[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 44 of about 44
1. Schuetze SM, Patel S: Should patients with high-risk soft tissue sarcoma receive adjuvant chemotherapy? Oncologist; 2009 Oct;14(10):1003-12
Hazardous Substances Data Bank. IFOSFAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Should patients with high-risk soft tissue sarcoma receive adjuvant chemotherapy?
  • Soft tissue sarcoma is a malignant connective tissue tumor that may arise anywhere in the body and from diverse mesenchymal elements.
  • The majority of patients with soft tissue sarcoma present with potentially life-threatening disease, and complete resection to obtain specimen margins free of tumor and radiation offer the best chance for local disease control.
  • Adjuvant chemotherapy has been studied as a means to decrease the risk for disease recurrence in patients with localized soft tissue sarcoma at diagnosis, but the majority of trials reported on have been hampered by patient heterogeneity, low patient accrual, and short follow-up.
  • Meta-analysis and reviews of institutional large series, in efforts to overcome some of the limitations, suggest that doxorubicin with ifosfamide reduces the risk for sarcoma recurrence and death in selected patients with high-grade, large, and chemotherapy-sensitive sarcoma subtypes to a clinically meaningful degree.
  • In multiple analyses, patients with high-risk soft tissue sarcoma treated with chemotherapy have a >10% absolute lower risk for disease recurrence and longer disease-specific survival than patients treated without chemotherapy.
  • In the absence of conclusive results from an adequately powered, randomized, controlled clinical trial, the available data support the use of chemotherapy in the management of high-risk, localized, soft tissue sarcoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Sarcoma / drug therapy. Sarcoma / mortality. Soft Tissue Neoplasms / drug therapy. Soft Tissue Neoplasms / mortality
  • [MeSH-minor] Anthracyclines / administration & dosage. Anthracyclines / therapeutic use. Chemotherapy, Adjuvant. Combined Modality Therapy. Humans. Ifosfamide / administration & dosage. Ifosfamide / therapeutic use. Meta-Analysis as Topic. Neoplasm Recurrence, Local. Neoplasm Staging. Risk Factors

  • Genetic Alliance. consumer health - Soft tissue 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 = 19808770.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; UM20QQM95Y / Ifosfamide
  •  go-up   go-down


2. Tejwani A, Kobayashi W, Chen YL, Rosenberg AE, Yoon S, Raskin KA, Rosenthal DI, Nielsen GP, Hornicek FJ, Delaney TF: Management of acral myxoinflammatory fibroblastic sarcoma. Cancer; 2010 Dec 15;116(24):5733-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of acral myxoinflammatory fibroblastic sarcoma.
  • BACKGROUND: Acral myxoinflammatory fibroblastic sarcoma (AMFS) is a rare, low-grade sarcoma that commonly affects the distal extremities.
  • From the published cases, therapy for AMFS to date has been comprised of excision or amputation, with limited use of radiotherapy (RT) or chemotherapy.
  • METHODS: A retrospective review of all cases of AMFS identified in the Sarcoma Database in the Department of Radiation Oncology at the study institution was conducted.
  • Treatment records and data from follow-up visits of patients were reviewed.
  • The average total dose was 56.4 Gray (Gy).
  • He was free of disease 23 months after his last treatment.
  • CONCLUSIONS: Data were consistent with local control of distal extremity sarcomas with resection and RT, suggesting that limb-sparing surgery with this treatment combination is an appropriate option in the limb-sparing control of patients with AMFS, even those with positive surgical margins.
  • [MeSH-major] Extremities. Histiocytoma, Malignant Fibrous / radiotherapy. Histiocytoma, Malignant Fibrous / surgery. Sarcoma / radiotherapy. Sarcoma / surgery

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 American Cancer Society.
  • (PMID = 20737559.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


3. Cassier P, Pissaloux D, Alberti L, Ray-Coquard I, Blay JY: [Targeted treatment of rare connective tissue tumors and sarcomas]. Bull Cancer; 2010 Jun;97(6):693-700
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] [Targeted treatment of rare connective tissue tumors and sarcomas].
  • [Transliterated title] Traitements ciblés des sarcomes et des tumeurs conjonctives rares.
  • The recent progress of the biology of the locally aggressive sarcomas of soft tissues and related connective tissue tumors enabled to reclassify molecular and histological entities of the disease.
  • Six subgroups of sarcomas are identified with specific molecular alterations, the targeted treatments of which are the object of this article:.
  • 3) tumors with deletion of tumor suppressor genes (TSC in the PEComes, NF1 involved in type 1 neurofibromatosis;.
  • The identification of these abnormal ways of road marking to licence the development of effective targeted therapeutic agents against certain rare histological connective subcategories of sarcomas and tumors with local aggressiveness, in particular DFSP, PVNS, GCST, PEComes, endometrial stromal sarcomas, Ewing sarcomas, etc.
  • Imatinib is used in the treatment of DFSP, characterized by a translocation of the gene PDGF, or in pigmented villonodular synovitis (PVNS), a tumor of soft part also locally aggressive, caused by an abnormality of the gene coding for the M-CSF.
  • The molecular characterization of sarcomas allowed to develop therapeutic targeted to correct the responsible abnormalities.
  • Translational research is and will be an essential tool for the development of new treatments and the identification of the mechanisms of answer and resistance set up by these tumors.
  • [MeSH-major] Neoplasms, Connective Tissue / drug therapy. Rare Diseases / drug therapy. Sarcoma / drug therapy

  • MedlinePlus Health Information. consumer health - Rare Diseases.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20497911.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases
  •  go-up   go-down


Advertisement
4. Hohenberger P, Wysocki WM: Neoadjuvant treatment of locally advanced soft tissue sarcoma of the limbs: which treatment to choose? Oncologist; 2008 Feb;13(2):175-86
Genetic Alliance. consumer health - Soft tissue sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neoadjuvant treatment of locally advanced soft tissue sarcoma of the limbs: which treatment to choose?
  • Soft tissue sarcomas (STSs) form a heterogeneous group of malignant neoplasms arising in the mesenchymal connective tissues.
  • Initially, treatment of STS relied solely on excision.
  • In the 1970s, Enneking et al. developed the concept of compartmental resection to reduce the local failure rate.
  • Later, Rosenberg et al. demonstrated, in a randomized study, that there was no difference in local tumor control and disease-free survival (DFS) in patients treated with amputation versus limb-saving surgery followed by 50-70 Gy external-beam radiotherapy (EBRT).
  • High-dose preoperative EBRT for high-grade STS was developed, and its combination with intra-arterial or i.v. chemotherapy was reported to be effective.
  • Recently, systemic chemotherapy combined with deep wave hyperthermia was shown to result in a longer DFS time in a large, randomized, phase III study.
  • Treatment concepts differ significantly among centers and are influenced more by availability of technical equipment than by data.
  • [MeSH-major] Extremities / pathology. Limb Salvage. Neoadjuvant Therapy / methods. Soft Tissue Neoplasms / drug therapy
  • [MeSH-minor] Chemotherapy, Adjuvant. Chemotherapy, Cancer, Regional Perfusion / methods. Fever. Humans. Mesoderm / pathology. Radiotherapy, Adjuvant. Recombinant Proteins. Tumor Necrosis Factor-alpha / therapeutic use

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18305063.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 83
  •  go-up   go-down


5. Jayaraman S, Rao SD, Govindarajan M: Synovial sarcoma of anterior abdominal wall. Indian J Surg; 2010 Jul;72(Suppl 1):293-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synovial sarcoma of anterior abdominal wall.
  • Sarcomas are connective tissue tumours, and can arise in any part of the body, more commonly in the extremities.
  • Histological types and clinical presentation of truncal sarcomas are similar to those seen in any other anatomic locations.
  • Surgical resection with wide margins is the initial standard treatment, however a multimodal approach including radiotherapy and chemotherapy is often favoured.
  • Because of the high recurrence rate regardless of therapy, close follow-up is imperative.
  • We present a case of synovial sarcoma of the anterior abdominal wall.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Surg. 1995 Feb;221(2):185-95 [7857146.001]
  • [Cites] Am J Pathol. 1996 Feb;148(2):601-9 [8579122.001]
  • [Cites] Ann Surg Oncol. 1997 Jul-Aug;4(5):425-31 [9259971.001]
  • [Cites] Arch Surg. 2001 Jan;136(1):70-9 [11146782.001]
  • [Cites] Virchows Arch. 2006 Sep;449(3):367-72 [16855839.001]
  • [Cites] Surg Clin North Am. 2008 Jun;88(3):539-57, vi [18514697.001]
  • [Cites] Surg Clin North Am. 2008 Jun;88(3):571-82, vi-vii [18514699.001]
  • [Cites] Adv Surg. 2008;42:219-28 [18953820.001]
  • (PMID = 23133275.001).
  • [ISSN] 0972-2068
  • [Journal-full-title] The Indian journal of surgery
  • [ISO-abbreviation] Indian J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3451847
  • [Keywords] NOTNLM ; Abdominal wall / Synovial sarcoma
  •  go-up   go-down


6. BaniHani MN, Al Manasra AR: Spontaneous regression in alveolar soft part sarcoma: case report and literature review. World J Surg Oncol; 2009;7:53
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] Spontaneous regression in alveolar soft part sarcoma: case report and literature review.
  • BACKGROUND: Sarcomas are a type of malignant tumors that arise from connective tissue.
  • They are most of the time found in extremities CASE PRESENTATION: We are presenting a case of adult male patient, who was found to have huge abdominal mass and multiple gastric and duodenal polyps.
  • Pathological diagnosis for all lesions was Alveolar soft part sarcoma.
  • No chemotherapy or radiotherapy was given.
  • CONCLUSION: ASPS is a rare type of sarcomas that affect primarily the lower limbs.
  • [MeSH-major] Neoplasm Regression, Spontaneous. Sarcoma, Alveolar Soft Part / pathology
  • [MeSH-minor] Adult. Brain Neoplasms / secondary. Humans. Lung Neoplasms / secondary. Male. Tomography, X-Ray Computed

  • Genetic Alliance. consumer health - Alveolar Soft Part Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Diagn Pathol. 2003 Oct;7(5):306-9 [14571434.001]
  • [Cites] Ann N Y Acad Sci. 1964 Apr 2;114(2):721-35 [5220109.001]
  • [Cites] J Neurooncol. 2005 Jan;71(1):43-8 [15719274.001]
  • [Cites] Postgrad Med J. 1988 May;64(751):386-8 [3200782.001]
  • [Cites] Histopathology. 1997 Nov;31(5):469-73 [9416489.001]
  • [Cites] Pathol Res Pract. 1998;194(1):59-63 [9542749.001]
  • [Cites] Cancer. 1952 Jan;5(1):100-11 [14886902.001]
  • [Cites] Pathol Res Pract. 2000;196(7):519-25 [10926330.001]
  • [Cites] Cancer. 2001 Feb 1;91(3):585-91 [11169942.001]
  • [Cites] Int J Gynecol Pathol. 1995 Oct;14(4):283-92 [8598329.001]
  • (PMID = 19515237.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2703639
  •  go-up   go-down


7. van Oosterom AT, Judson IR, Verweij J, Stroobants S, Dumez H, Donato di Paola E, Sciot R, Van Glabbeke M, Dimitrijevic S, Nielsen OS, European Organisation for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Group: Update of phase I study of imatinib (STI571) in advanced soft tissue sarcomas and gastrointestinal stromal tumors: a report of the EORTC Soft Tissue and Bone Sarcoma Group. Eur J Cancer; 2002 Sep;38 Suppl 5:S83-7
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update of phase I study of imatinib (STI571) in advanced soft tissue sarcomas and gastrointestinal stromal tumors: a report of the EORTC Soft Tissue and Bone Sarcoma Group.
  • In a phase I study conducted by the EORTC Soft Tissue and Bone Sarcoma Group, 40 patients with advanced soft tissue sarcomas, most of whom had gastrointestinal stromal tumors (GISTs), received imatinib at doses of 400 mg q.d., 300 mg b.i.d., 400 mg b.i.d., or 500 mg b.i.d.
  • The most common side effects seen in patients continuing on therapy have been periorbital edema (40%), peripheral edema (37.5%), fatigue (30%), skin rash (30%) and nausea/vomiting (25%).
  • Thus, 82% of patients with GISTs are still obtaining clinically important benefits with continued imatinib therapy.
  • On the other hand, following drug withdrawal, 2 patients had reductions in tumor burden and remain alive without drug therapy.
  • In summary, imatinib is generally well tolerated and has significant activity during long-term treatment of patients with advanced GISTs.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Enzyme Inhibitors / administration & dosage. Gastrointestinal Neoplasms / drug therapy. Neoplasms, Connective Tissue / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Sarcoma / drug therapy
  • [MeSH-minor] Adult. Aged. Benzamides. Dose-Response Relationship, Drug. Female. Humans. Imatinib Mesylate. Male. Maximum Tolerated Dose. Middle Aged. Stromal Cells. Treatment Outcome


8. Chugh R, Baker LH: Pharmacotherapy of sarcoma. Expert Opin Pharmacother; 2009 Aug;10(12):1953-63
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] Pharmacotherapy of sarcoma.
  • BACKGROUND: Comprising < 1% of adult malignancies and approximately 12% of pediatric malignancies, sarcomas are derived from a variety of connective tissues and exhibit highly variable responsiveness to therapy.
  • The clinical and biologic heterogeneity of the > 50 histologic subtypes of sarcomas often require different therapeutic approaches.
  • OBJECTIVE: This review describes the use of therapeutic agents in the management of bone and soft-tissue sarcomas.
  • RESULTS/CONCLUSIONS: Chemotherapy has improved outcomes over the past few decade, particularly in patients with certain bone sarcomas and gastrointestinal stromal tumors; while in the majority of patients, additional strategies are necessary.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / drug therapy. Sarcoma / drug therapy

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19558336.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 117
  •  go-up   go-down


9. Fanucchi M: Update on the management of connective tissue malignancies. Semin Oncol; 2004 Apr;31(2 Suppl 4):16-9
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] Update on the management of connective tissue malignancies.
  • Approximately 11,000 new cases of connective tissue malignancies are anticipated in 2004.
  • These diseases can be divided into soft-tissue sarcomas, sarcomas of bone, and gastrointestinal stromal tumors.
  • Optimal management of these diseases requires a multidisciplinary team with expertise in surgery, pathology, radiotherapy, and chemotherapy.
  • Over half of patients with stage III soft tissue and bone sarcomas are cured, as are some patients with metastatic disease.
  • Imatinib mesylate has been an important advance in the treatment of gastrointestinal stromal tumors.
  • [MeSH-major] Sarcoma / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Bone Neoplasms / therapy. Combined Modality Therapy. Gastrointestinal Neoplasms / therapy. Humans. Soft Tissue Neoplasms / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15124129.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 27
  •  go-up   go-down


10. Thornton K: Chemotherapeutic management of soft tissue sarcoma. Surg Clin North Am; 2008 Jun;88(3):647-60, viii
Hazardous Substances Data Bank. IFOSFAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapeutic management of soft tissue sarcoma.
  • Soft tissue sarcomas are a heterogeneous group of connective tissue tumors, with more than 50 different subtypes.
  • Given the heterogeneity, and the relative small numbers of patients, performing large adequately powered clinical trials in which one can glean any overall broad treatment decisions based on outcome is difficult at best.
  • There is controversy on which chemotherapeutic agents to use in the adjuvant and metastatic settings, or even if to use chemotherapy in the adjuvant setting.
  • This review discusses the data on chemotherapy for treatment of metastatic sarcomas and the utility of chemotherapy in the adjuvant and neoadjuvant settings.
  • In addition, the utility of newer biologic agents in the treatment for sarcomas is considered.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Doxorubicin / therapeutic use. Ifosfamide / therapeutic use. Sarcoma / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Chemotherapy, Adjuvant. Dioxoles / therapeutic use. Humans. Neoadjuvant Therapy. Neovascularization, Pathologic / drug therapy. TNF-Related Apoptosis-Inducing Ligand / therapeutic use. Tetrahydroisoquinolines / therapeutic use

  • Genetic Alliance. consumer health - Soft tissue sarcoma.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18514704.001).
  • [ISSN] 0039-6109
  • [Journal-full-title] The Surgical clinics of North America
  • [ISO-abbreviation] Surg. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / Dioxoles; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tetrahydroisoquinolines; 114899-77-3 / trabectedin; 80168379AG / Doxorubicin; UM20QQM95Y / Ifosfamide
  • [Number-of-references] 87
  •  go-up   go-down


11. Brecht IB, Treuner J: [Soft tissue sarcoma in children and adolescents: experiences of the cooperative Soft Tissue Sarcoma Group Studies (CWS-81 - 96)]. Handchir Mikrochir Plast Chir; 2004 Oct;36(5):275-81
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] [Soft tissue sarcoma in children and adolescents: experiences of the cooperative Soft Tissue Sarcoma Group Studies (CWS-81 - 96)].
  • The very heterogeneous group of paediatric soft tissue sarcomas account for approximately 7 % of all malignant childhood tumours.
  • The prognosis and biology of soft tissue sarcomas in children and adolescents vary greatly depending on histological subtype, the age of the patient, the primary site, the tumour size, tumour invasiveness and the extent of disease at diagnosis.
  • Since 1981, 2918 children and adolescents with soft tissue sarcomas were treated prospectively according to the common treatment protocols of the Cooperative Soft Tissue Sarcoma Study Group (CWS-81 - 96).
  • The multimodal treatment includes the use of surgery, chemotherapy and radiotherapy and should be planned by a multidisciplinary team.
  • [MeSH-major] Sarcoma / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Protocols. Child. Child, Preschool. Combined Modality Therapy. Connective Tissue / pathology. Female. Germany. Humans. Infant. Interdisciplinary Communication. Male. Muscle, Skeletal / pathology. Neoplasm Invasiveness / pathology. Neoplasm Staging. Patient Care Team. Prognosis. Prospective 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 = 15503257.001).
  • [ISSN] 0722-1819
  • [Journal-full-title] Handchirurgie, Mikrochirurgie, plastische Chirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft für Handchirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft für Mikrochirurgie der Peripheren Nerven und Gefässe : Organ der Vereinigung der Deutschen Plastischen Chirurgen
  • [ISO-abbreviation] Handchir Mikrochir Plast Chir
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


12. Louthrenoo W, Kasitanon N, Mahanuphab P, Bhoopat L, Thongprasert S: Kaposi's sarcoma in rheumatic diseases. Semin Arthritis Rheum; 2003 Apr;32(5):326-33
MedlinePlus Health Information. consumer health - Kaposi's Sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Kaposi's sarcoma in rheumatic diseases.
  • OBJECTIVE: To review the clinical features and outcome of all reported cases of Kaposi's sarcoma in patients with rheumatic diseases.
  • Rheumatoid arthritis was present in 8 cases, polymyositis/dermatomyositis in 5, vasculitis syndromes in 5, systemic lupus erythematosus in 3, polymyalgia rheumatica in 2, and 1 each of undifferentiated connective tissue disease and Behcet disease.
  • All but 1 patient had been given systemic corticosteroids for a duration that ranged from 6 weeks to 22 years, and immunosuppressive drugs from 25 days to 3.5 years.
  • Most lesions responded to a decreasing dosage of corticosteroids and immunosuppressive drugs, or to the administration of radiation or cytotoxic therapy.
  • Six patients died, 4 of which were related to the progression of Kaposi's sarcoma.
  • CONCLUSION: Kaposi's sarcoma in patients with rheumatologic conditions is rare.
  • The clinical features are similar to those with classical Kaposi's sarcoma.
  • Tumor regression usually occurs with decreasing corticosteroids and/or immunosuppressive drugs, local irradiation, or cytotoxic therapy.
  • [MeSH-major] Anti-Inflammatory Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Immunosuppressive Agents / therapeutic use. Rheumatic Diseases / complications. Sarcoma, Kaposi / complications. Sarcoma, Kaposi / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Steroids. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003, Elsevier Inc. All rights reserved.
  • [CommentIn] Semin Arthritis Rheum. 2004 Apr;33(5):352; author reply 352-3 [15079765.001]
  • (PMID = 12701043.001).
  • [ISSN] 0049-0172
  • [Journal-full-title] Seminars in arthritis and rheumatism
  • [ISO-abbreviation] Semin. Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 0 / Steroids
  • [Number-of-references] 36
  •  go-up   go-down


13. Thomas DM, Wagner AJ: Specific targets in sarcoma and developmental therapeutics. J Natl Compr Canc Netw; 2010 Jun;8(6):677-85; quiz 686
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] Specific targets in sarcoma and developmental therapeutics.
  • Connective tissue tumors comprise a rich array of subtypes, many of which possess strong pathognomonic phenotypes and genotypes of therapeutic significance.
  • This article describes recent applications of targeted and nontargeted therapeutic agents in connective tissue tumors that illustrate important themes in drug development.
  • Targeted therapy has exploited the paradigms of oncogene and lineage addiction.
  • In other cases, potential targets are more difficult to classify, such as the role of the insulin-like growth factor 1 pathway in Ewing's sarcoma.
  • Understanding why these pathways seem critical in some cancers, and in some individuals but not others, is important in identifying novel therapeutic opportunities in an age of personalized medicine.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / antagonists & inhibitors. Neoplasm Proteins / antagonists & inhibitors. Oncogene Proteins, Fusion / antagonists & inhibitors. Precision Medicine. Sarcoma / drug therapy. Sarcoma / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20581299.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion
  •  go-up   go-down


14. Baker LH, Wathen K, Chugh R, Thomas D, Thall PF, Maki RG, Samuels BL, Meyers PA, Priebat DA, Benjamin RS: Activity of imatinib mesylate in desmoid tumors: Interim analysis of a Sarcoma Alliance for Research thru Collaboration (SARC) phase II trial. J Clin Oncol; 2004 Jul 15;22(14_suppl):9013

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of imatinib mesylate in desmoid tumors: Interim analysis of a Sarcoma Alliance for Research thru Collaboration (SARC) phase II trial.
  • : 9013 Background: Desmoid tumors (aggressive fibromatosis) are rare clonal neoplastic proliferations of connective tissues.
  • Standard treatment involves wide surgical resection and/or radiation therapy.
  • In cases of unresectable or recurrent disease, tamoxifen, chemotherapy, and NSAIDs have been used with varying success.
  • SARC, in association with the Connective Tissue Oncology Society, initiated a prospective phase II trial in patients with desmoid tumors, or one of nine sarcoma subtypes.
  • Rules for early termination within each disease type were based on a hierarchical Bayesian probability model accounting for correlation of the responses of the 10 disease types.
  • Tissue specimens were analyzed by immunohistochemistry for expression of c-kit, PDGFRα, PDGFRß, AKT, PTEN, FKHR, and beta catenin.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28013675.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Sampo M, Tarkkanen M, Huuhtanen R, Tukiainen E, Böhling T, Blomqvist C: Impact of the smallest surgical margin on local control in soft tissue sarcoma. Br J Surg; 2008 Feb;95(2):237-43
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] Impact of the smallest surgical margin on local control in soft tissue sarcoma.
  • BACKGROUND: The aim was to review a single-institution experience of a prospective treatment protocol for soft tissue sarcoma of the extremity and trunk wall, with particular focus on the smallest surgical margin leading to local control.
  • METHODS: The study included 270 patients who had surgery for soft tissue sarcoma at Helsinki University Central Hospital between 1987 and 1997.
  • On multivariable analysis, the smallest surgical margin around the sarcoma (after radiotherapy) was prognostic for local control.
  • A surgical margin of 2-3 cm provided reasonable local control of soft tissue sarcoma, even without radiotherapy.
  • [MeSH-major] Neoplasms, Connective Tissue / surgery. Sarcoma / surgery
  • [MeSH-minor] Abdominal Wall. Adult. Aged. Amputation / statistics & numerical data. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Protocols. Extremities. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / surgery. Prospective Studies. Radiotherapy, Adjuvant. Treatment Outcome

  • Genetic Alliance. consumer health - Soft tissue sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2007 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
  • (PMID = 17703500.001).
  • [ISSN] 1365-2168
  • [Journal-full-title] The British journal of surgery
  • [ISO-abbreviation] Br J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


16. Del Frari B, Zelger BG, Piza-Katzer H: [Epithelioid sarcoma of the hand, a seldomly recognized tumor]. Handchir Mikrochir Plast Chir; 2004 Oct;36(5):313-7
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] [Epithelioid sarcoma of the hand, a seldomly recognized tumor].
  • BACKGROUND: The epithelioid sarcoma of the hand is often misdiagnosed.
  • The characteristic histopathology is helpful in establishing the correct diagnosis.
  • Differential diagnosis includes synovialoma, fibromatosis and Dupuytren's contracture.
  • PATIENTS AND METHOD: Three young patients (one male and two female) were operated on the hand for treatment of Dupuytren's contracture, synovialoma and fibromas, respectively.
  • The original diagnosis having been found to be incorrect, the correct diagnosis was established namely, epithelioid sarcoma.
  • None of the patients underwent adjuvant radio- or chemotherapy.
  • Adequate treatment requires early radical excision; amputation may be required if the primary tumor is located in the fingers or treatment of recurrent growth.
  • Patients must be monitored with yearly lung X-rays since recurrence or metastasis may occur many years after the initial diagnosis and treatment.
  • [MeSH-major] Hand / surgery. Sarcoma / diagnosis. Sarcoma / surgery. Soft Tissue Neoplasms / diagnosis. Soft Tissue Neoplasms / surgery
  • [MeSH-minor] Adult. Amputation. Biopsy. Child. Connective Tissue / pathology. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Male. Muscle, Skeletal / pathology. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery

  • Genetic Alliance. consumer health - Epithelioid Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15503263.001).
  • [ISSN] 0722-1819
  • [Journal-full-title] Handchirurgie, Mikrochirurgie, plastische Chirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft für Handchirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft für Mikrochirurgie der Peripheren Nerven und Gefässe : Organ der Vereinigung der Deutschen Plastischen Chirurgen
  • [ISO-abbreviation] Handchir Mikrochir Plast Chir
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


17. Ganjavi H, Gee M, Narendran A, Freedman MH, Malkin D: Adenovirus-mediated p53 gene therapy in pediatric soft-tissue sarcoma cell lines: sensitization to cisplatin and doxorubicin. Cancer Gene Ther; 2005 Apr;12(4):397-406
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] Adenovirus-mediated p53 gene therapy in pediatric soft-tissue sarcoma cell lines: sensitization to cisplatin and doxorubicin.
  • Sarcomas, or tumors of connective tissue, represent roughly 20% of childhood cancers.
  • High-grade or metastatic soft-tissue sarcomas and rhabdomyosarcomas (RMS) of the extremities remain therapeutic challenges and their prognosis is often poor.
  • The future of sarcoma therapy will likely include molecular approaches including gene/protein expression profiling and gene-based therapy.
  • The tumor suppressor p53 is central to regulation of cell growth and tumor suppression and restoring wild-type p53 function in pediatric sarcomas may be of therapeutic benefit.
  • Studies with adenoviral-mediated p53 gene transfer have been conducted in many cancer types including cervical, ovarian, prostatic and head and neck tumors.
  • Using three viral constructs containing cDNA for wild-type p53, mutant p53 (C135S) and lacZ, we studied the effect of adenoviral-mediated gene therapy in four pediatric sarcoma cell lines, RD and Rh4 (RMS), Rh1 (Ewing's sarcoma) and A204 (undifferentiated sarcoma).
  • Using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, we have shown a dose-dependent decrease in cell viability 72 h post-treatment that occurs with Ad-wtp53 but not with Ad-mutp53.
  • Our results indicate that restoration of wild-type p53 function in pediatric sarcoma cells could provide a basis for novel approaches to treatment of this disease.
  • [MeSH-major] Adenoviridae / genetics. Cisplatin / pharmacology. Doxorubicin / pharmacology. Genes, p53 / genetics. Genetic Therapy / methods
  • [MeSH-minor] Apoptosis. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. Cell Survival. Child. Cyclin-Dependent Kinase Inhibitor p21. Dose-Response Relationship, Drug. Gene Transfer Techniques. Humans. In Situ Nick-End Labeling. Mutation. Prognosis. RNA, Messenger / metabolism. Retinoblastoma Protein / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Rhabdomyosarcoma / therapy. Sarcoma / metabolism. Sarcoma / therapy. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. Time Factors. Tumor Suppressor Protein p53 / metabolism

  • Genetic Alliance. consumer health - Soft tissue sarcoma.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. METHYLTHIAZOLETETRAZOLIUM .
  • 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 = 15618970.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / RNA, Messenger; 0 / Retinoblastoma Protein; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Tumor Suppressor Protein p53; 298-93-1 / thiazolyl blue; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


18. Dim DC, Cooley LD, Miranda RN: Clear cell sarcoma of tendons and aponeuroses: a review. Arch Pathol Lab Med; 2007 Jan;131(1):152-6
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] Clear cell sarcoma of tendons and aponeuroses: a review.
  • Clear cell sarcoma of tendons and aponeuroses, also referred to as malignant melanoma of soft parts, is a rare malignancy derived from neural crest cells.
  • It usually presents in the distal lower extremities of young adults, frequently attached to tendons or aponeuroses.
  • It behaves like a high-grade soft tissue sarcoma and is associated with poor overall survival.
  • The mainstay of treatment is wide excision of the tumor.
  • The use of sentinel lymph node biopsy may become an important procedure in detecting occult regional metastasis and guiding the extent of surgery.
  • The beneficial effects of adjuvant chemotherapy and radiotherapy have not been fully evaluated.
  • This article provides a short overview of the current knowledge of clear cell sarcoma of tendons and aponeuroses.
  • [MeSH-major] Neoplasms, Connective Tissue. Sarcoma, Clear Cell
  • [MeSH-minor] Activating Transcription Factor 1. Antigens, Neoplasm. Calmodulin-Binding Proteins / genetics. DNA-Binding Proteins / genetics. Diagnosis, Differential. Humans. Melanoma-Specific Antigens. Neoplasm Proteins / metabolism. Nuclear Proteins / genetics. Prognosis. RNA-Binding Proteins / genetics. S100 Proteins / metabolism. Tendons / pathology. Transcription Factors. Translocation, Genetic

  • Genetics Home Reference. consumer health - chromosome 12.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17227118.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATF1 protein, human; 0 / Activating Transcription Factor 1; 0 / Antigens, Neoplasm; 0 / Calmodulin-Binding Proteins; 0 / DNA-Binding Proteins; 0 / EWSR1 protein, human; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA-Binding Proteins; 0 / S100 Proteins; 0 / Transcription Factors; 0 / regulatory factor X transcription factors
  • [Number-of-references] 31
  •  go-up   go-down


19. Veldwijk MR, Berlinghoff S, Laufs S, Hengge UR, Zeller WJ, Wenz F, Fruehauf S: Suicide gene therapy of sarcoma cell lines using recombinant adeno-associated virus 2 vectors. Cancer Gene Ther; 2004 Aug;11(8):577-84
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] Suicide gene therapy of sarcoma cell lines using recombinant adeno-associated virus 2 vectors.
  • Soft-tissue sarcomas are mesenchymal tumors that respond poorly to systemic chemotherapy.
  • Suicide gene therapy may be an alternative treatment strategy.
  • Here we show a high susceptibility of human sarcoma cell lines for recombinant adeno-associated virus 2 (rAAV-2) suicide vectors: connective tissue sarcoma (HS-1), fibrosarcoma (HT-1080), Ewing sarcoma (RD-ES), Askin tumor (SK-N-MC), rhabdomyosarcoma (A-204) and soft-tissue sarcoma (WSKL-1).
  • Higher expression levels of the transgene were observed in the sarcoma lines when using the EF1alpha-suicide gene-containing vectors.
  • Xenotransplantation tumor models (intraperitoneal, subcutaneous) for the human sarcoma cell line HS-1 were established in nonobese diabetic/severe-combined immunodeficient mice.
  • These data hold promise for further development of rAAV-2-based suicide gene therapy of sarcomas.
  • [MeSH-major] Dependovirus / genetics. Genes, Transgenic, Suicide / genetics. Genetic Therapy / methods. Genetic Vectors. Sarcoma / therapy. Thymidine Kinase / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytomegalovirus / genetics. Ganciclovir / therapeutic use. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Peptide Elongation Factor 1 / genetics. Promoter Regions, Genetic / genetics. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • Hazardous Substances Data Bank. GANCICLOVIR .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15280909.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptide Elongation Factor 1; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
  •  go-up   go-down


20. Taeger G, Ruchholtz S, Schütte J, Nast-Kolb D: [Diagnostics and treatment strategies for soft tissue sarcomas]. Unfallchirurg; 2004 Jul;107(7):601-15; quiz 616-7
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] [Diagnostics and treatment strategies for soft tissue sarcomas].
  • Soft tissue sarcomas (STS) represent a rare entity of all malignant tumors (1%).
  • Thus, an in-depth understanding of multidisciplinary treatment strategies may not be sufficiently present at all operative units.
  • Magnetic resonance imaging (MRI) is the procedure of choice in diagnosing STS.
  • Management of STS should employ multimodal treatment concepts (Oncology, Radiotherapy, Surgical Oncology).
  • The decision on whether radiotherapy, chemotherapy or another option is indicated should be taken by an interdisciplinary tumor board, which also determines the sequence of treatment in relation to resection.
  • Tumor resection alone, without previous evaluation and where appropriate adopting multimodal treatment strategies, no longer meets modern standards.
  • After primary treatment is complete, patients have to be enrolled in a standardized follow-up program.
  • [MeSH-major] Extremities / surgery. Sarcoma / surgery. Soft Tissue Neoplasms / surgery
  • [MeSH-minor] Biopsy. Chemotherapy, Adjuvant. Combined Modality Therapy. Connective Tissue / pathology. Diagnostic Imaging. Follow-Up Studies. Humans. Neoplasm Staging. Patient Care Team. Radiotherapy, Adjuvant

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2001 Mar 1;19(5):1238-47 [11230464.001]
  • [Cites] Eur J Surg Oncol. 2000 Nov;26(7):669-78 [11078614.001]
  • [Cites] Cancer. 2003 May 15;97(10):2544-53 [12733154.001]
  • [Cites] Chirurg. 2000 Jul;71(7):787-94 [10986600.001]
  • [Cites] Ann Surg. 1999 May;229(5):602-10; discussion 610-2 [10235518.001]
  • [Cites] J Surg Oncol. 2004 Feb;85(2):68-76 [14755506.001]
  • [Cites] AJR Am J Roentgenol. 1988 Mar;150(3):615-20 [3257620.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Jul 15;56(4):1117-27 [12829150.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Jun 1;56(2):482-8 [12738324.001]
  • [Cites] Arch Surg. 1999 Feb;134(2):190-4 [10025462.001]
  • [Cites] Acta Oncol. 2003;42(5-6):516-31 [14596510.001]
  • [Cites] J Clin Oncol. 1996 May;14(5):1679-89 [8622088.001]
  • [Cites] Cancer. 1987 Oct 15;60(8):1800-8 [3308055.001]
  • [Cites] Cancer. 1985 Aug 1;56(3):475-9 [4005809.001]
  • [Cites] J Clin Oncol. 1992 Aug;10(8):1317-29 [1634922.001]
  • [Cites] Lancet. 2002 Jun 29;359(9325):2235-41 [12103287.001]
  • [Cites] Clin Cancer Res. 1998 Oct;4(10):2377-82 [9796968.001]
  • [Cites] Ann Surg. 1998 Sep;228(3):355-65 [9742918.001]
  • [Cites] Eur J Surg Oncol. 1995 Oct;21(5):471-4 [7589587.001]
  • [Cites] Lancet. 1997 Dec 6;350(9092):1647-54 [9400508.001]
  • [Cites] Surg Oncol Clin N Am. 2002 Jan;11(1):11-22 [11928795.001]
  • [Cites] J Clin Oncol. 1996 Oct;14(10):2653-65 [8874324.001]
  • [Cites] Cancer. 1986 Jul 15;58(2):306-9 [3719523.001]
  • [Cites] J Bone Joint Surg Am. 1996 May;78(5):656-63 [8642021.001]
  • [Cites] Ann Surg. 2000 May;231(5):655-63 [10767786.001]
  • [Cites] Chirurg. 2001 Feb;72(2):138-48 [11253672.001]
  • [Cites] Eur J Cancer. 2003 Sep;39(13):1872-80 [12932665.001]
  • [Cites] Am J Pathol. 1994 Jun;144(6):1121-34 [8203453.001]
  • [Cites] Ann Surg. 1982 Sep;196(3):305-15 [7114936.001]
  • [Cites] Ann Surg. 2002 Mar;235(3):424-34 [11882765.001]
  • (PMID = 15252710.001).
  • [ISSN] 0177-5537
  • [Journal-full-title] Der Unfallchirurg
  • [ISO-abbreviation] Unfallchirurg
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


21. Luis ÁM, Aguilar DP, Martín JA: Multidisciplinary management of soft tissue sarcomas. Clin Transl Oncol; 2010 Aug;12(8):543-53
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] Multidisciplinary management of soft tissue sarcomas.
  • Musculoskeletal sarcomas are a heterogeneous group of malignant neoplasms derived from connective tissue.
  • The annual incidence in adults in Europe is around 14,000 new cases of soft tissue sarcomas (STS) and 4,800 new cases of bone sarcomas.
  • The aim of treatment should be focused on four main aspects: improving survival, avoiding local recurrence, maximising organ function and, finally, minimising morbidity.
  • Surgery, radiotherapy and, sometimes though increasingly, chemotherapy are the pillars on which rests the modern treatment of sarcomas.
  • The optimal management of musculoskeletal tumour requires a multidisciplinary integration of these different approaches in treatment planning right from the initial diagnoses.
  • [MeSH-major] Sarcoma / therapy. Soft Tissue Neoplasms / therapy
  • [MeSH-minor] Biopsy. Combined Modality Therapy. Humans. Patient Care Team

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Surg. 1975 Nov;182(5):597-602 [1190864.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):859-68 [8622034.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 Mar 15;49(4):1033-43 [11240245.001]
  • [Cites] J Clin Oncol. 2002 Nov 15;20(22):4472-7 [12431971.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2010 May 1;77(1):203-9 [19679403.001]
  • [Cites] Surg Clin North Am. 2008 Jun;88(3):629-46, viii [18514703.001]
  • [Cites] Int J Clin Oncol. 2003 Jun;8(3):174-9 [12851842.001]
  • [Cites] Ann Surg. 1991 Sep;214(3):328-36; discussion 336-8 [1929613.001]
  • [Cites] Clin Orthop Relat Res. 2004 Feb;(419):165-72 [15021149.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Jul 15;32(4):969-76 [7607971.001]
  • [Cites] J Bone Joint Surg Br. 1997 Jul;79(4):553-7 [9250737.001]
  • [Cites] Cancer Treat Rev. 2008 Jun;34(4):339-47 [18313854.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):869-77 [8622035.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 Jul 1;65(3):773-9 [16682152.001]
  • [Cites] Cancer. 1999 Jan 15;85(2):396-408 [10023708.001]
  • [Cites] Ann Surg. 1996 Dec;224(6):756-64; discussion 764-5 [8968230.001]
  • [Cites] Radiother Oncol. 1996 Dec;41(3):209-14 [9027935.001]
  • [Cites] Acta Orthop Scand. 1990 Dec;61(6):475-86 [2281753.001]
  • [Cites] Recent Results Cancer Res. 2009;179:211-28 [19230542.001]
  • [Cites] Strahlenther Onkol. 2004 Jun;180(6):365-70 [15175871.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2008 Nov 15;72(4):1146-53 [18394818.001]
  • [Cites] J Vasc Interv Radiol. 1992 Nov;3(4):659-63 [1332791.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1986 Oct;12(10):1729-34 [3759524.001]
  • [Cites] J Bone Joint Surg Am. 1976 Apr;58(3):317-27 [177425.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2007 Jan 1;67(1):158-63 [17084545.001]
  • [Cites] Cancer. 2008 Mar 15;112(6):1197-205 [18224666.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 Apr 1;64(5):1416-23 [16413697.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1984 Jun;10(6):825-30 [6735766.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Nov 1;57(3):739-47 [14529779.001]
  • [Cites] Sarcoma. 2000;4(3):103-12 [18521288.001]
  • [Cites] Arch Surg. 1981 Jun;116(6):765-9 [7235973.001]
  • [Cites] Crit Rev Oncol Hematol. 2006 Aug;59(2):106-15 [16844383.001]
  • [Cites] Cancer. 1985 Aug 1;56(3):475-9 [4005809.001]
  • [Cites] Clin Orthop Relat Res. 1980 Nov-Dec;(153):106-20 [7449206.001]
  • [Cites] Radiother Oncol. 2003 Jun;67(3):331-7 [12865183.001]
  • [Cites] Ann Surg. 1992 Mar;215(3):269-75 [1543400.001]
  • [Cites] CA Cancer J Clin. 2004 Mar-Apr;54(2):94-109 [15061599.001]
  • [Cites] J Bone Joint Surg Am. 1996 May;78(5):650-5 [8642020.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2001 May 1;50(1):127-31 [11316555.001]
  • [Cites] Eur J Surg Oncol. 1991 Feb;17(1):71-80 [1995362.001]
  • [Cites] Br J Surg. 1995 Feb;82(2):278-9 [7749711.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2007 Jun 1;68(2):458-64 [17363186.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Nov 1;48(4):1051-8 [11072162.001]
  • [Cites] Eur J Surg Oncol. 2003 Oct;29(8):676-81 [14511617.001]
  • [Cites] Cancer. 1994 Mar 15;73(6):1652-9 [8156492.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):573-81 [18521899.001]
  • [Cites] Lancet. 1997 Dec 6;350(9092):1647-54 [9400508.001]
  • [Cites] Radiother Oncol. 2005 Apr;75(1):48-53 [15948265.001]
  • [Cites] Sarcoma. 1998;2(3-4):183-91 [18521252.001]
  • [Cites] BMJ. 1998 Jul 11;317(7151):93-4 [9657781.001]
  • [Cites] Lancet Oncol. 2007 Sep;8(9):773-83 [17714991.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Nov 1;63(3):852-9 [16199316.001]
  • [Cites] J Surg Oncol. 1993 Apr;52(4):223-30 [8468983.001]
  • [Cites] J Clin Oncol. 1996 Feb;14(2):473-8 [8636760.001]
  • [Cites] J Clin Oncol. 1990 Nov;8(11):1818-29 [2121910.001]
  • [Cites] Cancer Control. 2005 Jan-Feb;12(1):27-35 [15668650.001]
  • [Cites] Clin Transl Oncol. 2008 Feb;10(2):102-10 [18258509.001]
  • [Cites] Sarcoma. 2002;6(1):5-18 [18521341.001]
  • [Cites] Ann Oncol. 2008 May;19 Suppl 2:ii89-93 [18456783.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2000 Apr 1;47(1):157-63 [10758318.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Feb 1;52(2):469-75 [11872294.001]
  • [Cites] Acta Orthop Scand Suppl. 1997 Feb;273:4-8 [9057580.001]
  • [Cites] J Bone Joint Surg Br. 1993 Jul;75(4):658-60 [8331127.001]
  • [Cites] Ann Surg. 1982 Sep;196(3):305-15 [7114936.001]
  • [Cites] Ann Oncol. 2010 May;21 Suppl 5:v198-203 [20555081.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):197-203 [9440743.001]
  • [Cites] Sarcoma. 2006;2006(1):91671 [17040093.001]
  • [Cites] Cancer. 1975 Aug;36(2):759-64 [1157035.001]
  • [Cites] Cancer Treat Rev. 1977 Jun;4(2):67-86 [329988.001]
  • [Cites] Sarcoma. 2010;2010:506182 [20634933.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Jan 1;31(1):129-34 [7995743.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Apr 1;61(5):1439-45 [15817348.001]
  • [Cites] Ann Oncol. 1992 Apr;3 Suppl 2:S57-8 [1622868.001]
  • [Cites] Cancer. 2007 Feb 1;109(3):598-602 [17183556.001]
  • (PMID = 20709652.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  •  go-up   go-down


22. Aguiar Junior S, Ferreira Fde O, Rossi BM, Santos EM, Salvajoli JV, Lopes A: Neoadjuvant chemoradiation therapy for soft tissue sarcomas of the extremities. Clinics (Sao Paulo); 2009;64(11):1059-64
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neoadjuvant chemoradiation therapy for soft tissue sarcomas of the extremities.
  • INTRODUCTION AND OBJECTIVE: Neoadjuvant and adjuvant therapies for soft tissue sarcomas of the extremities are still controversial.
  • The aim of this study was to analyze the results of a protocol of neoadjuvant chemoradiation therapy for extremity sarcomas.
  • METHODS: A retrospective analysis was carried out in a consecutive series of 49 adult patients with advanced extremity soft tissue sarcomas that could not be resected with adequate margins during the primary resection.
  • All patients were treated with a protocol of preoperative radiation therapy at a total dose of 30 Gy, concomitant with doxorubicin (60 mg/m(2)) chemotherapy.
  • The median follow-up time was 32.1 months.
  • These complications precluded adjuvant chemotherapy in 73.7% (14/19) of the patients eligible to receive it.
  • CONCLUSIONS: In this study, neoadjuvant chemoradiation therapy was associated with a good local control rate, but the distant relapse-free rate and overall survival rate were still poor.
  • The high rate of wound complications modified the planning of adjuvant treatment in most patients.
  • [MeSH-major] Neoadjuvant Therapy / adverse effects. Sarcoma / mortality. Soft Tissue Neoplasms / mortality
  • [MeSH-minor] Adolescent. Adult. Aged. Chemotherapy, Adjuvant / adverse effects. Doxorubicin / adverse effects. Epidemiologic Methods. Extremities. Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Radiotherapy, Adjuvant / adverse effects. Treatment Outcome. Young Adult

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Cancer. 2001 Jun;37(9):1096-103 [11378339.001]
  • [Cites] Ann Oncol. 2009 Mar;20(3):425-30 [19088169.001]
  • [Cites] Ann Surg Oncol. 2002 Jul;9(6):535-42 [12095968.001]
  • [Cites] Lancet. 2002 Jun 29;359(9325):2235-41 [12103287.001]
  • [Cites] CA Cancer J Clin. 2004 Mar-Apr;54(2):94-109 [15061599.001]
  • [Cites] Cancer. 1981 May 15;47(10):2391-7 [7272893.001]
  • [Cites] Ann Surg. 1991 Sep;214(3):328-36; discussion 336-8 [1929613.001]
  • [Cites] Cancer Treat Res. 1993;67:135-41 [8102870.001]
  • [Cites] Hematol Oncol Clin North Am. 1995 Aug;9(4):817-23 [7490243.001]
  • [Cites] J Clin Oncol. 1996 Mar;14(3):859-68 [8622034.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):197-203 [9440743.001]
  • [Cites] Semin Surg Oncol. 1999 Jul-Aug;17(1):66-71 [10402639.001]
  • [Cites] J Clin Oncol. 2006 Feb 1;24(4):619-25 [16446334.001]
  • [Cites] Cancer Treat Rev. 2006 Feb;32(1):9-27 [16338075.001]
  • [Cites] Ann Surg Oncol. 2006 Sep;13(9):1209-15 [16952046.001]
  • [Cites] J Surg Oncol. 2007 Feb 1;95(2):135-41 [17262730.001]
  • [Cites] J Clin Oncol. 2007 Mar 10;25(8):1003-8 [17350950.001]
  • [Cites] Ann Surg Oncol. 2007 Apr;14(4):1254-6 [17103260.001]
  • [Cites] Oncologist. 2008 Feb;13(2):175-86 [18305063.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):573-81 [18521899.001]
  • [Cites] Ann Surg Oncol. 2001 Jul;8(6):484-95 [11456048.001]
  • (PMID = 19936179.001).
  • [ISSN] 1980-5322
  • [Journal-full-title] Clinics (São Paulo, Brazil)
  • [ISO-abbreviation] Clinics (Sao Paulo)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2780522
  • [Keywords] NOTNLM ; Adjuvant treatment / Chemotherapy / Connective tissue neoplasms / Radiotherapy / Survival
  •  go-up   go-down


23. Inoue K, Saito M, Kanai T, Kawata T, Shigematsu N, Uno T, Isobe K, Liu CH, Ito H: Anti-tumor effects of water-soluble propolis on a mouse sarcoma cell line in vivo and in vitro. Am J Chin Med; 2008;36(3):625-34

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-tumor effects of water-soluble propolis on a mouse sarcoma cell line in vivo and in vitro.
  • The tumor cell line used was mouse sarcoma 180 (S-180), and its growth was determined in vitro and in vivo with exposure to different concentrations of WSP.
  • WSP was administered to the mice 5 times, every other day for 10 days.
  • Furthermore, histological findings revealed a significant reduction in mitotic cells and tumor invasion of the muscular tissue at both dose-levels of WSP.
  • [MeSH-major] Anti-Infective Agents / therapeutic use. Neoplasms, Connective Tissue / drug therapy. Propolis / therapeutic use. Sarcoma, Experimental / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Male. Mice. Neoplasm Transplantation. Xenograft Model Antitumor Assays

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18543394.001).
  • [ISSN] 0192-415X
  • [Journal-full-title] The American journal of Chinese medicine
  • [ISO-abbreviation] Am. J. Chin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 9009-62-5 / Propolis
  •  go-up   go-down


24. Ray-Coquard I, Ranchère-Vince D, Thiesse P, Ghesquières H, Biron P, Sunyach MP, Rivoire M, Lancry L, Méeus P, Sebban C, Blay JY: Evaluation of core needle biopsy as a substitute to open biopsy in the diagnosis of soft-tissue masses. Eur J Cancer; 2003 Sep;39(14):2021-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of core needle biopsy as a substitute to open biopsy in the diagnosis of soft-tissue masses.
  • Open biopsy is recommended for a soft-tissue sarcoma (s-t-S) diagnosis.
  • Core needle biopsy (CNB) was recently associated with minimal morbidity, cost and time-consumption, but also potential inaccuracy.
  • Its diagnostic utility was investigated retrospectively in 110 patients with soft-tissue masses (s-t-M) undergoing CNB between September 1994 and September 2000.
  • Sensitivity (Se), specificity (Sp), positive (PPV) and negative (NPV) predictive values were determined for malignancy (benign/malign), soft-tissue tumour (yes/no), and sarcoma diagnosis (yes/no), comparing CNB and the best standard test available; concordance was evaluated.
  • Final diagnosis was 23 benign tumours (19%), 65 s-t-S (59%), 9 lymphomas (8%), 6 fibromatoses (desmoid) (5%) and 7 carcinomas (6%).
  • CNB Sp and PPV were 100%, Se was 95, 99 and 92%, and NPV 85, 95 and 88% for diagnosing malignancy, soft-tissue tumour and sarcoma.
  • CNB Se and NPV were 100% for malignancy, connective tumour and sarcoma in lymphomas, high-grade sarcomas and desmoid tumours.
  • In low grade sarcomas, Se was 94 and 85%, and NPV 84 and 77% for malignancy and sarcoma.
  • CNB is accurate, not misleading for s-t-M diagnosis, avoids open biopsy complications, and allows one-surgery or neo-adjuvant chemotherapy planning when combined with appropriate imaging.
  • [MeSH-major] Biopsy / methods. Soft Tissue Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Biopsy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12957456.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  •  go-up   go-down


25. Chugh R, Wathen JK, Patel SR, Maki RG, Meyers PA, Schuetze SM, Priebat DA, Thomas DG, Jacobson JA, Samuels BL, Benjamin RS, Baker LH, Sarcoma Alliance for Research through Collaboration (SARC): Efficacy of imatinib in aggressive fibromatosis: Results of a phase II multicenter Sarcoma Alliance for Research through Collaboration (SARC) trial. Clin Cancer Res; 2010 Oct 1;16(19):4884-91
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] Efficacy of imatinib in aggressive fibromatosis: Results of a phase II multicenter Sarcoma Alliance for Research through Collaboration (SARC) trial.
  • PURPOSE: Aggressive fibromatoses (AF; desmoid tumors) are rare clonal neoplastic proliferations of connective tissues that can be locally aggressive despite wide surgical resection and/or radiation therapy.
  • The Sarcoma Alliance for Research through Collaboration (SARC) initiated a prospective phase II trial to investigate the outcome of patients treated with imatinib, a multiple tyrosine kinase inhibitor, in patients with AF, or 1 of 10 sarcoma subtypes.
  • Tissue specimens were analyzed by immunohistochemistry for expression of cKIT, platelet-derived growth factor receptor α (PDGFRα), PDGFRβ, AKT, PTEN, FKHR, and β-catenin.
  • Expression and polymorphisms of target proteins were identified in tissue samples, but no significant correlation with outcome was observed using the samples available.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Fibromatosis, Aggressive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Child. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Imatinib Mesylate. Immunohistochemistry. Kaplan-Meier Estimate. Male. Maximum Tolerated Dose. Middle Aged. Treatment Outcome. Young Adult


26. Duan Z, Choy E, Hornicek FJ: NSC23925, identified in a high-throughput cell-based screen, reverses multidrug resistance. PLoS One; 2009 Oct 12;4(10):e7415
Hazardous Substances Data Bank. TAXOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Multidrug resistance (MDR) is a major factor which contributes to the failure of cancer chemotherapy, and numerous efforts have been attempted to overcome MDR.
  • To date, none of these attempts have yielded a tolerable and effective therapy to reverse MDR; thus, identification of new agents would be useful both clinically and scientifically.
  • METHODOLOGY/PRINCIPAL FINDINGS: To identify small molecule compounds that can reverse chemoresistance, we developed a 96-well plate high-throughput cell-based screening assay in a paclitaxel resistant ovarian cancer cell line.
  • CONCLUSIONS/SIGNIFICANCE: The ability of NSC23925 to restore sensitivity to the cytotoxic effects of chemotherapy or to prevent resistance could significantly benefit cancer patients.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Drug Metab Dispos. 2000 May;28(5):522-8 [10772630.001]
  • [Cites] Gene. 1999 Mar 18;229(1-2):75-81 [10095106.001]
  • [Cites] Ann Oncol. 2000 Nov;11(11):1471-6 [11142488.001]
  • [Cites] EMBO J. 2001 Oct 15;20(20):5615-25 [11598005.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1999;39:361-98 [10331089.001]
  • [Cites] Cancer Chemother Pharmacol. 2005 Mar;55(3):277-85 [15565326.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):275-84 [15803154.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4852-60 [15930306.001]
  • [Cites] Lung Cancer. 2005 Sep;49(3):337-43 [15955594.001]
  • [Cites] Anticancer Res. 2005 May-Jun;25(3B):1953-62 [16158930.001]
  • [Cites] Carcinogenesis. 2006 Jan;27(1):1-22 [16195239.001]
  • [Cites] Nat Rev Drug Discov. 2006 Mar;5(3):219-34 [16518375.001]
  • [Cites] Int J Cancer. 2007 Feb 1;120(3):611-22 [17096323.001]
  • [Cites] Adv Cancer Res. 2007;96:145-73 [17161679.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):749-57 [17429392.001]
  • [Cites] Cancer Chemother Pharmacol. 2007 Oct;60(5):741-50 [17273824.001]
  • [Cites] Mol Pharmacol. 2007 Nov;72(5):1137-45 [17675586.001]
  • [Cites] Pharmacology. 2008;81(4):275-300 [18259091.001]
  • [Cites] J Clin Oncol. 2008 Jun 1;26(16):2616-8 [18509172.001]
  • [Cites] Biochem J. 2009 Jan 1;417(1):361-70 [18976239.001]
  • [Cites] Nat Rev Cancer. 2009 Mar;9(3):167-81 [19238149.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 May;63(6):1121-9 [18828019.001]
  • [Cites] Br J Haematol. 2001 Dec;115(4):895-902 [11843823.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585.001]
  • [Cites] Anal Biochem. 2002 Jun 1;305(1):106-14 [12018951.001]
  • [Cites] J Bioenerg Biomembr. 2002 Aug;34(4):235-50 [12392187.001]
  • [Cites] Curr Cancer Drug Targets. 2003 Feb;3(1):1-19 [12570657.001]
  • [Cites] J Med Chem. 2003 Apr 24;46(9):1716-25 [12699389.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2200-5 [12727840.001]
  • [Cites] Trends Biochem Sci. 2003 Nov;28(11):581-4 [14607087.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Dec;307(3):846-53 [14534356.001]
  • [Cites] Chemotherapy. 2004 Apr;50(1):43-50 [15084806.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Jul 30;320(3):672-9 [15240100.001]
  • [Cites] Cancer Cell. 2004 Aug;6(2):129-37 [15324696.001]
  • [Cites] J Clin Oncol. 2004 Nov 1;22(21):4290-301 [15514371.001]
  • [Cites] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100.001]
  • [Cites] Cancer Res. 1988 Sep 1;48(17):4926-32 [2900677.001]
  • [Cites] Eur J Cancer. 1991;27(12):1639-42 [1816768.001]
  • [Cites] Cancer Chemother Pharmacol. 1992;30(3):238-42 [1352739.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Sep 15;89(18):8472-6 [1356264.001]
  • [Cites] Br J Cancer. 1993 May;67(5):1031-5 [8388231.001]
  • [Cites] Eur J Cancer. 1996 Jun;32A(6):1070-81 [8763349.001]
  • [Cites] Cancer Res. 1996 Sep 15;56(18):4171-9 [8797588.001]
  • [Cites] Semin Hematol. 1997 Oct;34(4 Suppl 5):40-7 [9408960.001]
  • [Cites] Eur J Pharm Sci. 2000 Oct;11(4):265-83 [11033070.001]
  • (PMID = 19823672.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA119617; United States / NCI NIH HHS / CA / R01-CA119617
  • [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 / (2-(4-methoxyphenyl)-4-quinolinyl)(2-piperidinyl)methanol; 0 / Antineoplastic Agents; 0 / Fluoresceins; 0 / P-Glycoprotein; 0 / Piperidines; 0 / Quinolines; 148504-34-1 / calcein AM; EC 3.6.1.- / Adenosine Triphosphatases; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC2757897
  •  go-up   go-down


27. Duan Z, Weinstein EJ, Ji D, Ames RY, Choy E, Mankin H, Hornicek FJ: Lentiviral short hairpin RNA screen of genes associated with multidrug resistance identifies PRP-4 as a new regulator of chemoresistance in human ovarian cancer. Mol Cancer Ther; 2008 Aug;7(8):2377-85
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.
  • Published reports implicate a variety of mechanisms that may contribute to drug resistance in ovarian cancer.
  • The chief aim of this study is to understand the relationship between overexpression of drug resistance associated genes and multidrug resistance in ovarian cancer.
  • Using lentiviral short hairpin RNA collections targeting 132 genes identified from transcriptional profiling of drug-resistant cancer cell lines, individual knockdown experiments were done in the presence of sublethal doses of paclitaxel.
  • Both MDR1 and survivin have been reported previously to play a role in multidrug resistance and chemotherapy-induced apoptosis; however, the effect of PRP-4 expression on drug sensitivity is currently unrecognized.
  • Finally, overexpression of PRP-4 in drug-sensitive cells could induce a modest level of drug resistance to paclitaxel, doxorubicin, and vincristine.

  • Genetic Alliance. consumer health - Ovarian cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAXOL .
  • 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
  • [Cites] Cancer Res. 1991 Nov 1;51(21):5903-9 [1657373.001]
  • [Cites] J Biol. 2003;2(4):27 [14527345.001]
  • [Cites] Cancer Res. 1993 Jan 1;53(1):16-8 [8416741.001]
  • [Cites] EMBO J. 1993 Feb;12(2):461-8 [8440237.001]
  • [Cites] Breast Cancer Res Treat. 1992;24(2):85-95 [8095168.001]
  • [Cites] Cancer Res. 1994 Feb 1;54(3):794-9 [8306343.001]
  • [Cites] J Cell Biol. 1994 Nov;127(3):609-22 [7525595.001]
  • [Cites] Biochemistry. 1995 Jan 10;34(1):32-9 [7819214.001]
  • [Cites] Br J Cancer. 1996 Oct;74(8):1263-8 [8883415.001]
  • [Cites] Nucleic Acids Res. 1997 Mar 1;25(5):1028-35 [9102632.001]
  • [Cites] Gene. 2004 Sep 29;340(1):53-9 [15556294.001]
  • [Cites] Cancer Chemother Pharmacol. 2005 Mar;55(3):277-85 [15565326.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1283-98 [16564017.001]
  • [Cites] Trends Mol Med. 2007 Jan;13(1):4-11 [17118707.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):1988-96 [17332326.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4843-50 [17510414.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5831-9 [17575151.001]
  • [Cites] Cancer Res. 2007 Jul 15;67(14):6657-64 [17638875.001]
  • [Cites] Am J Clin Pathol. 2007 Sep;128(3):389-97 [17709312.001]
  • [Cites] Transgenic Res. 2007 Oct;16(5):571-80 [17682833.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Dec;46(12):1069-79 [17726699.001]
  • [Cites] J Cell Biol. 2007 Nov 19;179(4):601-9 [17998396.001]
  • [Cites] Nat Rev Cancer. 2004 Sep;4(9):677-87 [15343274.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3445-53 [10589757.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Dec 20;266(2):291-5 [10600495.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):E31-6 [10655601.001]
  • [Cites] Cell Mol Life Sci. 2001 Jun;58(7):931-59 [11497241.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):32247-56 [11418604.001]
  • [Cites] Cytokine. 2002 Mar 7;17(5):234-42 [12027404.001]
  • [Cites] Drug Resist Updat. 2002 Apr;5(2):65-72 [12135582.001]
  • [Cites] Anticancer Res. 2002 Jul-Aug;22(4):1933-41 [12174867.001]
  • [Cites] Curr Cancer Drug Targets. 2003 Feb;3(1):1-19 [12570657.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2200-5 [12727840.001]
  • [Cites] Mod Pathol. 2003 Jun;16(6):574-83 [12808063.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2778-85 [12855658.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7280-95 [14576838.001]
  • [Cites] Int J Gynecol Cancer. 2003 Nov-Dec;13(6):701-34 [14675307.001]
  • [Cites] Curr Drug Metab. 2004 Feb;5(1):21-53 [14965249.001]
  • [Cites] Mol Cancer Ther. 2004 Jul;3(7):833-8 [15252144.001]
  • [Cites] Nat Rev Drug Discov. 2006 Mar;5(3):219-34 [16518375.001]
  • [Cites] Gene Ther. 2006 Mar;13(6):503-8 [16195700.001]
  • [Cites] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100.001]
  • [Cites] Mol Gen Genet. 1991 Apr;226(1-2):305-9 [2034223.001]
  • [Cites] Cancer Res. 1992 Oct 1;52(19):5407-11 [1394146.001]
  • (PMID = 18687998.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA119617-01; United States / NCI NIH HHS / CA / R01 CA119617; United States / NCI NIH HHS / CA / R01 CA 119617; United States / NCI NIH HHS / CA / R01 CA119617-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / DNA Primers; 0 / PRPF4 protein, human; 0 / RNA, Viral; 0 / Ribonucleoprotein, U4-U6 Small Nuclear; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS66400; NLM/ PMC2597512
  •  go-up   go-down


28. Duan Z, Choy E, Harmon D, Yang C, Ryu K, Schwab J, Mankin H, Hornicek FJ: Insulin-like growth factor-I receptor tyrosine kinase inhibitor cyclolignan picropodophyllin inhibits proliferation and induces apoptosis in multidrug resistant osteosarcoma cell lines. Mol Cancer Ther; 2009 Aug;8(8):2122-30
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.
  • Insulin-like growth factor-I receptor (IGF-IR) is an important mediator of tumor cell survival and shows prognostic significance in sarcoma.
  • To explore potential therapeutic strategies for interrupting signaling through this pathway, we assessed the ability of cyclolignan picropodophyllin (PPP), a member of the cyclolignan family, to selectively inhibit the receptor tyrosine kinase activity of IGF-IR in several sarcoma cell line model systems.
  • Of the diverse sarcoma subtypes studied, osteosarcoma cell lines were found to be particularly sensitive to IGF-IR inhibition, including several multidrug resistant osteosarcoma cell lines with documented resistance to various conventional anticancer drugs.
  • These studies show that PPP significantly inhibits IGF-IR expression and activation in both chemotherapy-sensitive and chemotherapy-resistant osteosarcoma cell lines.
  • Furthermore, small interfering RNA down-regulation of IGF-IR expression in drug-resistant cell lines also caused resensitization to doxorubicin.
  • Our data suggest that inhibition of IGF-IR with PPP offers a novel and selective therapeutic strategy for ostosarcoma, and at the same time, PPP is effective at reversing the drug-resistant phenotype in osteosarcoma cell lines.

  • Genetic Alliance. consumer health - Osteosarcoma.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PODOFILOX .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Growth Horm IGF Res. 2001 Dec;11(6):336-8 [11914020.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 Aug;64(3):607-14 [19125251.001]
  • [Cites] Cancer Lett. 2003 Jun 10;195(2):127-37 [12767520.001]
  • [Cites] Oncogene. 2003 Sep 29;22(42):6589-97 [14528284.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):236-42 [14729630.001]
  • [Cites] Lancet. 2004 Apr 24;363(9418):1346-53 [15110491.001]
  • [Cites] Oncogene. 2004 Oct 14;23(47):7854-62 [15334055.001]
  • [Cites] Cancer Res. 1982 Aug;42(8):3232-9 [7046921.001]
  • [Cites] EMBO J. 1986 Oct;5(10):2503-12 [2877871.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2803-7 [8168113.001]
  • [Cites] Cancer Res. 1995 Jan 15;55(2):249-52 [7812953.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3588-91 [10446966.001]
  • [Cites] Int J Oncol. 2005 Dec;27(6):1605-16 [16273217.001]
  • [Cites] Clin Cancer Res. 2006 Feb 15;12(4):1383-91 [16489097.001]
  • [Cites] Expert Rev Anticancer Ther. 2006 Jul;6(7):1075-85 [16831079.001]
  • [Cites] Br J Cancer. 2006 Jul 17;95(2):172-80 [16819546.001]
  • [Cites] Biochim Biophys Acta. 2006 Aug;1766(1):1-22 [16844299.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5055-63 [16951221.001]
  • [Cites] Int J Cancer. 2007 Feb 1;120(3):611-22 [17096323.001]
  • [Cites] Mol Cancer Ther. 2007 Jan;6(1):1-12 [17237261.001]
  • [Cites] Clin Cancer Res. 2007 Feb 15;13(4):1322-30 [17317844.001]
  • [Cites] Int J Cancer. 2007 Oct 15;121(8):1857-61 [17546599.001]
  • [Cites] J Cell Biochem. 2007 Sep 1;102(1):28-40 [17372931.001]
  • [Cites] Clin Cancer Res. 2008 Mar 1;14(5):1581-9 [18316583.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Oncogene. 2008 Mar 6;27(11):1629-38 [17828296.001]
  • [Cites] Front Biosci. 2008;13:3273-87 [18508432.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Jun;49(6):2337-42 [18515579.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Jun;49(6):2620-6 [18515591.001]
  • [Cites] Curr Opin Oncol. 2008 Jul;20(4):393-4 [18525333.001]
  • [Cites] Expert Rev Anticancer Ther. 2008 Aug;8(8):1257-69 [18699764.001]
  • [Cites] Cancer Res. 2008 Aug 15;68(16):6661-8 [18701490.001]
  • [Cites] Paediatr Drugs. 2008;10(5):315-27 [18754698.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6364-70 [18927274.001]
  • [Cites] Nat Rev Cancer. 2008 Dec;8(12):915-28 [19029956.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2008 Dec;13(4):371-9 [19030972.001]
  • [Cites] Apoptosis. 2009 Jan;14(1):124-33 [19052873.001]
  • [Cites] Oncologist. 2009 Jan;14(1):83-91 [19126579.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2359-64 [19174523.001]
  • [Cites] Int J Cancer. 2009 May 15;124(10):2416-29 [19142965.001]
  • [Cites] Radiat Res. 2002 Aug;158(2):174-80 [12105987.001]
  • (PMID = 19638450.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA119617-01; United States / NCI NIH HHS / CA / R01 CA119617; United States / NCI NIH HHS / CA / R01 CA119617-01; United States / NCI NIH HHS / CA / R01-CA119617
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 0F35AOI227 / picropodophyllin; EC 2.7.10.1 / Receptor, IGF Type 1; L36H50F353 / Podophyllotoxin
  • [Other-IDs] NLM/ NIHMS125962; NLM/ PMC2766237
  •  go-up   go-down


29. 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).
  • 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


30. Feng X, Zhang L, Zhu H: Comparative anticancer and antioxidant activities of different ingredients of Ginkgo biloba extract (EGb 761). Planta Med; 2009 Jun;75(8):792-6
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.
  • We have investigated the anticancer effects of three analogues of EGb 761 samples on sarcoma 108 (S180)-bearing mice and leukemic 1210 (L1210) cell lines.
  • The EGb 761, EGb 761-H (containing mainly flavonoid aglycones and terpene trilactones), and EGb 761-DT-H (containing mainly flavonoid aglycones) samples exhibited cytotoxicity and inhibitory activity with IC (50) values of 46.36 +/- 2.43 microM, 10.27 +/- 0.88 microM, and 14.93 +/- 0.73 microM in L1210 cell-based assays, respectively.
  • This resulted in 41.74 %, 60.72 %, and 63.76 % reductions in tumor weight after 10 days of treatment, respectively.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Antioxidants / therapeutic use. Flavonoids / therapeutic use. Ginkgo biloba / chemistry. Neoplasms, Connective Tissue / drug therapy. Phytotherapy. Plant Extracts / therapeutic use
  • [MeSH-minor] Animals. Catalase / blood. Cell Line, Tumor. Dose-Response Relationship, Drug. Glutathione / blood. Glycosides / analysis. Glycosides / pharmacology. Glycosides / therapeutic use. Lactones / analysis. Lactones / pharmacology. Lactones / therapeutic use. Leukemia / drug therapy. Lipid Peroxidation / drug effects. Mice. Organ Size. Sarcoma / drug therapy. Superoxide Dismutase / blood. Terpenes / analysis. Terpenes / pharmacology. Terpenes / therapeutic use

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • MedlinePlus Health Information. consumer health - Herbal Medicine.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19288403.001).
  • [ISSN] 1439-0221
  • [Journal-full-title] Planta medica
  • [ISO-abbreviation] Planta Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Antioxidants; 0 / Flavonoids; 0 / Ginkgo biloba extract 761; 0 / Glycosides; 0 / Lactones; 0 / Plant Extracts; 0 / Terpenes; 0 / trilactone; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; GAN16C9B8O / Glutathione
  •  go-up   go-down


31. Joyner DE, Damron TA, Aboulafia A, Bokor W, Bastar JD, Randall RL: Heterogeneous expression of melanoma antigen (hMAGE) mRNA in mesenchymal neoplasia. Tissue Antigens; 2006 Jul;68(1):19-27
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.
  • CT antigens are encoded by cancer-germline genes (e.g., hMAGE family) that are expressed in tumors and male germline cells but typically not in normal tissues.
  • At present, little information is available regarding CT expression in mesenchymal neoplasms, and it remains uncertain whether CT immunotherapy will serve as a viable alternative or adjunct to current sarcoma therapies involving resection, followed by adjuvant radiotherapy and/or chemotherapy.
  • In this study, hMAGEA2, hMAGEA3, hMAGEA4, and hMAGEC1 mRNA content in 21 benign mesenchymal tumors (representing seven histotypes) and 28 primary sarcomas (10 histotypes) was inventoried using real-time-PCR and then compared against hMAGE mRNA expression in non-sarcomatous malignancies, three cell lines, and muscle. hMAGEA2, hMAGEA3, and hMAGEC1 transcripts were infrequent in mesenchymal tissues in general, whereas hMAGEA4 mRNA was present in 84% of all mesenchymal tumors, 100% of non-sarcomatous tumors, all three cell lines, and in four of five muscle samples.
  • The presence of hMAGEA4 mRNA in muscle, plus the inconsistent and infrequent occurrence of hMAGEA2, hMAGEA3, and hMAGEC1 mRNA within and among mesenchymal tumor histotypes, makes these four hMAGE antigens unlikely candidates for sarcoma-specific immunotherapy.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Neoplasm Proteins / metabolism. Neoplasms / metabolism. Neoplasms, Connective Tissue / metabolism. Sarcoma / metabolism. Testis / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Tissue Antigens. 2006 Aug;68(2):192
  • (PMID = 16774536.001).
  • [ISSN] 0001-2815
  • [Journal-full-title] Tissue antigens
  • [ISO-abbreviation] Tissue Antigens
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MAGEA1 protein, human; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  •  go-up   go-down


32. Sinkovics JG: Adult human sarcomas. I. Basic science. Expert Rev Anticancer Ther; 2007 Jan;7(1):31-56
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.
  • When connective tissue undergoes malignant transformation, glioblastomas and sarcomas arise.
  • Immune lymphocytes that kill autologous sarcoma cells in vitro commonly fail to do so in vivo.
  • Sarcoma vaccines generate immune T- and natural killer cell reactions; even when vaccinated patients do not show a clinical response, their tumors become more sensitive to chemotherapy.
  • The aim of this review is to lay a solid molecular biological foundation for the conclusion that targeting the sarcoma oncogenes will result in regression of the disease.
  • [MeSH-major] Cancer Vaccines. Sarcoma / pathology. Sarcoma / physiopathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Expert Rev Anticancer Ther. 2007 Feb;7(2):247-8
  • (PMID = 17187519.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines
  • [Number-of-references] 272
  •  go-up   go-down


33. Susa M, Choy E, Yang C, Schwab J, Mankin H, Hornicek F, Duan Z: Multidrug resistance reversal agent, NSC77037, identified with a cell-based screening assay. J Biomol Screen; 2010 Mar;15(3):287-96
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.
  • The development of multidrug resistance (MDR) remains a significant obstacle in treating cancer patients with chemotherapy.
  • The cytotoxic activity of NSC77037 and the duration of its effect were evaluated in vitro using a panel of cancer cell lines expressing permeability glycoprotein (Pgp), multiple drug resistance protein 1 (MRP 1), and breast cancer resistance protein (BCRP).
  • The use of NSC77037 to restore sensitivity to chemotherapy or to prevent resistance could be a potential treatment strategy for cancer patients.
  • [MeSH-major] Benzylisoquinolines / analysis. Benzylisoquinolines / pharmacology. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm / drug effects. Drug Screening Assays, Antitumor / methods
  • [MeSH-minor] Adenosine Triphosphatases / metabolism. Cell Line, Tumor. Fluoresceins / metabolism. Humans. P-Glycoprotein / metabolism. Paclitaxel / pharmacology. Substrate Specificity / drug effects. Time Factors. Verapamil / pharmacology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. VERAPAMIL HYDROCHLORIDE .
  • Hazardous Substances Data Bank. TAXOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20150589.001).
  • [ISSN] 1552-454X
  • [Journal-full-title] Journal of biomolecular screening
  • [ISO-abbreviation] J Biomol Screen
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA119617
  • [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 / Benzylisoquinolines; 0 / Fluoresceins; 0 / P-Glycoprotein; 148504-34-1 / calcein AM; 29EX23D5AJ / tetrandrine; CJ0O37KU29 / Verapamil; EC 3.6.1.- / Adenosine Triphosphatases; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


34. Duan Z, Ames RY, Ryan M, Hornicek FJ, Mankin H, Seiden MV: CDDO-Me, a synthetic triterpenoid, inhibits expression of IL-6 and Stat3 phosphorylation in multi-drug resistant ovarian cancer cells. Cancer Chemother Pharmacol; 2009 Mar;63(4):681-9
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] CDDO-Me, a synthetic triterpenoid, inhibits expression of IL-6 and Stat3 phosphorylation in multi-drug resistant ovarian cancer cells.
  • Activation of the IL-6-Stat3 pathway contributes to tumor cell growth, survival and drug resistance in several cancers, including ovarian cancer.
  • To explore potential therapeutic strategies for interrupting signaling through this pathway, we assessed the ability of CDDO-Me, a synthetic triterpenoid, to inhibit IL-6 secretion, Stat3 phosphorylation, Stat3 nuclear translocation and paclitaxel sensitivity in several cell line model systems.
  • Treatment with CDDO-Me significantly decreases the levels of Stat3, Jak2, and Src phosphorylation in ovarian and breast cancer cell lines with constitutively activated Stat3.
  • In a model system of established acquired drug resistance, CCDO-Me is effective at partially reversing the drug-resistance phenotype.

  • Genetic Alliance. consumer health - Ovarian cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3445-53 [10589757.001]
  • [Cites] Blood. 2002 Jan 1;99(1):326-35 [11756188.001]
  • [Cites] J Biol Chem. 2002 May 10;277(19):16639-47 [11872748.001]
  • [Cites] Cytokine. 2002 Mar 7;17(5):234-42 [12027404.001]
  • [Cites] Cytokine. 2002 Mar 21;17(6):324-34 [12061840.001]
  • [Cites] Curr Cancer Drug Targets. 2003 Feb;3(1):1-19 [12570657.001]
  • [Cites] Nat Rev Cancer. 2004 Feb;4(2):97-105 [14964307.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3550-8 [15150111.001]
  • [Cites] Cancer Res. 1987 Feb 15;47(4):943-6 [3802101.001]
  • [Cites] Cancer. 1994 Apr 1;73(7):1882-8 [8137215.001]
  • [Cites] Blood. 1996 Feb 1;87(3):1104-12 [8562936.001]
  • [Cites] Science. 1997 Sep 12;277(5332):1630-5 [9287210.001]
  • [Cites] Cancer Chemother Pharmacol. 2005 Mar;55(3):277-85 [15565326.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):192-7 [15618392.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1053-65 [15558012.001]
  • [Cites] Eur J Cancer. 2005 Nov;41(16):2502-12 [16199153.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10794-800 [16322225.001]
  • [Cites] Clin Cancer Res. 2006 Jan 1;12(1):11-9 [16397018.001]
  • [Cites] Clin Cancer Res. 2006 Jan 1;12(1):20-8 [16397019.001]
  • [Cites] Clin Cancer Res. 2006 Mar 15;12(6):1828-38 [16551868.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5055-63 [16951221.001]
  • [Cites] J Biol Chem. 2006 Nov 24;281(47):35764-9 [16998237.001]
  • [Cites] Cancer. 2006 Dec 1;107(11):2730-40 [17063503.001]
  • [Cites] Mol Cancer Ther. 2006 Dec;5(12):3232-9 [17148759.001]
  • [Cites] Nat Rev Immunol. 2007 Jan;7(1):41-51 [17186030.001]
  • [Cites] Trends Mol Med. 2007 Jan;13(1):4-11 [17118707.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2414-9 [17363558.001]
  • [Cites] Nat Rev Cancer. 2007 May;7(5):357-69 [17446857.001]
  • (PMID = 18587580.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1P50CA105009; United States / NCI NIH HHS / CA / K24 CA109416; United States / NCI NIH HHS / CA / P50 CA105009; United States / NCI NIH HHS / CA / P50 CA105009-040004; United States / NCI NIH HHS / CA / CA105009-040004
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / IL6 protein, human; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 6SMK8R7TGJ / Oleanolic Acid; CEG1Q6OGU1 / methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate
  • [Other-IDs] NLM/ NIHMS193288; NLM/ PMC2875930
  •  go-up   go-down


35. Guerrero MA, Ballard BR, Grau AM: Malignant phyllodes tumor of the breast: review of the literature and case report of stromal overgrowth. Surg Oncol; 2003 Jul;12(1):27-37
MedlinePlus Health Information. consumer health - Breast Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The term "sarcoma" was initially used because of its fleshy appearance, a more modern term is Phyllodes tumor (PT).
  • The microscopic appearance of PT is that of epithelial elements and connective tissue stroma.
  • Wide local excision with 2 cm margins is the treatment of choice.
  • There is no proven benefit of radiation or chemotherapy, although radiotherapy may be useful in selected cases.
  • We present a case of a sarcomatous overgrowth in a malignant phyllodes tumor involving multiple histologic types.
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Treatment Outcome

  • Genetic Alliance. consumer health - Phyllodes Tumor.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12689668.001).
  • [ISSN] 0960-7404
  • [Journal-full-title] Surgical oncology
  • [ISO-abbreviation] Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 56
  •  go-up   go-down


36. Yang C, Hornicek FJ, Wood KB, Schwab JH, Choy E, Mankin H, Duan Z: Blockage of Stat3 with CDDO-Me inhibits tumor cell growth in chordoma. Spine (Phila Pa 1976); 2010 Aug 15;35(18):1668-75
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.
  • STUDY DESIGN: An experimental study to investigate the activation of Src/Stat3 pathways in chordomas and blockage of this pathway as a potential strategy for chordoma treatment.
  • OBJECTIVE: To investigate the activation of Src/Stat3 pathway in chordomas cells and to determine the efficiency of inhibiting this pathway by 2-cyano-3,12-dioxooleana-1,9 (11)-dien-28-oic acid-methyl ester (CDDO-Me) as a potential chemotherapeutic agent for chordoma treatment.
  • SUMMARY OF BACKGROUND DATA: The advent of molecularly targeted therapies has raised interest for their use in the treatment of chordomas.
  • METHODS: The expression of key components of the Src/Stat3 signaling cascade was evaluated by Western blot in chordoma tissues and chordoma cell lines.
  • Expression of the key components of the Src/Stat3 signaling cascade was inhibited in chordoma cells after treatment with CDDO-Me.
  • The growth of chordoma cells was inhibited and apoptosis associated poly (ADP-ribose) polymerase cleavage was detected after treatment with CDDO-Me.
  • Finally, expression of pSrc and pStat3 and chordoma cell growth was inhibited by treatment of CDDO-Me using 3D culture.
  • Blockage of Src/Stat3 pathway by CDDO-Me is a potential strategy for chordoma treatment and may be focus for future research.
  • [MeSH-major] Chordoma / drug therapy. Chordoma / pathology. Growth Inhibitors / therapeutic use. Oleanolic Acid / analogs & derivatives. STAT3 Transcription Factor / antagonists & inhibitors. Spinal Neoplasms / drug therapy. Spinal Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / therapeutic use. Humans. Organ Culture Techniques

  • Genetic Alliance. consumer health - Chordoma.
  • COS Scholar Universe. author profiles.
  • 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 = 20386502.001).
  • [ISSN] 1528-1159
  • [Journal-full-title] Spine
  • [ISO-abbreviation] Spine
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA119617
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Growth Inhibitors; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 6SMK8R7TGJ / Oleanolic Acid; CEG1Q6OGU1 / methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate
  •  go-up   go-down


37. Confavreux C, Lurkin A, Mitton N, Blondet R, Saba C, Ranchère D, Sunyach MP, Thiesse P, Biron P, Blay JY, Ray-Coquard I: Sarcomas and malignant phyllodes tumours of the breast--a retrospective study. Eur J Cancer; 2006 Nov;42(16):2715-21
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Although most breast cancers are adenocarcinomas of the mammary gland, primary breast sarcomas may also arise from mammary gland mesenchymal tissue.
  • The annual incidence of primary breast sarcoma is low and has been estimated at 45 new cases per 10 million women.
  • Phyllodes tumours represent a specific subset of these breast soft tissue tumours.
  • They are composed of a connective tissue stroma and epithelial elements.
  • Pathological presentation ranges from grade I to malignant phyllodes tumours (grade III) where the stromal component clearly exhibits a sarcoma pattern.
  • MATERIALS AND METHODS: SAPHYR (SArcoma and PHYllode Retrospective) is a retrospective study of the experience of Leon Bérard Cancer Centre (Lyon, France) from 1966 to August 2004.
  • The first goal of treatment is to achieve negative margins (R0).
  • We propose to treat the patients according to the clinical practice guidelines in use for soft tissue sarcomas and address them to a reference centre for sarcoma.
  • Treating rare tumours in the same place should permit us to standardise pathological data and to include patients into multicentric radiotherapy or chemotherapy protocols to improve overall survival.
  • [MeSH-major] Breast Neoplasms. Phyllodes Tumor. Sarcoma

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17023158.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


38. Conway JG, Pink H, Bergquist ML, Han B, Depee S, Tadepalli S, Lin P, Crumrine RC, Binz J, Clark RL, Selph JL, Stimpson SA, Hutchins JT, Chamberlain SD, Brodie TA: Effects of the cFMS kinase inhibitor 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine (GW2580) in normal and arthritic rats. J Pharmacol Exp Ther; 2008 Jul;326(1):41-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The cFMS (cellular homolog of the V-FMS oncogene product of the Susan McDonough strain of feline sarcoma virus) (Proc Natl Acad Sci U S A 83:3331-3335, 1986) kinase inhibitor 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine (GW2580) inhibits colony-stimulating factor (CSF)-1-induced monocyte growth and bone degradation in vitro and inhibits CSF-1 signaling through cFMS kinase in 4-day models in mice (Proc Natl Acad Sci U S A 102:16078, 2005).
  • In the present study, the kinase selectivity of GW2580 was further characterized, and the effects of chronic treatment were evaluated in normal and arthritic rats.
  • In a 21-day adjuvant arthritis model, GW2580 dosed twice a day (b.i.d.) from days 0 to 21, 7 to 21, or 14 to 21 inhibited joint connective tissue and bone destruction as assessed by radiology, histology and bone mineral content measurements.
  • GW2580 administered to normal rats for 21 days showed no effects on tissue histology and only modest changes in serum clinical chemistry and blood hematology.
  • [MeSH-major] Anisoles / therapeutic use. Arthritis, Experimental / drug therapy. Arthritis, Experimental / enzymology. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Receptor, Macrophage Colony-Stimulating Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Cells, Cultured. Humans. Male. Rats. Rats, Inbred Lew. Sarcoma Viruses, Feline / drug effects. Sarcoma Viruses, Feline / enzymology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18434589.001).
  • [ISSN] 1521-0103
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine; 0 / Anisoles; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  •  go-up   go-down


39. Siddiqi S, Mills J, Matushansky I: Epigenetic remodeling of chromatin architecture: exploring tumor differentiation therapies in mesenchymal stem cells and sarcomas. Curr Stem Cell Res Ther; 2010 Mar;5(1):63-73
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epigenetic remodeling of chromatin architecture: exploring tumor differentiation therapies in mesenchymal stem cells and sarcomas.
  • Sarcomas are the mesenchymal-derived malignant tumors of connective tissues (e.g., fat, bone, and cartilage) presumed to arise from aberrant development or differentiation of mesenchymal stem cells (MSCs).
  • Appropriate control of stem cell maintenance versus differentiation allows for normal connective tissue development.
  • Current theories suggest that loss of this control--through accumulation of genetic lesions in MSCs at various points in the differentiation process--leads to development of sarcomas, including undifferentiated, high grade sarcoma tumors.
  • This review will focus on the importance of epigenetic chromatin remodeling in the context of mesenchymal stem cells, sarcoma tumorigenesis and differentiation therapy.

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Lett. 2004 Jan 20;203(2):217-24 [14732230.001]
  • [Cites] Mol Cell. 2004 Mar 26;13(6):887-93 [15053881.001]
  • [Cites] J Cell Biochem. 2004 Jul 1;92(4):691-700 [15211567.001]
  • [Cites] Genes Dev. 2004 Jul 1;18(13):1592-605 [15231737.001]
  • [Cites] Stem Cells. 2004;22(5):823-31 [15342946.001]
  • [Cites] Biochim Biophys Acta. 1968 Jun 26;160(2):252-5 [5658127.001]
  • [Cites] J Mol Biol. 1971 Jun 28;58(3):651-9 [5104701.001]
  • [Cites] CRC Crit Rev Biochem. 1974 Jan;2(1):67-112 [4360087.001]
  • [Cites] Biochem Biophys Res Commun. 1975 May 19;64(2):514-8 [1147941.001]
  • [Cites] Nature. 1977 May 26;267(5609):364-6 [68440.001]
  • [Cites] Cell. 1978 Oct;15(2):393-403 [214238.001]
  • [Cites] Nature. 1978 Dec 7;276(5688):565-70 [103000.001]
  • [Cites] Biochem Biophys Res Commun. 1979 Jan 30;86(2):340-9 [284780.001]
  • [Cites] Mol Cell Biochem. 1982 Feb 5;42(2):65-82 [6174854.001]
  • [Cites] Nature. 1983 Jan 6;301(5895):89-92 [6185846.001]
  • [Cites] Biochim Biophys Acta. 1984 Sep 10;782(4):331-42 [6383476.001]
  • [Cites] Cancer Res. 1988 Apr 15;48(8):1996-2004 [2450643.001]
  • [Cites] N Engl J Med. 1991 May 16;324(20):1385-93 [1850498.001]
  • [Cites] Cell. 1992 Jun 12;69(6):915-26 [1606615.001]
  • [Cites] Mol Biol Cell. 1992 Jun;3(6):593-602 [1498368.001]
  • [Cites] Leukemia. 1994;8 Suppl 3:S50-4 [7808025.001]
  • [Cites] Muscle Nerve. 1995 Dec;18(12):1417-26 [7477065.001]
  • [Cites] Dev Biol. 1996 Jan 10;173(1):2-13 [8575621.001]
  • [Cites] Physiol Rev. 1996 Apr;76(2):593-629 [8618964.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5705-8 [8650156.001]
  • [Cites] Reprod Nutr Dev. 1996;36(6):619-35 [9021873.001]
  • [Cites] Curr Biol. 1997 Mar 1;7(3):157-65 [9395433.001]
  • [Cites] Genes Dev. 1997 Sep 15;11(18):2383-95 [9308966.001]
  • [Cites] Nat Genet. 1998 Jun;19(2):187-91 [9620779.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] J Clin Invest. 1999 Mar;103(5):697-705 [10074487.001]
  • [Cites] Science. 1999 Apr 2;284(5411):143-7 [10102814.001]
  • [Cites] Cell. 1999 Jul 9;98(1):37-46 [10412979.001]
  • [Cites] Clin Chem. 1999 Oct;45(10):1708-17 [10508115.001]
  • [Cites] Proc Natl Acad Sci U S A. 1962 Jul 15;48:1216-22 [14036409.001]
  • [Cites] Proc Natl Acad Sci U S A. 1963 Dec;50:1018-26 [14096173.001]
  • [Cites] DNA Cell Biol. 2005 Feb;24(2):117-25 [15699631.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 8;102(6):1859-64 [15684044.001]
  • [Cites] Cancer Lett. 2005 Jun 28;224(2):311-9 [15914281.001]
  • [Cites] Int J Cancer. 2005 Aug 20;116(2):226-35 [15800932.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3923-31 [15897550.001]
  • [Cites] Cell. 1999 Oct 29;99(3):247-57 [10555141.001]
  • [Cites] Cell. 1999 Nov 24;99(5):451-4 [10589672.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14967-72 [10611321.001]
  • [Cites] Proc Nutr Soc. 2000 Feb;59(1):65-73 [10828175.001]
  • [Cites] Science. 2000 Aug 11;289(5481):950-3 [10937998.001]
  • [Cites] Nature. 2000 Nov 23;408(6811):495-8 [11100734.001]
  • [Cites] Curr Opin Genet Dev. 2001 Feb;11(1):91-7 [11163157.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):116-20 [11242053.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):120-4 [11242054.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2409-12 [11289106.001]
  • [Cites] Br J Haematol. 2001 Mar;112(4):950-8 [11298590.001]
  • [Cites] Mol Cell Biol. 2001 May;21(10):3598-603 [11313485.001]
  • [Cites] Curr Opin Cell Biol. 2001 Jun;13(3):263-73 [11343896.001]
  • [Cites] Br J Cancer. 2001 May 18;84(10):1372-6 [11355949.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1074-80 [11498575.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Nature. 2001 Nov 15;414(6861):277-83 [11713521.001]
  • [Cites] Cancer Res. 2001 Dec 1;61(23):8492-7 [11731433.001]
  • [Cites] Cell. 2001 Dec 14;107(6):727-38 [11747809.001]
  • [Cites] Mol Cell. 2001 Nov;8(5):933-5 [11741529.001]
  • [Cites] Genes Dev. 2002 Jan 1;16(1):6-21 [11782440.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 15;30(2):475-81 [11788710.001]
  • [Cites] Exp Cell Res. 2007 Mar 10;313(5):975-83 [17239852.001]
  • [Cites] Biochem Pharmacol. 2007 May 1;73(9):1297-307 [17276411.001]
  • [Cites] Clin Cancer Res. 2007 May 1;13(9):2541-8 [17473182.001]
  • [Cites] Cancer Cell. 2007 May;11(5):421-9 [17482132.001]
  • [Cites] Eur Urol. 2007 Aug;52(2):455-63 [17134822.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):553-60 [17603471.001]
  • [Cites] J Cell Physiol. 2007 Nov;213(2):384-90 [17708532.001]
  • [Cites] Mol Cancer Ther. 2007 Sep;6(9):2525-34 [17876049.001]
  • [Cites] Mol Cancer Res. 2007 Oct;5(10):981-9 [17951399.001]
  • [Cites] J Clin Invest. 2007 Nov;117(11):3248-57 [17948129.001]
  • [Cites] Front Biosci. 2008;13:1568-77 [17981649.001]
  • [Cites] Nature. 2007 Nov 15;450(7168):440-4 [18004385.001]
  • [Cites] Toxicol Appl Pharmacol. 2007 Dec 15;225(3):300-9 [17904174.001]
  • [Cites] Mutat Res. 2008 Jan 1;637(1-2):1-15 [17850830.001]
  • [Cites] Prostate. 2008 Feb 1;68(2):210-22 [18092350.001]
  • [Cites] Semin Hematol. 2008 Jan;45(1):23-30 [18179966.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1060-6 [17962510.001]
  • [Cites] Br J Pharmacol. 2008 Feb;153(4):657-68 [18059320.001]
  • [Cites] Int J Oncol. 2008 Apr;32(4):821-7 [18360709.001]
  • [Cites] Am J Pathol. 2008 Apr;172(4):1069-80 [18310505.001]
  • [Cites] Oncogene. 2008 Apr 10;27(17):2412-21 [17968314.001]
  • [Cites] Cell Cycle. 2008 Mar 15;7(6):720-4 [18239459.001]
  • [Cites] Cancer Res. 2008 Jun 1;68(11):4303-10 [18519690.001]
  • [Cites] Clin Orthop Relat Res. 2008 Sep;466(9):2114-30 [18563507.001]
  • [Cites] Mutat Res. 2008 Jul-Aug;659(1-2):40-8 [18407786.001]
  • [Cites] Curr Drug Targets. 2008 Jul;9(7):571-80 [18673243.001]
  • [Cites] Cell Stem Cell. 2008 Sep 11;3(3):301-13 [18786417.001]
  • [Cites] Nat Chem Biol. 2008 Oct;4(10):590-7 [18800048.001]
  • [Cites] Mol Cell Biol. 2008 Oct;28(19):6123-33 [18644860.001]
  • [Cites] Curr Drug Targets. 2008 Nov;9(11):1013-24 [18991612.001]
  • [Cites] Ann Rheum Dis. 2008 Dec;67 Suppl 3:iii97-100 [19022824.001]
  • [Cites] Blood. 2008 Dec 15;112(13):4793-807 [19064739.001]
  • [Cites] Nat Rev Genet. 2009 Jan;10(1):32-42 [19065135.001]
  • [Cites] Methods Mol Biol. 2008;468:5-15 [19099242.001]
  • [Cites] Neuropharmacology. 2009 Feb;56(2):473-80 [19007798.001]
  • [Cites] Nat Genet. 2009 Feb;41(2):246-50 [19151716.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2009 Mar 1;73(3):904-12 [19215824.001]
  • [Cites] Cell Mol Life Sci. 2009 Feb;66(4):596-612 [18985277.001]
  • [Cites] Cell Cycle. 2009 Mar 15;8(6):809-17 [19229128.001]
  • [Cites] Stem Cells Dev. 2009 Jun;18(5):725-36 [18771397.001]
  • [Cites] Stem Cells. 2009 May;27(5):1142-51 [19418444.001]
  • [Cites] Cell. 2002 Feb 22;108(4):489-500 [11909520.001]
  • [Cites] Biochem Pharmacol. 2002 Mar 1;63(5):933-43 [11911845.001]
  • [Cites] Science. 2002 Jul 5;297(5578):102-4 [12098700.001]
  • [Cites] Genes Dev. 2002 Jul 15;16(14):1779-91 [12130538.001]
  • [Cites] EMBO J. 2002 Aug 1;21(15):4183-95 [12145218.001]
  • [Cites] Mol Cell Biol. 2002 Sep;22(17):6070-8 [12167701.001]
  • [Cites] Tsitologiia. 2002;44(7):649-55 [12455373.001]
  • [Cites] Mol Biol Cell. 2002 Dec;13(12):4279-95 [12475952.001]
  • [Cites] J Biol Chem. 2003 Feb 7;278(6):4035-40 [12427740.001]
  • [Cites] J Biol Chem. 2003 Feb 14;278(7):4806-12 [12473678.001]
  • [Cites] Zhonghua Xue Ye Xue Za Zhi. 2002 Dec;23(12):628-30 [12667344.001]
  • [Cites] Nucleic Acids Res. 2003 May 1;31(9):2305-12 [12711675.001]
  • [Cites] Trends Genet. 2003 Jun;19(6):321-9 [12801725.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Jul 4;306(3):650-9 [12810068.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3464-8 [12839926.001]
  • [Cites] J Nutr. 2003 Jul;133(7 Suppl):2485S-2493S [12840228.001]
  • [Cites] Mol Cell Biol. 2003 Aug;23(16):5594-605 [12897133.001]
  • [Cites] Best Pract Res Clin Haematol. 2003 Sep;16(3):453-61 [12935962.001]
  • [Cites] EMBO J. 2003 Oct 1;22(19):5154-62 [14517253.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(23):8795-808 [14612419.001]
  • [Cites] Cancer Sci. 2003 Dec;94(12):1059-65 [14662021.001]
  • [Cites] Mol Cell. 2003 Dec;12(6):1577-89 [14690609.001]
  • [Cites] EMBO J. 2004 Jan 14;23(1):138-49 [14685282.001]
  • [Cites] Mol Cell. 2005 Aug 5;19(3):381-91 [16061184.001]
  • [Cites] Expert Opin Ther Targets. 2005 Aug;9(4):809-24 [16083344.001]
  • [Cites] Endocrinology. 2005 Dec;146(12):5365-73 [16123169.001]
  • [Cites] Cell Mol Biol Lett. 2005;10(4):631-47 [16341272.001]
  • [Cites] Nat Rev Genet. 2006 Jan;7(1):21-33 [16369569.001]
  • [Cites] Nat Rev Cancer. 2006 Jan;6(1):38-51 [16397526.001]
  • [Cites] Dev Cell. 2006 Jan;10(1):105-16 [16399082.001]
  • [Cites] EMBO J. 2006 Jan 25;25(2):335-45 [16395332.001]
  • [Cites] Pediatr Res. 2006 Apr;59(4 Pt 2):21R-5R [16549544.001]
  • [Cites] Cell. 2006 Apr 21;125(2):315-26 [16630819.001]
  • [Cites] J Clin Invest. 2006 May;116(5):1202-9 [16670761.001]
  • [Cites] Nature. 2006 May 18;441(7091):349-53 [16625203.001]
  • [Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]
  • [Cites] Biochem Cell Biol. 2006 Aug;84(4):463-76 [16936820.001]
  • [Cites] Bone. 2006 Oct;39(4):678-83 [16765663.001]
  • [Cites] Mol Cancer Ther. 2006 Dec;5(12):3096-104 [17172412.001]
  • [Cites] Clin Orthop Relat Res. 2007 Jan;454:237-46 [17075380.001]
  • [Cites] Hum Cell. 2006 Aug;19(3):98-117 [17204093.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):232-6 [17200670.001]
  • [Cites] DNA Cell Biol. 2007 Jan;26(1):1-18 [17263592.001]
  • [Cites] Cell. 2007 Feb 23;128(4):735-45 [17320510.001]
  • [Cites] Cell. 2007 Feb 23;128(4):747-62 [17320511.001]
  • (PMID = 19807660.001).
  • [ISSN] 2212-3946
  • [Journal-full-title] Current stem cell research & therapy
  • [ISO-abbreviation] Curr Stem Cell Res Ther
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA132986; United States / NCI NIH HHS / CA / K08 CA132986-01A1; United States / NCI NIH HHS / CA / 1K08 CA132968-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 5688UTC01R / Tretinoin
  • [Number-of-references] 153
  • [Other-IDs] NLM/ NIHMS173280; NLM/ PMC2842459
  •  go-up   go-down


40. Yang C, Schwab JH, Schoenfeld AJ, Hornicek FJ, Wood KB, Nielsen GP, Choy E, Mankin H, Duan Z: A novel target for treatment of chordoma: signal transducers and activators of transcription 3. Mol Cancer Ther; 2009 Sep;8(9):2597-605
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] A novel target for treatment of chordoma: signal transducers and activators of transcription 3.
  • A major obstacle in the effective treatment of chordoma is that there are no identifiable biomarkers capable of predicting prognosis.
  • In this study, the expression of Stat3 was evaluated in chordoma tissue microarray that contains 70 chordoma samples.
  • Cells in the tissue microarray showed nuclear staining for phosphorylated Stat3 in all instances.
  • The expression of Stat3 signaling cascade was inhibited in all chordoma cell lines after treatment with SD-1029.
  • The cytotoxicity of the combination of SD-1029 and chemotherapeutic drugs is significantly better than either agent alone.
  • Blockade of the Stat3 pathway represents a potential strategy for future treatment.
  • [MeSH-major] Chordoma / drug therapy. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cisplatin / administration & dosage. Cisplatin / pharmacology. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Female. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Tissue Array Analysis. Tumor Cells, Cultured. Xanthenes / administration & dosage. Xanthenes / pharmacology


41. Susa M, Choy E, Liu X, Schwab J, Hornicek FJ, Mankin H, Duan Z: Cyclin G-associated kinase is necessary for osteosarcoma cell proliferation and receptor trafficking. Mol Cancer Ther; 2010 Dec;9(12):3342-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The advent of neoadjuvant chemotherapy significantly improved the prognosis of patients with osteosarcoma in the 1980s, but it has since plateaued in the past decades.
  • Recently, one of the most researched areas in sarcoma treatment is tyrosine kinases.
  • The level of GAK expression and its correlation to prognosis was analyzed in osteosarcoma tissue microarray.
  • We observed that GAK was overexpressed in both osteosarcoma cell lines and tissue samples when compared with human osteoblasts.
  • GAK knockdown by siRNA decreased cell proliferation in both drug-sensitive and multidrug-resistant osteosarcoma cell lines.
  • Immunohistochemistry of osteosarcoma tissue microarray revealed that overexpression of GAK was associated with poor prognosis.
  • These findings may lead to the development of new therapeutic options for osteosarcoma.

  • Genetic Alliance. consumer health - Osteosarcoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • 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] ©2010 AACR.
  • (PMID = 20881269.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA119617
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Cell Surface; EC 2.7.11.1 / GAK protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  •  go-up   go-down


42. Brassens S, Chevalier JM, Leblainvaux M: [A strange case of phlebitis]. Ann Cardiol Angeiol (Paris); 2003 Dec;52(6):375-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This sarcoma developed from the smooth muscle of a leg vessel, probably a vein.
  • Leiomyosarcoma is a malignant mesenchymal tumor of specialized connective tissue, with a strong potential for local proliferation and metastatic spread.
  • The diagnosis suggested by imaging techniques (in particular MRI) is first and foremost immunohistochemical.
  • The treatment is surgical when possible, associated with radiotherapy and chemotherapy as appropriate.
  • The prognosis is especially poor when the diagnosis is made at the metastatic stage.
  • [MeSH-major] Leiomyosarcoma / diagnosis. Popliteal Vein / pathology. Thrombophlebitis / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14752921.001).
  • [ISSN] 0003-3928
  • [Journal-full-title] Annales de cardiologie et d'angéiologie
  • [ISO-abbreviation] Ann Cardiol Angeiol (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


43. Guo Y, Nemeth J, O'Brien C, Susa M, Liu X, Zhang Z, Choy E, Mankin H, Hornicek F, Duan Z: Effects of siltuximab on the IL-6-induced signaling pathway in ovarian cancer. Clin Cancer Res; 2010 Dec 1;16(23):5759-69
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.
  • PURPOSE: To explore potential therapeutic strategies for interrupting the interleukin-6 (IL-6) signaling pathway, we measured IL-6 expression in ovarian cancer tissues, and evaluated the effects of a monoclonal anti-IL-6 antibody; siltuximab (CNTO 328), on levels of IL-6-induced Stat3 phosphorylation, Stat3 nuclear translocation, and Stat3 downstream antiapoptotic genes.
  • Effects of siltuximab on IL-6-induced activation of Stat3 in an ovarian cancer cell line were determined by Western blot and real-time analysis of Stat3 nucleocytoplasmic translocation.
  • RESULTS: Metastatic and drug-resistant recurrent tumors have significantly higher IL-6 expression when compared with the matched primary tumors.
  • Treatment with siltuximab significantly decreased the levels of Stat3 downstream proteins such as MCL-1, Bcl-X(L), and survivin.
  • Treatment with siltuximab reduced expression of multiple IL-6-induced genes in these cell lines.
  • Furthermore, siltuximab increased the cytotoxic effects of paclitaxel in a paclitaxel resistant ovarian cancer cell line in vitro, but combination therapy with siltuximab did not have a significant effect on paclitaxel resistant tumor growth in vivo.
  • Blockage of IL-6 signaling may provide benefits for the treatment of ovarian cancer.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Carcinoma / drug therapy. Carcinoma / pathology. Interleukin-6 / pharmacology. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / pathology
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mice, Nude. Paclitaxel / administration & dosage. STAT3 Transcription Factor / metabolism. STAT3 Transcription Factor / physiology. Signal Transduction / drug effects. Signal Transduction / genetics. Validation Studies as Topic. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Ovarian cancer.
  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAXOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • (PMID = 20699329.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Interleukin-6; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 0 / siltuximab; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


44. Duan Z, Choy E, Harmon D, Yang C, Ryu K, Schwab J, Mankin H, Hornicek FJ: ZNF93 increases resistance to ET-743 (Trabectedin; Yondelis) and PM00104 (Zalypsis) in human cancer cell lines. PLoS One; 2009 Sep 09;4(9):e6967
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • ET-743 and PM00104 exposure over sustained periods of treatment will result in the development of drug resistance, but the mechanisms which lead to resistance are not yet understood.
  • These genes have not been previously associated with drug resistance in tumor cells.
  • Differential expressions of ZNF93 and ZNF43 genes were confirmed in both CS-1/ER and CS-1/PR resistant cell lines by real-time RT-PCR.
  • ZNF93 was overexpressed in two ET-743 resistant Ewing sarcoma cell lines as well as in a cisplatin resistant ovarian cancer cell line, but was not overexpressed in paclitaxel resistant cell lines.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Med Chem Anticancer Agents. 2005 Jan;5(1):15-27 [15720258.001]
  • [Cites] Rapid Commun Mass Spectrom. 2005;19(5):689-95 [15702485.001]
  • [Cites] Mol Cancer Ther. 2006 May;5(5):1239-47 [16731756.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):8155-62 [16912194.001]
  • [Cites] Prog Mol Subcell Biol. 2006;43:363-79 [17153351.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13062-7 [17656556.001]
  • [Cites] Oncogene. 2007 Aug 9;26(36):5194-203 [17297437.001]
  • [Cites] Mol Biotechnol. 2008 Feb;38(2):137-44 [18219593.001]
  • [Cites] Nat Prod Rep. 2009 Mar;26(3):322-37 [19240944.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 May;63(6):1121-9 [18828019.001]
  • [Cites] Anticancer Res. 2009 Jun;29(6):1879-88 [19528443.001]
  • [Cites] Curr Treat Options Oncol. 2009 Apr;10(1-2):94-106 [19238552.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3445-53 [10589757.001]
  • [Cites] Med Res Rev. 2000 Jan;20(1):1-27 [10608919.001]
  • [Cites] Br J Cancer. 2000 May;82(10):1732-9 [10817511.001]
  • [Cites] Int J Cancer. 2001 May 15;92(4):583-8 [11304695.001]
  • [Cites] Mol Cancer Ther. 2002 Dec;1(14):1327-34 [12516966.001]
  • [Cites] Clin Cancer Res. 2003 Mar;9(3):1211-7 [12631627.001]
  • [Cites] Ann Oncol. 2003 Nov;14(11):1607-15 [14581267.001]
  • [Cites] Biochem Pharmacol. 2003 Dec 15;66(12):2381-95 [14637196.001]
  • [Cites] Int J Cancer. 2004 Oct 10;111(6):900-9 [15300802.001]
  • [Cites] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100.001]
  • [Cites] Clin Cancer Res. 1998 Aug;4(8):1977-83 [9717828.001]
  • [Cites] Gene. 1999 Mar 18;229(1-2):75-81 [10095106.001]
  • [Cites] Cancer Chemother Pharmacol. 2005 Mar;55(3):277-85 [15565326.001]
  • [Cites] Eur J Cancer. 2005 Jan;41(2):323-33 [15661559.001]
  • [Cites] Int J Oncol. 2005 Dec;27(6):1605-16 [16273217.001]
  • (PMID = 19742314.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA119617; United States / NCI NIH HHS / CA / R01-CA119617
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Dioxoles; 0 / PM 00104; 0 / Tetrahydroisoquinolines; 114899-77-3 / trabectedin
  • [Other-IDs] NLM/ PMC2734182
  •  go-up   go-down






Advertisement