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Hepatocarcinogenesis in p53‐deficient mice
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| Zeitschriftentitel: | Molecular Carcinogenesis |
|---|---|
| Personen und Körperschaften: | |
| In: | Molecular Carcinogenesis, 12, 1995, 3, S. 132-136 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Kemp, Christopher J. Kemp, Christopher J. |
|---|---|
| author |
Kemp, Christopher J. |
| spellingShingle |
Kemp, Christopher J. Molecular Carcinogenesis Hepatocarcinogenesis in p53‐deficient mice Cancer Research Molecular Biology |
| author_sort |
kemp, christopher j. |
| spelling |
Kemp, Christopher J. 0899-1987 1098-2744 Wiley Cancer Research Molecular Biology http://dx.doi.org/10.1002/mc.2940120304 <jats:title>Abstract</jats:title><jats:p>To determine whether a constitutive <jats:italic>p53</jats:italic> deficiency would enhance the rate of development of chemically induced hepatocellular carcinoma, we treated groups of wild‐type, <jats:italic>p53</jats:italic>‐heterozygous (+/‐), and null (‐/‐) male mice with a single dose of diethylnitrosamine at 12 d of age. Although the null mice had to be killed very early, at 15 wk of age because of the development of nonliver tumors, hemangosarcoma of the liver had already developed in two of seven mice. More detailed analysis of the wild‐type and heterozygous mice showed no difference in the number, size, or growth rate of early microscopic lesions or in the number or apparent malignancy of hepatocellular adenomas or carcinomas at later time points. Thus, germline <jats:italic>p53</jats:italic> deficiency does not enhance the rate of development of diethylnitrosamine‐induced hepatocellular adenoma or carcinoma but may instead favor development of hepatic hemangiosarcoma. © 1995 Wiley‐Liss Inc.</jats:p> Hepatocarcinogenesis in <i>p53</i>‐deficient mice Molecular Carcinogenesis |
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Molecular Carcinogenesis |
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| title |
Hepatocarcinogenesis in p53‐deficient mice |
| title_unstemmed |
Hepatocarcinogenesis in p53‐deficient mice |
| title_full |
Hepatocarcinogenesis in p53‐deficient mice |
| title_fullStr |
Hepatocarcinogenesis in p53‐deficient mice |
| title_full_unstemmed |
Hepatocarcinogenesis in p53‐deficient mice |
| title_short |
Hepatocarcinogenesis in p53‐deficient mice |
| title_sort |
hepatocarcinogenesis in <i>p53</i>‐deficient mice |
| topic |
Cancer Research Molecular Biology |
| url |
http://dx.doi.org/10.1002/mc.2940120304 |
| publishDate |
1995 |
| physical |
132-136 |
| description |
<jats:title>Abstract</jats:title><jats:p>To determine whether a constitutive <jats:italic>p53</jats:italic> deficiency would enhance the rate of development of chemically induced hepatocellular carcinoma, we treated groups of wild‐type, <jats:italic>p53</jats:italic>‐heterozygous (+/‐), and null (‐/‐) male mice with a single dose of diethylnitrosamine at 12 d of age. Although the null mice had to be killed very early, at 15 wk of age because of the development of nonliver tumors, hemangosarcoma of the liver had already developed in two of seven mice. More detailed analysis of the wild‐type and heterozygous mice showed no difference in the number, size, or growth rate of early microscopic lesions or in the number or apparent malignancy of hepatocellular adenomas or carcinomas at later time points. Thus, germline <jats:italic>p53</jats:italic> deficiency does not enhance the rate of development of diethylnitrosamine‐induced hepatocellular adenoma or carcinoma but may instead favor development of hepatic hemangiosarcoma. © 1995 Wiley‐Liss Inc.</jats:p> |
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| description | <jats:title>Abstract</jats:title><jats:p>To determine whether a constitutive <jats:italic>p53</jats:italic> deficiency would enhance the rate of development of chemically induced hepatocellular carcinoma, we treated groups of wild‐type, <jats:italic>p53</jats:italic>‐heterozygous (+/‐), and null (‐/‐) male mice with a single dose of diethylnitrosamine at 12 d of age. Although the null mice had to be killed very early, at 15 wk of age because of the development of nonliver tumors, hemangosarcoma of the liver had already developed in two of seven mice. More detailed analysis of the wild‐type and heterozygous mice showed no difference in the number, size, or growth rate of early microscopic lesions or in the number or apparent malignancy of hepatocellular adenomas or carcinomas at later time points. Thus, germline <jats:italic>p53</jats:italic> deficiency does not enhance the rate of development of diethylnitrosamine‐induced hepatocellular adenoma or carcinoma but may instead favor development of hepatic hemangiosarcoma. © 1995 Wiley‐Liss Inc.</jats:p> |
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| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTAwMi9tYy4yOTQwMTIwMzA0 |
| imprint | Wiley, 1995 |
| imprint_str_mv | Wiley, 1995 |
| institution | DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1 |
| issn | 0899-1987, 1098-2744 |
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| physical | 132-136 |
| publishDate | 1995 |
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| publisher | Wiley |
| record_format | ai |
| recordtype | ai |
| series | Molecular Carcinogenesis |
| source_id | 49 |
| spelling | Kemp, Christopher J. 0899-1987 1098-2744 Wiley Cancer Research Molecular Biology http://dx.doi.org/10.1002/mc.2940120304 <jats:title>Abstract</jats:title><jats:p>To determine whether a constitutive <jats:italic>p53</jats:italic> deficiency would enhance the rate of development of chemically induced hepatocellular carcinoma, we treated groups of wild‐type, <jats:italic>p53</jats:italic>‐heterozygous (+/‐), and null (‐/‐) male mice with a single dose of diethylnitrosamine at 12 d of age. Although the null mice had to be killed very early, at 15 wk of age because of the development of nonliver tumors, hemangosarcoma of the liver had already developed in two of seven mice. More detailed analysis of the wild‐type and heterozygous mice showed no difference in the number, size, or growth rate of early microscopic lesions or in the number or apparent malignancy of hepatocellular adenomas or carcinomas at later time points. Thus, germline <jats:italic>p53</jats:italic> deficiency does not enhance the rate of development of diethylnitrosamine‐induced hepatocellular adenoma or carcinoma but may instead favor development of hepatic hemangiosarcoma. © 1995 Wiley‐Liss Inc.</jats:p> Hepatocarcinogenesis in <i>p53</i>‐deficient mice Molecular Carcinogenesis |
| spellingShingle | Kemp, Christopher J., Molecular Carcinogenesis, Hepatocarcinogenesis in p53‐deficient mice, Cancer Research, Molecular Biology |
| title | Hepatocarcinogenesis in p53‐deficient mice |
| title_full | Hepatocarcinogenesis in p53‐deficient mice |
| title_fullStr | Hepatocarcinogenesis in p53‐deficient mice |
| title_full_unstemmed | Hepatocarcinogenesis in p53‐deficient mice |
| title_short | Hepatocarcinogenesis in p53‐deficient mice |
| title_sort | hepatocarcinogenesis in <i>p53</i>‐deficient mice |
| title_unstemmed | Hepatocarcinogenesis in p53‐deficient mice |
| topic | Cancer Research, Molecular Biology |
| url | http://dx.doi.org/10.1002/mc.2940120304 |