Immunohistochemical Analysis of<i>p53</i>in Gynecologic Tumors

Inoue, Masakí; Fujita, Masami; Enomoto, Takayuki; Morimoto, Hideki; Monden, Takushi; Shimano, Takashi; Tanizawa, O

doi:10.1093/ajcp/102.5.665

Cited by 61 publications

(47 citation statements)

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“…We evaluated data from the USA (Mok et al 1992;Kupryjanczyk et al 1993;1995, Kohler et al 1993a, 1993bTeneriello et al 1993;Wertheim et al 1994;Zheng et al 1995;Casey et al 1996;Skilling et al 1996;DiCioccio et al 1998;Rhei et al 1998;Shigemasa et al 1999;Wen et al 1999;Tworek et al 1999;Leitao et al 2004), Eastern Asia (Japan and Korea) (Kihana et al 1992;Naito et al 1992;Fujita et al 1994;Inoue et al 1994;Niwa et al 1994;Kim et al 1995;Lee et al 1995;Sakamoto et al 1996;Sato et al 1999;Otsuka et al 2004) and Europe. Within Europe, the data from the following countries/regions were available: Poland, Germany (Kappes et al 1995;Meinhold-Heerlein et al 2001), Norway (Skomedal et al 1997;Smith-Sorensen et al 1998;Wang et al 2004aWang et al , 2004b, the United Kingdom (Jacobs et at.…”

Section: Comparative Analysis Of the Tp53 Gene Mutational Spectrummentioning

confidence: 99%

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

Dansonka-Mieszkowska

Ludwig

Kraszewska

et al. 2006

Annals of Human Genetics

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SummaryThe TP53 gene mutational spectrum in human tumours shows variations related to tissue of origin, carcinogen exposure or molecular background. We have compared TP53 mutations in ovarian carcinomas from different geographical regions; this study was based on data extracted and verified from the IARC database (R10, 2005), and on our results from 127 carcinomas. In total 873 mutations were evaluated. Tumours from Japan and Korea had a higher frequency of exon 7 mutations (38% vs 25%, p = 0.011) and lower frequency of exon 8 mutations (11% vs 29%, p = 0.0003) than those from Western countries; they were particularly different from Norwegian tumours which showed the lowest proportion of exon 7 (19%, p = 0.001) and highest proportion of exon 8 (37%, p < 0.0001) mutations. There were also differences in the profile of TP53 hotspots. The third hotspot in tumours from Poland was amino acid (AA) 176 (8.2% of substitutions vs 1.7% in other countries, p < 0.001), while in tumours from the UK it was AA 220 (8.9% vs 2.3%, p < 0.001). Codon 273 was the only apparent hotspot in the Norwegian tumours, while it was rarely mutated in Polish and Asian tumours. In contrast to other data tumours from Norway presented with 273 HIS codon (82% of mutations at AA 273, p = 0.002), while tumours from the UK shared the 273 CYS codon (80%, p < 0.001). Further analysis of TP53 gene mutations in ovarian cancer by geography could provide greater insights.

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Section: Comparative Analysis Of the Tp53 Gene Mutational Spectrummentioning

confidence: 99%

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

Dansonka-Mieszkowska

Ludwig

Kraszewska

et al. 2006

Annals of Human Genetics

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“…Similar to carcinomas, various definitions were used to classify the tumors of LMP as positive for p53. Few studies described their samples using specific percentages of positively stained tumor cells; however, 9 studies 16,21,31,37,40,45,48,58,59 provided information regarding the proportion of tumors that demonstrated staining in Ն 50% of the cells. In contrast to the carcinomas, for which the prevalence of p53 expression in Ն 50% of the cells was 29%, the prevalence among the tumors of LMP was only 5% (95% CI, 3-8%).…”

Section: Lmp Tumorsmentioning

confidence: 99%

A review of p53 expression and mutation in human benign, low malignant potential, and invasive epithelial ovarian tumors

Kmet

Cook

Magliocco

2003

Cancer

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Das rationale Design niedermolekularer Verbindungen, die selektiv auf eine definierte RNA wirken, ist eine schwierige Aufgabe; solche Sonden könnten aber die zeitlich hochaufgelöste Untersuchung von RNA‐Funktionen in Zellen ermöglichen. In der Zuschrift auf identifizieren R. Rodriguez, S. Balasubramanian et al. mit In‐situ‐Klickchemie eine niedermolekulare Substanz, die selektiv mit Telomerwiederholungseinheiten enthaltender RNA (TERRA) über die Erkennung der G‐Quadruplex‐Struktur wechselwirkt. Mit demselben Ansatz wurde ein verwandtes Analogon erkannt, das hoch effizient die entsprechende DNA adressiert.

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“…p53 mutation and its overexpression are more common in PSCE than in endometrioid adenocarcinoma. p53 overexpression as assessed by immunostaining is seen in Յ85% of PSCE tumors, compared with in 20% of endometrioid adenocarcinomas, and correlates with mutation of the p53 gene (13)(14)(15)(16)(17)(18). We have previously reported that p53 overexpression is associated with a poor outcome for patients with lowrisk endometrial carcinoma (defined at our center as Stage Ia or Ib, Grade 1 or 2 endometrioid endometrial adenocarcinoma, without vascular invasion; 19).…”

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confidence: 96%

Markers of Proliferative Activity Are Predictors of Patient Outcome for Low-Grade Endometrioid Adenocarcinoma But Not Papillary Serous Carcinoma of Endometrium

et al. 2002

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On the basis of pathogenesis, two types of endometrial cancer can be recognized. Type 1 endometrial carcinomas are relatively indolent tumors that develop after prolonged estrogen stimulation, on a background of endometrial hyperplasia. Type 2 endometrial carcinomas are aggressive tumors that are not associated with hyperplasia or estrogen excess. The aim of this study is to evaluate the prognostic significance of tumor proliferative activity in early-stage endometrial cancer by using mitotic index and immunostaining, comparing Type 1 (endometrioid) and Type 2 (papillary serous carcinoma) tumors. The mitotic index, MIB-1, and p53 immunostaining in 39 tumors from patients with lowgrade Stage Ia or Ib endometrioid adenocarcinoma; as well as 23 tumors from patients with Stage I papillary serous carcinoma. In low-grade endometrioid adenocarcinoma, mitotic and MIB-1 indices were statistically significant independent prognostic indicators (P ‫؍‬ .004 and P ‫؍‬ .018, respectively), and both were strongly correlated with p53 expression (P ‫؍‬ .01 and P ‫؍‬ .006, respectively). The mean mitotic index was 5 mitoses/10 high-power fields, and mean MIB-1 index was 27.5%. There was no significant correlation between mitotic or MIB-1 indices and patient outcome or p53 expression in papillary serous carcinoma. The mean mitotic index was 31 mitoses/10 high-power fields, and mean MIB-1 index was 30.5% in these tumors. p53 expression and proliferative indices are strongly correlated in low-grade endometrioid adenocarcinoma. MIB-1 and mitotic indices are independent prognostic indicators in these tumors. Papillary serous carcinoma of endometrium is rapidly proliferative in tumors even at an early stage, and quantification of proliferative activity in these tumors does not allow prediction of patient outcome. KEY WORDS: Endometrial carcinoma, MIB-1, Mitotic index, p53, Papillary serous carcinoma, Proliferative activity. Mod Pathol 2002;15(4):365-371Endometrial cancer is the fourth most common malignancy in North American women. In the United States, there are 33,000 newly diagnosed cases and 4,000 deaths per year (1, 2). On the basis of the proposed dualistic model of endometrial carcinogenesis, there are two types of endometrial carcinoma that differ with regard to epidemiologic risk factors, histopathologic lesions, and molecular events (3). Type 1 endometrial carcinomas are relatively indolent tumors that develop after prolonged estrogenic stimulation. Low-grade endometrioid adenocarcinoma is the prototype of Type 1 endometrial carcinoma. Although most of these patients do well, recurrence and death due to disease can occur. Type 2 endometrial carcinomas are more aggressive tumors that are not associated with endometrial hyperplasia or estrogen excess. These tumors develop de novo in the atrophic endometrium of older postmenopausal women (4 -7). Papillary serous carcinoma of endometrium (PSCE) is the prototype of Type 2 endometrial carcinoma and is an uncommon aggressive variant of endometrial cancer. It accounts for 1-10% of cas...

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Immunohistochemical Analysis ofp53in Gynecologic Tumors

Cited by 61 publications

References 0 publications

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

Geographical Variations in TP53 Mutational Spectrum in Ovarian Carcinomas

A review of p53 expression and mutation in human benign, low malignant potential, and invasive epithelial ovarian tumors

Markers of Proliferative Activity Are Predictors of Patient Outcome for Low-Grade Endometrioid Adenocarcinoma But Not Papillary Serous Carcinoma of Endometrium

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