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1. Thompson JF, Siebert GA, Anissimov YG, Smithers BM, Doubrovsky A, Anderson CD, Roberts MS: Microdialysis and response during regional chemotherapy by isolated limb infusion of melphalan for limb malignancies. Br J Cancer; 2001 Jul 20;85(2):157-65
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  • [Title] Microdialysis and response during regional chemotherapy by isolated limb infusion of melphalan for limb malignancies.
  • This study sought to use a microdialysis technique to relate clinical and biochemical responses to the time course of melphalan concentrations in the subcutaneous interstitial space and in tumour tissue (melanoma, malignant fibrous histiocytoma, Merkel cell tumour and osteosarcoma) in patients undergoing regional chemotherapy by Isolated Limb Infusion (ILI).
  • 19 patients undergoing ILI for treatment of various limb malignancies were monitored for intra-operative melphalan concentrations in plasma and, using microdialysis, in subcutaneous and tumour tissues.
  • Peak and mean concentrations of melphalan were significantly higher in plasma than in subcutaneous or tumour microdialysate.
  • There was no significant difference between drug peak and mean concentrations in interstitial and tumour tissue, indicating that there was no preferential uptake of melphalan into the tumours.
  • The time course of melphalan in the microdialysate could be described by a pharmacokinetic model which assumed melphalan distributed from the plasma into the interstitial space.
  • Tumour response in the whole group to treatment was partial response: 53.8% (n = 7); complete response: 33.3% (n = 5); no response: 6.7% (n = 1).
  • There was a significant association between tumour response and melphalan concentrations measured over time in subcutaneous microdialysate (P< 0.01).
  • No significant relationship existed between the severity of toxic reactions in the limb or peak plasma creatine phosphokinase levels and peak melphalan microdialysate or plasma concentrations.
  • It is concluded that microdialysis is a technique well suited for measuring concentrations of cytotoxic drug during ILI.
  • The possibility of predicting actual concentrations of cytotoxic drug in the limb during ILI using our model opens an opportunity for improved drug dose calculation.
  • The combination of predicting tissue concentrations and monitoring in microdialysate of subcutaneous tissue could help optimise ILI with regard to post-operative limb morbidity and tumour response.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Chemotherapy, Cancer, Regional Perfusion. Extremities / pathology. Melphalan / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Carcinoma, Merkel Cell / drug therapy. Histiocytoma, Benign Fibrous / drug therapy. Humans. Melanoma / drug therapy. Microdialysis. Middle Aged. Osteosarcoma / drug therapy. Treatment Outcome

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  • (PMID = 11461070.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ PMC2364039
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2. de Gorter DJ, Reijmers RM, Beuling EA, Naber HP, Kuil A, Kersten MJ, Pals ST, Spaargaren M: The small GTPase Ral mediates SDF-1-induced migration of B cells and multiple myeloma cells. Blood; 2008 Apr 1;111(7):3364-72
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  • Chemokine-controlled migration plays a critical role in B-cell development, differentiation, and function, as well as in the pathogenesis of B-cell malignancies, including the plasma cell neoplasm multiple myeloma (MM).
  • Here, we demonstrate that stimulation of B cells and MM cells with the chemokine stromal cell-derived factor-1 (SDF-1) induces strong migration and activation of the Ras-like GTPase Ral.
  • We have recently shown that Btk, PLCgamma2, and Lyn/Syk mediate SDF-1-controlled B-cell migration; however, SDF-1-induced Ral activation is not affected in B cells deficient in these proteins.
  • In addition, treatment with pharmacological inhibitors against PI3K and PLC or expression of dominant-negative Ras did not impair SDF-1-induced Ral activation.
  • Taken together, these results reveal a novel function for Ral, that is, regulation of SDF-1-induced migration of B cells and MM cells, thereby providing new insights into the control of B-cell homeostasis, trafficking, and function, as well as into the pathogenesis of MM.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Movement. Chemokine CXCL12 / metabolism. Leukemia, Plasma Cell / metabolism. ral GTP-Binding Proteins / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Chickens. Enzyme Activation / drug effects. Enzyme Activation / genetics. Genes, Dominant / genetics. Homeostasis / drug effects. Homeostasis / genetics. Humans. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Mutation. Oncogene Protein p21(ras) / genetics. Oncogene Protein p21(ras) / metabolism. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. Phospholipase C gamma / genetics. Phospholipase C gamma / metabolism. Protein Isoforms / genetics. Protein Isoforms / metabolism. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. src-Family Kinases / genetics. src-Family Kinases / metabolism

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  • (PMID = 18227351.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Intracellular Signaling Peptides and Proteins; 0 / Protein Isoforms; 0 / Ralb protein, human; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Agammaglobulinaemia tyrosine kinase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; EC 2.7.10.2 / lyn protein-tyrosine kinase; EC 2.7.10.2 / src-Family Kinases; EC 3.1.4.3 / Phospholipase C gamma; EC 3.6.1.- / RALA protein, human; EC 3.6.5.2 / Oncogene Protein p21(ras); EC 3.6.5.2 / ral GTP-Binding Proteins
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3. Knobel D, Zouhair A, Tsang RW, Poortmans P, Belkacémi Y, Bolla M, Oner FD, Landmann C, Castelain B, Ozsahin M, Rare Cancer Network: Prognostic factors in solitary plasmacytoma of the bone: a multicenter Rare Cancer Network study. BMC Cancer; 2006;6:118
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  • BACKGROUND: Solitary plasmacytoma (SP) of the bone is a rare plasma-cell neoplasm.
  • There are no conclusive data in the literature on the optimal radiation therapy (RT) dose in SP.
  • Histopathological diagnosis was obtained for all patients.
  • The majority (n = 169) of the patients received RT alone; 32 chemotherapy and RT, and 5 surgery.
  • Median time to MM development was 21 months (2-135) with a 5-year probability of 51%.
  • In multivariate analyses, favorable factors were younger age and tumor size < 5 cm for survival; younger age for DFS; anatomic localization (vertebra vs. other) for local control.
  • There was no dose-response relationship for doses 30 Gy or higher, even for larger tumors.
  • Further investigation should focus on adjuvant chemotherapy and/or novel therapeutic agents.
  • [MeSH-minor] Actuarial Analysis. Adult. Age Factors. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Cohort Studies. Combined Modality Therapy. Dexamethasone / administration & dosage. Disease Progression. Disease-Free Survival. Dose-Response Relationship, Radiation. Doxorubicin / administration & dosage. Europe / epidemiology. Female. Follow-Up Studies. Humans. Male. Melphalan / administration & dosage. Middle Aged. Multiple Myeloma / epidemiology. North America / epidemiology. Prednisone / administration & dosage. Prognosis. Proportional Hazards Models. Radiotherapy Dosage. Retrospective Studies. Spinal Neoplasms / drug therapy. Spinal Neoplasms / mortality. Spinal Neoplasms / pathology. Spinal Neoplasms / radiotherapy. Spinal Neoplasms / surgery. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 16677383.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; Q41OR9510P / Melphalan; VB0R961HZT / Prednisone; VAD I protocol
  • [Other-IDs] NLM/ PMC1479355
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4. Megat Shiraz MA, Jong YH, Primuharsa Putra SH: Extramedullary plasmacytoma in the maxillary sinus. Singapore Med J; 2008 Nov;49(11):e310-1
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  • Extramedullary plasmacytoma is a rare malignant plasma cell tumour.
  • Magnetic resonance imaging revealed a right maxillary tumour with extension to the ipsilateral nasal cavity, nasopharynx, right sphenoid and ethmoidal sinuses.
  • Histopathology examination of the maxillary mass revealed abundant plasma cells with kappa-chain restriction.
  • He was planned for four cycles of chemotherapy.
  • Unfortunately, in view of the advanced stage of disease, he succumbed to his disease during the first cycle of chemotherapy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Brain Neoplasms / pathology. Maxillary Sinus Neoplasms / diagnosis. Maxillary Sinus Neoplasms / radiography
  • [MeSH-minor] Anemia / complications. Antineoplastic Agents / therapeutic use. Fatal Outcome. Humans. Magnetic Resonance Imaging / methods. Male. Maxillary Sinus / pathology. Maxillary Sinus / radiography. Middle Aged. Nasopharynx / pathology. Neoplasm Metastasis. Plasmacytoma / diagnosis. Plasmacytoma / pathology. Plasmacytoma / radiography

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  • (PMID = 19037537.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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5. Danker K, Reutter W, Semini G: Glycosidated phospholipids: uncoupling of signalling pathways at the plasma membrane. Br J Pharmacol; 2010 May;160(1):36-47
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  • [Title] Glycosidated phospholipids: uncoupling of signalling pathways at the plasma membrane.
  • Cell expansion and metastasis are considered hallmarks of tumour progression.
  • Therefore, efforts have been made to develop novel anti-cancer drugs that inhibit both the proliferation and the motility of tumour cells.
  • Synthetic alkylphospholipids, compounds with aliphatic side chains that are ether linked to a glycerol backbone, are structurally derived from platelet-activating factor and represent a new class of drugs with anti-proliferative properties in tumour cells.
  • These compounds do not interfere with the DNA or mitotic spindle apparatus of the cell.
  • Instead, they are incorporated into cell membranes, where they accumulate and interfere with lipid metabolism and lipid-dependent signalling pathways.
  • Recently, it has been shown that the most commonly studied alkylphospholipids inhibit proliferation by inducing apoptosis in malignant cells while leaving normal cells unaffected.
  • Members of this subfamily also exhibit anti-proliferative capacity and modulate the cell adhesion, differentiation, and migration of tumour cells.
  • Apart from its anti-proliferative effect, Ino-C2-PAF strongly reduces cell motility via its inhibitory effect on the phosphorylation of the cytosolic tyrosine kinases FAK and Src.
  • Signalling pathways under the control of the FAK/Src complex are normally required for both migration and proliferation and play a prominent role in tumour progression.
  • We intend to highlight the potential of glycosidated phospholipids, especially Ino-C2-PAF, as a promising new group of drugs for the treatment of hyperproliferative and migration-based skin diseases.
  • [MeSH-minor] Animals. Cell Membrane / metabolism. Cell Movement / drug effects. Cell Proliferation / drug effects. Humans. Inositol / adverse effects. Inositol / analogs & derivatives. Inositol / pharmacology. Molecular Structure. Neoplasm Metastasis. Neoplasms / drug therapy. Neoplasms / pathology. Platelet Activating Factor / adverse effects. Platelet Activating Factor / analogs & derivatives. Platelet Activating Factor / pharmacology. Signal Transduction

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  • (PMID = 20331609.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glycosides; 0 / Phospholipids; 0 / Platelet Activating Factor; 4L6452S749 / Inositol
  • [Number-of-references] 116
  • [Other-IDs] NLM/ PMC2860204
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6. Health Quality Ontario: Extracorporeal photophoresis: an evidence-based analysis. Ont Health Technol Assess Ser; 2006;6(6):1-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To assess the effectiveness, safety and cost-effectiveness of extracorporeal photophoresis (ECP) for the treatment of refractory erythrodermic cutaneous T cell lymphoma (CTCL) and refractory chronic graft versus host disease (cGvHD).
  • BACKGROUND: CUTANEOUS T CELL LYMPHOMA: Cutaneous T cell lymphoma (CTCL) is a general name for a group of skin affecting disorders caused by malignant white blood cells (T lymphocytes).
  • Cutaneous T cell lymphoma is relatively uncommon and represents slightly more than 2% of all lymphomas in the United States.
  • The relative frequency and disease-specific 5-year survival of 1,905 primary cutaneous lymphomas classified according to the World Health Organization-European Organization for Research and Treatment of Cancer (WHO-EORTC) classification (Appendix 1).
  • Cutaneous T cell lymphoma has an annual incidence of approximately 0.4 per 100,000 and it mainly occurs in the 5(th) to 6(th) decade of life, with a male/female ratio of 2:1.
  • Mycosis fungoides is an indolent lymphoma with patients often having several years of eczematous or dermatitic skin lesions before the diagnosis is finally established.
  • Early in the disease biopsies are often difficult to interpret and the diagnosis may only become apparent by observing the patient over time.
  • A particular syndrome in these patients involves erythroderma (intense and usually widespread reddening of the skin from dilation of blood vessels, often preceding or associated with exfoliation), and circulating tumour cells.
  • CHRONIC GRAFT VERSUS HOST DISEASE: Allogeneic hematopoietic cell transplantation (HCT) is a treatment used for a variety of malignant and nonmalignant disease of the bone marrow and immune system.
  • The procedure is often associated with serious immunological complications, particularly graft versus host disease (GvHD).
  • Of the patients with extensive disease, approximately 60% will respond to treatment and eventually be able to discontinue immunosuppressive therapy.
  • The remaining patients will develop opportunistic infection, or require prolonged treatment with immunosuppressive agents.
  • The most commonly involved tissues are the skin, liver, mouth, and eyes.
  • TREATMENT:   CUTANEOUS T CELL LYMPHOMA: The optimal management of MF is undetermined because of its low prevalence, and its highly variable natural history, with frequent spontaneous remissions and exacerbations and often prolonged survival.
  • Nonaggressive approaches to therapy are usually warranted with treatment aimed at improving symptoms and physical appearance while limiting toxicity.
  • Given that multiple skin sites are usually involved, the initial treatment choices are usually topical or intralesional corticosteroids or phototherapy using psoralen (a compound found in plants which make the skin temporarily sensitive to ultraviolet A) (PUVA).
  • "Second line" therapy for early stage disease is often topical chemotherapy, radiotherapy or total skin electron beam radiation (TSEB).
  • Treatment of advanced stage (IIB-IV) MF usually consists of topical or systemic therapy in refractory or rapidly progressive SS.
  • Bone marrow transplantation and peripheral blood stem cell transplantation have been used to treat many malignant hematologic disorders (e.g., leukemias) that are refractory to conventional treatment.
  • Reports on the use of these procedures for the treatment of CTCL are limited and mostly consist of case reports or small case series.
  • CHRONIC GRAFT VERSUS HOST DISEASE: Patients who develop cGvHD require reinstitution of immunosuppressive medication (if already discontinued) or an increase in dosage and possibly addition of other agents.
  • The current literature regarding cGvHD therapy is less than optimal and many recommendations about therapy are based on common practices that await definitive testing.
  • Numerous salvage therapies have been considered in patients with refractory cGvHD, including ECP.
  • Due to uncertainty around salvage therapies, Bhushan and Collins suggested that ideally, patients with refractory cGvHD should be entered into clinical trials.
  • Two Ontario expert consultants jointly estimated that there may be approximately 30 new erythrodermic treatment resistant CTCL patients and 30 new treatment resistant cGvHD patients per year who are unresponsive to other forms of therapy and may be candidates for ECP.
  • Extracorporeal photopheresis is a procedure that was initially developed as a treatment for CTCL, particularly SS.
  • The lymphocyte layer is treated with methoxsalen (a drug that sensitizes the lymphocytes to light) and exposed to UVA, following which the lymphocytes are returned to the patient.
  • Red blood cells and plasma are returned to the patient between each cycle.
  • Photosensitization is achieved by administering methoxsalen to the patient orally 2 hours before the procedure, or by injecting methoxsalen directly ino the leucocyte rich fraction.
  • The latter approach avoids potential side effects such as nausea, and provides a more consistent drug level within the machine.
  • In general, from the time the intravenous line is inserted until the white blood cells are returned to the patient takes approximately 2.5-3.5 hours.
  • For CTCL, the treatment schedule is generally 2 consecutive days every 4 weeks for a median of 6 months.
  • For cGvHD, an expert in the field estimated that the treatment schedule would be 3 times a week for the 1(st) month, then 2 consecutive days every 2 weeks after that (i.e., 4 treatments a month) for a median of 6 to 9 months.
  • REGULATORY STATUS: The UVAR XTS Photopheresis System is licensed by Health Canada as a Class 3 medical device (license # 7703) for the "palliative treatment of skin manifestations of CTCL."
  • It is not licensed for the treatment of cGvHD.

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  • (PMID = 23074497.001).
  • [Journal-full-title] Ontario health technology assessment series
  • [ISO-abbreviation] Ont Health Technol Assess Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3379535
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7. Biecker E, Fischer HP, Strunk H, Sauerbruch T: Benign hepatic tumours. Z Gastroenterol; 2003 Feb;41(2):191-200
MedlinePlus Health Information. consumer health - Liver Diseases.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Due to advances in imaging procedures like MRI, Cf-scan and ultrasound as well as progress in immunohistochemistry, the appropriate diagnosis is made ina high percentage of patients without laparotomy and resection.
  • Most important in clinical practice is the differential diagnosis of focal nodular hyperplasia and hepatocellular adenoma because of the risk of rupture and bleeding in the latter.
  • Cavernous haemangioma, the most common benign hepatic tumour, rarely needs treatment.
  • The diagnosis of nodular regenerative hyperplasia is often missed and patients present with secondary complications and signs of portal hypertension that necessitate treatment.
  • The main problem in angiomyolipoma is to distinguish it from malignant processes which do require treatment.
  • Because of its clinical presentation, inflammatory pseudotumour is also sometimes confused with a malignant tumour.
  • Therapeutic options are drug therapy or surgical resection.
  • [MeSH-major] Liver Diseases / diagnosis. Liver Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Liver Cell / diagnosis. Adenoma, Liver Cell / pathology. Adult. Aged. Diagnostic Imaging. Focal Nodular Hyperplasia / diagnosis. Focal Nodular Hyperplasia / pathology. Granuloma, Plasma Cell / diagnosis. Granuloma, Plasma Cell / pathology. Hemangioendothelioma / diagnosis. Hemangioendothelioma / pathology. Hemangioma, Cavernous / diagnosis. Hemangioma, Cavernous / pathology. Humans. Infant. Liver / pathology. Liver Regeneration / physiology. Middle Aged

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  • (PMID = 12650132.001).
  • [ISSN] 0044-2771
  • [Journal-full-title] Zeitschrift für Gastroenterologie
  • [ISO-abbreviation] Z Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 138
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8. Engineer L, Dow EC, Braverman IM, Ahmed AR: Epidermolysis bullosa acquisita and multiple myeloma. J Am Acad Dermatol; 2002 Dec;47(6):943-6
Hazardous Substances Data Bank. DEXAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The coexistence in the same patient of epidermolysis bullosa acquisita (a rare, autoimmune, acquired mucocutaneous blistering disorder) and multiple myeloma (a plasma cell neoplasm) is extremely uncommon.
  • [MeSH-minor] Biopsy, Needle. Dexamethasone / administration & dosage. Drug Therapy, Combination. Follow-Up Studies. Humans. Immunoglobulins, Intravenous / administration & dosage. Immunohistochemistry. Male. Middle Aged. Risk Assessment


9. Tageja N, Nagi J, Valent J, Zonder J: Plasma cell leukemia presenting as organizing pneumonia refractory to high-dose steroid therapy. South Med J; 2010 Jul;103(7):706-10
Genetic Alliance. consumer health - Plasma cell leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plasma cell leukemia presenting as organizing pneumonia refractory to high-dose steroid therapy.
  • A case of steroid-refractory organizing pneumonia (OP) as the initial presentation of plasma cell leukemia (PCL) in a patient who had no prior exposure to chemotherapy or radiation is described.
  • Since OP is traditionally a steroid-responsive disease, this case raises the possibility of a previously unknown patient subgroup with variable disease pattern and/or behavior in patients with plasma cell neoplasm.
  • [MeSH-major] Cryptogenic Organizing Pneumonia / diagnosis. Leukemia, Plasma Cell / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Female. Glucocorticoids / therapeutic use. Humans. Lung / pathology. Middle Aged. Multiple Myeloma / diagnosis

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  • (PMID = 20531051.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids
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10. Wiesenthal AA, Nguyen BD: F-18 FDG PET/CT staging of multiple myeloma with diffuse osseous and extramedullary lesions. Clin Nucl Med; 2007 Oct;32(10):797-801
MedlinePlus Health Information. consumer health - Multiple Myeloma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Multiple myeloma is the most common plasma cell neoplasm, with abnormal clonal proliferation of B cells in bone marrow.
  • Its staging is important for therapeutic management and prognosis.
  • Through imaging integration, PET provides functional detection of high metabolic lesions whereas CT provides correlated anatomic localization.
  • The authors present a case of multiple myeloma status post chemotherapy and stem cell transplant with diffuse osseous and extramedullary lesions evaluated by PET/CT.
  • [MeSH-major] Bone Neoplasms / diagnosis. Fluorodeoxyglucose F18. Multiple Myeloma / diagnosis. Positron-Emission Tomography / methods. Soft Tissue Neoplasms / diagnosis. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Humans. Male. Middle Aged. Neoplasm Staging. Radiopharmaceuticals. Subtraction Technique

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  • (PMID = 17885362.001).
  • [ISSN] 0363-9762
  • [Journal-full-title] Clinical nuclear medicine
  • [ISO-abbreviation] Clin Nucl Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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11. Turk HM, Komurcu S, Ozet A, Kuzhan O, Günhan O: An unusual presentation of extramedullary plasmacytoma in testis and review of the literature. Med Oncol; 2010 Dec;27(4):1378-80
MedlinePlus Health Information. consumer health - Testicular Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Extramedullary plasmacytoma is a rare plasma cell neoplasm, and it is extremely uncommon in the testicles.
  • Multiple lytic bone lesions were seen in bone survey scans, serum immunoelectrophoresis and bone marrow aspiration aided to the diagnosis of multiple myeloma.
  • He received chemotherapy, melphalan and prednisolone, and palliative radiotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multiple Myeloma / diagnosis. Orchiectomy. Plasmacytoma / diagnosis. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Humans. Male. Prognosis. Radiotherapy Dosage

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  • (PMID = 20035386.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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12. Pratibha CB, Sreenivas V, Babu MK, Rout P, Nayar RC: Plasmacytoma of larynx--a case report. J Voice; 2009 Nov;23(6):735-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Plasma cell myeloma, the most common plasma cell neoplasm, is characterized by the presence of multiple lesions in the bone marrow.
  • A single isolated lesion may occur either in bone (solitary plasmacytoma of bone) or in soft tissue (extramedullary plasmacytoma).
  • The diagnosis is established by histopathology and immunohistochemistry.
  • A detailed evaluation for lesions at other sites is recommended as extramedullary plasmacytoma treated by radiation therapy has better survival rates than plasma cell myeloma, which is treated by chemotherapy.
  • A case of plasmacytoma of the larynx is presented highlighting clinical and histological features with a review of literature.
  • [MeSH-minor] Diagnosis, Differential. Follow-Up Studies. Humans. Immunohistochemistry. Laryngoscopy. Larynx / pathology. Male. Middle Aged. Treatment Outcome. Vocal Cords / pathology

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  • (PMID = 18619786.001).
  • [ISSN] 1873-4588
  • [Journal-full-title] Journal of voice : official journal of the Voice Foundation
  • [ISO-abbreviation] J Voice
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 19
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13. Karunakaran S, Umapathy NS, Thangaraju M, Hatanaka T, Itagaki S, Munn DH, Prasad PD, Ganapathy V: Interaction of tryptophan derivatives with SLC6A14 (ATB0,+) reveals the potential of the transporter as a drug target for cancer chemotherapy. Biochem J; 2008 Sep 15;414(3):343-55
Xenbase. Xenbase .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interaction of tryptophan derivatives with SLC6A14 (ATB0,+) reveals the potential of the transporter as a drug target for cancer chemotherapy.
  • 1-Methyltryptophan is an inducer of immune surveillance against tumour cells through its ability to inhibit indoleamine dioxygenase.
  • In the present study, we investigated the role of ATB(0,+) in the uptake of 1-methyltryptophan as a potential mechanism for entry of this putative anticancer drug into tumour cells.
  • ATB(0,+) can transport 18 of the 20 proteinogenic amino acids. alpha-Methyltryptophan blocks the transport function of ATB(0,+) with an IC(50) value of approximately 250 muM under conditions simulating normal plasma concentrations of all these 18 amino acids.
  • Screening of several mammary epithelial cell lines shows that ATB(0,+) is expressed robustly in some cancer cell lines, but not in all; in contrast, non-malignant cell lines do not express the transporter.
  • Treatment of ATB(0,+)-positive tumour cells with alpha-methyltryptophan leads to suppression of their colony-forming ability, whereas ATB(0,+)-negative cell lines are not affected.
  • The blockade of ATB(0,+) in these cells with alpha-methyltryptophan is associated with cell cycle arrest.
  • These studies reveal the potential of ATB(0,+) as a drug target for cancer chemotherapy.
  • [MeSH-minor] Amino Acid Transport Systems / metabolism. Animals. Biological Transport, Active / drug effects. Cell Line. Cell Line, Tumor. Humans. Large Neutral Amino Acid-Transporter 1 / genetics. Large Neutral Amino Acid-Transporter 1 / metabolism. Mice. Oocytes / metabolism. Plasma Membrane Neurotransmitter Transport Proteins / metabolism. Xenopus laevis

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  • (PMID = 18522536.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1-methyltryptophan; 0 / Amino Acid Transport Systems; 0 / Amino Acid Transport Systems, Neutral; 0 / Antineoplastic Agents; 0 / Large Neutral Amino Acid-Transporter 1; 0 / Plasma Membrane Neurotransmitter Transport Proteins; 0 / SLC6A14 protein, human; 0 / Slc6A14 protein, mouse; 13510-08-2 / alpha-methyltryptophan; 8DUH1N11BX / Tryptophan
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14. Jimenez-Zepeda VH, Domínguez-Martínez VJ: Vincristine, doxorubicin, and dexamethasone or thalidomide plus dexamethasone for newly diagnosed patients with multiple myeloma? Eur J Haematol; 2006 Sep;77(3):239-44
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  • Multiple myeloma (MM) is a malignant plasma cell tumor that is distributed at multiple sites within the bone marrow compartments.
  • High-dose dexamethasone regimens [including vincristine, doxorubicin, and dexamethasone (VAD) chemotherapy] induce rapid responses, and have resulted in improved survival for many patients when followed by intensive therapy with autologous stem cell support early in the disease course.
  • P = 0.0005. In summary, we conclude Thal/dex is an effective therapy in newly diagnosed MM inducing objective responses in over 84.3%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Multiple Myeloma / drug therapy

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  • (PMID = 16856924.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 4Z8R6ORS6L / Thalidomide; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; VAD I protocol
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15. Bruno B, Giaccone L, Rotta M, Anderson K, Boccadoro M: Novel targeted drugs for the treatment of multiple myeloma: from bench to bedside. Leukemia; 2005 Oct;19(10):1729-38
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel targeted drugs for the treatment of multiple myeloma: from bench to bedside.
  • Multiple myeloma remains an incurable plasma cell neoplasm.
  • New insights into its pathogenesis have identified signaling pathways that have become potential therapeutic targets.
  • It has clearly been established that intracellular regulatory proteins and interactions between malignant plasma cells and the bone marrow microenvironment play an important role in their survival and drug resistance.
  • Several new agents associated with molecular targets are currently being investigated to design new treatment strategies aimed at prolonging survival and improving quality of life.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Multiple Myeloma / drug therapy

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  • (PMID = 16094421.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 58
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16. Sze DM, Brown R, Yang S, Ho PJ, Gibson J, Joshua D: The use of thalidomide in myeloma therapy as an effective anticancer drug. Curr Cancer Drug Targets; 2006 Jun;6(4):325-31
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  • [Title] The use of thalidomide in myeloma therapy as an effective anticancer drug.
  • Thalidomide and its immunomodulatory derivatives have provided the most significant advance in the therapy of myeloma since the introduction of high dose chemotherapy followed by stem cell transplantation nearly 20 years ago.
  • The mechanism of action of thalidomide is complex and involves many aspects of malignant plasma cell growth and bone marrow stromal cell microenvironment interaction.
  • Thalidomide was first used because of its anti-angiogenic properties, however it is the immunomodulatory actions that involve increasing host tumour-specific immunosurveillance by both T cell and natural killer cells which may be the most important mode of action.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Multiple Myeloma / drug therapy. Thalidomide / therapeutic use
  • [MeSH-minor] Animals. Bone Remodeling. Bone and Bones / drug effects. Bone and Bones / metabolism. Bone and Bones / pathology. Cell Proliferation / drug effects. Humans. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Neovascularization, Pathologic / prevention & control. T-Lymphocytes / drug effects. T-Lymphocytes / immunology

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  • (PMID = 16848723.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 84
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17. Yakushijin Y, Sakai I, Takada K, Yasukawa M, Fujita S: [Double B-cell malignancies with simultaneous onset]. Rinsho Ketsueki; 2004 Mar;45(3):218-22
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  • [Title] [Double B-cell malignancies with simultaneous onset].
  • We encountered a case of a 59-year-old female who simultaneously contracted a non-Hodgkin lymphoma (NHL) and a plasma cell neoplasm.
  • The patient consulted her physician about her abdominal tumor and anemia in March 1999.
  • She was diagnosed as having NHL (follicular center lymphoma, grade I, stage IIA) after an open tumor biopsy, and treated by cycles of CHOP chemotherapy which resulted in complete remission.
  • However, the patient's abdominal tumor appeared again in March 2000 and she was hospitalized at the Ehime University Hospital.
  • A tumor biopsy was performed laparoscopically at that time.
  • This diagnosis was made after the presence of IgG-lambda M protein when the marrow showed an increase in the number of plasma cells.
  • In a Southern blot analysis which studied the abdominal tumor and the bone marrow cells, each B-cell tumor had a different IgH gene rearrangement pattern.
  • Therefore, this case was diagnosed as an example of the simultaneous existence of two different B-cell tumors.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. B-Lymphocytes / pathology. Fatal Outcome. Female. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Humans. Middle Aged. Neoplasm Recurrence, Local

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  • (PMID = 15103935.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 17
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18. Pratt G, Goodyear O, Moss P: Immunodeficiency and immunotherapy in multiple myeloma. Br J Haematol; 2007 Sep;138(5):563-79
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  • Multiple myeloma is a malignant tumour of plasma cells that remains incurable for the vast majority of patients, with a median survival of 2-3 years.
  • It is characterized by the patchy accumulation of tumour cells within bone marrow leading to variable anaemia, bone destruction, hypercalcaemia, renal failure and infections.
  • Immune dysfunction is an important feature of the disease and leads to infections that are both a major cause of morbidity and mortality and may promote tumour growth and resistance to chemotherapy.
  • Although T cells and humoral responses directed against myeloma-associated antigens have been described, it is uncertain if the immune system plays a role in preventing or controlling myeloma cell growth.

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  • (PMID = 17686051.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 175
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19. Matsui W, Huff CA, Vala M, Barber J, Smith BD, Jones RJ: Anti-tumour activity of interferon-alpha in multiple myeloma: role of interleukin 6 and tumor cell differentiation. Br J Haematol; 2003 Apr;121(2):251-8
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  • [Title] Anti-tumour activity of interferon-alpha in multiple myeloma: role of interleukin 6 and tumor cell differentiation.
  • In vitro, IFN-alpha has diverse effects on both normal and malignant cells, however, the exact mechanisms responsible for its clinical anti-tumour activity remain unclear.
  • We found that IFN-alpha inhibited MM cell proliferation in association with cell cycle arrest at G1 and limited the clonogenic growth of both MM cell lines and primary patient specimens.
  • At the doses tested, IFN-alpha was not cytotoxic, but induced terminal plasma cell differentiation resulting in the loss of clonogenicity.
  • IL-6 also induced MM cell terminal differentiation when combined with a second, unrelated, antiproliferative agent bryostatin-1, suggesting that its differentiating activities are preferentially enhanced in the presence of agents that inhibit cell cycling.
  • These results suggest that the differentiating activities of IFN-alpha may play a role in its clinical antimyeloma activity and provide the rationale for clinical differentiation therapy in MM.
  • [MeSH-major] Interferon-alpha / therapeutic use. Interleukin-6 / therapeutic use. Multiple Myeloma / therapy
  • [MeSH-minor] Analysis of Variance. Apoptosis / drug effects. Bryostatins. Cell Differentiation / drug effects. Cell Division / drug effects. Clone Cells. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Humans. Immune Sera / pharmacology. Lactones / pharmacology. Macrolides. Mitogens / pharmacology. Tumor Cells, Cultured

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  • (PMID = 12694246.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA153962
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bryostatins; 0 / Immune Sera; 0 / Interferon-alpha; 0 / Interleukin-6; 0 / Lactones; 0 / Macrolides; 0 / Mitogens; 37O2X55Y9E / bryostatin 1
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20. Paterson JL, Li Z, Wen XY, Masih-Khan E, Chang H, Pollett JB, Trudel S, Stewart AK: Preclinical studies of fibroblast growth factor receptor 3 as a therapeutic target in multiple myeloma. Br J Haematol; 2004 Mar;124(5):595-603
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  • [Title] Preclinical studies of fibroblast growth factor receptor 3 as a therapeutic target in multiple myeloma.
  • Dysregulation of fibroblast growth factor receptor 3 (FGFR3) by the translocation t(4;14)(p16;q32) occurs in 15% of multiple myeloma (MM) patients and confers a growth and survival advantage to malignant plasma cells.
  • As FGFR3 is a molecular target, we assessed the therapeutic potential of the FGFR-specific tyrosine kinase inhibitors SU5402 and SU10991 in MM.
  • SU5402 inhibited FGFR3 phosphorylation in vitro and in murine MM tumour models.
  • A panel of 11 human myeloma cell lines was studied, five bearing the t(4;14) translocation.
  • The KMS11 human myeloma cell line, which expresses constitutively active mutant FGFR3, displayed an 85% decrease in S-phase cells, a 95% increase in G0/G1 cells, and 4.5-fold increase in apoptotic cells after 72 h treatment with 10 micromol/l SU5402.
  • Activated extracellular signal-regulated kinases 1 and 2 and signal transducer and activator of transcription 3 were rapidly down-regulated after SU5402 treatment.
  • In human myeloma cell lines expressing wild-type FGFR3 the stimulating effect of aFGF ligand was abrogated by SU5402 treatment.
  • Myeloma cells lacking the t(4;14) or with the t(4;14) and a secondary RAS mutation did not respond to therapy.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins. Multiple Myeloma / drug therapy. Protein-Tyrosine Kinases. Pyrroles / pharmacology. Receptors, Fibroblast Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Carrier Proteins / antagonists & inhibitors. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. DNA-Binding Proteins / antagonists & inhibitors. Humans. Mice. Mice, Inbred BALB C. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mutation / genetics. Phosphorylation. Receptor, Fibroblast Growth Factor, Type 3. Repressor Proteins / antagonists & inhibitors. STAT3 Transcription Factor. Suppressor of Cytokine Signaling Proteins. Trans-Activators / antagonists & inhibitors

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  • (PMID = 14871245.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Pyrroles; 0 / Receptors, Fibroblast Growth Factor; 0 / Repressor Proteins; 0 / SOCS1 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / SU 5402; 0 / Socs1 protein, mouse; 0 / Stat3 protein, mouse; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Trans-Activators; EC 2.7.10.1 / FGFR3 protein, human; EC 2.7.10.1 / Fgfr3 protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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21. Jansen B, Wacheck V, Heere-Ress E, Schlagbauer-Wadl H, Hoeller C, Lucas T, Hoermann M, Hollenstein U, Wolff K, Pehamberger H: Chemosensitisation of malignant melanoma by BCL2 antisense therapy. Lancet; 2000 Nov 18;356(9243):1728-33
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  • [Title] Chemosensitisation of malignant melanoma by BCL2 antisense therapy.
  • BACKGROUND: Chemoresistance of malignant melanoma has been linked to expression of the proto-oncogene BCL2.
  • Antisense oligonucleotides (ASO) targeted against BCL2 mRNA decreased BCL2 protein concentrations, increased tumour-cell apoptosis, and led to tumour responses in a mouse xenotransplantation model when combined with systemic dacarbazine.
  • This phase I-II clinical study investigated the combination of BCL2 ASO (augmerosen, Genasense, G3139) and dacarbazine in patients with advanced malignant melanoma expressing BCL2.
  • METHODS: In a within-patient dose-escalation protocol, 14 patients with advanced malignant melanoma were given augmerosen intravenously or subcutaneously in daily doses of 0.6-6.5 mg/kg plus standard dacarbazine treatment (total doses up to 1000 mg/m2 per cycle).
  • Plasma augmerosen concentrations were assayed by high-performance liquid chromatography.
  • In serial tumour biopsy samples, BCL2 protein concentrations were measured by western blotting and tumour-cell apoptosis was assessed.
  • Steady-state plasma concentrations of augmerosen were attained within 24 h, and increased with administered dose.
  • By day 5, daily doses of 1.7 mg/kg and higher led to a median 40% decrease in BCL2 protein in melanoma samples compared with baseline, concomitantly with increased tumour-cell apoptosis, which was greatly increased after dacarbazine treatment.
  • Such downregulation of BCL2, combined with standard anticancer therapy, offers a new approach to the treatment of patients with resistant neoplasms.
  • [MeSH-major] DNA, Antisense / therapeutic use. Melanoma / drug therapy. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / therapeutic use. Dacarbazine / adverse effects. Dacarbazine / therapeutic use. Dose-Response Relationship, Drug. Drug Therapy, Combination. Female. Fever / chemically induced. Follow-Up Studies. Hematologic Diseases / chemically induced. Humans. Male. Middle Aged. Skin / drug effects. Skin / pathology. Skin Neoplasms / prevention & control. Skin Neoplasms / secondary. Survival Analysis. Treatment Outcome

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  • (PMID = 11095261.001).
  • [ISSN] 0140-6736
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / DNA, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 7GR28W0FJI / Dacarbazine
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22. Raab MS, Podar K, Breitkreutz I, Richardson PG, Anderson KC: Multiple myeloma. Lancet; 2009 Jul 25;374(9686):324-39
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  • Multiple myeloma is characterised by clonal proliferation of malignant plasma cells, and mounting evidence indicates that the bone marrow microenvironment of tumour cells has a pivotal role in myeloma pathogenesis.
  • This knowledge has already expanded treatment options for patients with multiple myeloma.
  • Prototypic drugs thalidomide, bortezomib, and lenalidomide have each been approved for the treatment of this disease by targeting both multiple myeloma cells and the bone marrow microenvironment.
  • Although benefit was first shown in relapsed and refractory disease, improved overall response, duration of response, and progression-free and overall survival can be achieved when these drugs are part of first-line regimens.
  • This treatment framework promises to improve outcome not only for patients with multiple myeloma, but also with other haematological malignancies and solid tumours.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Multiple Myeloma / drug therapy. Pyrazines / therapeutic use. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use
  • [MeSH-minor] Bortezomib. Clinical Trials as Topic. Combined Modality Therapy. Genetic Predisposition to Disease / genetics. Humans. Melphalan / therapeutic use. Neoplasm Staging. Protease Inhibitors / therapeutic use. Remission Induction. Stem Cell Transplantation. Survival Rate. Treatment Outcome

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  • (PMID = 19541364.001).
  • [ISSN] 1474-547X
  • [Journal-full-title] Lancet (London, England)
  • [ISO-abbreviation] Lancet
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 4Z8R6ORS6L / Thalidomide; 69G8BD63PP / Bortezomib; F0P408N6V4 / lenalidomide; Q41OR9510P / Melphalan
  • [Number-of-references] 148
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23. Economou MA: Uveal melanoma and macular degeneration: molecular biology and potential therapeutic applications. Acta Ophthalmol; 2008 Dec;86(8):930-1
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  • [Title] Uveal melanoma and macular degeneration: molecular biology and potential therapeutic applications.
  • Uveal melanoma is the most common primary intraocular malignant tumor in adults with 30% to 50% of patients that ultimately succumb to metastatic disease, mainly to the liver. (Shields et al.
  • 1991) Although new diagnostic and therapeutic tools have been developed during the most recent years, only the eye conservation rate has been achieved, while the survival rate remains poor.
  • It has been shown to be crucial for tumor transformation, maintenance of malignant phenotype, promotion of cell growth, and prevention of apoptosis. (Baserga 1995) The hepatocyte growth factor/scatter factor (HGF/SF) is another growth factor produced in the liver and exerts its biological effects through binding to the plasma membrane receptor c-Met.
  • The activation of this receptor by HGF/SF ligand can induce proliferation, motility, adhesion, and invasion of tumor cells. (Cruz et al.
  • 2003) Metastasis is a process involving many components, including tumor cell adhesion, migration, extracellular matrix (ECM) proteolysis, and invasion.
  • The tumor cells undergo intravasation, disperse via the vascular and the lymphatic systems, and finally extravasate to invade the secondary sites.
  • The migration of a malignant cell through the ECM and the basement membrane requires proteolytic activities. (Stetler-Stevenson et al. 1993).
  • Efforts to target the IGF-I system has been made with different types of cancer but not with uveal melanoma.
  • [MeSH-major] Macular Degeneration / drug therapy. Melanoma / drug therapy. Melanoma / metabolism. Molecular Biology / methods. Uveal Neoplasms / drug therapy. Uveal Neoplasms / metabolism
  • [MeSH-minor] Animals. Biomarkers. Humans. Mice. Podophyllotoxin / analogs & derivatives. Podophyllotoxin / therapeutic use. Prognosis. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, IGF Type 1 / metabolism. Signal Transduction. Vascular Endothelial Growth Factor A / metabolism


24. Campbell RA, Sanchez E, Steinberg JA, Baritaki S, Gordon M, Wang C, Shalitin D, Chen H, Pang S, Bonavida B, Said J, Berenson JR: Antimyeloma effects of arsenic trioxide are enhanced by melphalan, bortezomib and ascorbic acid. Br J Haematol; 2007 Aug;138(4):467-78
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  • Arsenic trioxide (ATO) induces apoptosis of malignant plasma cells through multiple mechanisms, including inhibition of DNA binding by nuclear factor kappa-B, a key player in the development of chemoresistance in multiple myeloma (MM).
  • This activity suggests that ATO may be synergistic when combined with other active antimyeloma drugs.
  • Animals treated with any of these drugs alone showed tumour growth and increases in paraprotein levels similar to control mice, whereas animals treated with ATO-containing combinations showed markedly suppressed tumour growth and significantly reduced serum paraprotein levels.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arsenicals / therapeutic use. Multiple Myeloma / drug therapy. Oxides / therapeutic use
  • [MeSH-minor] Animals. Antioxidants / therapeutic use. Apoptosis / drug effects. Ascorbic Acid / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Enzyme-Linked Immunosorbent Assay. Humans. Immunoglobulin G / analysis. Melphalan / therapeutic use. Mice. Mice, SCID. Pyrazines / therapeutic use. Xenograft Model Antitumor Assays

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  • (PMID = 17587338.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Arsenicals; 0 / Boronic Acids; 0 / Immunoglobulin G; 0 / Oxides; 0 / Pyrazines; 69G8BD63PP / Bortezomib; PQ6CK8PD0R / Ascorbic Acid; Q41OR9510P / Melphalan; S7V92P67HO / arsenic trioxide
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25. Tomassetti P, Salomone T, Migliori M, Campana D, Corinaldesi R: Optimal treatment of Zollinger-Ellison syndrome and related conditions in elderly patients. Drugs Aging; 2003;20(14):1019-34
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  • [Title] Optimal treatment of Zollinger-Ellison syndrome and related conditions in elderly patients.
  • Zollinger-Ellison syndrome is characterised by refractory peptic ulcer disease, severe diarrhoea and gastric acid hypersecretion associated with an islet-cell tumour of the pancreas (gastrinoma).
  • Zollinger-Ellison syndrome is sporadic in 62-80% of cases and in 20-38% of cases is associated with multiple endocrine neoplasia type 1 (MEN 1).
  • The diagnosis of Zollinger-Ellison syndrome is certain when the plasma gastrin is >1000 pg/mL and the basal acid output is >15 mEq/h in patients with an intact stomach, >5 mEq/h in gastrectomised patients, or when this hypergastrinemia is associated with a pH <2.
  • The treatment is based on control of gastric acid hypersecretion and of the malignant tumour and its possible metastases.
  • Proton pump inhibitors are the most effective antisecretory drugs and can be administered in the elderly at high dosages without drug-related adverse effects.
  • As an initial therapy, daily dosages of omeprazole 80-100 mg or pantoprazole 40-160 mg are employed.
  • In long-term treatment the doses can be greatly reduced once effective control of the gastric output has been established.
  • Intravenous proton pump inhibitors may be administered when patients cannot take oral therapy, particularly in acute conditions.
  • When liver metastases are also present, their debulking may improve symptoms and survival, and facilitate medical treatment.
  • Chemotherapy is not the therapy of choice in patients with gastrinomas and is indicated only in those with malignant progressive disease; interferon alpha, embolisation and chemoembolisation are not advisable for the elderly.
  • The treatment of elderly Zollinger-Ellison syndrome patients, similarly to all elderly oncological patients, should be based on the use of comprehensive geriatric assessment.
  • This will enable the clinician to define the functional status of the elderly person, to decide whether the patient can tolerate surgery and/or the stress of antineoplastic therapy, and finally, to determine whether this patient can tolerate an aggressive treatment for Zollinger-Ellison syndrome or whether the only possible choice is palliative relief of symptoms.
  • [MeSH-major] Geriatrics. Helicobacter pylori. Histamine H2 Antagonists / therapeutic use. Proton Pump Inhibitors. Zollinger-Ellison Syndrome
  • [MeSH-minor] Aged. Carcinoid Tumor / complications. Helicobacter Infections / complications. Humans. Multiple Endocrine Neoplasia Type 1 / complications

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  • (PMID = 14651442.001).
  • [ISSN] 1170-229X
  • [Journal-full-title] Drugs & aging
  • [ISO-abbreviation] Drugs Aging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 0 / Proton Pump Inhibitors
  • [Number-of-references] 143
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26. Lawson MA, Ashcroft J, Croucher PI: Bisphosphonate therapy in the treatment of multiple myeloma. Curr Pharm Des; 2010;16(27):3028-36
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  • [Title] Bisphosphonate therapy in the treatment of multiple myeloma.
  • Multiple myeloma is an incurable B cell neoplasm caused by the monoclonal expansion of malignant plasma cells in the bone marrow, often resulting in devastating bone disease.
  • For over 2 decades bisphosphonates have been successfully used to treat the tumour-induced bone disease associated with multiple myeloma.
  • Major advances in the use of bisphosphonates, including findings that they may have additional benefits such as anti-tumour effects and promoting patient survival will be discussed.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Diseases / drug therapy. Bone Diseases / etiology. Diphosphonates / pharmacology. Diphosphonates / therapeutic use. Multiple Myeloma / drug therapy
  • [MeSH-minor] Animals. Bone Density Conservation Agents / adverse effects. Bone Density Conservation Agents / pharmacology. Bone Density Conservation Agents / therapeutic use. Drug Design. Humans. Osteoclasts / drug effects

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  • (PMID = 20722619.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates
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27. Prabhakara S, Kalia VK: Optimizing radiotherapy of brain tumours by a combination of temozolomide & lonidamine. Indian J Med Res; 2008 Aug;128(2):140-8
Hazardous Substances Data Bank. DACARBAZINE .

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  • BACKGROUND & OBJECTIVE: Temozolomide (TMZ), a second generation alkylating drug, an effective cytotoxic agent as well as radiosensitizer for malignant brain tumours, has side effects like myelosuppression.
  • Lonidamine (LND) increases the effectiveness of several experimental multiple chemotherapy protocols, without increasing bone marrow toxicities and is effective in brain tumour patients.
  • The objective of the present studies was to investigate whether combining clinically relevant doses of LND and TMZ could increase the proliferation and radiation response of malignant human brain tumour cells in vitro.
  • METHODS: A malignant human glioma (U373MG) cell line was used in these studies.
  • The effects of continuous treatment for two days on proliferation response and cytotoxicity were studied after trypsinization; by cell counts and the uptake of trypan blue dye (0.5%).
  • For the study of radiation (60Co-Gamma-rays, 2 Gy) response, drugs were removed 4 h after irradiation and cultures were grown further in drug free, normal growth medium for another 20 h or 44 h.
  • RESULTS: Continuous presence of TMZ or LND for two days significantly inhibited cell proliferation in a concentration dependent manner.
  • Combination of 20 microM TMZ with 100 microM LND had additive effects on proliferation response, without affecting cell viability.
  • Short-term drug treatments without irradiation did not induce micronuclei formation.
  • Cell proliferation and viability were also not affected.
  • However, post-irradiation presence of either of these drugs for 4 h significantly reduced the proliferation response, 24 and 48 h after treatments.
  • It was further inhibited by the combination treatment.
  • On the contrary, radiation induced micronuclei formation was enhanced by either of the drugs; which was significantly increased by the combined treatment, 24 h as well as 48 h after irradiation.
  • No effects on cell viability were observed, immediately after these treatments as well as at later time points.
  • INTERPRETATION & CONCLUSION: Our findings showed that combination of TMZ and LND at clinically achievable, low plasma concentrations could inhibit tumour growth, and lonidamine could reduce the dose of temozolomide required for radiosensitization of brain tumours.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Brain Neoplasms / drug therapy. Brain Neoplasms / radiotherapy. Cell Proliferation / drug effects. Radiation-Sensitizing Agents / pharmacology. Radiotherapy / methods
  • [MeSH-minor] Acridine Orange. Analysis of Variance. Cell Line, Tumor. Dacarbazine / analogs & derivatives. Dacarbazine / pharmacology. Gamma Rays. Humans. Indazoles / pharmacology

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  • (PMID = 19001677.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Indazoles; 0 / Radiation-Sensitizing Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; F30N4O6XVV / Acridine Orange; U78804BIDR / lonidamine
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28. Fullerton NE, Boyd M, Ross SC, Pimlott SL, Babich J, Kirk D, Zalutsky MR, Mairs RJ: Comparison of radiohaloanalogues of meta-iodobenzylguanidine (MIBG) for a combined gene- and targeted radiotherapy approach to bladder carcinoma. Med Chem; 2005 Nov;1(6):611-8
The Lens. Cited by Patents in .

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  • Targeted radiotherapy using radiolabelled meta-iodobenzylguanidine (MIBG) is a promising treatment option for bladder cancer, restricting the effects of radiotherapy to malignant cells thereby increasing efficacy and decreasing morbidity of radiotherapy.
  • We investigated the efficacy of a combined gene therapy and targeted radiotherapy approach for bladder cancer using radiolabelled MIBG.
  • The effectiveness of alternative radiohalogens and alternative preparations of radiolabelled MIBG for this therapeutic strategy were compared.
  • Bladder cancer cells, EJ138, were transfected with a gene encoding the noradrenaline transporter (NAT) under the control of a tumour specific telomerase promoter, enabling them to actively take up radiolabelled MIBG.
  • This resulted in tumour-specific cell kill.
  • [211At] meta-astatobenzylguanidine (MABG)) were compared with respect to efficiency of induction of cell kill.
  • However, the alpha-emitter [211At]MABG was, by three orders of magnitude, more effective in causing tumour cell kill than the beta-emitter [131I]MIBG.
  • [131I]MIBG or [211At]MABG, is a promising novel treatment approach for bladder cancer therapy.
  • [MeSH-major] 3-Iodobenzylguanidine / therapeutic use. Astatine / therapeutic use. Genetic Therapy / methods. Iodine Radioisotopes / therapeutic use. Radiopharmaceuticals / therapeutic use. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Alpha Particles / therapeutic use. Beta Particles / therapeutic use. Cell Line, Tumor. Cell Survival / drug effects. Combined Modality Therapy / methods. Dose-Response Relationship, Radiation. Humans. Iodates / chemistry. Iodates / therapeutic use. Norepinephrine Plasma Membrane Transport Proteins / biosynthesis. Norepinephrine Plasma Membrane Transport Proteins / genetics. Structure-Activity Relationship. Symporters / biosynthesis. Symporters / genetics. Tumor Cells, Cultured

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  • (PMID = 16787344.001).
  • [ISSN] 1573-4064
  • [Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))
  • [ISO-abbreviation] Med Chem
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Iodates; 0 / Iodine Radioisotopes; 0 / Norepinephrine Plasma Membrane Transport Proteins; 0 / Radiopharmaceuticals; 0 / Symporters; 0 / sodium-iodide symporter; 35MRW7B4AD / 3-Iodobenzylguanidine; U558PCS5Z9 / sodium iodate; XI595HAL7H / Astatine
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29. Quigg M, Mairs RJ, Brown SM, Harland J, Dunn P, Rampling R, Livingstone A, Wilson L, Boyd M: Assessment in vitro of a novel therapeutic strategy for glioma, combining herpes simplex virus HSV1716-mediated oncolysis with gene transfer and targeted radiotherapy. Med Chem; 2005 Sep;1(5):423-9
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  • [Title] Assessment in vitro of a novel therapeutic strategy for glioma, combining herpes simplex virus HSV1716-mediated oncolysis with gene transfer and targeted radiotherapy.
  • Genetically engineered herpes simplex virus ICP34.5 null mutants replicate only in dividing cells and have shown potential for the treatment of malignant disease, including glioma.
  • Phase I trials have demonstrated the safety of these viruses in various clinical settings but it is envisaged that for full efficacy they will be used in combination with other therapeutic modalities.
  • To enhance virus-induced tumour cytotoxicity, we have engineered an ICP34.5 null mutant (HSV1716) of HSV1 which expresses the noradrenaline transporter gene (NAT).
  • We have shown previously that introduction of the NAT gene into a range of tumour cells, via plasmid-mediated transfection, conferred the capacity for active uptake of the radiopharmaceutical [131I]MIBG and resulted in dose-dependent toxicity.
  • In this study, combination therapy utilising HSV1716/NAT and [131I]MIBG was assessed in vitro by the MTT assay.
  • The combination of viral oncolysis and induced radiopharmaceutical uptake resulted in significantly enhanced cytotoxicity compared to either agent alone and the response was dose- and time-dependent.
  • These studies show that the combination of oncolytic HSV therapy with targeted radiotherapy has the potential for effective tumour cell kill and warrants further investigation as a treatment for malignant glioma.
  • [MeSH-major] 3-Iodobenzylguanidine / pharmacokinetics. Gene Transfer Techniques. Glioma / therapy. Herpesvirus 1, Human / physiology. Oncolytic Virotherapy / methods
  • [MeSH-minor] Animals. Cell Line. Cell Survival / drug effects. Combined Modality Therapy. Cricetinae. Dose-Response Relationship, Drug. Genetic Engineering. Humans. In Vitro Techniques. Kinetics. Mice. Norepinephrine Plasma Membrane Transport Proteins / genetics. Norepinephrine Plasma Membrane Transport Proteins / physiology. Radiotherapy / methods. Structure-Activity Relationship. Time Factors. Transduction, Genetic. Tumor Cells, Cultured

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  • (PMID = 16787326.001).
  • [ISSN] 1573-4064
  • [Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))
  • [ISO-abbreviation] Med Chem
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Norepinephrine Plasma Membrane Transport Proteins; 35MRW7B4AD / 3-Iodobenzylguanidine
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30. Mueller S, Holdenrieder S, Stieber P, Haferlach T, Schalhorn A, Braess J, Nagel D, Seidel D: Early prediction of therapy response in patients with acute myeloid leukemia by nucleosomal DNA fragments. BMC Cancer; 2006;6:143
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  • [Title] Early prediction of therapy response in patients with acute myeloid leukemia by nucleosomal DNA fragments.
  • BACKGROUND: Elevated levels of nucleosomal DNA fragments can be detected in plasma and sera of patients with malignant diseases.
  • METHODS: We investigated the course of nucleosomal DNA, thymidine kinase, lactate dehydrogenase and leukocytes in sera of 25 patients with acute myeloid leukemia during the first cycle of induction chemotherapy and tested their power to distinguish between patients with complete remission and those with no remission.
  • The area under the curve of DNA values of days 2-4 after start of therapy (AUC 2-4) discriminated between both groups with a sensitivity of 56% at a specificity of 100%.
  • CONCLUSION: Our results indicate that nucleosomal DNA fragments are valuable markers for the early prediction of therapeutic efficacy in patients with acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Cytarabine / administration & dosage. DNA Fragmentation. Daunorubicin / administration & dosage. Female. Humans. L-Lactate Dehydrogenase / analysis. L-Lactate Dehydrogenase / blood. Leukocytes. Male. Middle Aged. Mitoxantrone / administration & dosage. Nucleosomes / chemistry. Predictive Value of Tests. Prognosis. Thioguanine / administration & dosage. Thymidine Kinase / blood. Treatment Outcome

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  • (PMID = 16734907.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nucleosomes; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.7.1.21 / Thymidine Kinase; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DAT protocol 1; MAC chemotherapy protocol
  • [Other-IDs] NLM/ PMC1555596
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31. D'Cruz OJ, Uckun FM: Metvan: a novel oxovanadium(IV) complex with broad spectrum anticancer activity. Expert Opin Investig Drugs; 2002 Dec;11(12):1829-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • At nanomolar and low micromolar concentrations, metvan induces apoptosis in human leukaemia cells, multiple myeloma cells and solid tumour cells derived from breast cancer, glioblastoma, ovarian, prostate and testicular cancer patients.
  • It is highly effective against cisplatin-resistant ovarian cancer and testicular cancer cell lines.
  • Metvan-induced apoptosis is associated with a loss of mitochondrial transmembrane potential, the generation of reactive oxygen species and depletion of glutathione.
  • Treatment of leukaemia cells from acute lymphoblastic leukaemia, acute myeloid leukaemia and chronic acute myeloid leukaemia patients with metvan inhibits the constitutive expression as well as the gelatinolytic activities of matrix metalloproteinase-9 and -2.
  • Treatment of human malignant glioblastoma and breast cancer cells with metvan at concentrations > 1 microM is associated with a nearly complete loss of the adhesive, migratory and invasive properties of the treated cancer cell populations.
  • Therapeutic plasma concentrations > or = 5 microM, which are highly cytotoxic against human cancer cells, can be rapidly achieved and maintained in mice for at least 24 h after intraperitoneal bolus injection of a single 10 mg/kg non-toxic dose of metvan.
  • Metvan exhibits significant antitumour activity, delays tumour progression and prolongs survival time in severe combined immunodeficient mouse xenograft models of human malignant glioblastoma and breast cancer.
  • Metvan could represent the first vanadium complex as an alternative to platinum-based chemotherapy.
  • [MeSH-minor] Animals. Humans. Mice. Tumor Cells, Cultured

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  • (PMID = 12457442.001).
  • [ISSN] 1354-3784
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organometallic Compounds; 0 / bis(4,7-dimethyl-1,10-phenanthroline)sulfatooxovanadium(IV); 20644-97-7 / oxovanadium IV; 3WHH0066W5 / Vanadates
  • [Number-of-references] 65
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32. Boyd M, Mairs RJ, Keith WN, Ross SC, Welsh P, Akabani G, Owens J, Vaidyanathan G, Carruthers R, Dorrens J, Zalutsky MR: An efficient targeted radiotherapy/gene therapy strategy utilising human telomerase promoters and radioastatine and harnessing radiation-mediated bystander effects. J Gene Med; 2004 Aug;6(8):937-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An efficient targeted radiotherapy/gene therapy strategy utilising human telomerase promoters and radioastatine and harnessing radiation-mediated bystander effects.
  • BACKGROUND: Targeted radiotherapy achieves malignant cell-specific concentration of radiation dosage by tumour-affinic molecules conjugated to radioactive atoms.
  • Combining gene therapy with targeted radiotherapy is attractive because the associated cross-fire irradiation of the latter induces biological bystander effects upon neighbouring cells overcoming low gene transfer efficiency.
  • METHODS: We sought to maximise the tumour specificity and efficacy of noradrenaline transporter (NAT) gene transfer combined with treatment using the radiopharmaceutical meta-[(131)I]iodobenzylguanidine ([(131)I]MIBG).
  • Cell-kill was achieved by treatment with the beta-decay particle emitter [(131)I]MIBG or the alpha-particle emitter [(211)At]MABG.
  • We utilised our novel transfected mosaic spheroid model (TMS) to determine whether this treatment strategy could result in sterilisation of spheroids containing only a small proportion of NAT-expressing cells.
  • The concentrations of radiopharmaceutical required to reduce to 0.1% the survival of clonogens derived from 5% RSV/NAT and 5% hTERT/NAT TMS were 14 and 23 MBq/ml, respectively, for treatment with [(131)I]MIBG and 0.018 and 0.028 MBq/ml, respectively, for treatment with [(211)At]MABG.
  • Spheroids composed of only 5% of cells expressing NAT under the control of the RSV or hTERT promoter were sterilised by radiopharmaceutical treatment.
  • This observation is indicative of bystander cell-kill.
  • [MeSH-major] Astatine / pharmacology. Bystander Effect. Genetic Therapy / methods. Promoter Regions, Genetic. Radiopharmaceuticals / pharmacology. Radiotherapy / methods. Telomerase / genetics
  • [MeSH-minor] Cell Death. Cell Survival. Dose-Response Relationship, Drug. Humans. Norepinephrine Plasma Membrane Transport Proteins. Plasmids. Spheroids, Cellular. Symporters / genetics. Transfection. Transgenes. Tumor Cells, Cultured

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  • (PMID = 15293352.001).
  • [ISSN] 1099-498X
  • [Journal-full-title] The journal of gene medicine
  • [ISO-abbreviation] J Gene Med
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA42324; United States / NINDS NIH HHS / NS / NS20023
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Norepinephrine Plasma Membrane Transport Proteins; 0 / Radiopharmaceuticals; 0 / SLC6A2 protein, human; 0 / Symporters; EC 2.7.7.49 / Telomerase; XI595HAL7H / Astatine
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33. Helige C, Hofmann-Wellenhof R, Fink-Puches R, Smolle J: Mofarotene-induced inhibition of melanoma cell motility by increasing vinculin-containing focal contacts. Melanoma Res; 2004 Dec;14(6):547-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mofarotene-induced inhibition of melanoma cell motility by increasing vinculin-containing focal contacts.
  • Tumour cell motility, which is dependent on the organization of the cytoskeleton, is considered to play an important role in the spread of malignant melanoma.
  • In this study, the effects of the arotinoid mofarotene on single cell motility and vinculin organization of the highly metastatic melanoma cell line K-1735-M2 were determined.
  • Cell movements were evaluated quantitatively from time-lapse video recordings using an IBAS image analysis system.
  • Vinculin distribution was evaluated using confocal laser scanning microscopy and a specially developed computerized image analysing program.
  • In addition, melanoma cell invasion was tested on the embryonic chick heart model.
  • Although 10 microM mofarotene did not reduce the translocative movements of melanoma cells, it significantly inhibited stationary motility, including fast plasma membrane movements and changes in shape.
  • Mofarotene also showed a pronounced effect on the organization of vinculin-containing cell-substratum adhesion plaques.
  • In retinoid-treated cells, the numbers of vinculin plaques per cell, and particularly those in the marginal areas of the cells, were significantly increased compared with untreated controls.
  • Furthermore, the compound reduced the invasiveness of melanoma cells in a three-dimensional tissue culture model.
  • In conclusion, our data demonstrate that mofarotene, an already almost forgotten synthetic retinoid, shows interesting effects on melanoma cells, which may be relevant for a slowdown of tumour spread.
  • [MeSH-major] Cell Movement / drug effects. Focal Adhesions / drug effects. Melanoma, Experimental / drug therapy. Morpholines / pharmacology. Retinoids / pharmacology. Vinculin / metabolism
  • [MeSH-minor] Actins / metabolism. Animals. Cell Adhesion / drug effects. Chick Embryo. Chickens. Collagen / metabolism. Drug Combinations. Heart / drug effects. Laminin / metabolism. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Mice. Neoplasm Invasiveness / pathology. Proteoglycans / metabolism. Skin Neoplasms. Spheroids, Cellular / drug effects. Tumor Cells, Cultured

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  • (PMID = 15577329.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Drug Combinations; 0 / Laminin; 0 / Morpholines; 0 / Proteoglycans; 0 / Retinoids; 119978-18-6 / matrigel; 125361-02-6 / Vinculin; 8K3CVY8F8V / mofarotene; 9007-34-5 / Collagen
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34. Ruf P, Kluge M, Jäger M, Burges A, Volovat C, Heiss MM, Hess J, Wimberger P, Brandt B, Lindhofer H: Pharmacokinetics, immunogenicity and bioactivity of the therapeutic antibody catumaxomab intraperitoneally administered to cancer patients. Br J Clin Pharmacol; 2010 Jun;69(6):617-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacokinetics, immunogenicity and bioactivity of the therapeutic antibody catumaxomab intraperitoneally administered to cancer patients.
  • AIMS: Catumaxomab is the first EMEA approved trifunctional anti-EpCAMxanti-CD3 antibody for the treatment of cancer patients with malignant ascites.
  • A phase II pharmacokinetic study was conducted to determine local and systemic antibody concentrations and anti-drug antibody (ADA) development.
  • METHODS: Thirteen cancer patients with symptomatic malignant ascites were treated with four ascending doses of 10, 20, 50, and 150 microg catumaxomab intraperitoneally (i.p.) infused on days 0, 3, 6 or 7 and 10.
  • The pharmacokinetics of catumaxomab were studied by implementation of supportive data from a non clinical mouse tumour model.
  • Catumaxomab became increasingly concentrated in ascites during the course of treatment, attaining effective concentrations in the ng ml(-1) range.
  • The observed systemic catumaxomab exposure was low (<1%), with a maximal median plasma concentration (C(max)) of 403 pg ml(-1).
  • The mean elimination half-life in the plasma was 2.13 days.
  • All patients developed ADA, but not before the last infusion.
  • High observed inter-individual variability and low systemic exposure may be explained by the inverse correlation between tumour burden, effector cell numbers and systemic antibody bioavailability as demonstrated in a defined mouse tumour model.
  • CONCLUSIONS: Based on the high and effective local concentrations, low systemic exposure and acceptable safety profile, we confirmed that the i.p. application scheme of catumaxomab for the treatment of malignant ascites is appropriate.
  • [MeSH-major] Antibodies, Bispecific / pharmacokinetics. Immunologic Factors / pharmacokinetics. Neoplasms / drug therapy

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  • (PMID = 20565453.001).
  • [ISSN] 1365-2125
  • [Journal-full-title] British journal of clinical pharmacology
  • [ISO-abbreviation] Br J Clin Pharmacol
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / Immunologic Factors; 0 / catumaxomab
  • [Other-IDs] NLM/ PMC2878603
  • [Keywords] NOTNLM ; catumaxomab / immunogenicity / intraperitoneal infusion / malignant ascites / pharmacokinetics
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