Histopathological characteristics and coexpression of p53 and p16INK4a proteins in renal cancer

被引:0
|
作者
Zivkovic, Sladana [1 ]
Kostov, Milos [2 ]
Pavlovic, Svetlana [3 ]
Mijovic, Zaklina [4 ]
机构
[1] Vojna Boln, Odsek Urol, Nish 18000, Serbia
[2] Vojna Boln, Odsek Patol, Nish 18000, Serbia
[3] Klinicki Ctr, Klin Urol, Nish, Serbia
[4] Klin Ctr, Inst Patol, Nish, Serbia
关键词
carcinoma; renal cells; tumor suppressor protein p53; cyclindependent kinase inhibitor P16; immunohistochemistry;
D O I
10.2298/VSP0811820Z
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Results. In 9 (75%) of the cases was detected mutated protein p53, of whom 66.6% had higher histological gradus of tumor (G3-4) and higher pathological stadium of the disease (pT3a-b)) at the same time. In 7 (58.3%) and 5 (41.7%) of the cases expression of protein p16, the loss of expression of protein p16 were detected respectively A statistically significant positive correlation was determined between pathological stadium of disease (TNM) and the degree of tumor differentiation (G) (rho = 0.834; p < 0.001), as well as between TNM and mitotic kidex (rho = 0.622; p = 0.031). Conclusion. A mutated form of protein p53 exists in 75% of the cases with the renal carcinoma and 66.6% of then have higher histological gradus of tumor and higher stadium of tumor disease at the same time. Coexpression of mutated protein p53 and protein p16(INK4a) in renal carcinoma is not statistically significant and it is not in correlation with clinicopathological parameters. Immunohistochemical analysis of mutated protein p53 in renal carcinoma can have predictive significance. Methods. The examination included 12 patients (6607% men, 33.3% women), with patohistologically verified renal carcinoma. Expression of mutated form of protein p53 and protein p16 was determined in tissue samples, by immunohistochemical analysis using of mice monoclinical antibodies produced by DAKO, Denmark. Background/Aim. Renal carcinoma represents histological heterogeneous group of malignant tumors, with various clinical aggressiveness. The frequency of p53 mutation in primal renal carcinoma is rare, although there are information about its heterogenous accumulation. The loss of protein p16 expression in primal renal carcinoma is detected in 20-30% of the cases. The aim of this paper was to determine frequency of mutated protein p53 and expression of protein protein p16(INK4a) in renal carcinoma, to analyze their correlative relation and relation with the examined clinicopathological parameters.
引用
收藏
页码:820 / 824
页数:5
相关论文
共 50 条
  • [21] Adenovirus-mediated transfer of p53 and p16INK4a results in pancreatic cancer regression in vitro and in vivo
    Ghaneh, P
    Greenhalf, W
    Humphreys, M
    Wilson, D
    Zumstein, L
    Lemoine, NR
    Neoptolemos, JP
    GENE THERAPY, 2001, 8 (03) : 199 - 208
  • [22] The prevalence and clinicopathologic correlate of p16INK4a, retinoblastoma and p53 immunoreactivity in locally advanced urinary bladder cancer
    Tzai, TS
    Tsai, YS
    Chow, NH
    UROLOGIC ONCOLOGY-SEMINARS AND ORIGINAL INVESTIGATIONS, 2004, 22 (02) : 112 - 118
  • [23] Human papillomavirus infection and immunohistochemical expression of cell cycle proteins pRb, p53, and p16INK4a in sinonasal diseases
    Yamashita, Yukashi
    Hasegawa, Masahiro
    Deng, Zeyi
    Maeda, Hiroyuki
    Kondo, Shunsuke
    Kyuna, Asanori
    Matayoshi, Sen
    Agena, Shinya
    Uehara, Takayuki
    Kouzaki, Hideaki
    Shimizu, Takeshi
    Ikegami, Taro
    Ganaha, Akira
    Suzuki, Mikio
    INFECTIOUS AGENTS AND CANCER, 2015, 10
  • [24] Real-time in vivo imaging of p16Ink4a reveals cross talk with p53
    Yamakoshi, Kimi
    Takahashi, Akiko
    Hirota, Fumiko
    Nakayama, Rika
    Ishimaru, Naozumi
    Kubo, Yoshiaki
    Mann, David J.
    Ohmura, Masako
    Hirao, Atsushi
    Saya, Hideyuki
    Arase, Seiji
    Hayashi, Yoshio
    Nakao, Kazuki
    Matsumoto, Mitsuru
    Ohtani, Naoko
    Hara, Eiji
    JOURNAL OF CELL BIOLOGY, 2009, 186 (03): : 393 - 407
  • [25] Dioxin-induced immortalization of normal human keratinocytes and silencing of p53 and p16INK4a
    Ray, SS
    Swanson, HI
    JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (26) : 27187 - 27193
  • [26] The inherent instability of mutant p53 is alleviated by Mdm2 or p16INK4a loss
    Terzian, Tamara
    Suh, Young-Ah
    Iwakuma, Tomoo
    Post, Sean M.
    Neumann, Manja
    Lang, Gene A.
    Van Pelt, Carolyn S.
    Lozano, Guillermina
    GENES & DEVELOPMENT, 2008, 22 (10) : 1337 - 1344
  • [27] Expression of P16INK4a, p53 AND COX-2 in colorectal carcinoma and their clinical significance
    Abdennadher, I. Miladi
    Ayadi, L.
    Khabir, A.
    Frikha, F.
    Kallel, L.
    Makni, S.
    Frikha, M.
    Gargouri, A.
    Gargouri, R.
    Boudawara, T. Sellami
    HISTOPATHOLOGY, 2008, 53 : 149 - 149
  • [28] Survey of familial glioma and role of germline p16INK4A/p14ARF and p53 mutation
    Lindsay B. Robertson
    Georgina N. Armstrong
    Bianca D. Olver
    Amy L. Lloyd
    Sanjay Shete
    Ching Lau
    Elizabeth B. Claus
    Jill Barnholtz-Sloan
    Rose Lai
    Dora Il’yasova
    Joellen Schildkraut
    Jonine L. Bernstein
    Sara H. Olson
    Robert B. Jenkins
    Ping Yang
    Amanda L. Rynerason
    Margaret Wrensch
    Lucie McCoy
    John K. Wienkce
    Bridget McCarthy
    Faith Davis
    Nicholas A. Vick
    Christoffer Johansen
    Hanne Bødtcher
    Siegal Sadetzki
    Revital Bar-Sade Bruchim
    Galit Hirsh Yechezkel
    Ulrika Andersson
    Beatrice S. Melin
    Melissa L. Bondy
    Richard S. Houlston
    Familial Cancer, 2010, 9 : 413 - 421
  • [29] Loss of p16Ink4a
    Weitzman J.B.
    Genome Biology, 2 (1)
  • [30] Predictive value of expression of p16INK4A, retinoblastoma and p53 proteins for the prognosis of non-small cell lung cancers
    Hommura, F
    Dosaka-Akita, H
    Kinoshita, I
    Mishina, T
    Hiroumi, H
    Ogura, S
    Katoh, H
    Kawakami, Y
    BRITISH JOURNAL OF CANCER, 1999, 81 (04) : 696 - 701