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Effect of recombinant human granulocyte-macrophage colony-stimulating factor on hematopoietic reconstitution after high-dose chemotherapy and autologous bone marrow transplantation.
Brandt SJ, Peters WP, Atwater SK, Kurtzberg J, Borowitz MJ, Jones RB, Shpall EJ, Bast RC, Gilbert CJ, Oette DH
(1988) N Engl J Med 318: 869-76
MeSH Terms: Adult, Alkylating Agents, Antineoplastic Agents, Bone Marrow, Bone Marrow Transplantation, Breast Neoplasms, Colony-Stimulating Factors, Combined Modality Therapy, Drug Evaluation, Granulocyte-Macrophage Colony-Stimulating Factor, Growth Substances, Hematopoiesis, Humans, Leukocyte Count, Melanoma, Middle Aged, Platelet Count, Recombinant Proteins
Show Abstract · Added March 5, 2014
Recombinant human granulocyte-macrophage colony-stimulating factor (rHuGM-CSF) has been reported to increase the leukocyte count in subhuman primates subjected to total-body irradiation and in patients with the acquired immunodeficiency syndrome. We administered this substance to 19 patients with breast cancer or melanoma treated with high-dose combination chemotherapy and autologous bone marrow support. Groups of three or four patients were treated with 2.0, 4.0, 8.0, 16.0, or 32.0 micrograms per kilogram of body weight per day of glycosylated rHuGM-CSF by continuous intravenous infusion for 14 days, beginning three hours after bone marrow infusion. Total leukocyte and granulocyte recovery was accelerated in these patients as compared with 24 historical controls matched for age, diagnosis, and treatment. Leukocyte counts (mean +/- SD) obtained 14 days after transplantation were 1511 +/- 1003 per microliter in patients given 2 to 8 micrograms per kilogram per day, 2575 +/- 2304 in those given 16 micrograms, and 3120 +/- 1744 in those given 32 micrograms, as compared with 863 +/- 645 per microliter in the controls. No consistent effect on platelet counts was noted. Toxic effects were generally mild and not clearly dose-related in patients given 2 to 16 micrograms per kilogram per day. Edema, weight gain, or myalgias occurred in all patients given 32 micrograms per kilogram; marked weight gain, generalized edema, pleural effusions, and hypotension developed in two patients, one of whom also had acute renal failure. Our results indicate that rHuGM-CSF can accelerate myeloid recovery after high-dose chemotherapy and autologous bone marrow transplantation, over a range of doses that can be tolerated. In this setting the ability to increase the dose is limited by the development of myalgias and fluid retention.
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18 MeSH Terms
Phase I clinical study of N-[(4-chlorophenyl)amino]carbonyl-2,3-dihydro-1H-indene-5-sulfonamide (LY186641).
Hainsworth JD, Hande KR, Satterlee WG, Kuttesch J, Johnson DH, Grindey G, Jackson LE, Greco FA
(1989) Cancer Res 49: 5217-20
MeSH Terms: Antineoplastic Agents, Drug Evaluation, Female, Humans, Male, Methemoglobinemia, Middle Aged, Neoplasms, Sulfonylurea Compounds, Time Factors
Show Abstract · Added March 5, 2014
Between February 1987 and July 1988, 45 patients with advanced refractory cancer were treated with LY186641, a diarylsulfonylurea that has shown a broad spectrum of activity in preclinical testing. Patients received a weekly p.o. dose of LY186641 for 6 consecutive weeks; responding and stable patients continued weekly therapy until progression occurred. Using a standard phase I study design, the first three patients received LY186641 at 30 mg/m2 week; the dose was escalated in subsequent patients until dose-limiting toxicity occurred. Methemoglobinemia was the major toxicity observed and was dose related. Methemoglobin levels peaked approximately 24 h after LY186641 was administered and fell to low levels after 48 h. Six patients developed fatigue, cyanosis, and dyspnea associated with serum methemoglobinemia levels of greater than 20%; four of these patients were subsequently removed from the study. Hemolytic anemia was also observed but was clinically significant in only 10 patients. Other side effects were mild and infrequent. The maximum tolerated dose of LY186641, when given at this schedule, was 2550 mg/m2/week. No objective tumor responses were observed.
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10 MeSH Terms
Conjugation of 9-deoxy-delta 9,delta 12(E)-prostaglandin D2 with intracellular glutathione and enhancement of its antiproliferative activity by glutathione depletion.
Atsmon J, Freeman ML, Meredith MJ, Sweetman BJ, Roberts LJ
(1990) Cancer Res 50: 1879-85
MeSH Terms: Animals, Antimetabolites, Antineoplastic Agents, Biological Transport, Biotransformation, Buthionine Sulfoximine, Cell Division, Cell Line, Glutathione, Maleates, Mass Spectrometry, Methionine Sulfoximine, Prostaglandin D2, Tritium
Show Abstract · Added December 10, 2013
The major dehydration product of prostaglandin D2, 9-deoxy-delta 9,delta 12(E)-prostaglandin D2, is a potent cytotoxic compound. Like other cytotoxic prostaglandins, this compound possesses an alpha, beta-unsaturated ketone group to which cytotoxic activity has been attributed. This prostaglandin was found to readily conjugate with glutathione (GSH) in vitro. When 9-deoxy-delta 9,delta 12(E)-prostaglandin D2 was incubated with Chinese hamster ovary or hepatoma tissue culture cells, it was rapidly taken up and was recovered in the cell lysate primarily as a GSH conjugate in which the keto group at C-11 and the delta 12 double bond had been reduced. Identification of the GSH conjugate was accomplished by analysis by fast atom bombardment mass spectrometry following purification by high performance liquid chromatography. This GSH conjugate and its cysteinylglycinyl and cysteinyl metabolites were also identified in the cell culture medium. 9-Deoxy-delta 9,delta 12(E)-prostaglandin D2 inhibited cell proliferation of these two cell lines in a concentration dependent manner. Depletion of intracellular glutathione by treatment with diethyl maleate and buthionine sulfoximine decreased the amount of intracellular conjugated prostaglandin recovered, and significantly enhanced the antiproliferative effect of 9-deoxy-delta 9-delta 12(E)-prostaglandin D2 on the growth of these cell lines in a concentration dependent fashion. We conclude that intracellular GSH may modulate the antiproliferative activity of 9-deoxy-delta 9,delta 12(E)-prostaglandin D2 and, possibly, of other cytotoxic prostaglandins.
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14 MeSH Terms
Stabilization of the topoisomerase II-DNA cleavage complex by antineoplastic drugs: inhibition of enzyme-mediated DNA religation by 4'-(9-acridinylamino)methanesulfon-m-anisidide.
Robinson MJ, Osheroff N
(1990) Biochemistry 29: 2511-5
MeSH Terms: Aminacrine, Aminoacridines, Amsacrine, Animals, Antineoplastic Agents, Culture Techniques, DNA, DNA Damage, DNA Polymerase II, DNA Topoisomerases, Type II, Drosophila melanogaster, Enzyme Stability
Show Abstract · Added March 5, 2014
In order to elucidate the mechanism by which the intercalative antineoplastic drug 4'-(9-acridinylamino)methanesulfon-m-anisidide (m-AMSA) stabilizes the covalent topoisomerase II-DNA cleavage complex, the effect of the drug on the DNA cleavage/religation reaction of the type II enzyme from Drosophila melanogaster was examined. At a concentration of 60 microM, m-AMSA enhanced topoisomerase II mediated double-stranded DNA breakage approximately 5-fold. Drug-induced stabilization of the enzyme-DNA cleavage complex was readily reversed by the addition of EDTA or salt. When a DNA religation assay was utilized, m-AMSA was found to inhibit the topoisomerase II mediated rejoining of cleaved DNA approximately 3.5-fold. This result is similar to that previously reported for the effects of etoposide on the activity of the Drosophila enzyme [Osheroff, N. (1989) Biochemistry 28, 6157-6160]. Thus, it appears that structurally disparate classes of topoisomerase II targeted antineoplastic drugs stabilize the enzyme's DNA cleavage complex primarily by interfering with the ability of topoisomerase II to religate DNA.
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12 MeSH Terms
Inhibition of prostatic tumor cell proliferation by suramin: alterations in TGF alpha-mediated autocrine growth regulation and cell cycle distribution.
Kim JH, Sherwood ER, Sutkowski DM, Lee C, Kozlowski JM
(1991) J Urol 146: 171-6
MeSH Terms: Antineoplastic Agents, Cell Cycle, Cell Division, Cell Line, Depression, Chemical, Dose-Response Relationship, Drug, Drug Screening Assays, Antitumor, ErbB Receptors, Humans, Male, Prostatic Neoplasms, Suramin, Transforming Growth Factor alpha, Tumor Cells, Cultured
Show Abstract · Added October 18, 2015
Suramin is a trypanocidal drug that has generated recent interest as an antineoplastic agent because of its ability to inhibit the binding of growth factors to their cell surface receptors. Our studies, and others, suggest that the androgen-independent human prostatic carcinoma cell lines PC3 and DU145 proliferate via autocrine growth mechanisms mediated by transforming growth factor alpha (TGFa) and its receptor, the epidermal growth factor (EGF) receptor. The present studies were designed to evaluate the ability of suramin to inhibit PC3 and DU145 proliferation by interfering with TGFa-mediated autocrine growth. Suramin induced a dose-dependent reduction of prostatic tumor cell proliferation which was reversed by removal of suramin from the culture medium. 3H-thymidine release studies showed that suramin had little direct cytotoxicity to either cell line. These findings suggest that the effects of suramin are mediated by cytostatic, rather than cytotoxic, mechanisms. Suramin also interfered with TGFa-mediated growth mechanisms. Specifically, suramin reduced the specific binding of TGFa to PC3 and DU145 cells. Additionally, the inhibitory effect of suramin on DU145 was reversed by cultivation of cells in the presence of excess TGFa. Further investigations revealed that suramin increased the percentage of cells in the S phase of the cell cycle for both cell lines. These studies show that the inhibitory effect of suramin on PC3 and DU145 cell growth is mediated, in part, by alteration of TGFa-mediated autocrine growth mechanisms and cell cycle kinetics.
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14 MeSH Terms
Desire for control and choice of antiemetic treatment for cancer chemotherapy.
Wallston KA, Smith RA, King JE, Smith MS, Rye P, Burish TG
(1991) West J Nurs Res 13: 12-23; discussion 23-9
MeSH Terms: Adult, Aged, Antiemetics, Antineoplastic Agents, Choice Behavior, Female, Humans, Internal-External Control, Male, Middle Aged, Nausea, Neoplasms, Patient Participation, Vomiting
Added July 28, 2015
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14 MeSH Terms
Vascular trauma as a result of therapeutic procedures for the treatment of malignancy.
Myers SI, Harward TR, Putnam JB, Frazier OH
(1991) J Vasc Surg 14: 314-9
MeSH Terms: Adolescent, Adult, Aged, Aneurysm, Antineoplastic Agents, Arteries, Blood Vessel Prosthesis, Catheters, Indwelling, Female, Follow-Up Studies, Hemorrhage, Humans, Iatrogenic Disease, Infusions, Intra-Arterial, Ischemia, Leg, Male, Middle Aged, Neoplasm Invasiveness, Neoplasm Metastasis, Neoplasms, Retrospective Studies, Thromboembolism, Vascular Diseases
Show Abstract · Added March 27, 2014
Twenty-two iatrogenic vascular injuries caused by resection of tumors with local recurrences or adjuvant chemotherapy were treated over a 42-month period in 11 female and 8 male patients with cancer (58% had documented metastases). Sixteen of 22 vascular injuries were caused by intraarterial administration of chemotherapy (8 emboli; 8 direct catheter trauma), and six were caused by resection of tumors with local invasion. The injuries were extremity ischemia (15 extremities in 13 patients), pseudoaneurysm (4), expanding hematoma (3 injuries in 2 patients). Twenty-two surgical repairs included bypass of severely damaged arteries in five, embolectomy in five, interposition grafts in three, pseudoaneurysm resection and primary repair in three, primary repair of three vascular injuries, and one patch angioplasty. Leg amputation was required in two patients. Seventeen of 19 patients had successful vascular repairs with resolution of preoperative indications for vascular repair without intraoperative or postoperative deaths. Long term follow-up (mean, 17 months) showed no recurrence of vascular problems; however, two patients died of metastatic cancer at 6 and 24 weeks after vascular repair. This study supports an aggressive approach to the management of vascular injuries caused by therapeutic interventions for malignancy despite the presence of metastatic disease.
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24 MeSH Terms
Modulation of the antiproliferative activity of 9-deoxy-delta 9,delta 12(E)-PGD2 by conjugation with intracellular glutathione.
Atsmon J, Freeman ML, Meredith MJ, Sweetman BJ, Roberts LJ
(1991) Adv Prostaglandin Thromboxane Leukot Res 21B: 887-90
MeSH Terms: Animals, Antineoplastic Agents, Cell Division, Cell Line, Glutathione, Molecular Structure, Prostaglandin D2, Tumor Cells, Cultured
Added December 10, 2013
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8 MeSH Terms
Catalytic function of DNA topoisomerase II.
Osheroff N, Zechiedrich EL, Gale KC
(1991) Bioessays 13: 269-73
MeSH Terms: Adenosine Triphosphate, Animals, Antineoplastic Agents, Base Sequence, Catalysis, Consensus Sequence, DNA, DNA Topoisomerases, Type II, DNA, Superhelical, Eukaryotic Cells, Humans, Molecular Sequence Data, Nucleic Acid Conformation, Phosphorylation, Protein Binding, Recombination, Genetic, Substrate Specificity, Topoisomerase II Inhibitors
Show Abstract · Added March 5, 2014
Although the genetic code is defined by a linear array of nucleotides, it is the three-dimensional structure of the double helix that regulates most of its cellular functions. Over the past two decades, it has become increasingly clear that aspects of this three-dimensionality which reflect topological relationships within the double helix (i.e., superhelical twisting, knotting, or tangling) influence virtually every facet of nucleic acid physiology. In vivo, DNA topology is modulated by ubiquitous enzymes known as topoisomerases. The type II enzyme is essential to the eukaryotic cell and is required for unlinking daughter chromosomes and maintaining chromosome structure. Moreover, topoisomerase II also has been identified as the primary cellular target for several widely used antineoplastic drugs. Before the physiological functions of topoisomerase II can be effectively dissected or its drug interactions fully exploited, it is imperative to understand the mechanism by which this important enzyme carries out its catalytic cycle.
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18 MeSH Terms
Current research in side effects of high-dose chemotherapy.
Wujcik D
(1992) Semin Oncol Nurs 8: 102-12
MeSH Terms: Antineoplastic Agents, Cystitis, Gastrointestinal Diseases, Heart Diseases, Humans, Kidney Diseases, Nervous System Diseases, Oncology Nursing, Research
Show Abstract · Added March 27, 2014
The toxicities of chemotherapy continue to hamper dose escalation of specific chemotherapeutic agents. The impact of dose intensification upon survival will be assessed as clinical studies continue. Strategies to support chemotherapy dose intensification include BMT, use of CSFs and antiemetic drug combinations. Advances in symptom management will hopefully enhance quality of life for patients, whereas the development of chemoprotectant agents may allow specific organ toxicities to be avoided.
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9 MeSH Terms