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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lethally irradiated mice pretreated with a wide range of Adriamycin (ADM) doses were tested for their in vivo antitumor response against transplanted lymphoma cells. Tumor growth, as assessed by 125IUdR uptake, was markedly impaired by treatment with ADM by a variety of different administration schedules. This ADM-induced antitumor response was largely dose-dependent, occurred regardless of route of administration, and was detectable as late as 15-30 days following drug treatment. No genetic restriction could be found to regulate the development of this response, since tumor growth inhibition occurred in syngeneic as well as allogeneic tumor-host combinations. ADM-induced antitumor response did not appear to be due to direct antitumor action by the drug, but rather to some interaction with host immune mechanisms. Antimacrophage agents, such as silica or carrageenan, abrogated the response. The possible implication of different cells as effectors of this response is discussed.
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PMID:Adriamycin-induced antitumor response in lethally irradiated mice. 23 85

The Nb rat prostatic adenocarcinoma is a well-characterized, hormonally induced family of tumors that are all readily transplantable into congenitally athymic (nude) mice. Because of this versatile heterotransplantation model, multiple replicate copies of individual tumors can be studied "in rodent." We have extended this by studying the chemotherapeutic response of such tumors and believe that this provides a useful avenue for evaluation of cytotoxic agents. Indeed, this combination of both animal model systems may provide a useful experimental tool to evaluate tumor growth, histopathologic changes and responsiveness to appropriate therapy. We report herein that two Nb rat prostatic carcinomas (2 Pr-129-D-11A and Pr-90) and thie responsiveness to Adriamycin and 5-fluorouracil are objective by studying both growth rates and tumor histology.
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PMID:The effect of 5-fluorouracil and adriamycin on heterotransplantation of Noble rat prostatic tumors in congenitally athymic (nude) mice. 47 60

The effect of methylprednisolone (MP) on the cell kinetic response to cyclophosphamide (CP) and Adriamycin (ADR) in C3H/HeJ spontaneous mammary tumors and hematopoietic tissue was investigated. The [3H]deoxythymidine labelingg index, the primer-dependent DNA polymerase labeling index (an estimate of tumor growth fraction), and the mitotic index were determined at various intervals after treatment. Treatment consisted of CP (200 mg/kg) on Day 0 plus ADR (2 mg/kg) on Day 1 with or without MP every 12 hr for 9 doses beginning on Day 2. In tumors treated with CP and ADR alone, changes in the kinetic parameters suggested proliferative recovery between Days 3 and 4 which coincided with bone marrow recovery. In tumors treated with CP, ADR, and MP, although the timing of the hematopoietic recovery was not affected by MP, the overshoot of the [3H]deoxythymidine labelin index on Days 3 and 4 was abolished. Proliferative recovery in the tumor was delayed until after cessation of MP treatments. Cell kinetic changes in the tumor after CP, ADR, and MP were used to design effective sequential chemotherapy which obviated the hematopoietic toxicity associated with sequential therapy designed from cell kinetic changes after CP and ADR alone.
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PMID:Effect of methylprednisolone on the cell kinetic response of C3H/HeJ mammary tumors to cyclophosphamide and adriamycin. 47 17

A treatment concept for the control of tumor growth utilized weekday radiotherapy and weekend chemotherapy. Mice were given sc injections of P815X2 mastocytoma cells on the lower back (day 0) and separated into the following treatment groups: 5-day/week X-irradiation, adriamycin alone at either 5 mg/kg body wt (days 6 and 13) or 2 mg/kg (days 5, 12, and 19), and combined radiotherapy and chemotherapy. Untreated controls had a mean tumor volume of 2.77 cm-3 and a mean survival time of 24 days. Adriamycin alone at 5 mg/kg resulted in an eventual tumor of 70 percent of the control value at death, whereas at 2mg/kg the tumor volume was 60 percent of control. After radiotherapy only, tumor size was 52 percent of control. Irradiation plus either 5 or 2 mg drug per kg body wt resulted in tumor volumes of 23 and 30 percent, respectively, of control values. Although no treatment regimen prolonged survival, the marked reduction in local tumor growth with combination therapy indicates that it may be a useful concept in future cancer therapy.
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PMID:Control of local tumor growth with combined fractionated radiotherapeutic and chemotherapeutic regimens. 80 53

The transplantable C1300 murine neuroblastoma has been characterized biochemically and an in vivo model for the screening of new therapeutic approaches to the treatment of neuroblastoma developed. Subcutaneous inoculation of A/J mice with 10)6) C1300 cells results in predictable tumor growth and animal death in 25 +/- 4 days. Tumor growth is Gompertzian, correlates with increases in tumor RNA and DNA content and with the rate of tumor DNA synthesis as measured by [3H] thymidine incorporation. The model proposed is based on the degree to which various therapeutic options are able to inhibit tumor DNA synthesis, and these observations have been confirmed autoradiographically. A single course of either cyclophosphamide (25, 50, 100 or 200 mg/kg), BCNU (2, 7.5, 15, or 30 mg/kg) or cytosine arabinoside (15, 30, 60, 90 mg/kg) resulted in dose-related inhibition of tumor DNA synthesis. The maximum decline in DNA synthesis that was produced by the highest dose of each agent was by 81%, 77% and 68% of untreated tumor values respectively. Adriamycin, however, even at lethal levels (10 mg/kg), did not elicit significant inhibition of tumor DNA synthesis. Radiotherapy (200 R, 500 R or 1000 R) also produced graded inhibition of tumor DNA synthesis. This model is potentially useful for the preclinical screening of therapuetic options in the treatment of neuroblastoma. Thus, single agent therapy, combination chemotherapy and combined radiotherapy and chemotherapy may be rapidly evaluated for possible clinical use.
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PMID:Pharmacokinetic studies in the chemotherapy of neuroblastoma using the C1300 murine system. 101 81

HeLa cells were heterotransplanted to nude mice and their response to some of antitumor agents was investigated. HeLa cell-tumor readily grew in nude mice and no regression was observed. Metastases to the lung and other organs were noticed in some of the animals. Histopathological examination revealed that the tumor retained the original characteristics of human epidermoid carcinoma. Standardization of HeLa cell-tumor in nude mice for the screening and evaluation of antitumor chemotherapeutics was attempted. Marked inhibition of tumor growth was observed with lower doses of Mitomycin-C, 5-fluorouracil, Adriamycin, and Bleomycin. The tumor regression was observed with high doses of Mitomycin-C, Adriamycin, and 5-fluorouracil. However, cyclophosphamide, cytosine arabinoside, and daunorubicin had little effect on the tumor growth. Complete regression was not obtained with any of the test agents and active regrowth took place even with the most effective compound. Considerable variation in the effect on tumor growth was observed among the test compounds, while histopathological findings were much alike; few mitotic figures, vacuolization, and pyknosis were main changes in tumor cells, and large foci of necrosis and hemorrhage were present in the degenerative areas. The regrowth was initiated around the capillaries in the necrotic tumor tissue.
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PMID:HeLa cell-tumor in nude mice and its response to antitumor agents. 103 Jun 74

Single and combination chemotherapy was evaluated for antitumor activity against N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT)-induced bladder carcinoma in syngeneic mice. Two hundred fifty C3H/He mice having ingested FANFT for 10 months were randomly divided into groups of 30, and the following regimens initiated: cyclophosphamide (Cy), cis-diam-minedichloroplatinum (cis-Pt-II), dactinomycin, adriamycin, Cy plus cis-Pt-II, Cy plus 5-fluorouracil, and Cy plus adriamycin. The drugs were administered for 3 weeks. Each regimen was capable of producing a significant reduction in the mean bladder weight (MBW) when compared to a groups not receiving therapy (108.3 mg). Adriamycin (MBW equal 69.5), dactinomycin (49.6), and cyclophosphamide (42.9) were the best single agents, but the greatest inhibition of tumor growth was achieved by the combination of cyclophosphamide with 5-fluorouracil (38.3) or adriamycin (37.3). These combination chemotherapeutic regimens were able to effect a significant reduction in the number of bladders with Stage C tumors. It is hoped that information gained from this new animal model which allows evaluation of many antitumor drugs within a relatively short period of time will lead to therapeutic trials in patients with locally advanced or metastatic bladder cancer.
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PMID:Single and combination chemotherapy for primary murine bladder cancer. 115 4

Adriamycin (ADM), an anthracycline cytotoxic agent, was conjugated with monoclonal antibody 3H11 against gastric cancer via the dextran bridge method. The conjugate 3H11-DEX-ADM, with molar ratio of 3H11 to ADM being 1:73, retained antibody activity to 86%. In the cytotoxicity assay, 3H11-DEX-ADM was shown to exhibit increased cytotoxicity against the target cell line BGC 823. Its IC50 was 3.75 fold less than that of free ADM. The antitumor effect of the conjugate was evaluated in tumor-bearing nude mice. The results indicate that the specific antibody conjugate 3H11-DEX-ADM can significantly inhibit the tumor growth. At the dosage level used in the present study (5 micrograms/mouse x 6), 3H11-DEX-ADM showed an inhibition rate of 51.5%, whereas only moderate inhibition rates were observed with free ADM and the control conjugate NIgG-DEX-ADM. In addition, experiment was performed to evaluate the combined cytotoxicity of 3H11-DEX-ADM and the conjugate of mitomycin C (3H11-HSA-MMC) at different ratios. It was shown that the combination has no synergistic effect when their IC50 was compared with that of the two conjugates used alone. The same result was observed on combinations of the two corresponding free drugs.
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PMID:[The antitumor effect of adriamycin conjugated with monoclonal antibody against gastric cancer in vitro and in vivo]. 144 51

Treosulfan (L-threitol-1,4-bismethanesulfonate, Ovastat) is a bifunctional alkylating agent that shows a formal structural similarity to busulfan and is applied clinically to patients suffering from ovarian cancer. The present study demonstrated the pronounced antitumor activity of this drug against three of five human breast carcinomas xenografted to athymic mice. It was shown that treosulfan is capable of inducing irreversible and complete remission of the heterotransplanted human breast carcinomas MDA-MB-436 and MX-1 within 14 days after drug application and of effecting growth inhibition by more than 90% in the MDA-MB-435S xenograft. In all three carcinomas, treosulfan caused more pronounced growth reduction than did equitoxic doses of the alkylator cyclophosphamide. Adriamycin, an intercalating cytostatic agent that is an important component of clinical nonhormonal chemotherapy of breast carcinomas, induced only partial remission of these three xenografts and inhibited the tumor growth by 80%-90% (MDA-MB-436, MX-1) and by 70%-80% (MDA-MB-435S), respectively. In the M 3 xenograft, treosulfan just led to a retardation and stagnation of tumor growth; it was again more effective than Adriamycin but was clearly less active than cyclophosphamide. The FM 2 breast carcinoma, finally, was the only xenograft whose growth was not influenced by treosulfan at doses up to that which was lethal to 50% of the treated mice (LD50 value). These results confirm that treosulfan is effective against human breast carcinomas. Because of this activity as well as the known low toxicity and good clinical compatibility of treosulfan, it should be considered for introduction into nonendocrine chemotherapeutic regimens against human breast carcinomas and investigation in clinical trials.
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PMID:Antitumor activity of treosulfan against human breast carcinomas. 145 Dec 31

In the present study the potential of minocycline, a semisynthetic tetracycline that inhibits collagenase activity in vivo, as an adjuvant to standard anticancer therapies was explored in vitro and in vivo. In EMT-6 cells, minocycline proved to be only minimally cytotoxic, producing a 50% cell kill at concentrations of 132 and 220 microM in normally oxygenated and hypoxic cells, respectively, after 24 h exposure to the drug. In vitro, there appeared to be no interaction between minocycline and cisplatin (CDDP), melphalan, 4-hydroperoxycyclophosphamide, or radiation. In tumor-cell survival studies using the FSaIIC murine fibrosarcoma, short-term treatment with minocycline (5 x 5 mg/kg given over 24 h) was only minimally cytotoxic and did not alter the tumor response to a range of radiation doses. However, when minocycline (5 x 5 mg/kg given over 24 h) was added to treatment with cyclophosphamide, there was a 4-fold increase in FSaIIC tumor-cell killing across the dose range of cyclophosphamide doses tested, whereas the killing of bone marrow granulocyte macrophage colony-forming units (CFU-GM) remained unchanged. The Lewis lung carcinoma was used to assess the response of both the primary tumor and metastatic lung disease to treatment with minocycline (14 x 5 mg/kg) given alone or in combination with several cytotoxic anticancer drugs or with radiation delivered locally to the primary tumor. Of the various therapies tested, minocycline proved to be especially effective as an addition to treatment with cyclophosphamide both in increasing the response of the primary tumor and in reducing the number of lung metastases. The tumor growth delay produced by melphalan, radiation, Adriamycin, and bleomycin was also increased by the addition of minocycline to these therapies. These results indicate that minocycline given in clinically achievable doses may be an effective addition to some standard therapeutic regimens and that the mechanism of modulation by minocycline is likely to involve an effect of the drug on the host and not its direct interaction with other therapeutic modalities at the level of the tumor cell.
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PMID:Minocycline in combination with chemotherapy or radiation therapy in vitro and in vivo. 150 76


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