Expression of p21 and mutant p53 gene products in residual prostatic tumor cells after radical radiotherapy

Ljung, Gunilla; Egevad, Lars; Norberg, M.; Holmberg, Lars; Nilsson, Sten; Busch, Christer

doi:10.1002/(sici)1097-0045(19970701)32:2<99::aid-pros4>3.0.co;2-a

Cited by 10 publications

(4 citation statements)

References 42 publications

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“…These observations are consistent with observations in other tumour types (McKay et al, 2000;Holland et al, 2001;Tut et al, 2001) and support its role in promoting cyclin D1/CDK4 activity. Second, we showed that p21 Cip1 levels correlate with proliferation ( Figure 5B), thus confirming other reports (Ljung et al, 1997;Baretton et al, 1999;Osman et al, 1999;Fizazi et al, 2002). Collectively, these data indicate that p21 Cip1 action in this tumour type likely favours proliferation.…”

Section: Discussionsupporting

confidence: 91%

Impact of differential cyclin D1 expression and localisation in prostate cancer

et al. 2007

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Cyclin D1 is a critical regulator of androgen-dependent transcription and cell cycle progression in prostate cancer cells. Despite the influence of D-type cyclins on prostate cancer proliferation, few studies have examined the expression of cyclin D1 in localised tumours or challenged its relevance to disease progression. Cyclin D1 status was characterised using immunohistochemistry in 38 non-neoplastic prostate samples, 138 primary human prostate carcinomas, and three lymph node metastatic specimens. Relevance of cyclin D1 to preoperative prostate-specific antigen (PSA) levels, Ki-67 index, and p21 Cip1 status was also examined. Cyclin D1-positive phenotype was increased in primary carcinoma compared to non-neoplastic tissue, and was evident in all lymph node metastases cases. Interestingly, at least three distinct localisation patterns were observed in the cyclin D1-positive cohort, wherein cytoplasmic localisation was identified in a large fraction, and this pattern was predominant in lower grade tumours. Relevance of altered cyclin D1 status was observed, wherein cyclin D1-positive tumours were associated with low preoperative PSA levels, consistent with in vitro reports that cyclin D1 may alter the expression of this tumour marker. Moreover, tumours with predominantly cytoplasmic cyclin D1 showed the lowest Ki-67 index, whereas nuclear cyclin D1 was associated with higher grade, elevated Ki-67, and increased nuclear p21 Cip1 . These data demonstrate that differential cyclin D1 status may influence clinicopathological parameters, and reveal new insight as to the regulation and potential consequence of cyclin D1 expression in prostate cancer.

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Section: Discussionsupporting

confidence: 91%

Impact of differential cyclin D1 expression and localisation in prostate cancer

et al. 2007

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“…The morphology of tumor cells in postradiotherapy biopsies was not found to be a useful predicting factor. Other predictive assays such as direct measurement of the proliferative activity of tumor cells10, 11 or other measurements of oncogene expression12, 13 should be explored.…”

Section: Discussionmentioning

confidence: 99%

The time course of histologic remission after treatment of patients with nasopharyngeal carcinoma

Kwong

Nicholls

Wei

et al. 1999

Cancer

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BACKGROUND The objective of this study was to define the time course of histologic remission and to evaluate the prognostic significance of delayed histologic remission of patients with nasopharyngeal carcinoma (NPC). METHODS Between 1986‐1994, 803 patients underwent serial postradiotherapy nasopharyngeal biopsies. Patients with positive histology underwent repeated biopsies every 2 weeks until the biopsies were found to be negative or, if remission did not occur by the 12th week after radiotherapy, treatment was initiated for persistent disease. Patients with positive histology found after the fifth week but who achieved spontaneous remission before the twelfth week were considered to have delayed histologic remission. Negative histology by the sixth week was considered early histologic remission. The outcome of patients with delayed histologic remission, early histologic remission, and persistent disease were compared. RESULTS Six hundred and seventeen patients (76.8%) had negative histology within 12 weeks of the completion of radiotherapy and 55 (6.9%) had persistent disease at Week 12. In 131 patients (16.3%) spontaneous remission was observed in repeat biopsies after initial positive histology. With increasing time after radiotherapy, the incidence of positive histology decreased but more patients were found to have persistent disease. Patients with early and delayed histologic remission had 5‐year NPC control rates of 82.4% and 76.8%, respectively (P = 0.35) versus a 40% NPC control rate among patients with persistent disease (P < 0.001). The 5‐year survival rates were 75.3%, 79.4%, and 54.2%, respectively, for the 3 groups (P < 0.001). CONCLUSIONS A high proportion of early positive histology remitted spontaneously. Delayed histologic remission in NPC patients is not a poor prognostic factor and additional treatment is not necessary. A confirmatory biopsy at 10 weeks is recommended before the initiation of salvage treatment. Cancer 1999;85:1446–53. © 1999 American Cancer Society.

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“…For example, p53 mutations are uncommon (3%) in clinically localized prostate carcinoma in some studies (120) but up to 40% in another study which combined several techniques to identify mutations (121). p53 mutations are detected with increased frequency in more advanced metastatic prostate cancers (122), occurring at up to twice the frequency in metastases compared to primary tumors (123,124). Furthermore, multifocal tumors within a prostate differ in whether or not they harbor the mutant TP53 gene (123), prostate tumors have been documented to contain more than one p53 mutation (119), and within a single tumor, there is heterogeneity of distribution of mutant p53 (123).…”

Section: Myc Ras P53 Bcl-2 and Telomerasementioning

confidence: 99%

“…Furthermore, multifocal tumors within a prostate differ in whether or not they harbor the mutant TP53 gene (123), prostate tumors have been documented to contain more than one p53 mutation (119), and within a single tumor, there is heterogeneity of distribution of mutant p53 (123). The increased p53 mutation frequency found post-androgen ablation (124) and low p53 levels found after radical radiotherapy (125) indicate that abnormalities in p53 may lead to tumor progression, therapy resistance and association with a more invasive phenotype.…”

Section: Myc Ras P53 Bcl-2 and Telomerasementioning

confidence: 99%