Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1140680 (ovarian cancer)
28,141 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

4'-Epi-doxorubicin (4'-epi-DX) is a new doxorubicin derivative that in phase II human studies has been demonstrated to be less toxic than doxorubicin. Sixty-four patients with advanced solid tumors were treated with the drug combination of 4'-epi-DX and cis-dichlorodiammineplatinum (CDDP) at the doses of 40-60 and 50 mg/m2, respectively, every 21-28 days. Out of 52 evaluable patients, complete remission (CR) was recorded in 5, partial remission (PR) in 12, minor remission (MR) in 7, no change (NC) in 16 and progression (P) in 12. The median duration of remission in patients who achieved a CR and PR was 9+ months. In particular, out of 19 patients with ovarian cancer, 2 CR (second look) and 7 PR have been documented. One CR and 3 PR also have been observed in 21 patients with lung carcinoma. Complete and partial responses also have been documented in breast cancer (1 CR/1), in bladder carcinoma (1 CR/2), in renal cancer (1 PR/5) and in testicular cancer (1 PR/1). Hematologic toxicity was generally mild to moderate (leukopenia less than or equal to 1500 cells/mm3 in 3% of the patients; thrombocytopenia less than or equal to 120,000 cells/mm3 in 2% of the patients). Vomiting was present in almost all patients while alopecia has been recorded in 63% of the patients. No case of cardiac toxicity had been observed up to now (median cumulative dose of 4'-epi-DX:240 mg/m2, range 40-650 mg/m2). The combination of 4'-epi-DX with CDDP appears to be an active and well-tolerated regimen in ovarian cancer and lung cancer.
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PMID:A phase II study of 4'-epi-doxorubicin plus cis-platinum in advanced solid tumors. 658 74

We have explored the use of data from the Commission on Professional and Hospital Activities-Professional Activity Study ( CPHA -PAS) for ascertaining information on cancer incidence, with regional breakdowns. Extirpative surgical procedures were linked with discharge diagnoses to provide estimates of numbers of incident cases. We calculated incidence rates for four cancers: breast, colon, ovary, and testis. CPHA -PAS inferred rates corresponded closely to those of other reporting systems for breast cancer in most age groups, and for colonic and testicular cancer in some age groups. Ovarian cancer rates were consistently underestimated. We conclude that a cancer incidence reporting scheme based on hospital discharge data can work for certain cancers, and be very inexpensive and efficient. It must, however, be used with care.
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PMID:Cancer of the breast, colon, ovary, and testis in the United States: rates 1970-78 from a hospital reporting system. 672 Oct 14

The treatment of solid tumours with high-dose chemotherapy using alkylating agents either as single agents or in combination schedules has received increasing attention from clinical investigators in recent years. This has frequently been given in association with autologous bone marrow support, a technique which appears to ameliorate myelosuppression that might otherwise be dose-limiting, and which thus may allow dose escalation into a range previously not reached. Despite this ability, and in spite of much experimental evidence from drug-sensitive animal tumours that increasing doses result in increased response rates, no major impact has yet been made in the therapy of solid tumours using this form of therapy. In addition, the use of high-dose schedules has seen the emergence of extramedullary manifestations of drug toxicity which were not encountered at conventional doses. Nevertheless, there are some encouraging data from reports in certain tumours, including small cell lung cancer, testicular cancer, ovarian cancer, and lymphoma, and further studies are clearly indicated. These should probably be restricted to certain drug-sensitive tumours, and should include an examination of the role of high-dose chemotherapy as consolidation treatment, following conventional induction therapy for selected tumour types. This form of treatment may yet provide an important contribution to the control of human solid tumours, but much further work, probably with combination drug schedules, is required.
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PMID:Intensive chemotherapy for solid tumours--current clinical applications. 676 Oct 9

The effects of chemotherapy for lung metastasis in 284 cancer patients using various anti-tumor drugs, including classic ones and modern active agents for the past 18 years, were presented. Lung metastasis for lung cancer was excluded. The response was achieved in cervical carcinoma of the uterus (17/62, 27%), endometrial carcinoma of the uterus (1/7, 14%), colorectal cancer (6/39, 15%), breast cancer (5/28, 18%) and stomach cancer (4/28, 14%). A high response was achieved in myosarcoma (5/12, 42%), testicular cancer (5/11, 45%) and also in ovarian cancer (3/10, 30%). Though there were few cases, a high response was achieved in malignant melanoma (2/3), choriocarcinoma (2/4) and esophageal cancer (1/3). In total patients the response rate was 20%. In these cases a complete response was achieved in 4 cervical cancers; one testicular cancer, ovarian cancer, esophageal cancer and renal cancer, respectively. However, the effect was temporary and no longterm survivor was observed except for one case of renal cancer treated continuously with interferon (3 X 10(6) units daily) and showing complete remission after 7 months of therapy. The effect of chemotherapy for lung metastasis was compared between nodular metastasis (NM) and lymphagiosis carcinomatosa (LC). In cervical carcinoma of the uterus, the response rate in NM (39%) was higher than in LC (11%). However, no difference was observed in breast cancer (NM 15%, LC 13%) nor in stomach cancer (NM 13%, LC 18%).
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PMID:[Chemotherapy for metastatic lung cancer]. 687 21

Screening for cancer should not be offered routinely to a symptomatic people on a population basis unless it has been shown to be effective in reducing mortality in randomised controlled trials. A suitable screening test should have high sensitivity and specificity and a high positive predictive value. There is an ethical imperative to ensure that the benefit to each person from screening is likely to outweight the possible harm. Preliminary studies have identified suitable screening tests for ovarian cancer, and a randomised controlled trail is about to start. There is considerable controversy about whether to screen for prostatic cancer. Likewise, there is uncertainty about the best means of treating localised prostatic cancer. Screening for prostatic cancer raises important ethical considerations which should not be ignored. Testicular self examination is of unproved benefit. Although there is a need for education about the early signs and symptoms of testicular cancer to reduce delay at presentation, a case cannot be made for screening.
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PMID:Screening for ovarian, prostatic, and testicular cancers. 808 99

Risk of cancer mortality from 1973 to 1985 in persons born in the Indian subcontinent who migrated to England and Wales was analysed by ethnicity, and compared with cancer mortality in the England and Wales native population, using data from England and Wales death certificates. There were substantial highly significant raised risks in Indian ethnic migrants for cancers of the mouth and pharynx, gall bladder, and liver in each sex, larynx and thyroid in males, and oesophagus in females. There were also substantial raised risks in these migrants of each sex for non-Hodgkin's lymphoma and myeloma. For the mouth and pharynx, and liver in each sex, and gall bladder in females, there were also raised risks of lesser magnitude in British ethnic migrants. For colon and rectal cancer and cutaneous melanoma in each sex, ovarian cancer in women and bladder cancer in men, there were appreciable significantly reduced risks in the Indian ethnic migrants not shared by those of British ethnicity. Appreciable raised risks in British ethnic migrants not shared by those of Indian ethnicity occurred for nasopharyngeal cancer in males, soft tissue malignancy in both sexes and non-melanoma skin cancer in males. In migrants of both ethnicities there were appreciable significantly raised risks in each sex for leukaemia and decreased risks in each sex for gastric cancer, for lung cancer except in females of British ethnicity and in males for testicular cancer. The results suggest the need for public health measures to combat the high risks of oral and pharyngeal cancers and liver cancer in the Indian ethnic immigrant population of England and Wales, by prevention of betel quid chewing and hepatitis transmission respectively. The data also imply that early exposures or early acquired behaviours in India, or exposures during migration, may increase the risk of leukaemia and reduce the risks of gastric and testicular cancers in the migrants irrespective of their ethnicity. Aetiological studies would be worthwhile to investigate the reasons for the sizeable decreased risk of colon and rectal cancer and increased risk of gall bladder cancer in each sex and the increased risk of thyroid and laryngeal cancer in males and oesophageal cancer in females of Indian ethnicity but not of British ethnicity who have migrated from the Indian subcontinent.
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PMID:Cancer mortality in Indian and British ethnic immigrants from the Indian subcontinent to England and Wales. 757 89

Paclitaxel represents a novel antitumour agent with demonstrated activity in cisplatin-sensitive tumours, particularly ovarian cancer. In addition, responses to paclitaxel have been observed in patients with cisplatin-refractory ovarian cancer. The role of paclitaxel in the treatment of testicular cancer has not been explored so far. Despite the generally high cure rates in patients with metastatic testicular cancer, patients with relapsed disease not responding to platin-based salvage chemotherapy have an extremely poor prognosis. In a phase I/II trial 10 patients with relapsed, cisplatin-refractory malignant germ-cell tumours were treated with paclitaxel as 6-h infusions (8 patients) or 3-h infusions (2 patients) at doses from 135 mg/m2 to 310 mg/m2 at 3-week intervals. Three patients achieved a response to paclitaxel, but disease recurred shortly in two patients after two and four cycles of therapy, respectively. One patient has remained in marker-negative partial response for more than 5 months. The toxicity of paclitaxel was tolerable for a dose range from 135 mg/m2 to 225 mg/m2. Granulocytopenia, WHO grades 3 and 4, occurred in all patients but was of short duration (median 3 days; range: 2-7 days). Other toxicities such as mucositis (5 patients grade 1), neurotoxicity (1 patient grade 1, 2 patients grade 2), infection (1 patient grade 3) and diarrhoea (1 patient grade 2) were not dose-limiting. There were no hypersensitivity reactions, but 1 patient developed severe myalgias during therapy with paclitaxel. Six patients with documented cisplatin-refractory disease were retreated with cisplatin-based chemotherapy after paclitaxel treatment and, in 4 of these, tumour responses of 3, 4, 5 and more than 5 months duration were achieved. In order to explore the role of paclitaxel in relapsed and/or cisplatin-refractory testicular cancer a phase II study using a 3-h infusion of 225 mg/m2 paclitaxel every 3 weeks, conducted by the German Testicular Cancer Study Group, is ongoing.
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PMID:Preliminary results of a phase I/II trial of paclitaxel in patients with relapsed or cisplatin-refractory testicular cancer. 779 4

Anti-tumour monoclonal murine and humanised (reshaped human) antibodies (H17E2 and Hu2PLAP, respectively) against placental alkaline phosphatase (PLAP), radioactively labelled with indium-111 (111In) and iodine-123 (123I), were evaluated for their ability to localise mainly testicular and ovarian tumours in sequential pilot studies of the Hammersmith Oncology Group. 33 patients with active primary and/or metastatic testicular cancer were studied with the [111In]- or [123I]H17E2 antibody. 8 patients with testicular cancer were studied with the same antibody after being rendered free of disease after induction chemotherapy and surgical resection of residual tumour. 3 additional patients, 2 with ovarian cancer and 1 with testicular seminoma, were studied with [111In]H17E2 via a macrocyclic chelating agent (DOTA). 7 patients; 5 with ovarian cancer, 1 with breast cancer, and 1 with gastric cancer, received the reshaped human Hu2PLAP antibody [111In]DOTA labelled. One of these was imaged twice, with H17E2- and Hu2PLAP-DOTA-111In, respectively. In the initial 33 patients with active primary and/or metastatic testicular cancer, the presence of tumour was confirmed and correlated well with conventional radiological diagnostic methods, and in addition, the antibody scan revealed the presence of active disease in 2 patients with negative conventional imaging, but elevated serum tumour markers. In the 8 patients with complete remission (CR), imaging studies with the radiolabelled antibody did not show any localisation. The best images were obtained at 24 and 48 h after the [123I]- and [111In]H17E2, respectively. None of these patients developed human anti-mouse antibody responses (HAMA). Successful imaging with the reshaped human antibody, Hu2PLAP-DOTA-111In, was seen in 3 patients with PLAP-positive tumours (2 ovarian and 1 gastric cancer). The 3 negative patients were 1 in complete remission, 1 with PLAP-negative tumour and 1 who cleared the Hu2PLAP antibody immediately after infusion due to the presence of anti-chelating agent (anti-DOTA) antibodies from a previous H17E2-DOTA-111In scan. One patient with PLAP-negative breast carcinoma had a false-positive scan with Hu2PLAP, showing localisation to the pleural effusion. Antibody pharmacokinetics showed a mean t1/2 beta = 73.1 +/- 30.2 h (n = 5) for Hu2PLAP versus t1/2 beta = 27.2 +/- 5.9 h (n = 3) for H17E2 (P < 0.05). 2 patients receiving Hu2PLAP were excluded due to the rapid clearance of the radiolabel as a result of the presence of high HAMA and anti-chelate antibody levels, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Targeting of tumours with murine and reshaped human monoclonal antibodies against placental alkaline phosphatase: immunolocalisation, pharmacokinetics and immune response. 788 Jun 16

Cisplatin is one of the most important anticancer drugs yet developed. It proved critical in the development of curative programs for testicular cancer and in life-prolonging regimens for such diseases as small cell lung cancer, ovarian cancer, and metastatic bladder cancer. Cisplatin currently remains the recommended agent of choice for treatment of several malignancies and is a major reagent in the design of existing clinical trials. Although its analogue, carboplatin, has a constitutional and nonhematologic toxicity profile clearly superior to that of cisplatin, thrombocytopenia associated with carboplatin remains a problem, particularly since it can only be circumvented by means of cellular support, with or without growth factors. Continued laboratory investigations exploring new hypotheses concerning the pharmacodynamics of platinating agents emphasize the importance of the parent compound as well. Thus, in the short term, cisplatin will continue to be used in the therapy of certain major cancers. Ultimately, however, it will be replaced by compounds that both obviate its toxicity and increase its spectrum of activity.
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PMID:Cisplatin: the future. 799 62

In the nonprotocol, clinical arena, carboplatin is supplanting cisplatin due to its more favorable toxicity profile and lower overall cost. A review of the presentations from "The Role of Platinum Compounds in Cancer Treatment" (February 24 to 28, 1993, Kona, Hawaii) suggests that carboplatin can replace cisplatin for dose-intensification studies and treatment of ovarian cancer. Carboplatin (rather than cisplatin) is recommended for chemotherapy of palliative or noncurative intent (ie, for most solid tumors where cisplatin has activity), for the reasons mentioned above. In potentially curative settings (eg, testicular cancer) and in combination with radiation, results obtained with carboplatin are less clear and further study will be required.
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PMID:The future role of carboplatin. 799 63


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