Mutant p53 in Patients with Invasive Cervical Cancer Stages IB to IIB

Kainz, Ch.; Kohlberger, Petra; Gitsch, G.; Sliutz, Gerhard; Breitenecker, G.; Reinthaller, Alexander

doi:10.1006/gyno.1995.1127

Cited by 24 publications

(13 citation statements)

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“…However, using immunohistochemical staining, overexpression of p53 was found in 20.2-30.7% of cervical cancers [16][17][18]. Most studies failed to show a prognostic significance of overexpression of p53 in cervical cancer [16,17]. Apart from mutation, a loss of p53 function could also occur as a result of degradation of p53 by the HPV16/18 protein [2].…”

Section: Discussionmentioning

confidence: 99%

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Homozygous Arginine at Codon 72 of p53 Has No Prognostic Significance in Cervical Cancer

Ngan

Liu

et al. 2000

Tumor Biol

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Mutation of p53, a tumour suppressor gene, is uncommon in cervical cancer but the detection of human papillomavirus (HPV) DNA in cervical cancer is common. The findings of increased susceptibility to degradation of p53 by E6 protein of HPV16/18 in cervical cancer with homozygous arginine at codon 72 (HA72) of p53 led to this study on whether cervical cancers with HA72 were more aggressive with the increase in the rate of loss of p53 function. In 102 cervical cancers, 76.5% were HPV16/18 positive and 30% had HA72. No survival difference was detected between HA72 and non-HA72 tumours irrespective of HPV16/18 status. Furthermore, the detection of HPV16/18 in cervical cancer was found not to be of prognostic significance in this study.

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Section: Discussionmentioning

confidence: 99%

“…Since p53 mutation is infrequent in cervical cancer [1], it is difficult to study its effect on prognosis. However, using immunohistochemical staining, overexpression of p53 was found in 20.2-30.7% of cervical cancers [16][17][18]. Most studies failed to show a prognostic significance of overexpression of p53 in cervical cancer [16,17].…”

Section: Discussionmentioning

confidence: 99%

Homozygous Arginine at Codon 72 of p53 Has No Prognostic Significance in Cervical Cancer

Ngan

Liu

et al. 2000

Tumor Biol

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“…[29] While analyzing p53 in patients with invasive cervical cancer stages IB to IIB, Kainz et al, reported no prognostic significance of p53 in surgically treated cervical cancer. [30] However, some studies have demonstrated an association between p53 protein accumulation and aggressive behavior of carcinoma, including a genetic propensity towards metastasis and recurrence. [31] Tilting the balance in favor of p53 by novel treatment protocols might reestablish the tumor suppressor function of p53 in cervical carcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

High-risk human papillomavirus, tumor suppressor protein p53 and mitomycin-C in invasive squamous cell carcinoma cervix

et al. 2006

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BACKGROUND: Clinical data relating to human papillomavirus (HPV) infection and p53 status in cervical cancer has been sparse and confusing. AIM: To evaluate high-risk HPV and expression of tumor suppressor protein p53 in squamous cell carcinoma of cervix and to assess response to mitomycin-C in neo-adjuvant chemotherapy. SETTING AND DESIGN: RESULTS:All patients with cancer cervix were positive for high-risk HPV DNA having relative light units/cut off values ranging from 3.4-2389.21 (P value = 0.006). High viral load of high risk HPV DNA was seen in advanced stages (P= 0.05) and an association of viral load with tumor volume was also seen (r=0.361, P=0.05). Analysis of p53 protein in cervical carcinoma patient showed expression in 50% of cancer specimens (P value < 0.001).McNemar's and Fischer's exact test showed no change in p53 status post-chemotherapy; however 66% of stage II B patients in VBP-M group became operable. CONCLUSION: High-risk HPV was universally present in all cases of cancer cervix and viral load was associated with stage and tumor volume while p53 protein was expressed in 50% of cases suggesting deregulation. More studies using mitomycin-C in cervical cancer treatment protocols are needed.

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“…En extrapolant les données précé-demment exposées d'hybridation in situ et de biologie moléculaire, on peut en effet penser que dans les CIN de grade élevé, les liaisons E6-p53 et E7-pRb indiquées par l'hybridation in situ ne seraient que rarement à prendre en considération dans les cellules atypiques [47]. Dans les cancers, cette liaison pourrait l'être plus fréquemment dans les cellules tumorales et métastasiques [49][50][51]. Toutefois, en toute rigueur, on ne peut suggérer cette association dans les cellules où on ne détec-te pas leur présence simultanée.…”

Section: Applications Des Données Biologiques Aux Aspectsunclassified

“…Toutefois, en toute rigueur, on ne peut suggérer cette association dans les cellules où on ne détec-te pas leur présence simultanée. La p53 s'accumule anormalement dans les cellules atypiques au fur et à mesure que la lésion s'aggrave [50][51][52][53][54]. A la différence de la cellule normale, dans laquelle la protéine p53 est présente à faible concentration et a une courte durée de vie, dans les cellules cancéreuses, la protéine p53 mutante a une durée de vie plus longue ; elle s'accumule ainsi dans le noyau des cellules atypiques et peut être aisément détec-tée en immunohistochimie [55].…”

Section: Applications Des Données Biologiques Aux Aspectsunclassified

Pathogénie cellulaire et moléculaire du cancer du col.

Monsonégo¹

1996

Med Sci (Paris)

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SYNTHÈSE médecine/sciences 1996 ; 12 : 733-44 m/s n°6-7, vol. 12, juin-juillet 96 Joseph MonsonegoDe nombreuses études indiquent que les papillomavirus à risque sont impliqués dans la carcinogenèse des cancers épidermoïdes ano-génitaux, et particulièrement dans celle des cancers du col utérin. Trois notions fondamentales se déga-gent de la biologie moléculaire de ces cancers [2] : (1) Régulation du cycle cellulaireLe gène RB a un rôle régulateur néga-tif dans la réplication de l'ADN et le cycle mitotique [9, 10]. Le gène p53 semble impliqué dans le contrôle de la croissance cellulaire des cellules « agressées » ; on le considère comme un gène suppresseur de la transformation. Il est exprimé dans tous les tissus

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Mutant p53 in Patients with Invasive Cervical Cancer Stages IB to IIB

Cited by 24 publications

References 0 publications

Homozygous Arginine at Codon 72 of p53 Has No Prognostic Significance in Cervical Cancer

Homozygous Arginine at Codon 72 of p53 Has No Prognostic Significance in Cervical Cancer

High-risk human papillomavirus, tumor suppressor protein p53 and mitomycin-C in invasive squamous cell carcinoma cervix

Pathogénie cellulaire et moléculaire du cancer du col.

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