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p16 and p53 after different treatments in human-tumour cells.

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p16 and p53 after different treatments in human-tumour cells. / Valenzuela, M. T.; Núñez, M. I.; Siles, E. et al.
In: European Journal of Cancer, Vol. 31, No. Supple, 1995, p. S175-S175.

Research output: Contribution to Journal/Magazine › Journal article

Harvard

Valenzuela, MT, Núñez, MI, Siles, E, Villalobos, M, Pedraza, V, Gordon, AT, McMillan, TJ & de Almodóvar, JMR 1995, 'p16 and p53 after different treatments in human-tumour cells.', European Journal of Cancer, vol. 31, no. Supple, pp. S175-S175. https://doi.org/10.1016/0959-8049(95)96085-R

APA

Valenzuela, M. T., Núñez, M. I., Siles, E., Villalobos, M., Pedraza, V., Gordon, A. T., McMillan, T. J., & de Almodóvar, J. M. R. (1995). p16 and p53 after different treatments in human-tumour cells. European Journal of Cancer, 31(Supple), S175-S175. https://doi.org/10.1016/0959-8049(95)96085-R

Vancouver

Valenzuela MT, Núñez MI, Siles E, Villalobos M, Pedraza V, Gordon AT et al. p16 and p53 after different treatments in human-tumour cells. European Journal of Cancer. 1995;31(Supple):S175-S175. doi: 10.1016/0959-8049(95)96085-R

Author

Valenzuela, M. T. ; Núñez, M. I. ; Siles, E. et al. / p16 and p53 after different treatments in human-tumour cells. In: European Journal of Cancer. 1995 ; Vol. 31, No. Supple. pp. S175-S175.

Bibtex

@article{6d77c0aea25844bea6f2ae863a56219d,
title = "p16 and p53 after different treatments in human-tumour cells.",
abstract = "It has been suggested that the product of p53 gene inhibits cellular growth by stimulating the production of p16 protein. We have examined by ELISA the protein levels of p16 (ranged 0.80-3.44 O.D. unit per 106 cells) and p53 (ranged 2.20-4.65 O.D. unit per 106 cells) in human tumour cell lines. We have not found a quantitative relationship between these protein levels: neither in standard growth conditions nor after 6 Gy of radiation. The p53 product function has been surveyed by flow cytometry studying cell cycle arrest after irradiation of the cells at 6 Gy. Taking into account that concept we have divided our cell lines in two groups (A) cells with functional p53 protein and (B) cells with functional inactivation of the p53 gene product. Higher constitutive levels of p16 product were found in group A cells. Intracellular p16 levels change after 6 Gy but not a defined time course profile has been found. We have identified that p16 levels change markedly with growth conditions, ie, age of culture, growth rate modified by use of differents serum levels or after hormonal synchronization of human breast cancer cell lines. The implications of this for the radiation response and cellular proliferation of human tumour cell lines remains to be determined.",
author = "Valenzuela, {M. T.} and N{\'u}{\~n}ez, {M. I.} and E. Siles and M. Villalobos and V. Pedraza and Gordon, {A. T.} and McMillan, {T. J.} and {de Almod{\'o}var}, {J. M. R.}",
year = "1995",
doi = "10.1016/0959-8049(95)96085-R",
language = "English",
volume = "31",
pages = "S175--S175",
journal = "European Journal of Cancer",
publisher = "Elsevier Limited",
number = "Supple",

}

RIS

TY - JOUR

T1 - p16 and p53 after different treatments in human-tumour cells.

AU - Valenzuela, M. T.

AU - Núñez, M. I.

AU - Siles, E.

AU - Villalobos, M.

AU - Pedraza, V.

AU - Gordon, A. T.

AU - McMillan, T. J.

AU - de Almodóvar, J. M. R.

PY - 1995

Y1 - 1995

N2 - It has been suggested that the product of p53 gene inhibits cellular growth by stimulating the production of p16 protein. We have examined by ELISA the protein levels of p16 (ranged 0.80-3.44 O.D. unit per 106 cells) and p53 (ranged 2.20-4.65 O.D. unit per 106 cells) in human tumour cell lines. We have not found a quantitative relationship between these protein levels: neither in standard growth conditions nor after 6 Gy of radiation. The p53 product function has been surveyed by flow cytometry studying cell cycle arrest after irradiation of the cells at 6 Gy. Taking into account that concept we have divided our cell lines in two groups (A) cells with functional p53 protein and (B) cells with functional inactivation of the p53 gene product. Higher constitutive levels of p16 product were found in group A cells. Intracellular p16 levels change after 6 Gy but not a defined time course profile has been found. We have identified that p16 levels change markedly with growth conditions, ie, age of culture, growth rate modified by use of differents serum levels or after hormonal synchronization of human breast cancer cell lines. The implications of this for the radiation response and cellular proliferation of human tumour cell lines remains to be determined.

AB - It has been suggested that the product of p53 gene inhibits cellular growth by stimulating the production of p16 protein. We have examined by ELISA the protein levels of p16 (ranged 0.80-3.44 O.D. unit per 106 cells) and p53 (ranged 2.20-4.65 O.D. unit per 106 cells) in human tumour cell lines. We have not found a quantitative relationship between these protein levels: neither in standard growth conditions nor after 6 Gy of radiation. The p53 product function has been surveyed by flow cytometry studying cell cycle arrest after irradiation of the cells at 6 Gy. Taking into account that concept we have divided our cell lines in two groups (A) cells with functional p53 protein and (B) cells with functional inactivation of the p53 gene product. Higher constitutive levels of p16 product were found in group A cells. Intracellular p16 levels change after 6 Gy but not a defined time course profile has been found. We have identified that p16 levels change markedly with growth conditions, ie, age of culture, growth rate modified by use of differents serum levels or after hormonal synchronization of human breast cancer cell lines. The implications of this for the radiation response and cellular proliferation of human tumour cell lines remains to be determined.

U2 - 10.1016/0959-8049(95)96085-R

DO - 10.1016/0959-8049(95)96085-R

M3 - Journal article

VL - 31

SP - S175-S175

JO - European Journal of Cancer

JF - European Journal of Cancer

IS - Supple

ER -