Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this pilot study was to estimate the toxicity and response rate of an alternating chemotherapeutic program in chemotherapy-naive metastatic breast cancer patients. Treatment consisted of regimen A (given days 1-28): cyclophosphamide 100 mg/m2 PO days 1-14, doxorubicin 30 mg/m2 i.v. days 1 and 8, and 5-fluorouracil 500 mg/m2 i.v. days 1 and 8 (CAF regimen); regimen B (given days 29-56): dibromodulcitol 135 mg/m2 p.o. days 30-39, mitoxantrone 9 mg/m2 i.v. day 29, and vincristine 1.2 mg/m2 i.v. (maximum 2.0 mg) day 29 (DMV regimen); and regimen C (given days 57-84): thiotepa 12 mg/m2, doxorubicin 45 mg/m2 and vinblastine 4.5 mg/m2 all i.v. on day 57. There were 27 eligible patients with a median age of 51 years (range 34-78). On 14 episodes the leukocyte count fell to less than 1 X 10(9)/L during the first six cycles of treatment (14% of 99 cycles). There were no treatment-related deaths. Common non-life-threatening toxicities included thrombocytopenia, anemia, vomiting, and alopecia. Despite having no drugs in common, the leukocyte and platelet nadirs after CAF correlated with the nadir counts after DMV (r values of 0.6829 and 0.5892, respectively; p = 0.01). Among the 23 patients with measurable and/or evaluable disease there were five complete responses (22%) and nine partial responses (39%), with a median time to treatment failure of 29 weeks. The overall median survival was 19 months.
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PMID:A pilot study of three sequential chemotherapeutic regimens in metastatic breast cancer. 189 99

Due to the favourable results previously obtained with cisplatin in breast cancer (54% response rate), we studied a second-generation platinum analogue, carboplatin, in patients with previously untreated breast cancer. A total of 20 patients were entered in the study and all were evaluable. The median age was 57 years and all patients were in menopause. Karnofsky scores of 80-100 and 40-70 were registered in 14 and 6 cases, respectively. The predominant metastatic site was soft tissue in 12 subjects, visceral organs in 5 and bone in 3; 14 patients had greater than 2 metastatic sites. Carboplatin was given i.v. at a dose of 400 mg/m2 on day 1, with a 3-week rest period. In 13 patients who did not respond or whose disease recurred after carboplatin treatment, the CMFVP, CAP or FAC regimen was given as second line treatment. Carboplatin activity was observed in 4 patients [2 complete remissions (CRs) and 2 partial responses (PRs)], for a response rate of 20% (4/20); the 2 PRs were observed in soft tissue and bone and the 2 CRs, in lung, liver and bone. Remission lasted 2-10 months (mean, 4 months). CMFVP given as second-line chemotherapy to 13 patients produced 7 PRs (7/13, 54%). Toxicity was moderate, producing no drug-related deaths. Anemia (grade I-II) was recorded in seven patients; grade I-II leukopenia, in six; and grade III-IV leukopenia in two (median leukocyte nadir, 1,600/mm3). Thrombocytopenia was observed in three cases (grades I, II and III; median platelet nadir, 47,800/mm3). Unpleasant nausea/vomiting was pronounced (12 cases of grade III-IV) in 19 subjects. There were no cases of neuro- or nephrotoxicity. Due to permanent myelosuppression, no more than five cycles could be given. Our study showed that, unlike cisplatin, carboplatin given at a dose of 400 mg/m2 has low antitumorigenic activity in breast cancer patients and produces pronounced myelotoxicity. Additional first-line chemotherapy studies using carboplatin are needed to define the antitumorigenic activity of this platinum analogue.
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PMID:Carboplatin activity in untreated metastatic breast cancer patients--results of a phase II study. 199 4

Twelve patients with advanced or relapsed head and neck adenocarcinoma received a combination chemotherapy regimen of either cyclophosphamide (C), tetrahydropyranyl-adriamycin (T), and cis-platinum (P) (CTP) or cyclophosphamide, adriamycin (A), and cis-platinum (CAP). Cyclophosphamide (300 mg/sq m), either etrahydropyranyl-adriamycin (30 mg/sq m) or adriamycin (30 mg/sq m), and cis-platinum (50 mg/sq m) were administered intravenously in a single day. Nine patients received the CTP regimen, and three patients, the CAP regimen. Prior to chemotherapy, five patients had received surgery or radiation therapy, and the other seven patients received no special treatment. A response rate 75% was achieved (9/12); there were 7 complete responses, whose duration was a mean 6.8 months, ranging from 2 to 18 months, and 2 partial responses, whose duration was 2 months. Virtually all patients experienced nausea and vomiting. Alopecia developed in 7 patients; however, the patients with the CTP regimen experienced less alopecia, if any. Leucopenia and anemia of either a slight or moderate degree were observed, but there was no patient for whom it was necessary to discontinue the treatment. Both CTP and CAP regimens appear to be of significant value in controlling head and neck adenocarcinoma.
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PMID:Cyclophosphamide, tetrahydropyranyl-adriamycin, and cis-platinum in the treatment of head and neck adenocarcinoma. 260 11

A non-randomized clinical study on systemic combination chemotherapy was conducted by the Japanese Urological Cancer Research Group for Adriamycin to compare the effectiveness of CAP (cyclophosphamide 200-500 mg/m2, adriamycin 30-50 mg/m2 and cisplatin 30-50 mg/m2) and CAF (cyclophosphamide 200-500 mg/m2, adriamycin 30-50 mg/m2 and 5-fluorouracil 250 mg/m2) in 123 patients (104 evaluable) with advanced and/or metastatic cancer of the urinary bladder. Among 96 patients who were non-randomly selected to receive CAP, 4 achieved complete remission, 12 achieved partial remission, 7 achieved minor response, 30 had stable disease, and 43 had disease progression. The response in the 8 patients who received CAF were: partial remission in 1 and progressive disease in 7. The overall response rate to CAP therapy was 17%, as against 13% for CAF therapy. The median duration of survival with CAP was 29 weeks and with CAF, 22 weeks. The differences between the two groups in duration of survival and response rate were not statistically significant. Complete and/or partial remissions were observed in the lymph nodes, lung and liver in 32%, 24%, and 57% of cases, respectively. There was no objective response in bone metastasis. The main side effects of CAP were anorexia (88%), nausea and/or vomiting (81%), alopecia (65%), leukopenia (72%), anemia (48%), and renal dysfunction (17%). No patients died as a result of toxicity of these combination chemotherapy modalities.
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PMID:Phase III trial of the Japanese Urological Cancer Research Group for Adriamycin: cyclophosphamide, adriamycin and cisplatinum versus cyclophosphamide, adriamycin and 5-fluorouracil in patients with advanced transitional cell carcinoma of the urinary bladder. 331 45

Fludarabine is an antineoplastic agent which has been studied in patients with a variety of lymphoproliferative malignancies. Clinical evidence from comparative studies in chronic lymphocytic leukaemia (CLL) suggests that fludarabine is at least as effective as CAP (cyclophosphamide, doxorubicin and prednisone) or CHOP (cyclophosphamide, vincristine, doxorubicin and prednisone) in previously treated or chemotherapy-naive patients and significantly more effective than chlorambucil in terms of response rate and duration and survival in chemotherapy-naive patients. Promising results have also been reported with fludarabine-based combination therapy in the treatment of patients with CLL. In addition, sequential therapy with fludarabine and cytarabine has demonstrated good efficacy in the treatment of acute leukaemias, as has fludarabine monotherapy and combination therapy in low grade non-Hodgkin's lymphoma. A favourable cytoreductive response has been reported in patients with lymphoplasmacytoid lymphoma and in a smaller number of patients with cutaneous T cell lymphomas, CLL of T cell origin or prolymphocytic leukaemia. Recent data also support the use of fludarabine, either as a component of a nonmyeloablative conditioning regimen or in the attainment of minimal residual disease, in patients undergoing peripheral blood stem cell or bone marrow transplantation. The tolerability profile of fludarabine is similar to that of CAP, with the most common adverse events being granulocytopenia, thrombocytopenia, anaemia and infection. Alopecia and nausea/vomiting appear to be less frequent with fludarabine therapy than with CAP although the development of immune cytopenias is more frequent with fludarabine. Severe neurotoxicity has been reported with fludarabine but this is mostly confined to the use of high doses. Clinical experience therefore indicates that fludarabine is an effective and generally well-tolerated antineoplastic agent for the second-line treatment of advanced CLL. Recent data from comparative studies also support the earlier use of fludarabine in the treatment of chemotherapy-naive patients with CLL. Furthermore, results of available studies are increasingly highlighting an important future role for fludarabine in the treatment of acute leukaemias and low grade NHL and possibly other lymphoproliferative disorders, particularly when used as a component of combination chemotherapy.
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PMID:Fludarabine. An update of its pharmacology and use in the treatment of haematological malignancies. 917 29

The purpose of this phase II study was to evaluate the clinical efficacy of mitomycin C and vinblastine in patients with anthracycline-resistant metastatic breast cancer. This single-center, non-randomized trial enrolled 39 patients. Eligible patients must have received at least three chemotherapy regimens with epirubicin or CAF and had treatment failure while on chemotherapy or within 6 months of completing therapy. Treatment consisted of mitomycin C at a starting dose of 8 mg/m2 on day 1 and vinblastine (8 mg/m2, days 1 and 28). The regimen was repeated every 6 weeks with a 20% dose escalation of both drugs after the first cycle in the absence of grade III hematologic or other toxicity. On an intent-to-treat basis, 38 patients were eligible for assessment; 9 (23.7%, 95% confidence interval 1.92-2.45%) achieved a partial response and 13 (34.2%) had stable disease. The median time to disease progression was 6.21+/-4.26 months (range, 1-15; 95% confidence interval, 4.81-7.61), and the median survival was 10.76+/-7.6 (range, 1-29; 95% confidence interval 8.0-13.1%). Responsive patients had a significantly better survival than those with stable and progressive disease. Treatment was well tolerated. Anemia and neutropenia (grade I-III) developed in 28.9% and 26.3% of the patients, respectively. One patient with grade III granulocytopenia developed fever and infection that required hospitalization. Moderate neurotoxicity, myalgia, constipation, diarrhea and alopecia were observed. No toxic death occurred. Mitomycin C plus vinblastine is an effective and well-tolerated regimen for anthracycline resistant cancer.
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PMID:Mitomycin C and vinblastine in anthracycline-resistant metastatic breast cancer: a phase II study. 1198 93

The therapeutic efficacy and adverse reactions were compared between 14 patients who received TJ therapy using paclitaxel (PTX) and carboplatin (CBDCA) and 39 who received CAP therapy using cyclophosphamide (CPA), doxorubicin (DXR) and cisplatin (CDDP) as postoperative chemotherapy for cancer of the uterine body. In TJ therapy, PTX (175 mg/m(2)) and CBDCA (AUC 5) were administered on Day 1 (every 3 weeks), while in CAP therapy, CPA (500 mg/m(2)), DXR (40 mg/m(2)) and CDDP (50 mg/m(2)) were administered on Day 1 (every 4 weeks). Grade 3 or more severe hematotoxicity included leukocytopenia (incidence in the TJ and CAP groups: 71.4% and 64.1%, respectively), neutropenia (100%, 87.1%), thrombocytopenia (0%, 12.8%), and anemia (0%, 20.5%). No significant differences were noted between the two groups. Grade 3 or severe non-hematologic toxicities included nausea (0%, 15.4%) and vomiting (0%, 12.8%) with significantly higher incidence in the CAP therapy group (p=0.0000736, p=0.000736), peripheral sensory disturbance (7.1%, 0%) and arthralgia (7.1%, 0%) with significantly higher incidence in the TJ therapy group (p=0.00129, p=0.00000538). The survival rate and disease-free survival rate showed no significant differences between the two groups. TJ therapy is thought to be as effective as CAP therapy, and can be safely conducted, although precautions are required regarding arthralgia and neuropathy.
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PMID:[Adjuvant chemotherapy of paclitaxel plus carboplatin in uterine corpus cancer--comparison with cisplatin, adriamycin plus cyclophosphamide]. 1683 85

ICON3 trial results have suggested that CAP and carboplatin-taxol regimens as first-line treatment of advanced ovarian cancer (AOC) yield similar survival. We explored the impact of increased dose of cyclophosphamide in a modified CAP regimen on the disease-free survival (DFS) and overall survival (OS) of AOC patients. From February 1994 to June 1997, 164 patients were randomised to receive six cycles every 3 weeks of either standard CEP (S) combining cyclophosphamide (C), 500 mg m(-2), epirubicin (E) 50 mg m(-2), and cisplatin (P) 75 mg m(-2) or intensive CEP (I) with E and P at the same doses, but with (C) 1800 mg m(-2) and filgrastim 5 mug kg(-1) per day x 10 days. Response was evaluated at second-look surgery. Patient characteristics were well balanced. Except for grade 3-4 neutropaenia (S: 54%, I: 38% of cycles), Arm1 presented a significantly more important toxicity: infection requiring antibiotics, grade 3-4 thrombocytopaenia, anaemia, nausea-vomiting, diarrhoea, mucositis. Median follow-up was 84 months. DFS (15.9 vs 14.8 months) and OS (33 vs 30 months) were not significantly different between S and I (P>0.05). Increasing cyclophosphamide dose by more than 3 times with filgrastim support in the modified CAP regimen CEP induces more toxicity but not better efficacy in AOC.
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PMID:Intensified dose of cyclophosphamide with G-CSF support versus standard dose combined with platinum in first-line treatment of advanced ovarian cancer a randomised study from the GINECO group. 1792 67

Ovary cancer treatment often presents clinical promlems due to frequent occurence of late diagnostics (III-IV stages), severe treatment complications in patients with ascitis and tumor intoxication. Reamberin can be used as supportive therapy aimed at decrease of intoxication, which is one of the main hindrances for antitumor therapy. In the current study reamberin was used in 89 stage III-IV (FIGO) ovary cancer patients with ascitis, age 42 to 79, CP or CAP chemotherapy recipients after prior cytoreductive surgery. The occurrence of hematological complications (grade 1-2 anemia and neutropenia) and cardiac dysfunctions in the study group was much lower, than in the control group. This difference is statistically valid (p < 0.01 and p < 0.05). The patients receiving reamberin prior to chemotherapy or during chemotherapy rarely (in 3.7% of cases) displayed raised creatinine values. In the control group grade 1-3 renal impairment was observed in 41.4% cases, in 12 cases the therapy had to be ceased. This difference between the groups is statistically valid (p < 0.001). Patients receiving reamberin displayed more rapid rate of CA-125 tumor marker serum concentration decrease. Therefore, reamberin is an effective drug for prevention of chemotherapy side effects and alleviation of intoxication allowing the more rigid chemotherapy schedule without an increase in toxicity.
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PMID:[Use of Reamberin for the prevention of adverse effects of combined antineoplastic agents in stage III-IV ovarian cancer during induction treatment]. 2262 39

Paroxysmal nocturnal hemoglobinuria (PNH) is a hematological disorder characterized by complement-mediated hemolytic anemia, thrombophilia, and bone marrow failure. PNH is due to a somatic, acquired mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene, which impairs the membrane expression on affected blood cells of a number of proteins, including the complement regulators CD55 and CD59. The most evident clinical manifestations of PNH arise from dysregulated complement activation on blood cells; in fact, the hallmark of PNH is chronic, complement-mediated, intravascular hemolysis, which results in anemia, hemoglobinuria, fatigue, and other hemolysis-related disabling symptoms. In addition, the peculiar thromboembolic risk typical of PNH patients is thought as secondary to the complement-mediated hemolysis itself and/or to a complement-mediated activation of platelets. Thus, as a complement-mediated disease, PNH was an appropriate medical condition to develop and to investigate therapeutical complement inhibitors. Indeed, the first complement inhibitor eculizumab, a humanized anti-C5 monoclonal antibody, has been proven safe and effective for the treatment of PNH patients. Chronic treatment with eculizumab results in sustained control of intravascular hemolysis, leading to hemoglobin stabilization and transfusion independence in more than half of the patients. However, recent observations have demonstrated that residual anemia may persist in some patients regardless of sustained fluid-phase terminal complement inhibition. Indeed, persistent dysregulated activation of the early phases of the complement cascade on PNH erythrocytes may lead to progressive C3 deposition on affected cells, which become susceptible to subsequent extravascular hemolysis through the reticuloendothelial system. These findings have renewed the interest for the development of novel complement inhibitors which aim to modulate early phases of complement activation, more specifically at the level of C3 activation. As proof of principle of this concept, an anti-C3 monoclonal antibody has been proven effective in vitro to prevent hemolysis of PNH erythrocytes. More intriguingly, a human fusion protein consisting of the iC3b/ C3d-binding region of complement receptor 2 and of the inhibitory domain of the CAP regulator factor H has been recently shown effective in inhibiting, in vitro, both intravascular hemolysis of and surface C3-deposition on PNH erythrocytes, and is now under investigation in phase 1 clinical trials.
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PMID:Paroxysmal nocturnal hemoglobinuria and the complement system: recent insights and novel anticomplement strategies. 2340 25


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