged. Neoplasm Invasiveness. Remission Induction. Treatment Outcome. Vincristine / administration & dosage

  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20379108.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate; CVAD protocol
  •  go-up   go-down


26. Ludwig K: [Musculoskeletal lymphomas]. Radiologe; 2002 Dec;42(12):988-92
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary lymphomas of bone or skeletal muscle are rare entities.
  • The most frequent among these diseases are primary non-Hodgkin's lymphomas of bone.
  • They account for 3-5% of all bone tumors and 5% of all primary extranodal non-Hodgkin's lymphomas.
  • Primary manifestations of Hodgkin's disease in bone or skeletal muscle are rarities.
  • Primary non-Hodgkin's lymphomas of bone can be found in any patient age.
  • The radiographic appearance of these entities resembles other aggressive bone tumors.
  • Their differential diagnosis includes -- depending on the patient's age -- Ewing's sarcoma,malignant fibrous histiocytoma,metastases of small cell tumors and osteomyelitis.Further differential diagnoses are the peripheral primitive neuroectodermal tumor (PNET), osteosarcoma, eosinophilic granuloma and fibrosarcoma.
  • Treatment of primary non-Hodgkin's lymphomas uses combinations of chemotherapy and radiation therapy.
  • Operative treatment is reserved for the treatment of complications.
  • [MeSH-major] Bone Neoplasms / diagnosis. Hodgkin Disease / diagnosis. Lymphoma, Non-Hodgkin / diagnosis. Magnetic Resonance Imaging. Muscle Neoplasms / diagnosis. Tomography, X-Ray Computed
  • [MeSH-minor] Bone and Bones / pathology. Humans. Muscle, Skeletal / pathology. Neoplasm Staging. Prognosis. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - CT Scans.
  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
  • MedlinePlus Health Information. consumer health - MRI Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12486552.001).
  • [ISSN] 0033-832X
  • [Journal-full-title] Der Radiologe
  • [ISO-abbreviation] Radiologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 0
  •  go-up   go-down


27. Kunisaki Y, Muta T, Yamano Y, Kobayashi Y: Detection of two cell populations corresponding to distinct maturation stages in API-2/MLT-positive mucosa-associated lymphoid tissue lymphoma cells proliferating in pleural effusion. Int J Hematol; 2003 Nov;78(4):357-61

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of two cell populations corresponding to distinct maturation stages in API-2/MLT-positive mucosa-associated lymphoid tissue lymphoma cells proliferating in pleural effusion.
  • Abnormal plasmacytoid cells were seen in both the peripheral blood (PB) and the bone marrow (BM).
  • Computed tomography scans showed extensive thickening of the gastric wall and bilateral massive PE without lymph node or pulmonary involvement.
  • A histologic examination of the gastric mucosa showed a diffuse infiltration of small- to medium-sized lymphoid CD20-bearing cells, some of which showed a plasmacytoid morphology.
  • The diagnosis was gastric mucosa-associated lymphoid tissue (MALT) lymphoma infiltrating to the PE, PB, and BM.
  • The patient had a good response to fludarabine treatment, which was followed with rituximab therapy.
  • In this article, we show that the cell character of API-2/MLT-positive MALT lymphoma is preserved even when the cells are disseminated.
  • [MeSH-major] Lymphoma, B-Cell, Marginal Zone / pathology. Oncogene Proteins, Fusion / analysis. Pleural Effusion, Malignant / pathology
  • [MeSH-minor] Aged. Antigens, Differentiation, B-Lymphocyte / analysis. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. B-Lymphocytes / pathology. Cell Adhesion Molecules / analysis. Cell Differentiation. Cell Division. Humans. Immunophenotyping. Male. Neoplasm, Residual. Stomach Neoplasms / diagnosis. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1997 Sep 15;57(18):3944-8 [9307277.001]
  • [Cites] Blood. 2002 Jan 1;99(1):3-9 [11756145.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Lancet. 1991 Nov 9;338(8776):1175-6 [1682595.001]
  • [Cites] Am J Pathol. 1999 Dec;155(6):2019-27 [10595932.001]
  • [Cites] Mod Pathol. 2001 Aug;14(8):798-805 [11504840.001]
  • [Cites] Int J Hematol. 2002 Dec;76(5):385-93 [12512832.001]
  • [Cites] Blood. 2000 Jul 15;96(2):410-9 [10887100.001]
  • [Cites] Rinsho Ketsueki. 2000 Nov;41(11):1183-8 [11193437.001]
  • [Cites] Br J Haematol. 2001 Dec;115(3):588-94 [11736940.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1 Suppl 2):36-40 [11842387.001]
  • [Cites] Am J Clin Pathol. 2001 Nov;116(5):683-90 [11710684.001]
  • [Cites] Gut. 2001 Oct;49(4):519-25 [11559649.001]
  • [Cites] Am J Clin Pathol. 1999 Jan;111(1 Suppl 1):S8-12 [9894466.001]
  • [Cites] Am J Pathol. 1997 May;150(5):1583-93 [9137085.001]
  • [Cites] Br J Haematol. 1997 Jun;97(3):515-22 [9207392.001]
  • [Cites] Jpn J Cancer Res. 2000 Mar;91(3):301-9 [10760689.001]
  • [Cites] Leuk Res. 1990;14(7):617-22 [2388473.001]
  • [Cites] Acta Otolaryngol Suppl. 1996;523:259-62 [9082801.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Mar;117(2):113-7 [10704680.001]
  • [Cites] Cell. 1993 Jul 16;74(1):185-95 [7687523.001]
  • (PMID = 14686495.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / API2-MALT1 fusion protein, human; 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Cell Adhesion Molecules; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


28. Demetri GD: Identification and treatment of chemoresistant inoperable or metastatic GIST: experience with the selective tyrosine kinase inhibitor imatinib mesylate (STI571). Eur J Cancer; 2002 Sep;38 Suppl 5:S52-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and treatment of chemoresistant inoperable or metastatic GIST: experience with the selective tyrosine kinase inhibitor imatinib mesylate (STI571).
  • Sequencing of c-kit complementary DNA from human GIST cells has demonstrated a high frequency of mutations that lead to constitutive activation of the KIT tyrosine kinase in the absence of stimulation by its physiologic ligand (stem cell factor).
  • Historically, malignant GIST has been highly refractory to conventional cytotoxic therapy.
  • Signal transduction inhibition as cancer therapy was first tested successfully with imatinib mesylate (formerly known as STI571), a selective small-molecule tyrosine kinase inhibitor, with the initial target being blockade of Bcr-Abl, the oncogene with tyrosine kinase activity responsible for the pathogenesis of chronic myelogenous leukemia (CML).
  • The first GIST patient to receive imatinib exhibited dramatic benefit despite far-advanced metastatic disease that was previously refractory to all chemotherapy.
  • The results from these studies have established imatinib as an effective new therapeutic alternative for the majority of patients with advanced GIST, a solid tumor for which no prior chemotherapy has ever shown antitumor efficacy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Gastrointestinal Neoplasms / drug therapy. Neoplasms, Connective Tissue / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Stromal Cells
  • [MeSH-minor] Benzamides. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Neoplasm Proteins / antagonists & inhibitors. Neoplasm Recurrence, Local / prevention & control. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit. Receptor Protein-Tyrosine Kinases. Tomography, Emission-Computed

  • Genetic Alliance. consumer health - Gastrointestinal Stromal Tumors.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12528773.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  • [Number-of-references] 28
  •  go-up   go-down


29. Yamamoto R, Hosokawa S, Yamatodani T, Morita S, Okamura J, Mineta H: [Eight cases of neuroendcrine carcinoma of the head and neck]. Nihon Jibiinkoka Gakkai Kaiho; 2008 Jul;111(7):517-22
Hazardous Substances Data Bank. EPIRUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Small cell neuroendocrine carcinoma of the head and neck is rare, and diagnosis may be difficult.
  • We reported eight cases of stage IV small cell neuroendocrine carcinoma of the head and neck, all in men with a mean onset age of 62 years (range: 45 to 80 years).
  • Histological analysis by hematoxylin-eosin staining tentatively revealed malignant lymphoma and undifferentiated carcinoma in two cases each, while immunohistological and/or electron microscopy analysis confirmed histological diagnosis.
  • All were treated by chemotherapy (VP-16, CDDP) and seven cases with radiotherapy based on the schedule of small cell carcinoma of the lung and two cases with lesional resection.
  • Chemotherapy and radiotherapy were effective locally.
  • Five patients died of distant metastasis to the brain, bone, lung, liver, or skin within 12 months.
  • Long-term survival thus requires the effective treatment of distant metastasis.
  • [MeSH-major] Carcinoma, Neuroendocrine / pathology. Carcinoma, Neuroendocrine / therapy. Head and Neck Neoplasms / pathology. Head and Neck Neoplasms / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Cisplatin / administration & dosage. Combined Modality Therapy. Diagnosis, Differential. Epirubicin / administration & dosage. Humans. Immunohistochemistry. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Staging. Prognosis. Radiotherapy

  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18697475.001).
  • [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; 3Z8479ZZ5X / Epirubicin; Q20Q21Q62J / Cisplatin; PE regimen
  •  go-up   go-down


30. Rousseau J, Escriou V, Perrot P, Picarda G, Charrier C, Scherman D, Heymann D, Rédini F, Trichet V: Advantages of bioluminescence imaging to follow siRNA or chemotherapeutic treatments in osteosarcoma preclinical models. Cancer Gene Ther; 2010 Jun;17(6):387-97
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advantages of bioluminescence imaging to follow siRNA or chemotherapeutic treatments in osteosarcoma preclinical models.
  • Osteosarcoma is the most common malignant primary bone tumor for which pertinent preclinical models are still needed to develop new therapeutic strategies.
  • As osteosarcoma growth is strongly supported by bone resorption, previous studies have inhibited the cytokine receptor activator of nuclear factor-kappaB ligand using antibodies or recombinant proteins.
  • However, its expression has not yet been inhibited using genetic approaches using small interfering RNA.
  • To optimize the delivery of small interfering RNA to its cellular target and demonstrate their efficiency in vivo, two new osteosarcoma models expressing the firefly luciferase enzyme were developed.
  • In comparison with measurement of tumor volume, bioluminescence analysis enabled earlier tumor detection and revealed extensive cell death in response to ifosfamide treatment.
  • Finally, by targeting the luciferase expression into osteosarcoma, we established a protocol for in vivo administration of small interfering RNA combined with cationic liposome.
  • [MeSH-major] Luminescent Proteins / metabolism. Osteosarcoma / metabolism. RNA Interference. RNA, Small Interfering / genetics
  • [MeSH-minor] Animals. Cell Line. Cell Line, Tumor. Flow Cytometry. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Lentivirus / genetics. Luciferases, Firefly / genetics. Luciferases, Firefly / metabolism. Male. Mice. Mice, Inbred C3H. Mice, Inbred Strains. Mice, Nude. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Rats. Transfection. Transplantation, Heterologous. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Osteosarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20075983.001).
  • [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] 0 / Luminescent Proteins; 0 / RNA, Small Interfering; 147336-22-9 / Green Fluorescent Proteins; EC 1.13.12.7 / Luciferases, Firefly
  •  go-up   go-down


31. Hornick JL, Jaffe ES, Fletcher CD: Extranodal histiocytic sarcoma: clinicopathologic analysis of 14 cases of a rare epithelioid malignancy. Am J Surg Pathol; 2004 Sep;28(9):1133-44
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Histiocytic sarcoma is a rare malignant neoplasm that occurs in lymph nodes, skin, and the gastrointestinal tract.
  • Only small numbers of bona fide examples exist in the world literature; cases arising primarily at extranodal sites are not well described and often seem to go unrecognized.
  • Seven tumors arose in soft tissue (6 lower limb; 1 upper limb), 5 in the gastrointestinal tract (1 involving both stomach and colon, 1 ileum, 2 rectum, 1 anus), 1 in the nasal cavity, and 1 in the lung.
  • Six patients were treated with postoperative radiation and 7 with chemotherapy (CHOP or ProMACE-MOPP).
  • Two tumors recurred locally, and 5 patients developed distant spread: 3 to lymph nodes, 1 to lung, and 1 to bone.
  • At the last follow-up, 2 patients have died of disseminated disease, 4 and 5 months following initial diagnosis.
  • Histiocytic sarcoma may arise primarily in soft tissue and shows reproducible histologic features, including abundant eosinophilic cytoplasm and a prominent inflammatory infiltrate.
  • Metastatic carcinoma, metastatic melanoma, and large cell non-Hodgkin lymphomas should be excluded by immunohistochemistry.

  • Genetic Alliance. consumer health - Epithelioid Sarcoma.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15316312.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


32. Katz BZ: Adhesion molecules--The lifelines of multiple myeloma cells. Semin Cancer Biol; 2010 Jun;20(3):186-95
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • As a common presentation of the disease, the malignant plasma cells accumulate and proliferate in the bone marrow, where they disrupt normal hematopoiesis and bone physiology.
  • Multiple myeloma cells and the bone marrow microenvironment are linked by a composite network of interactions mediated by soluble factors and adhesion molecules.
  • The SDF-1/CXCR4 axis is a key factor in the homing of multiple myeloma cells to the bone marrow.
  • Several signaling responses are activated by adhesive interactions of multiple myeloma cells, and their outcomes affect the survival, proliferation and migration of these cells, and in many cases generate a drug-resistant phenotype.
  • Hence, the adhesion systems of multiple myeloma cells are attractive potential therapeutic targets.
  • Several approaches are being developed to disrupt the activities of adhesion molecules in multiple myeloma cells, including small antagonist molecules, direct targeting by immunoconjugates, stimulation of immune responses against these molecules, and signal transduction inhibitors.
  • These potential novel therapeutics may be incorporated into current treatment schemes, or directed against minimal residual malignant cells during remission.
  • [MeSH-major] Cell Adhesion Molecules / physiology. Multiple Myeloma / pathology
  • [MeSH-minor] Animals. Cell Adhesion / genetics. Cell Communication / physiology. Cell Proliferation. Drug Resistance, Neoplasm / genetics. Humans. Models, Biological. Molecular Targeted Therapy. Tumor Microenvironment / genetics. Tumor Microenvironment / physiology

  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010. Published by Elsevier Ltd.
  • (PMID = 20416379.001).
  • [ISSN] 1096-3650
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules
  •  go-up   go-down


33. Ory B, Moriceau G, Trichet V, Blanchard F, Berreur M, Rédini F, Rogers M, Heymann D: Farnesyl diphosphate synthase is involved in the resistance to zoledronic acid of osteosarcoma cells. J Cell Mol Med; 2008 Jun;12(3):928-41
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We recently demonstrated original anti-tumor effects of zoledronic acid (Zol) on osteosarcoma cell lines independently of their p53 and Rb status.
  • The present study investigated the potential Zol-resistance acquired by osteosarcoma cells after prolonged treatment.
  • After 12 weeks of culture in the presence of 1 microm Zol, the effects of high doses of Zol (10-100 microm) were compared between the untreated rat (OSRGA, ROS) and human (MG63, SAOS2) osteosarcoma cells and Zol-pretreated cells in terms of cell proliferation, cell cycle analysis, migration assay and cytoskeleton organization.
  • Long-term treatment with 1 microm Zol reduced the sensitivity of osteosarcoma cells to high concentrations of Zol.
  • However, as similar experiments performed in the presence of clodronate and pamidronate evidenced that this drug resistance was restricted to the nitrogen-containing bisphosphonates, we then hypothesized that this resistance could be associated with a differential expression of farnesyl diphos-phate synthase (FPPS) also observed in human osteosarcoma samples.
  • This study demonstrates for the first time the induction of metabolic resistance after prolonged Zol treatment of osteosarcoma cells confirming the therapeutic potential of Zol for the treatment of bone malignant pathologies, but points out the importance of the treatment regimen may be important in terms of duration and dose to avoid the development of drug metabolic resistance.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Diphosphonates / pharmacology. Drug Resistance, Neoplasm / drug effects. Geranyltranstransferase / metabolism. Imidazoles / pharmacology. Osteosarcoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. RNA, Small Interfering / pharmacology. Time Factors. Transfection

  • Genetic Alliance. consumer health - Osteosarcoma.
  • HAL archives ouvertes. Full text from .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18494934.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphosphonates; 0 / Imidazoles; 0 / RNA, Small Interfering; 6XC1PAD3KF / zoledronic acid; EC 2.5.1.10 / Geranyltranstransferase
  • [Other-IDs] NLM/ PMC4401135
  •  go-up   go-down


34. Cambien B, Karimdjee BF, Richard-Fiardo P, Bziouech H, Barthel R, Millet MA, Martini V, Birnbaum D, Scoazec JY, Abello J, Al Saati T, Johnson MG, Sullivan TJ, Medina JC, Collins TL, Schmid-Alliana A, Schmid-Antomarchi H: Organ-specific inhibition of metastatic colon carcinoma by CXCR3 antagonism. Br J Cancer; 2009 Jun 2;100(11):1755-64

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent research has indicated that CXCR3/chemokines interactions that orchestrate haematopoetic cell movement are implicated in the metastatic process of malignant tumours, including that of CRC cells to lymph nodes.
  • To determine whether CXCR3 receptors regulate malignancy-related properties of CRC cells, we have used CXCR3-expressing CRC cell lines of human (HT29 cells) and murine (C26 cells) origins that enable the development of liver and lung metastases when injected into immunodeficient and immunocompetent mice, respectively, and assessed the effect of CXCR3 blockade using AMG487, a small molecular weight antagonist.
  • In vivo, systemic CXCR3 antagonism by preventive or curative treatments with AMG487 markedly inhibited the implantation and the growth of human and mouse CRC cells within lung without affecting that in the liver.
  • Altogether, our findings indicate that activation of CXCR3 receptors by its cognate ligands facilitates the implantation and the progression of CRC cells within lung tissues and that inhibition of this axis decreases pulmonary metastasis of CRC in two murine tumour models.
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Cell Movement. Humans. Ligands. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Mice. Neoplasm Transplantation. Organ Specificity. Survival Rate

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2000 Jan 15;95(2):627-32 [10627472.001]
  • [Cites] Oncol Rep. 2003 Jul-Aug;10(4):909-13 [12792744.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):50-6 [11242036.001]
  • [Cites] Lab Invest. 2001 Mar;81(3):409-18 [11310833.001]
  • [Cites] Arthritis Rheum. 2001 May;44(5):1022-32 [11352233.001]
  • [Cites] Cancer Res. 2002 Mar 15;62(6):1832-7 [11912162.001]
  • [Cites] J Immunol. 2003 Sep 15;171(6):2812-24 [12960302.001]
  • [Cites] Immunol Lett. 2004 Mar 29;92(1-2):171-8 [15081542.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):4010-7 [15173015.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):540-50 [15229479.001]
  • [Cites] J Exp Med. 1993 Sep 1;178(3):1057-65 [8350046.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13791-6 [8943014.001]
  • [Cites] J Exp Med. 1996 Sep 1;184(3):963-9 [9064356.001]
  • [Cites] J Clin Invest. 1998 Feb 15;101(4):746-54 [9466968.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23):8604-12 [15574767.001]
  • [Cites] J Bone Miner Res. 2005 Feb;20(2):318-29 [15647826.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):490-7 [15701832.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2428-35 [15536145.001]
  • [Cites] Clin Cancer Res. 2005 Mar 1;11(5):1743-50 [15755995.001]
  • [Cites] Life Sci. 2006 Mar 13;78(16):1784-93 [16263140.001]
  • [Cites] Cancer Res. 2006 Aug 1;66(15):7701-7 [16885372.001]
  • [Cites] Cancer Metastasis Rev. 2006 Sep;25(3):357-71 [17016763.001]
  • [Cites] Nat Rev Cancer. 2007 Feb;7(2):139-47 [17218951.001]
  • [Cites] Gut. 2007 Mar;56(3):365-72 [16870716.001]
  • [Cites] Cancer Res. 2007 Apr 1;67(7):3396-405 [17409450.001]
  • [Cites] J Immunother. 2007 Jul-Aug;30(5):490-8 [17589289.001]
  • [Cites] Oncogene. 2007 Jul 12;26(32):4679-88 [17297455.001]
  • [Cites] Cancer Sci. 2007 Nov;98(11):1652-8 [17894551.001]
  • [Cites] ChemMedChem. 2008 Jun;3(6):861-72 [18442035.001]
  • [Cites] Cancer Gene Ther. 2002 May;9(5):432-42 [11961666.001]
  • [Cites] Int J Cancer. 2002 May 1;99(1):149-53 [11948506.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2606-10 [11980656.001]
  • [Cites] J Invest Dermatol. 2002 Jun;118(6):915-22 [12060384.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]
  • [Cites] J Immunol. 2002 Nov 15;169(10):5546-54 [12421931.001]
  • [Cites] Hum Immunol. 2002 Dec;63(12):1164-71 [12480260.001]
  • [Cites] Hum Gene Ther. 2000 Jan 20;11(2):247-61 [10680839.001]
  • (PMID = 19436305.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Receptors, CXCR3
  • [Other-IDs] NLM/ PMC2695685
  •  go-up   go-down


35. Feldmann G, Habbe N, Dhara S, Bisht S, Alvarez H, Fendrich V, Beaty R, Mullendore M, Karikari C, Bardeesy N, Ouellette MM, Yu W, Maitra A: Hedgehog inhibition prolongs survival in a genetically engineered mouse model of pancreatic cancer. Gut; 2008 Oct;57(10):1420-30
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Current therapeutic strategies are virtually ineffective in controlling advanced, metastatic disease.
  • The effect of Hedgehog pathway inhibition on survival was determined by continuous application of the small molecule cyclopamine, a smoothened antagonist.
  • Microarray analysis was performed on non-malignant human pancreatic ductal cells overexpressing Gli1 in order to screen for downstream Hedgehog target genes likely to be involved in pancreatic cancer progression.
  • CONCLUSION: This study provides another line of evidence that Hedgehog signalling is a valid target for the development of novel therapeutics for pancreatic cancer that might be worth evaluating soon in a clinical setting.

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. CYCLOPAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Dev. 2006 Nov 15;20(22):3147-60 [17114585.001]
  • [Cites] Genes Dev. 2006 Nov 15;20(22):3130-46 [17114584.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):2187-96 [17332349.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):229-43 [17349581.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 20;104(12):5103-8 [17372229.001]
  • [Cites] J Biol Chem. 2007 May 11;282(19):14048-55 [17353198.001]
  • [Cites] Cancer Cell. 2007 Jul;12(1):66-80 [17613437.001]
  • [Cites] Cancer Res. 2007 Jul 15;67(14):6637-46 [17638874.001]
  • [Cites] J Clin Pathol. 2007 Aug;60(8):885-95 [16775116.001]
  • [Cites] Curr Cancer Drug Targets. 2007 Sep;7(6):559-65 [17896921.001]
  • [Cites] Endocr Relat Cancer. 2007 Sep;14(3):865-74 [17914115.001]
  • [Cites] PLoS One. 2007;2(11):e1155 [17982507.001]
  • [Cites] Br J Cancer. 1997;75(3):388-95 [9020484.001]
  • [Cites] Cell. 2000 Jul 7;102(1):109-26 [10929718.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Am J Pathol. 2002 Apr;160(4):1239-49 [11943709.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1151-62 [12651607.001]
  • [Cites] World J Gastroenterol. 2003 Apr;9(4):818-23 [12679940.001]
  • [Cites] Virchows Arch. 2003 May;442(5):444-52 [12692724.001]
  • [Cites] Cell Mol Life Sci. 2003 Jun;60(6):1180-99 [12861384.001]
  • [Cites] J Pathol. 2003 Sep;201(1):63-74 [12950018.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):846-51 [14520411.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]
  • [Cites] Nucleic Acids Res. 2003 Dec 15;31(24):e154 [14654707.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Oncogene. 2004 Mar 25;23(13):2385-400 [14767473.001]
  • [Cites] Eur J Cancer. 2004 Apr;40(6):827-36 [15120038.001]
  • [Cites] Eur J Cancer. 2004 Apr;40(6):852-7 [15120041.001]
  • [Cites] Int J Cancer. 2004 Oct 20;112(1):100-12 [15305381.001]
  • [Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14717-22 [9843955.001]
  • [Cites] Gastroenterology. 1999 May;116(5):1202-16 [10220513.001]
  • [Cites] Oncogene. 1999 Aug 12;18(32):4554-63 [10467400.001]
  • [Cites] Neoplasia. 2004 Sep-Oct;6(5):611-22 [15548371.001]
  • [Cites] Cancer Biol Ther. 2004 Nov;3(11):1081-9; discussion 1090-1 [15467436.001]
  • [Cites] Cancer Biol Ther. 2004 Dec;3(12):1254-61 [15477757.001]
  • [Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]
  • [Cites] Int J Oncol. 2005 Aug;27(2):401-7 [16010421.001]
  • [Cites] Neoplasia. 2005 Jun;7(6):556-62 [16036106.001]
  • [Cites] Lab Invest. 2005 Aug;85(8):1003-12 [15924149.001]
  • [Cites] Gastroenterology. 2005 Oct;129(4):1187-97 [16230073.001]
  • [Cites] J Biol Chem. 2005 Nov 11;280(45):37383-92 [16115895.001]
  • [Cites] Gastroenterology. 2005 Nov;129(5):1454-63 [16285947.001]
  • [Cites] Development. 2005 Dec;132(24):5601-11 [16314491.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] Bone. 2006 Feb;38(2):154-66 [16126463.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Endoscopy. 2006 Jun;38(6):604-9 [16673309.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8788-95 [16951195.001]
  • [Cites] Am J Hematol. 2006 Nov;81(11):824-31 [16929535.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1030-7 [17283135.001]
  • (PMID = 18515410.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA113669-02; United States / NCI NIH HHS / CA / P50CA62924; United States / NCI NIH HHS / CA / R01 CA113669-01; United States / NCI NIH HHS / CA / CA113669-02; United States / NCI NIH HHS / CA / CA113669-04; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / R01CA113669; United States / NCI NIH HHS / CA / CA113669-03; United States / NCI NIH HHS / CA / R01 CA113669-05; United States / NCI NIH HHS / CA / R01 CA113669-03; United States / NCI NIH HHS / CA / R01 CA113669; United States / NCI NIH HHS / CA / R01 CA113669-04; United States / NCI NIH HHS / CA / CA113669-05; United States / NCI NIH HHS / CA / CA113669-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Neoplasm Proteins; 0 / Veratrum Alkaloids; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ NIHMS97875; NLM/ PMC2707354
  •  go-up   go-down


36. Weber GF: The metastasis gene osteopontin: a candidate target for cancer therapy. Biochim Biophys Acta; 2001 Dec 28;1552(2):61-85
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The metastasis gene osteopontin: a candidate target for cancer therapy.
  • Malignant tumors are characterized by dysregulated growth control, overcoming of replicative senescence, and metastasis formation.
  • Current therapeutic regimens mostly exert their effects through inhibition of cell cycle progression, leaving two major components of transformation untouched.
  • The osteopontin receptor CD44 has been targeted by diverse therapeutic strategies, including cytotoxic and immunotherapeutic approaches.
  • The receptor integrin alpha(V)beta(3) contributes not only to tumor cell dissemination, but also to angiogenesis and osteolysis in bone metastases.
  • Small molecule inhibitors of this receptor are under study as drug candidates.
  • Because receptors and cytokine ligands that mediate metastasis formation are sparsely expressed in the adult healthy organism and are more readily reached by pharmaceuticals than intracellular drug targets they may represent a particularly suitable focus for therapeutic intervention.
  • [MeSH-major] Neoplasm Metastasis / genetics. Neoplasms / therapy. Receptors, Vitronectin / antagonists & inhibitors. Sialoglycoproteins / genetics
  • [MeSH-minor] Animals. Antigens, CD29 / drug effects. Antigens, CD44 / drug effects. Antigens, CD44 / metabolism. Binding Sites. Chemotaxis. Cytokines / metabolism. Drug Delivery Systems. Gene Expression Regulation, Neoplastic / drug effects. Genetic Therapy. Humans. Immunotherapy. Osteopontin. Stress, Physiological / metabolism

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11825687.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 76176
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD29; 0 / Antigens, CD44; 0 / Cytokines; 0 / Receptors, Vitronectin; 0 / SPP1 protein, human; 0 / Sialoglycoproteins; 106441-73-0 / Osteopontin
  • [Number-of-references] 157
  •  go-up   go-down






Advertisement