p53 expression, proliferation marker Ki-S5, DNA content and serum PSA: Possible biopotential markers in human prostatic cancer

Papadopoulos, I.; Rudolph, Pierre; Wirth, B.; Weichert-Jacobsen, K.

doi:10.1016/s0090-4295(96)00169-0

Cited by 19 publications

(10 citation statements)

References 32 publications

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“…This datum indicated a correlation between the increase of proliferating index and the accumulation of mutated p53. This is in agreement with Papadopoulos et al (1996) that found a highly significant correlation between p53 overexpression and tumor stage. They suggested the mutation of the p53 gene was not an initial event in prostate carcinogenesis.…”

supporting

confidence: 93%

“…It implied the existence of a strong correlation between p53 and tumor grade, suggesting also that aberrant p53 expression goes along with a loss of differentiation. Indeed, Papadopoulos et al (1996) found that tumors with increased p53 positivity also exhibited a significant higher proliferation index, this latter corroborating the former observation. In conclusion, in this work we studied a series of prostate adenocarcinomas with an intermediate grade of differentiation (Gleason 6: 3+3).There were simultaneously present both tubular and cribrous areas.…”

supporting

confidence: 84%

“…In this way, p53 immunoreactivity is likely to reflect p53 gene mutations (Papadopoulos et al, 1996). Numerous studies suggested the role of p53 mutation in the pathogenesis of prostate cancer, even if recent studies reported conflicting results about the incidence of nuclear p53 accumulation (Samaan et al, 1993;Kallakury et al, 1994;Fox et al, 1993;Shurbaji et al, 1995).…”

mentioning

confidence: 99%

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Biological aggressiveness evaluation in prostate carcinomas: immunohistochemical analysis of PCNA and p53 in a series of Gleason 6 (3+3) adenocarcinomas

Cappello

Palma²,

Martorana³

et al. 2009

Eur J Histochem

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We selected 63 prostate tumors with Gleason's grade 6 (3+3), commonly showing both tubular and cribrous patterns. We compared in both patterns the expression of two of the most used biologic markers: PCNA and p53, with the aim to verify the validity of the Gleason's grading system to compare the morphologic grade with biologic aggressiveness and prognostic value. We did not find any statistical difference in the protein immunopositivity, indicating that both patterns could have identical biologic behaviour; then we confirmed the validity of Gleason's system for considering both tubular and cribrous patterns as an intermediate grade of tumoral differentiation. Moreover, we found a linear relationship between the increase of PCNA and the accumulation of mutated p53; this datum could confirm the hypothesis that p53 mutation is a late event in prostate carcinogenesis.

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supporting

confidence: 93%

supporting

confidence: 84%

mentioning

confidence: 99%

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Biological aggressiveness evaluation in prostate carcinomas: immunohistochemical analysis of PCNA and p53 in a series of Gleason 6 (3+3) adenocarcinomas

Cappello

Palma²,

Martorana³

et al. 2009

Eur J Histochem

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“…We believe Overall survival Kaplan − Meier estimates that survival differences between patients treated in different decades may be explained by both an improvement in surgical techniques for metastases and the advent of supportive care measures, for example, the erythropoietins. In contrast to numerous prognostic factors, only two predictive factors for response to treatment have been identified yet: the proliferation status in terms of Ki-S5-immunoreactive scores (Papadopoulos et al, 1996) and the histological type of RCC (Upton et al, 2005). IL-2 responsiveness was shown to be predicted by clear-cell type, presence of more than 50% alveolar features and absence of papillary or granular features.…”

Section: Discussionmentioning

confidence: 96%

Prognostic factors in metastatic renal cell carcinoma: metastasectomy as independent prognostic variable

et al. 2006

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Prognostic and predictive factors in patients with metastatic renal cell carcinoma (MRCC) have been evaluated from untreated patients or patients on several different treatment approaches. The aim of this analysis was to define prognostic and predictive factors in patients treated uniformly with a low-dose outpatient cytokine combination. The relationship between patient-, tumour-, and treatment-related factors was analysed in 99 patients with MRCC. These features were first examined in univariate analyses, then a stepwise modelling approach based on Cox regression was used to form a multivariate model. Nuclear grade, metastasectomyeven incomplete -C-reactive protein and lactate dehydrogenase were identified as independent prognostic factors for survival. Patients assigned to three different risk groups had statistically significant survival differences (30, 22 and 6 months, respectively). A total of 43.4% had undergone metastasectomy, mostly incomplete. Risk group affiliation was correlated with response to treatment. Our findings strongly suggest the consideration of metastasectomy in the management of patients with metastatic renal cell cancer undergoing either immunotherapy or targeted treatment.

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“…This deregulation of cell-cycle control in the absence of p53 is readily observed in early-passage mouse p53-/-fibroblasts, which exhibit a higher rate of proliferation and a greater percentage of cells in S phase and mitosis than their p53+/+ counterparts [33]. Cellular proliferation markers are also expressed in human tumors with overexpressed mutant p53, suggesting that these tumors have a higher proliferation rate than tumors with wild-type p53 [34][35][36][37].…”

Section: Introductionmentioning

confidence: 99%

Increased tumor cell proliferation in murine tumors with decreasing dosage of wild-typep53

et al. 1999

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A number of transgenic animal model systems have addressed the mechanistic role of p53 loss in tumor progression. However, many of these tumor models have analyzed p53 function in the context of other transgenes expressing activated oncogenes or defective tumor suppressor genes generated by gene targeting. To examine the role of p53 loss independent of other exogenous oncogenic influences, we analyzed some of the biological aspects of tumor formation and progression in p53-knockout mice containing a null germline p53 allele. We analyzed tumors from p53-/-, p53+/-, and p53+/+ littermates. Some of the p53+/- tumors had lost the remaining p53 allele (p53+/- loss of heterozygosity), whereas others retained the allele (p53+/-). In this report, we show that loss or absence of p53 conferred a tumor growth advantage by increasing the rate of cellular proliferation in a p53 dosage-dependent manner. The apoptotic levels in tumor tissue were found to be modest and not significantly dependent on p53 status. These results contrast with those from some other p53-deficient tumor models, in which p53 loss was associated with more rapid tumor progression through abrogated apoptosis. Finally, as p53 has been shown to regulate certain angiogenic factors, we examined the levels of angiogenesis in p53-containing and p53-deficient tumors. We found no p53-dependent differences in the levels of tumor angiogenesis measured by intratumoral microvessel density.

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p53 expression, proliferation marker Ki-S5, DNA content and serum PSA: Possible biopotential markers in human prostatic cancer

Cited by 19 publications

References 32 publications

Biological aggressiveness evaluation in prostate carcinomas: immunohistochemical analysis of PCNA and p53 in a series of Gleason 6 (3+3) adenocarcinomas

Biological aggressiveness evaluation in prostate carcinomas: immunohistochemical analysis of PCNA and p53 in a series of Gleason 6 (3+3) adenocarcinomas

Prognostic factors in metastatic renal cell carcinoma: metastasectomy as independent prognostic variable

Increased tumor cell proliferation in murine tumors with decreasing dosage of wild-typep53

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