PROGNOSTIC VALUE OF CELL CYCLE PROTEINS p27kip1 AND MIB-1, AND THE CELL ADHESION PROTEIN CD44s IN SURGICALLY TREATED PATIENTS WITH PROSTATE CANCER

VIS, ANDR?? N.; Noordzij, Marinus A.; FITOZ, KUBILAY; Wildhagen, Mark F.; SCHR??DER, FRITZ H.; Kwast, Theo H. van der

doi:10.1097/00005392-200012000-00083

Cited by 14 publications

(20 citation statements)

References 22 publications

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“…This is contradictory to most tumors, where a low p27 Kip1 is associated with poor prognosis, e.g., colorectal, epithelial, ovarian, breast, gastric, Barrett's, esophageal, non-small cell lung, and prostatic carcinomas (18 -21, 32-37). The findings are, however, consistent with previous evidence that p27 Kip1 is often expressed at relatively high levels in human cancer cell lines, which are additionally characterized by increased the expression of cyclin D1 or cyclin E (38,39). Also, high levels of p27 Kip1 are associated with poor survival in invasive cervical carcinoma (16) High proliferative activity, as defined by expression of the Ki-67 analysis (MIB-1) antibody, has been shown to correlate with reduced p27 Kip1 in lymphoid neoplasms, carcinoma of the oral cavity, and endocrine tumors, including pituitary, thyroid, and parathyroid gland hyperplasia (14, 40 -43).…”

Section: Discussionsupporting

confidence: 91%

MIB-1 (KI-67) Proliferation Index and Cyclin-Dependent Kinase Inhibitor p27Kip1 Protein Expression in Nephroblastoma

Ghanem

Kwast

Sudaryo

et al. 2004

Clinical Cancer Research

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Purpose: A number of studies have indicated that the tumor proliferation marker MIB-1 and cell cycle inhibitor p27Kip1 expression are of prognostic importance in a variety of cancers. The present study was performed to evaluate the prognostic value of these molecules in Wilms' tumors.Experimental Design: MIB-1 and p27 Kip1 expressions were investigated by the means of immunohistochemical analysis of 62 Wilms' tumor. Patients were preoperatively treated by chemotherapeutic agents and had a mean follow-up of 5.7 years.Results: MIB-1 and p27 Kip1 were expressed in normal kidney tissues and in the three main components of Wilms' tumor, i.e., the blastemal, epithelial, and stromal cells. In Wilms' tumors, the percentage of MIB-1-positive cells in the blastema ranged between 0 and 42% (mean, 9.4%) and in the epithelial component between 0 and 53% (mean, 19.9%), with a significant difference (P < 0.01). The percentage of blastemal p27Kip1 -positive cells ranged between 3 and 85% (mean, 55.1%) and for the epithelial component between 1 and 87% (mean, 59%). There was a significant inverse relationship between blastemal MIB-1 and p27Kip1 expression in Wilms' tumor. Univariate analysis showed that blastemal MIB-1 and p27Kip1 expression were indicative for clinical progression and tumor-specific survival. In a multivariate analysis, blastemal MIB-1 and p27Kip1 protein expression proved to be an independent prognostic for clinical progression besides stage. Conclusions:It was concluded that both MIB-1-based proliferative activity and p27Kip1 protein expression in the blastema have prognostic impact in Wilms' tumor.

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Section: Discussionsupporting

confidence: 91%

MIB-1 (KI-67) Proliferation Index and Cyclin-Dependent Kinase Inhibitor p27Kip1 Protein Expression in Nephroblastoma

Ghanem

Kwast

Sudaryo

et al. 2004

Clinical Cancer Research

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“…Therefore, the identification of membrane antigens or biomarkers using immunohistochemical techniques has become important for the diagnosis, prognosis, classification and treatment evaluation. It was shown that it is possible to identify predictive markers for biochemical failure [3][4][5], disease recurrence and patient survival after radical prostatectomy [4,6,7]. However, there remains conflicting evidence regarding prognostic influence of an individual marker.…”

Section: Introductionmentioning

confidence: 99%

“…Some studies showed that the proliferation fraction of primary PC, as assessed by Ki-67 (MIB-1) expression was associated with the grade or stage of prostatic cancer and clinical outcome of patients after radical prostatectomy [1,5,10]. However, other authors [7,11] could not see prognostic impact of Ki-67 proliferative activity in their patients' set.…”

Section: Introductionmentioning

confidence: 99%

Expression of Ki-67 (MIB-1) and GLUT-1 proteins in non-advanced prostatic cancer

Łuczyńska

Gasińska²,

Wilk³

2012

pjp

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The expression of Ki-67 (MIB-1) and glucose transporter-1 (GLUT-1) were evaluated in patients with clinically localized prostate cancer (PC) who had undergone radical prostatectomy with curative intent. 140 low advanced PC specimens were studied. Protein expression was assessed immunohistochemically on tumour sections and expressed as a labelling index, i.e. the percentage of positively stained cells. In the case of Ki-67 nuclear staining and in the case of GLUT-1 membrane and cytoplasmic staining was considered as positive. The patients' mean age was 62.9 ±6.2 years. There were 13 (9.3%) at pTNM stage 1, 78 (55.7%) at stage 2, 40 (28.6%) at stage 3 and 9 (6.4%) at stage 4, respectively. 75 (53.6%) tumours were well differentiated (Gleason score ≤ 6), 52 (37.1%) moderately differentiated (Gleason score of 7) and 13 (9.3%) poorly differentiated (Gleason score 8-10). The mean pre-operative serum PSA was 9.9 ± SE 0.5 ng/ml, and the mean LI was equal to 8.1 ±0.6% and 29.7 ±2.0%, for MIB-1 and GLUT-1, respectively. Increase of pathological tumor volume and tumor grade was associated with statistically significant growth of PSA (p < 0.011) and MIB-1 LI (p < 0.003), however, for GLUT-1 LI the relation was not significant. Ki-67 expression was correlated with PSA levels (p = 0.013) and GLUT-1 scores (p = 0.04). In PC, an increase in the proliferation rate (higher MIB-1 LI) in higher pTNM stages and tumour grades may point to Ki-67 as a good marker of biological aggressiveness useful in selecting patients for more aggressive treatment. A correlation between proliferation and GLUT-1 score may be the evidence of active glycolytic metabolism in hypoxic regions.

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“…When both a non-invasive and invasive component coexist in the tumour, loss of p27 KIP1 protein is detected in both carcinoma in situ and invasive tumour, suggesting that events leading to deregulation of p27 KIP1 protein may precede invasion 59 . For example, p27 KIP1 protein is reduced in benign prostatic hypertrophy, a hyperplastic premalignant prostatic neoplasm [65][66][67] . Study of prostate carcinoma also showed variable degrees of reduction in p27 KIP1 staining was frequently observed in the prostatic intraepithelial neoplasia adjacent to invasive carcinoma 66 .…”

Section: P27mentioning

confidence: 99%

Cyclin D1 and P27KIP1: The Gatekeepers of Dysplasia

Love¹

2018

J Immunological Sci

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There is increasing evidence suggesting that cyclins, cyclin-dependent kinases (CDKs), and cyclin-dependent kinase inhibitors (CDIs) either are themselves targets for genetic change in cancer or are disrupted secondarily by other oncogenic events. Cyclin D1 and p27 KIP1 are two important regulators at the G1/S checkpoint. Cyclin D1 is an oncogene of cell cycle regulation with positive effect. Normally, cyclin D1 at G1 is constant or at a very low level and its excessive expression may be associated with the disordered proliferation of cells leading to malignant change. On the other hand, p27KIP1 is an antioncogene for cell cycle regulation, which functions as a negative regulator. Under the regulation of TGF-β, p27KIP1 inhibits the activity of oncogenes and controls the transition of the G1/S phase mainly by the interaction with CDK and CDK-Cyclin in order to inhibit cell proliferation and give cells opportunities to repair DNA. In addition, p27KIP1 not only acts as CDK inhibitor, but also promotes cell differentiation and induces the apoptosis of cells. In this article we review studies that have explored the effects of cyclin D1 and P27 KIP1 on cancer progression and dysplasia with a specific focus on oral dysplasia and oral squamous cell carcinoma (OSCC). We also aim to shed some light on the different means of evaluating the interaction between Cyclin D1 and P27 KIP1 as well as the immunohistochemical reactions associated with different forms of cyclin D1. CELL CYCLEThe cell cycle is the series of events that are required to create two daughter cells from a progenitor cell. The cell division cycle consists of four phases, i.e. G1, S, G2, and M. A cell that is not in the cell cycle is in a quiescent state named G0. G1 is the interval before DNA replication, S is the DNA replication phase, G2 is the interval after DNA replication, M is the mitotic phase. Progression through the cell cycle is governed by a family of cyclin-dependent kinases (CDKs), the activity of which is regulated by phosphorylation The orderly progression through the different phases is assured by proteins that regulate critical checkpoints. Several checkpoints have been identified such as the late G1 phase restriction point, the G1/S phase transition, and the G2/M phase transition. These checkpoints normally verify that the preceding events have been completed before progressing to the next monitor completion of DNA replication and produce signals that interrupt the cell cycle in the event of an error or damage to the genome. Abnormal functioning of checkpoints, such as incapacity in detecting damaged DNA, may play a significant role in tumour progression by permitting cells to progress through the cell cycle with damaged or abnormal DNA 4 .

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PROGNOSTIC VALUE OF CELL CYCLE PROTEINS p27kip1 AND MIB-1, AND THE CELL ADHESION PROTEIN CD44s IN SURGICALLY TREATED PATIENTS WITH PROSTATE CANCER

Cited by 14 publications

References 22 publications

MIB-1 (KI-67) Proliferation Index and Cyclin-Dependent Kinase Inhibitor p27Kip1 Protein Expression in Nephroblastoma

MIB-1 (KI-67) Proliferation Index and Cyclin-Dependent Kinase Inhibitor p27Kip1 Protein Expression in Nephroblastoma

Expression of Ki-67 (MIB-1) and GLUT-1 proteins in non-advanced prostatic cancer

Cyclin D1 and P27KIP1: The Gatekeepers of Dysplasia

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