Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multicellular tumour spheroids (MTS) from 4 mouse tumours (Line 1 lung carcinoma; a fibrosarcoma, FSA; a mammary carcinoma, MCa-11; and SV40-transformed fibroblasts, SV-A31) WEre injected into the abdominal cavity of normal, immunized or tumour-bearing syngeneic mice, recovered after 4-48 h, and their growth measured in vitro for 7-16 days. Both normal and immunized mice inhibited MTS growth, but there was no correlation between the two types of inhibition, suggesting that different immunological processes were involved. For example, the greatest inhibition by normal mice was seen for the weakly immunogenic MCa-11, and the highly immunogenic tumour, SV-A31, was only moderately inhibited. However, the summed inhibition of MTS growth in normal and sensitized hosts corresponded to the behaviour of tumours as s.c. transplants; i.e., was inversely related to the malignancy of the same tumours. The inhibition of MTS by mice bearing identical early tumours (FSA or MCa-11) was comparable to that in immunized mice. Histological sections of SV-A31 MTS in normal or immunized hosts revealed the infiltration of MTS by various types of host cells, mostly polymorphonuclears, macrophages and lymphocytes.
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PMID:Multicellular tumour spheroids: a model for combined in vivo/in vitro assay of tumour immunity. 736 71

The clinical development of radioprotectors, such as misoprostol, to protect normal tissue during cancer treatment must proceed with the assurance that tumors are not protected similarly or significantly. To provide data on this critical question, radiation-induced growth delay with or without the presence of misoprostol was measured in four murine tumors grown in the flanks of mice: the Lewis lung carcinoma, M-5076 ovarian sarcoma, FSA and NFSA. The effect of misoprostol on the tumor control dose (TCD50) of radiation was measured in FSA-bearing mice with or without prior treatment with the nonsteroidal anti-inflammatory agent, indomethacin. Misoprostol did not influence the in vivo growth of any of the four tumors, nor did it protect any of the tumors from radiation-induced growth delay. Likewise, there was no increase in the radiation TCD50 to treat the FSA in vivo in control or indomethacin-treated tumor-bearing mice. To measure any possible influence of tumor burden on the protective effect of misoprostol on normal tissue in mice, the protective effect of misoprostol on the survival of intestinal clonogenic cells was measured in M-5076-bearing mice and found to be the same as in non-tumor-bearing mice. These data suggest that misoprostol protects normal tissue in mice without protecting at least four experimental murine tumors. The data support the contention that misoprostol can achieve therapeutic gain by protecting normal tissues without protecting tumors.
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PMID:The prostaglandin E1 analog, misoprostol, a normal tissue protector, does not protect four murine tumors in vivo from radiation injury. 776 78