Expression of COX-2, PCNA, Ki-67 and p53 in gastrointestinal stromal tumors and its relationship with histopathological parameters

Gümürdülü, Derya; Erdoğan, Şeyda; Kayaselçuk, Fazi̇let; Seydaoğlu, Gülşah; Parsak, Cem Kaan; Demircan, Orhan; Tuncer, İlhan

doi:10.3748/wjg.v13.i3.426

Cited by 24 publications

(16 citation statements)

References 27 publications

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“…However, the majority of these studies, as well as ours, were limited by the fact that most of the statistically significant variables based on univariate statistics are not statistically strong enough to 'surviveʼ a further multivariate analysis, leading to the heretic question of whether IHC does actually provide additional prognostic data in GISTs (18). Furthermore, we were unable to confirm the role of differentiation and cell-cycle regulatory proteins, such as Bcl-2, P16 and P53, as well as CD44, as prognostic factors, similar to previous studies (8,(21)(22)(23)(24). The reasons may be different antibodies, antigen retrieval or inter-observer variations of the immunohistochemical staining (10,11,15).…”

Section: Discussioncontrasting

confidence: 41%

Back to the start: Evaluation of prognostic markers in gastrointestinal stromal tumors

Klieser

Pichelstorfer

Weyland

et al. 2016

Molecular and Clinical Oncology

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Abstract. The aim of this study was to provide a standardized risk stratification model for gastrointestinal stromal tumors (GISTs) based on tumor localization, tumor size, involved lymph nodes and metastases, as well as mitotic activity and other morphological and molecular markers, in order to improve the risk evaluation scheme for recurrence, metastatic spread and survival for patients with GIST. A total of 201 cases of patients with GIST were investigated according to standardized morphological markers, including nuclear pleomorphism, tumor cell necrosis, mucosal infiltration, ulceration, skeinoid fibers and growth pattern. In addition, all cases were immunohistochemically analyzed using a tissue microarray platform for various markers of differentiation (CD34, CD44, CD117, desmin, discovered on GIST 1, platelet-derived growth factor receptor α, S-100 and smooth muscle actin) and proliferation (B-cell lymphoma 2, P16, P53, phosphohistone H3 and Ki-67). These findings were correlated by uni-and multivariable analyses with clinicopathological characteristics, including recurrence, metastasis and survival. The general clinicopathological parameters of this GIST specimen cohort were comparable to previous studies. While several parameters exhibited clear associations to each other and to the defined clinical endpoints, the multivariate analysis reduced the number of relevant prognostic variables to localization, margin status, growth pattern and hematoxylin and eosin-based mitosis̸Ki-67-based proliferation of GISTs. With the exception of CD34, none of the applied markers of differentiation and proliferation were found to be independent prognostic markers in GIST and the classical risk factors of GIST remain important prognostic factors. Additionally, growth pattern may predict the risk of recurrence and metastasis in GIST patients. Additional independent molecular prognostic markers remain to be identified and validated.

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Section: Discussioncontrasting

confidence: 41%

Back to the start: Evaluation of prognostic markers in gastrointestinal stromal tumors

Klieser

Pichelstorfer

Weyland

et al. 2016

Molecular and Clinical Oncology

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“…Liu et al (2005) demonstrated that PCNA index was correlated with necrosis, high grade atypia, cellularity and mitotic rate. In contrast, Gumurdulu et al (2007) did not Wnd a correlation of PCNA expression with survival in GISTs. Our observation showed that PCNA expression was lower in imatinib-responsive GISTs than acquired resistance tumors, suggesting that PCNA may act as the marker of GIST imatinib response.…”

Section: Discussionmentioning

confidence: 57%

Molecular mechanisms of secondary imatinib resistance in patients with gastrointestinal stromal tumors

Wang

Huang

Zhou

et al. 2009

J Cancer Res Clin Oncol

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“…Ki-67 antigen is expressed in proliferative cells throughout the G1, S, G2, and M phases, and provides a reliable index of cellular proliferation 3,4 PCNA is an acidic nuclear protein, expressed mainly in phase S of the cellular cycle. It becomes active, in various tissues par-ticularly in nervous tissue, as a first response to multiple insults.…”

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confidence: 99%

Ki-67 and PCNA expression in prostate cancer and benign prostatic hyperplasia

Zhong¹,

Peng²,

He³

et al. 2008

CIM

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Clin Invest Med 2008; 31 (1): E8-E15. AbstractObjective: Ki-67 is a proliferation-associated nuclear antigen and is expressed in all cycling cells except for resting cells in the G0-phase. PCNA is an acidic nuclear protein and has been recognized as a histologic marker for the G1/ S phase in the cell cycle. Ki-67and PCNA labeling indices are considered to reflect cell proliferation, particularly, growth fraction. The purpose of this study is to investigate the expression levels of Ki-67 and PCNA in prostate cancer (PCa) and benign prostatic hyperplasia (BPH) and their potential on the early diagnosis of PCa. Methods: Human prostate cancer cell lines LNCaP and PC-3, human normal prostate epithelial cell line HuPEC, tissues from patients with PCa (121 cases) and BPH (45) and 36 normal cases were examined for the expression of Ki-67 and PCNA by Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Then, the association of Ki-67 and PCNA expression with clinical grading of PCa was analyzed by immunohistochemistry staining. Results: The ratios of PCNA and Ki-67 expression levels in LNCaP and PC-3 were higher (P<0.05, P<0.001) than that in HuPEC. The two markers were differentially expressed in three tissues and showed increased expression in PCa (P<0.05) and BPH (P<0.05), relative to human normal prostate tissues. Compared with BPH, the ratio of Ki-67 and PCNA expressed in tumour tissue was increased (P<0.05). The increase of Ki-67 was greater than that of PCNA. Expression of the two markers increased after different grading of PCa cases Prostate cancer (PCa) is the second most frequent cause of male cancer-related death in the United States of America (USA) and Western Europe. Its incidence is continuously rising, with over 200 000 new cancers and 35 000~40 000 deaths per year, 1 Carcinogenesis and the mechanisms influencing the progression and prognosis of PCa is a multistep process, involving both genetic insults to epithelial cells and changes in epithelial-stromal interactions. 2 Despite extensive research PCa is not understood.There are two proliferative markers-Ki-67 and proliferating cell nuclear antigen (PCNA). Ki-67 antigen is expressed in proliferative cells throughout the G1, S, G2, and M phases, and provides a reliable index of cellular proliferation 3,4 PCNA is an acidic nuclear protein, expressed mainly in phase S of the cellular cycle. It becomes active, in various tissues par-

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Expression of COX-2, PCNA, Ki-67 and p53 in gastrointestinal stromal tumors and its relationship with histopathological parameters

Cited by 24 publications

References 27 publications

Back to the start: Evaluation of prognostic markers in gastrointestinal stromal tumors

Back to the start: Evaluation of prognostic markers in gastrointestinal stromal tumors

Molecular mechanisms of secondary imatinib resistance in patients with gastrointestinal stromal tumors

Ki-67 and PCNA expression in prostate cancer and benign prostatic hyperplasia

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