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Query: UMLS:C0016632 (Fox)
 1,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mouse liver is a frequent target organ for chemical carcinogenesis (Huff et al., 1988, 1991; Gold et al., 1989) and tumor development exhibits preferential strain sensitivity (Dragani et al., 1992; Drinkwater and Bennett, 1991). In some reports a positive correlation has been observed between the degree of spontaneous liver tumor incidence and the propensity to develop liver tumors after treatment with chemical carcinogens (Della Porta et al., 1967; Flaks, 1968; Dragani et al., 1984, 1987; Diwan et al., 1986; Drinkwater and Ginsler, 1986), but this is not always the case (Grasso and Hardy, 1975; Hanigan et al., 1988; Dragani et al., 1992). Thus, the interpretation of this endpoint in assessing potential health hazards to humans continues to be the subject of active debate. Studies of molecular and genetic factors that modulate the genesis of mouse liver tumors should enhance our understanding of the relevance of this response following exposure to genotoxic as well as nongenotoxic chemicals. To utilize intelligently animal models as surrogates for human carcinogenesis, the validity of rodent tumor endpoints in assessing potential human health hazards from chemical exposure remains an important issue. One approach has been to understand the animal system itself and the mechanisms by which chemicals induce tumors in the animal model. Information regarding the molecular events associated with tumor induction should make the relevance of results from rodent carcinogenicity studies to human risk easier to assess. Results to date have identified activation of ras proto-oncogenes as one early event and an important factor associated with chemical induction of mouse liver neoplasia (Reynolds et al., 1986, 1987; Wiseman et al., 1986), although ras-independent pathways appear to account for an appreciable proportion of some chemically induced mouse liver tumors (Fox et al., 1990; Buchmann et al., 1991). Available data emphasize the complexity of H-ras activation in murine hepatocarcinogenesis. Not only the genetic background of the mouse but also the dose of the carcinogen may influence significantly the number of tumors containing activated H-ras. Both high sensitivity and low sensitivity strains of mice can develop liver tumors which contain activated H-ras oncogenes, showing that the ability to activate this gene does not in itself determine susceptibility to hepatocarcinogenesis. Ras gene mutational profiles in chemically induced liver tumors may be different and distinguishable from those in spontaneous tumors. Since multiple genetic as well as nongenetic events are associated with tumor development, defining a precise role for ras gene mutations when they occur in mouse liver tumors is often difficult.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mutations in the ras proto-oncogene: clues to etiology and molecular pathogenesis of mouse liver tumors. 767 62

We applied MRI to the in vivo detection of spontaneous colorectal tumors in a unique mouse model, the Fox Chase Cancer Center (FCCC) ApcMIN mouse. Unlike other Min (multiple intestinal neoplasia) strains, FCCC ApcMIN animals develop an appreciable number of tumors in the large intestine, which makes them an appropriate mouse model for colon cancer in humans. We describe a method for marking the colon on MRI data sets that involves a bowel-cleansing procedure and the insertion of a polyurethane tube (filled with an MRI contrast agent) fully into the colon. We found that tumors as small as 1.5 mm in diameter can be consistently identified from MRI datasets with a voxel size of 0.1 mm x 0.133 mm x 0.133 mm. Tumor volumes were determined from the MRM data sets with the use of a novel approach to planimetry in 3D data sets. We observed a correlation between tumor volume (as measured from the MRI datasets) and tumor weight of 0.942, and a P-value of 0.008, based on Spearman's test. These data show that MRI can be used to accurately monitor tumor growth in mouse models of colorectal carcinogenesis.
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PMID:Detection and volume determination of colonic tumors in Min mice by magnetic resonance micro-imaging. 1533 70

Forkhead Box m1b (Foxm1b) is a subtype of the Fox transcription factor family. It is detected in all proliferative cells, but disappears when cells enter into their terminal differentiation phase. Foxm1b is closely related to hepatocellular growth, mainly through inhibiting cyclin-dependent kinase (CDK) inhibitors to influence cell proliferation. It also participates in growth hormone (GH) mediated cell multiplication, but does not induce tumors. The expression of Foxm1b has been observed in many tumor cell lines and malignant tumors, indicating that it might be an essential proto-oncogene in carcinogenesis. Furthermore, Foxm1b may take part in liver regeneration after hepatectomy, hepatic failure and liver transplantation. Foxm1b is a new potential target for the treatment human hepatic cell carcinoma (HCC).
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PMID:[Significance of Forkhead Box m1b (Foxm1b) gene in cell proliferation and carcinogenesis]. 1871 Jun 29