The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Abrogation of p53-Induced Apoptosis by the Hepatitis B Virus X Gene
Open accessAbstract
Hepatocellular carcinoma (HCC) is one of the most prevalent malignant diseases worldwide and has become a leading cause for cancer-related deaths in adults from Asia and sub-Saharan Africa (1). The DNA tumor virus hepatitis B virus (HBV) has been implicated to play a major causative role in the development of HCC in man (2-4). The HBx gene, the smallest viral openreading frame that may be essential for the viral life cycle (5,6), largely contributes the oncogenecity of HBV. The selective retention and expression of the HBx gene during acute and chronic hepatitis as well as in a great majority of HCCs may constitute an important step during HCC development (7,8). The oncogenic potential of the HBx gene has been experimentally demonstrated in a transgenic mice model (9) and in cell culture systems (10,11). HBx alone can induce HCC in certain transgenic mice (9) or can increase susceptibility to chemical carcinogens (12) and accelerate c-myc-induced HCC (13). Consequently, as an oncoprotein, HBx has been reported to disregulate cell-cycle transition (14,15) to potentially target certain proteases and proteasome (16-18), to interact with DNA repair factors (19,20), or to interact with the p53 tumor suppressor gene product (21-24).
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Cites
p53 Mutations in Human Cancers
Hollstein, M., Sidransky, D., Vogelstein, B., & Harris, C. C. (1991) · Science · doi:10.1126/science.1905840 · Cited by 8,018
Lane, D. P. (1992) · Nature · doi:10.1038/358015a0 · Cited by 5,138
Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
Toshiyuki, M., & Reed, J. C. (1995) · Cell · doi:10.1016/0092-8674(95)90412-3 · Cited by 4,063
Kastan, M. B., Zhan, Q., El-Deiry, W. S., Carrier, F., Jacks, T., Walsh, W. V., Plunkett, B. S., Vogelstein, B., & Fornace, A. J. (1992) · Cell · doi:10.1016/0092-8674(92)90593-2 · Cited by 3,047
The human papilloma virus-16 E7-oncoprotein is able to bind to the retinoblastoma gene product
Dyson, N., Howley, P. M., Münger, K., & Harlow, E. (1989) · Science · doi:10.1126/science.2537532 · Cited by 3,017
p53 is required for radiation-induced apoptosis in mouse thymocytes
Lowe, S. W., Schmitt, E. M., Smith, S. W., Osborne, B. A., & Jacks, T. (1993) · Nature · doi:10.1038/362847a0 · Cited by 2,864
Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
Graeber, T. G., Osmanian, C., Jacks, T., Housman, D. E., Koch, C. J., Lowe, S. W., & Giaccia, A. J. (1996) · Nature · doi:10.1038/379088a0 · Cited by 2,300
p53-Dependent apoptosis suppresses tumor growth and progression in vivo
Symonds, H., Krall, L., Remington, L., Saenz-Robles, M., Lowe, S., Jacks, T., & Van Dyke, T. (1994) · Cell · doi:10.1016/0092-8674(94)90534-7 · Cited by 880
Cited by
Rushing, B. R., & Selim, M. I. (2019) · Food and Chemical Toxicology · doi:10.1016/j.fct.2018.11.047 · Cited by 989
Hepatocellular carcinoma (HCC): Epidemiology, etiology and molecular classification
(2021) · Advances in Cancer Research · doi:10.1016/bs.acr.2020.10.001 · Cited by 851
Hussain, S. P., Schwank, J., Staib, F., Wang, X. W., & Harris, C. C. (2007) · Oncogene · doi:10.1038/sj.onc.1210279 · Cited by 621
Self-citationFan, T., Lu, H., Hu, H., Shi, L., McClarty, G. A., Nance, D. M., Greenberg, A. H., & Zhong, G. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.187.4.487 · Cited by 587
Donato, F., Boffetta, P., & Puoti, M. (1998) · International Journal of Cancer · doi:10.1002/(sici)1097-0215(19980130)75:3<347::aid-ijc4>3.0.co;2-2 · Cited by 543
Metadata
- Authors
- Wang, X. W.
- Venue
- Hepatocellular Carcinoma
- Publisher
- Humana Press
- Published
- 2003-11-14
- Volume
- 45
- Issue
- 24
- Pages
- 57-70
- OpenAlex
- W2152175101
- Cited by
- 321
- References
- 8
- FWCI
- 101.70
- Type
- book chapter
- Language
- en
- Open access
- green
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