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Ie Ming Shih - One of the best experts on this subject based on the ideXlab platform.

  • Loss of ARID1A expression correlates with stages of tumor progression in uterine Endometrioid Carcinoma.
    The American journal of surgical pathology, 2013
    Co-Authors: Tsui Lien Mao, Laura Ardighieri, Ayse Ayhan, Kuan-ting Kuo, Tian-li Wang, Ie Ming Shih
    Abstract:

    ARID1A is a recently identified tumor suppressor that functions in chromatin remodeling. Inactivating mutations of ARID1A and loss of its expression most frequently occur in ovarian clear cell Carcinoma, ovarian Endometrioid Carcinoma, and uterine Endometrioid Carcinoma. In this study, we performed a detailed immunostaining analysis of ARID1A in 246 cases including benign endometrium and Endometrioid Carcinoma at different stages of progression. Special attention was paid to recording intratumoral heterogeneity of clonal loss of ARID1A immunoreactivity. All normal endometria (n=51) and endometrial polyps (n=14) retained ARID1A expression. Among complex atypical hyperplasias (n=38), 16% exhibited clonal loss of ARID1A, but none showed complete loss. Among low-grade Endometrioid Carcinomas (n=88), 25% exhibited complete loss and 24% exhibited clonal loss. In contrast, 44% of high-grade Endometrioid Carcinomas (n=55) showed complete loss of ARID1A, and 9% exhibited clonal loss. We found that 19 high-grade Carcinomas also contained concurrent low-grade Carcinomas. In the high-grade areas, 63% exhibited complete loss and 11% exhibited clonal loss, whereas in the low-grade areas, 37% exhibited complete loss and 42% clonal loss. In 5 of these 19 cases, progressive loss of ARID1A from retention or clonal loss to complete loss was observed between the low-grade and high-grade areas. Overall, the percentage of complete ARID1A loss increased from 0% in complex atypical hyperplasia, to 25% in low-grade Endometrioid Carcinoma, to 44% in high-grade Endometrioid Carcinoma. These findings suggest that loss of ARID1A expression, presumably due to mutation, plays an important role in tumor progression of uterine Endometrioid Carcinoma.

  • Evolution of a trophoblastic tumor from an Endometrioid Carcinoma--a morphological and molecular analysis.
    International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists, 2011
    Co-Authors: Mathew T. Olson, Christopher D. Gocke, Robert L. Giuntoli, Ie Ming Shih
    Abstract:

    We report the clinicopathological and molecular characteristics of a rare uterine Endometrioid Carcinoma with a nongestational trophoblastic neoplastic component that was composed of both chorioCarcinoma and epithelioid trophoblastic tumor. Molecular genetic analysis showed a clonal evolution from Endometrioid Carcinoma to trophoblastic tumor. The findings from this case have both diagnostic and biological implications that may inspire future studies on the pathogenic mechanisms by which cancer stem cells assume aberrant differentiation programs and the molecular switch(es) that initiates trophoblastic differentiation in adult tumor tissues.

  • Mutation and loss of expression of ARID1A in uterine low-grade Endometrioid Carcinoma
    The American journal of surgical pathology, 2011
    Co-Authors: Bin Guan, Tsui Lien Mao, Tian-li Wang, Pradeep K. Panuganti, Elisabetta Kuhn, Robert J. Kurman, Daichi Maeda, Elizabeth H. Chen, Yung-ming Jeng, Ie Ming Shih
    Abstract:

    ARID1A is a recently identified tumor suppressor gene that is mutated in approximately 50% of ovarian clear cell and 30% of ovarian Endometrioid Carcinomas. The mutation is associated with loss of protein expression as assessed by immunohistochemistry. In this study, we evaluated ARID1A immunoreactivity in a wide variety of Carcinomas to determine the prevalence of ARID1A inactivation in Carcinomas. Mutational analysis of ARID1A was carried out in selected cases. Immunoreactivity was not detected (corresponding to inactivation or mutation of ARID1A) in 36 (3.6%) of 995 tumors. Uterine low-grade Endometrioid Carcinomas showed a relatively high-frequency loss of ARID1A expression, as 15 (26%) of 58 cases were negative. The other tumor that had a relatively high-frequency loss of ARID1A expression was gastric Carcinoma (11%). Mutational analysis showed 10 (40%) of 25 uterine Endometrioid Carcinomas; none of 12 uterine serous Carcinomas and none of 56 ovarian serous and mucinous Carcinomas harbored somatic ARID1A mutations. All mutations in Endometrioid Carcinomas were nonsense or insertion/deletion mutations, and tumors with ARID1A mutations showed complete loss or clonal loss of ARID1A expression. In conclusion, this study is the first large-scale analysis of a wide variety of Carcinomas showing that uterine low-grade Endometrioid Carcinoma is the predominant tumor type harboring ARID1A mutations and frequent loss of ARID1A expression. These findings suggest that the molecular pathogenesis of low-grade uterine Endometrioid Carcinoma is similar to that of ovarian low-grade Endometrioid and clear cell Carcinoma, tumors that have previously been shown to have a high-frequency loss of expression and mutation of ARID1A.

Toshiro Niki - One of the best experts on this subject based on the ideXlab platform.

  • stromal p16 expression helps distinguish atypical polypoid adenomyoma from myoinvasive Endometrioid Carcinoma of the uterus
    The American Journal of Surgical Pathology, 2019
    Co-Authors: Atsushi Kihara, Yusuke Amano, Taichiro Yoshimoto, Daisuke Matsubara, Noriyoshi Fukushima, Hiroyuki Fujiwara, Toshiro Niki
    Abstract:

    Atypical polypoid adenomyoma (APA) is a polypoid lesion that is comprised of atypical endometrial glands and fibromuscular stroma, which pathologists often confuse with myoinvasive Endometrioid Carcinoma. Here, we characterized the immunohistochemical and molecular features of the stromal components of APA to find distinct markers between APA and myoinvasive Endometrioid Carcinoma. First, we examined the immunohistochemical expression and gene mutations that were previously investigated in uterine and breast fibroepithelial lesions using 12 cases of APA. α-smooth muscle actin was diffusely positive in the stromal component in all cases, whereas desmin and h-caldesmon were focally expressed in 8 cases. Positive expression was also observed in 9 cases for CD10, 12 cases for estrogen receptor, 3 cases for HMGA2, and 3 cases for MDM2. All cases showed normal p53 expression and negative staining of HMGA1 and nuclear β-catenin. No mutations in MED12 exon 2 and the TERT promoter were found in any cases. p16 was positive in all cases and showed diffuse expression in 10 cases. We assessed stromal p16 expression in 84 cases of myoinvasive Endometrioid Carcinoma. The stromal p16 status was negative in all myoinvasive Carcinomas, but there was 1 case with focal staining. There was a significant difference in stromal p16 expression between APA and myoinvasive Endometrioid Carcinoma (P<0.001). Stromal p16 expression was more suggestive of APA than myoinvasive Endometrioid Carcinoma among endometrial fibroepithelial lesions.

  • Stromal p16 Expression Helps Distinguish Atypical Polypoid Adenomyoma From Myoinvasive Endometrioid Carcinoma of the Uterus.
    The American journal of surgical pathology, 2019
    Co-Authors: Atsushi Kihara, Yusuke Amano, Taichiro Yoshimoto, Daisuke Matsubara, Noriyoshi Fukushima, Hiroyuki Fujiwara, Toshiro Niki
    Abstract:

    Atypical polypoid adenomyoma (APA) is a polypoid lesion that is comprised of atypical endometrial glands and fibromuscular stroma, which pathologists often confuse with myoinvasive Endometrioid Carcinoma. Here, we characterized the immunohistochemical and molecular features of the stromal components of APA to find distinct markers between APA and myoinvasive Endometrioid Carcinoma. First, we examined the immunohistochemical expression and gene mutations that were previously investigated in uterine and breast fibroepithelial lesions using 12 cases of APA. α-smooth muscle actin was diffusely positive in the stromal component in all cases, whereas desmin and h-caldesmon were focally expressed in 8 cases. Positive expression was also observed in 9 cases for CD10, 12 cases for estrogen receptor, 3 cases for HMGA2, and 3 cases for MDM2. All cases showed normal p53 expression and negative staining of HMGA1 and nuclear β-catenin. No mutations in MED12 exon 2 and the TERT promoter were found in any cases. p16 was positive in all cases and showed diffuse expression in 10 cases. We assessed stromal p16 expression in 84 cases of myoinvasive Endometrioid Carcinoma. The stromal p16 status was negative in all myoinvasive Carcinomas, but there was 1 case with focal staining. There was a significant difference in stromal p16 expression between APA and myoinvasive Endometrioid Carcinoma (P

Atsushi Kihara - One of the best experts on this subject based on the ideXlab platform.

  • stromal p16 expression helps distinguish atypical polypoid adenomyoma from myoinvasive Endometrioid Carcinoma of the uterus
    The American Journal of Surgical Pathology, 2019
    Co-Authors: Atsushi Kihara, Yusuke Amano, Taichiro Yoshimoto, Daisuke Matsubara, Noriyoshi Fukushima, Hiroyuki Fujiwara, Toshiro Niki
    Abstract:

    Atypical polypoid adenomyoma (APA) is a polypoid lesion that is comprised of atypical endometrial glands and fibromuscular stroma, which pathologists often confuse with myoinvasive Endometrioid Carcinoma. Here, we characterized the immunohistochemical and molecular features of the stromal components of APA to find distinct markers between APA and myoinvasive Endometrioid Carcinoma. First, we examined the immunohistochemical expression and gene mutations that were previously investigated in uterine and breast fibroepithelial lesions using 12 cases of APA. α-smooth muscle actin was diffusely positive in the stromal component in all cases, whereas desmin and h-caldesmon were focally expressed in 8 cases. Positive expression was also observed in 9 cases for CD10, 12 cases for estrogen receptor, 3 cases for HMGA2, and 3 cases for MDM2. All cases showed normal p53 expression and negative staining of HMGA1 and nuclear β-catenin. No mutations in MED12 exon 2 and the TERT promoter were found in any cases. p16 was positive in all cases and showed diffuse expression in 10 cases. We assessed stromal p16 expression in 84 cases of myoinvasive Endometrioid Carcinoma. The stromal p16 status was negative in all myoinvasive Carcinomas, but there was 1 case with focal staining. There was a significant difference in stromal p16 expression between APA and myoinvasive Endometrioid Carcinoma (P<0.001). Stromal p16 expression was more suggestive of APA than myoinvasive Endometrioid Carcinoma among endometrial fibroepithelial lesions.

  • Stromal p16 Expression Helps Distinguish Atypical Polypoid Adenomyoma From Myoinvasive Endometrioid Carcinoma of the Uterus.
    The American journal of surgical pathology, 2019
    Co-Authors: Atsushi Kihara, Yusuke Amano, Taichiro Yoshimoto, Daisuke Matsubara, Noriyoshi Fukushima, Hiroyuki Fujiwara, Toshiro Niki
    Abstract:

    Atypical polypoid adenomyoma (APA) is a polypoid lesion that is comprised of atypical endometrial glands and fibromuscular stroma, which pathologists often confuse with myoinvasive Endometrioid Carcinoma. Here, we characterized the immunohistochemical and molecular features of the stromal components of APA to find distinct markers between APA and myoinvasive Endometrioid Carcinoma. First, we examined the immunohistochemical expression and gene mutations that were previously investigated in uterine and breast fibroepithelial lesions using 12 cases of APA. α-smooth muscle actin was diffusely positive in the stromal component in all cases, whereas desmin and h-caldesmon were focally expressed in 8 cases. Positive expression was also observed in 9 cases for CD10, 12 cases for estrogen receptor, 3 cases for HMGA2, and 3 cases for MDM2. All cases showed normal p53 expression and negative staining of HMGA1 and nuclear β-catenin. No mutations in MED12 exon 2 and the TERT promoter were found in any cases. p16 was positive in all cases and showed diffuse expression in 10 cases. We assessed stromal p16 expression in 84 cases of myoinvasive Endometrioid Carcinoma. The stromal p16 status was negative in all myoinvasive Carcinomas, but there was 1 case with focal staining. There was a significant difference in stromal p16 expression between APA and myoinvasive Endometrioid Carcinoma (P

  • Clinicopathologic Association and Prognostic Value of Microcystic, Elongated, and Fragmented (MELF) Pattern in Endometrial Endometrioid Carcinoma.
    The American journal of surgical pathology, 2017
    Co-Authors: Atsushi Kihara, Hiroshi Yoshida, Reiko Watanabe, Kenta Takahashi, Tomoyasu Kato, Yoshinori Ino, Masanobu Kitagawa, Nobuyoshi Hiraoka
    Abstract:

    Microcystic, elongated, and fragmented (MELF) pattern is seen in the invasive front of some endometrial Endometrioid Carcinomas. Although MELF pattern can be expected as an indicator of patient outcomes, its prognostic significance remains unclear. This study was conducted to elucidate clinicopathologic features and the prognostic impact of MELF pattern in patients with endometrial Endometrioid Carcinoma. We retrospectively analyzed data of 479 consecutive patients with endometrial Endometrioid Carcinoma that had been surgically resected. In 45 of 427 patients (11%) with low-grade Endometrioid Carcinoma, MELF pattern was found, but it was found in none of the 52 patients with high-grade Endometrioid Carcinoma. Among the patients with low-grade Endometrioid Carcinoma, MELF pattern was associated significantly with larger tumor size, myometrial invasion of more than 50%, advanced International Federation of Gynecology and Obstetrics stages, lymphovascular space invasion, lymph node metastasis, papillary architecture, and mucinous differentiation. However, survival analysis revealed that the patients with MELF pattern showed no significantly worse prognosis than those without MELF pattern either in disease-specific survival or in recurrence-free survival. MELF was not a significant prognosticator after adjustment for International Federation of Gynecology and Obstetrics stage (disease-specific survival [hazard ratio, 1.47; 95% confidence interval, 0.28-7.67; P=0.64], recurrence-free survival [hazard ratio, 0.98, 95% confidence interval, 0.32-2.99, P=0.98]). Immunohistochemical analysis revealed that MELF pattern was positive for p16 and p21 and almost negative for Ki-67 labeling, which suggested that tumor cells in MELF pattern were involved in growth arrest or cellular senescence. We conclude that MELF pattern could have little impact on outcomes of patients with low-grade endometrial Endometrioid Carcinoma.

Martin Köbel - One of the best experts on this subject based on the ideXlab platform.

  • High-grade Endometrioid Carcinoma of the Ovary: A Clinicopathologic Study of 30 Cases.
    The American journal of surgical pathology, 2018
    Co-Authors: Hisham Assem, Peter F Rambau, Sandra Lee, Travis Ogilvie, Anna Sienko, Linda E Kelemen, Martin Köbel
    Abstract:

    Although infrequently encountered, the diagnosis of ovarian high-grade Endometrioid Carcinoma remains a diagnostic challenge with potential consequences for targeted therapies and genetic counselling. We studied the clinical, morphologic, and immunohistochemical features of ovarian high-grade Endometrioid Carcinomas and their diagnostic reproducibility compared with tuboovarian high-grade serous Carcinomas. Thirty cases confirmed as International Federation of Gynecology and Obstetrics grade 3 Endometrioid Carcinomas were identified from 182 ovarian Endometrioid Carcinomas diagnosed in Alberta, Canada, between 1978 and 2010, from the population-based Alberta Ovarian Tumor Types cohort. Cases of lower grade Endometrioid and high-grade serous Carcinoma served for comparison. Ten immunohistochemical markers were assessed on tissue microarrays. Clinical data were abstracted and survival analyses performed using Cox regression. Interobserver reproducibility for histologic type was assessed using 1 representative hematoxylin and eosin-stained slide from 25 randomly selected grade 3 Endometrioid Carcinomas and 25 high-grade serous Carcinomas. Histotype was independently assigned by 5 pathologists initially blinded to immunohistochemical WT1/p53 status, with subsequent reassessment unblinded to WT1/p53 status. Patients diagnosed with grade 3 Endometrioid Carcinoma had a significantly longer survival compared with high-grade serous Carcinoma in univariate analysis (hazard ratio [HR]=0.34, 95% confidence interval [CI]=0.16-0.67, P=0.0012) but not after adjusting for age, stage, treatment center, and residual tumor (HR=1.01, 95% CI=0.43-2.16, P=0.98). Grade 3 Endometrioid Carcinoma cases (N=30) were identical to grade 2 Endometrioid Carcinoma cases (N=23) with respect to survival in univariate analysis (HR=1.07, 95% CI=0.39-3.21, P=0.89) and immunohistochemical profile. Using histomorphology alone, interobserver agreement for the diagnosis of grade 3 Endometrioid or high-grade serous Carcinoma was 69%, which significantly increased (P

  • high grade Endometrioid Carcinoma of the ovary a clinicopathologic study of 30 cases
    The American Journal of Surgical Pathology, 2018
    Co-Authors: Hisham Assem, Peter F Rambau, Sandra Lee, Travis Ogilvie, Anna Sienko, Linda E Kelemen, Martin Köbel
    Abstract:

    Although infrequently encountered, the diagnosis of ovarian high-grade Endometrioid Carcinoma remains a diagnostic challenge with potential consequences for targeted therapies and genetic counselling. We studied the clinical, morphologic, and immunohistochemical features of ovarian high-grade Endometrioid Carcinomas and their diagnostic reproducibility compared with tuboovarian high-grade serous Carcinomas. Thirty cases confirmed as International Federation of Gynecology and Obstetrics grade 3 Endometrioid Carcinomas were identified from 182 ovarian Endometrioid Carcinomas diagnosed in Alberta, Canada, between 1978 and 2010, from the population-based Alberta Ovarian Tumor Types cohort. Cases of lower grade Endometrioid and high-grade serous Carcinoma served for comparison. Ten immunohistochemical markers were assessed on tissue microarrays. Clinical data were abstracted and survival analyses performed using Cox regression. Interobserver reproducibility for histologic type was assessed using 1 representative hematoxylin and eosin-stained slide from 25 randomly selected grade 3 Endometrioid Carcinomas and 25 high-grade serous Carcinomas. Histotype was independently assigned by 5 pathologists initially blinded to immunohistochemical WT1/p53 status, with subsequent reassessment unblinded to WT1/p53 status. Patients diagnosed with grade 3 Endometrioid Carcinoma had a significantly longer survival compared with high-grade serous Carcinoma in univariate analysis (hazard ratio [HR]=0.34, 95% confidence interval [CI]=0.16-0.67, P=0.0012) but not after adjusting for age, stage, treatment center, and residual tumor (HR=1.01, 95% CI=0.43-2.16, P=0.98). Grade 3 Endometrioid Carcinoma cases (N=30) were identical to grade 2 Endometrioid Carcinoma cases (N=23) with respect to survival in univariate analysis (HR=1.07, 95% CI=0.39-3.21, P=0.89) and immunohistochemical profile. Using histomorphology alone, interobserver agreement for the diagnosis of grade 3 Endometrioid or high-grade serous Carcinoma was 69%, which significantly increased (P<0.0001) to 96% agreement with the knowledge of WT1/p53 status. Our data support the diagnostic value of WT1/p53 status in differentiating between grade 3 Endometrioid Carcinoma and high-grade serous Carcinoma. However, grade 3 and grade 2 Endometrioid Carcinomas showed no differences in immunophenotype or clinical parameters, suggesting that they could be combined into a single group.

  • pik3ca missense mutation is associated with unfavorable outcome in grade 3 Endometrioid Carcinoma but not in serous endometrial Carcinoma
    Gynecologic Oncology, 2014
    Co-Authors: John B Mcintyre, Gregg Nelson, Prafull Ghatage, Don Morris, Maire A Duggan, Chenghan Lee, Corinne M Doll, Martin Köbel
    Abstract:

    Abstract Objective To evaluate the outcome association of PIK3CA mutational status within histological types of rigorously classified high-grade endometrial Carcinomas. Methods We assessed PIK3CA mutational status in exon 9 and exon 20 hot spots by Sanger sequencing of DNA derived from formalin fixed paraffin embedded tissue of 57 grade 3 Endometrioid, 26 serous, 11 clear cell and 5 dedifferentiated Carcinomas. We correlated PIK3CA mutation status with clinicopathological and other molecular parameters. Univariate and multivariate disease specific survival analysis was performed using Kaplan–Meier and Cox regression analyses. Results PIK3CA exon 9 or exon 20 missense mutations were identified in 20 of 99 (20%) high-grade endometrial Carcinomas without significant difference across histological types (p=0.22). Presence of PIK3CA exon 9 or exon 20 missense mutations was associated with shorter disease specific survival within grade 3 Endometrioid (p=0.0029) but not endometrial serous (p=0.57) Carcinoma based on univariate analysis. Within grade 3 Endometrioid Carcinoma, PIK3CA exon 9 or exon 20 missense mutations were more commonly observed in cases that were deficient for mismatch repair protein expression (p=0.0058) and showed loss of ARID1A expression (p=0.037). Conclusions PIK3CA exon 9 or exon 20 missense mutations are present across all histological types of high-grade endometrial Carcinomas but a significant outcome association is only seen in grade 3 Endometrioid Carcinoma, suggesting a greater biological importance in this tumor type.

  • Characterization of the molecular differences between ovarian Endometrioid Carcinoma and ovarian serous Carcinoma
    The Journal of Pathology, 2009
    Co-Authors: Jason Madore, Fengge Ren, A. Filali-mouhim, Lilia Sanchez, Martin Köbel, Patricia N. Tonin, David G. Huntsman, Diane Provencher, Anne-marie Mes-masson
    Abstract:

    The histopathological diagnosis of high-grade Endometrioid and serous Carcinoma of the ovary is poorly reproducible under the current morphology based classification system, especially for anaplastic, high-grade tumours. The transcription factor Wilms' tumour-1 (WT1) is differentially expressed among the gynaecological epithelia from which epithelial ovarian cancers (EOCs) are believed to originate. In EOCs, WT1 protein is observed in the majority of serous Carcinomas and in up to 30% of Endometrioid Carcinomas. It is unclear whether the latter is a reflection of the actual incidence of WT1 protein expression in Endometrioid Carcinomas, or whether a significant number of high-grade serous Carcinomas have been misclassified as Endometrioid Carcinoma. Several genetic aberrations are reported to occur in EOCs. These include mutation of the TP53 gene, aberrant activation of beta-catenin signalling and loss of PTEN protein expression, among others. It is unclear whether these aberrations are histotype-specific. The aim of this study was to better define the molecular characteristics of serous and Endometrioid Carcinomas in an attempt to address the problems with the current histopathological classification methods. Gene expression profiles were analysed to identify reproducible gene expression phenotypes for Endometrioid and serous Carcinomas. Tissue microarrays (TMA) were used to assess the incidence of TP53, beta-catenin and PTEN aberrations in order to correlate their occurrence with WT1 as an immunohistochemistry based biomarker of serous histotype. It was found that nuclear WT1 protein expression can identify misclassified high-grade Endometrioid Carcinomas and these tumours should be reassigned to serous histotype. Although low-grade Endometrioid Carcinomas rarely progress to high-grade Carcinomas, a combined WT1-negative, TP53-positive immunophenotype may identify an uncommon high-grade subtype of ovarian Endometrioid Carcinoma. GEO database: array data accession number GSE6008.

Hitoshi Tsuda - One of the best experts on this subject based on the ideXlab platform.

  • Aquaporin 3 Expression in Endometrioid Carcinoma of the Uterine Body Correlated With Early Stage and Lower Grade
    Pathology & Oncology Research, 2020
    Co-Authors: Takanori Watanabe, Kimiya Sato, Morikazu Miyamoto, Masashi Takano, Takako Kono, Yoji Yamagishi, Fumihisa Kumazawa, Hitoshi Tsuda
    Abstract:

    Aquaporins (AQPs) are a family of transmembrane water channel proteins distributed in various human tissues. Recent studies revealed that AQPs play important roles in cancer biology. Few studies have documented the relationship between the prognosis, stage, and histological grade of uterine Endometrioid Carcinoma, with AQP expression. Hence, the present study aimed to investigate this relationship between uterine Endometrioid Carcinoma and AQP expression. We retrospectively reviewed records of the patients who underwent surgery for uterine body cancer between 1990 and 2010 at the National Defense Medical College Hospital, Saitama, Japan. In 241 cases of Endometrioid Carcinoma, we immunohistochemically examined the expression of AQP 1, 2, 3, 4, and 5, and their relationship with clinicopathological parameters and the patients’ prognosis. We investigated the relationship between the clinicopathological parameters and AQP3 expression, and found that as the FIGO stage and histological grade progressed, the percentage of AQP3 expression tends to decrease. Furthermore, we analyzed progression-free survival/overall survival (PFS/OS) using the log-rank test, and found that the AQP3-positive group had a better prognosis than AQP3-negative group (PFS: P  

  • Aquaporin 3 Expression in Endometrioid Carcinoma of the Uterine Body Correlated With Early Stage and Lower Grade.
    Pathology oncology research : POR, 2020
    Co-Authors: Takanori Watanabe, Kimiya Sato, Morikazu Miyamoto, Masashi Takano, Takako Kono, Yoji Yamagishi, Fumihisa Kumazawa, Hitoshi Tsuda
    Abstract:

    Aquaporins (AQPs) are a family of transmembrane water channel proteins distributed in various human tissues. Recent studies revealed that AQPs play important roles in cancer biology. Few studies have documented the relationship between the prognosis, stage, and histological grade of uterine Endometrioid Carcinoma, with AQP expression. Hence, the present study aimed to investigate this relationship between uterine Endometrioid Carcinoma and AQP expression. We retrospectively reviewed records of the patients who underwent surgery for uterine body cancer between 1990 and 2010 at the National Defense Medical College Hospital, Saitama, Japan. In 241 cases of Endometrioid Carcinoma, we immunohistochemically examined the expression of AQP 1, 2, 3, 4, and 5, and their relationship with clinicopathological parameters and the patients' prognosis. We investigated the relationship between the clinicopathological parameters and AQP3 expression, and found that as the FIGO stage and histological grade progressed, the percentage of AQP3 expression tends to decrease. Furthermore, we analyzed progression-free survival/overall survival (PFS/OS) using the log-rank test, and found that the AQP3-positive group had a better prognosis than AQP3-negative group (PFS: P < 0.001, OS: P = 0.002, respectively). Using Cox's univariate proportional hazard model, we revealed that AQP3 had a low hazard ratio. However, according to Cox's multivariate proportional hazard model, AQP3 was not an independent prognostic factor. Among the Endometrioid Carcinoma patients, the AQP3-positive group was associated with early stage and lower grade compared to the AQP3-negative group. Therefore, AQP3 has the potential to serve as a predictor of prognosis, although further investigation is necessary to elucidate the biological mechanism of AQP3 in Endometrioid Carcinoma.

  • Correlation of high LAT1 expression with the prognosis of Endometrioid Carcinoma of the uterine corpus
    Virchows Archiv, 2020
    Co-Authors: Kimiya Sato, Morikazu Miyamoto, Masashi Takano, Hitoshi Tsuda
    Abstract:

    The expression of L-type amino acid transporter 1 (LAT1) has been described to play essential roles in cancer cell growth and survival. To determine the significance of LAT1 in the prognosis of endometrial Endometrioid Carcinoma, we investigated LAT1 expression in 353 Endometrioid Carcinoma patients by immunohistochemical analysis using tissue microarray. The tumors in which stained tumor cells made up more than 25% of the tumor were graded as high expression. High expression of LAT1 was detected in 29 (8.2%) of patients. The ratio of high LAT1 expression did not significantly differ by age (