Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49-year-old female presented with a low abdominal tumor. Before operation, she had neither evidence of androgen excess nor abnormal tumor marker values, but US, CT and MRI findings strongly suggested the possibility of a malignant ovarian tumor. Her operative findings were as follows: a goose egg-sized main tumor in the low abdomen, with a walnut-sized tumor in the right side, which grew around the right ureter, causing right non-functional kidney. Pathological examination revealed her tumor was a very rare type of malignant Sertoli-Leidig cell tumor with pelvic lymph nodes metastases. Most patients with this disease usually have good prognoses, but with metastasis or recurrence, no therapy is as effective as in epithelial ovarian cancer. In this case, we selected a new combination chemotherapy of CBDCA, Etoposide and Epirubicin, considering current changes in the chemotherapy for ovarian germ cell tumors and Sertoli-Leidig cell tumors of testis. Now, 1 year and 4 months after operation, she has no evidence of recurrence or metastasis. This study proposes a new, presumably more effective chemotherapy for an ovarian malignant Sertoli-Leidig cell tumor.
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PMID:[A case of ovarian malignant Sertoli-Leidig cell tumor treated with CBDCA, etoposide and epirubicin chemotherapy]. 757 20

Cyclophosphamide, an alkylating agent belonging to the family of nitrogen mustards, is commonly used to treat progressive autoimmune diseases in humans. At the molecular level, its cytotoxicity results from DNA double strand crosslinks and, at higher concentrations, from DNA strand breaks. At the cellular level, cyclophosphamide may selectively affect mature lymphocytes with relative sparing of the respective precursor cells. In this study, we show that 4-hydroxycyclophosphamide (4-OH-CP), the active metabolite of cyclophosphamide, induces apoptosis in mature human lymphocytes at concentrations that are achieved in vivo. Since cyclophosphamide requires enzymatic conversion in the liver to yield its active metabolite, 4-OH-CP was generated in vitro by non-enzymatic hydrolysis of mafosfamide. Apoptotic cell death of lymphocytes was characterized by typical morphological changes, nucleosomal DNA fragmentation, and quantified by 3'-OH end labeling of fragmented DNA. The percentage of apoptotic cells both depended on drug concentration and time of exposure. Cycloheximide or ZnSO4 did not suppress 4-OH-CP induced apoptosis. Etoposide, a topoisomerase II inhibitor known to induce apoptosis in human tumor cell lines like 4-OH-CP, did induce detectable DNA fragmentation in only a minor proportion of T-lymphocytes but suppressed T-cell proliferation.
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PMID:Mafosfamide induces DNA fragmentation and apoptosis in human T-lymphocytes. A possible mechanism of its immunosuppressive action. 759 14

This study was performed to evaluate the antimetastatic activity of antitumor agents against metastatic colon carcinoma 26 (Co 26Lu), and to investigate their mechanisms of action. Pirarubicin demonstrated the most striking antitumor activity in mice bearing intravenously injected Co 26Lu cells. Etoposide and mitoxantrone also showed marked antitumor activity. Pirarubicin and mitoxantrone also exerted remarkable inhibitory effect on spontaneous lung metastases from subcutaneously implanted Co 26Lu. Pirarubicin showed marked inhibition of both primary tumor growth and lung metastases. Mitoxantrone was effective in preventing lung metastases even at doses that did not exhibit an antitumor effect on the primary tumor. Moreover, mitoxantrone administered two days after intravenous injection of tumor cells obviously reduced the number of lung colonies, while simultaneous injection of the drug did not inhibit colony formation. Mitoxantrone effectively inhibited angiogenesis on the chorioallantoic membrane at doses that did not affect the growth rate of embryos. These results suggest that mitoxantrone, besides its direct antitumor effect on tumor cells, may inhibit lung metastases by inhibiting angiogenesis.
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PMID:Characteristics of the inhibitory effect of mitoxantrone and pirarubicin on lung metastases of colon carcinoma 26. 759 65

The case of a patient with a uterine leiomyosarcoma (LMS) that rapidly recurred in the pelvis following primary surgery is reported. The tumor was refractory to conventional multiagent chemotherapy that included intravenously administered etoposide (VP-16). Etoposide was then administered orally in a prolonged schedule; this resulted in a sustained partial response with palliation of symptoms. Thus, prolonged oral administration of etoposide may have antitumor activity against LMS despite that tumor's resistance to short-term infusion schedules of etoposide.
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PMID:Prolonged oral etoposide for refractory advanced uterine leiomyosarcoma. 762 13

Granulocyte-Colony Stimulating Factor (G-CSF) was administered to patients with bladder cancer, ureteral cancer and testicular cancer following chemotherapy. Chemotherapy included 23 courses of M-VAC (Methotrexate, Vinblastine, Adriamycin, Cisplatin) therapy to patients with bladder cancer or ureteral cancer and 10 courses of EP (Etoposide, Cisplatin) therapy to patients with testicular cancer. During M-VAC chemotherapy, about a half of the patients experienced leukopenia below 3000/mm3 until the 11th day. Leukopenia failed to improve promptly when G-CSF was started after leukocytes decreased below 3000/mm3. On the other hand, 5-days of prophylactic administrations of G-CSF from the 9th day of M-VAC therapy were able to increase leukocytes promptly. In EP chemotherapy against testicular tumor, G-CSF was started on the 9th day and continued for 5 days. Leukocytes increased immediately and the average duration of leukopenia below 3000/mm3 was only 1.2 day. These results indicate that a short term of prophylactic administration of G-CSF following these chemotherapies is able to accelerate a recovery from leukopenia and decrease a risk of bacterial infection. G-CSF is proposed to be enrolled in the treatment of urological cancer for the improvement of safety and the outcome of therapy.
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PMID:[Optimal way of administration of granulocyte colony stimulating factor in the treatment of urological cancer]. 768 99

Germ cell tumors of the central nervous system are histological identical to the extracranial tumor sites. According to the localisation germ cell tumors of the CNS are different in symptoms, diagnostic approaches, kind and location of metastases and stratification of therapy. Since 1986 patients with intracranial germ cell tumors are registered in the ongoing study for non-testicular germ cell tumors (MAKEI) of the German Society of Pediatric Oncology and Hematology, and are treated in accordance to therapy guidelines for extracranial sites. In MAKEI 89 therapy strategy was revised with a reduction of radiotherapy and an increased cumulative cisplatinum dose from 200 mg/m2 to 400 mg/m2. Patients with germinoma receive after histologic diagnosis radiotherapy consisting of 30 Gy craniospinal irradiation and 15 Gy tumorboost. Malignant non-germinoma receive after diagnosis by tumor marker in CSF and/or serum 2 courses bleomycin 15 mg/m2 day 1-3, Etoposide 150 mg/m2 day 1 + 2 and cisplatinum 20 mg/m2 days 4-8 (BEP), continued by 2 courses Vinblastine 3 mg/m2 day 1 + 2, Ifosfamide 1500 mg/m2 days 1-5 and cisplatinum 20 mg/m2 days 1-5 (VIP), followed by 30 Gy craniospinal irradiation and 20 Gy tumor boost. In teratoma first line therapy is complete resection. In incomplete resected cases adjuvant chemotherapy according to histological grading is administered. Until 31st January, 1993 101 patients (pts) were registered, containing 69 protocol pts. Diagnosis in protocol pts was teratoma in 8 cases, 2 pts died postnatal because of extended disease, 2/8 pts relapsed, but were salvaged by chemotherapy. 40 pts offered germinomas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Improved prognosis of intracranial germ cell tumors by intensified therapy: results of the MAKEI 89 therapy protocol]. 769 Aug 63

A 37-year-old man, who had been treated with inguinal orchiectomy and radiotherapy of retroperitoneal and iliac lymph node for r-testicular tumor 6 months earlier, was admitted with a complaint of left leg pain in May 1992. CT scan of pelvic bone revealed osteolytic change of left pubic bone with soft tissue mass. Bone scintigram showed significant uptake of radioisotope on left pubic bone. Biopsy of left pubic bone confirmed histologic findings compatible with that of previous testicular cancer. He was treated with PEB chemotherapy (CDDP, Etoposide and Bleomycin) and radiation therapy. After treatment, the majority of the tumor mass disappeared on CT scan. On repeat biopsy specimens, significant fibrotic change was observed and no cancer cells were recognized. He is alive with no evidence of disease.
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PMID:[A case of complete response with radiation and chemotherapy using cisplatin, etoposide and bleomycin]. 769 Oct 42

Antifolates have been shown to increase the DNA strand breaks produced by the topoisomerase inhibitor etoposide. PT523 is a potent new antifolate that cannot be polyglutamated. Human SCC-25 squamous carcinoma cells were exposed to methotrexate, trimetrexate or PT523 at a concentration of 5 microM for 24 h along with various concentrations of etoposide or novobiocin during the final 2 h. Isobologram analysis of the treatment combinations indicated that exposure of the cells to PT523/etoposide, methotrexate/etoposide, PT523/novobiocin, methotrexate/novobiocin and trimetrexate/novobiocin resulted in greater than additive cytotoxicity. DNA alkaline elution studies with the same drug combinations indicated that there were three- to four-fold increases in the radiation equivalent (rad equivalent) strand breaks in the cellular DNA with etoposide or novobiocin along with the antifolate compared with the topoisomerase II inhibitors alone. Tumor growth delay studies were carried out in the murine SCC VII squamous carcinoma. PT523 (0.5 mg/kg) and methotrexate (2 mg/kg) were administered by 7-day continuous infusion while trimetrexate (3.75 mg/kg) was administered intraperitoneally daily on days 7-9. Etoposide (10 mg/kg) and novobiocin (100 mg/kg) were administered intraperitoneally on alternate days (7, 9, 11). The combinations of PT523 with etoposide or novobiocin were significantly more effective than methotrexate and etoposide or novobiocin, producing tumor growth delays of 8.4 days and 6.9 days, respectively. Overall, the antifolate/topoisomerase II inhibitor treatment combinations produced tumor growth delays that were apparently additive to greater than additive.
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PMID:Antifolates can potentiate topoisomerase II inhibitors in vitro and in vivo. 776 54

A 48-year-old man was admitted to our hospital because of upper abdominal pain, and a cervical tumor, on Oct. 23, 1992. Chest X-ray, CT scan and MRI revealed a tumor (left-S10) and enlarged mediastinal lymph nodes. A pathological diagnosis of small cell lung cancer was made by transbronchial biopsy. Ultrasonography showed liver metastases. He received four courses of chemotherapy (Carboplatin, Ifosfamide, Etoposide). Three days after the completion of chemotherapy, his serum transaminase level was markedly increased, and he was disorientated on March 4, 1993. In spite of plasma exchange, the patient died due to hepatic failure on March 6, 1993. Fulminant hepatitis in a patient with lung cancer receiving chemotherapy is rarely reported.
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PMID:[A case of small cell lung cancer associated with fulminant hepatitis B]. 779 62

A new cell line (BRC-230) was established from surgical material of primary ductal infiltrating breast carcinoma. The epithelial nature of this cell line was confirmed by ultrastructural analysis and demonstrated the retention of structural properties characteristic of the original tumor. The BRC-230 cell line induced tumor in athymic Cr1:nu/nu(CD-1)BR nude mice, it possessed an abnormal karyotype with a modal chromosome number between 60-61 with eight recurrent marker chromosomes, and it presented a doubling time of 30.5 hr. Scatchard analysis demonstrated that both primary tumor and BRC-230 cells were estrogen and progesterone receptor negative. Immunoenzymatic and radioimmunoassays showed a production of marker antigens (CEA, TPA, CA125, CA15-3, CA19-9) which was similar in the patient's serum and BRC-230 cells. The in vitro drug sensitivity assay of the cell line and of the parental tumor tissue showed overlapping results to all tested antiblastic drugs. BRC-230 cells were resistant to 4-Idroperoxy-cyclophosphamide, Idarubicinol, Mitoxantrone, Etoposide, 4'Epidoxorubicin, and Doxorubicin, showing a multiple drug resistance phenotype. Amplification or rearrangement of Her-2neu, Ha-ras, and C-myc genes was observed neither in the original tumor nor in BRC-230 cells; the mdr-1 gene was also present in a single copy. We conclude from these studies that the BRC-230 cell line maintains the same characteristics as the original tumor and may provide us with a good model to study in vitro the biology of drug resistance of breast cancer.
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PMID:Establishment and characterization of a new cell line from primary human breast carcinoma. 801 54


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