Neoplastic Endometrial Tissues Research Articles

Diagnostic and Prognostic Values of PTEN Expression in Functional and Pathological Endometrial Biopsies

Background: Endometrial carcinoma is the most common gynecological malignancy in developed countries. About 80% of endometrial carcinomas are preceded by atypical endometrial hyperplasia. PTEN is a tumor suppressor gene involved in many vital intracellular biological processes. PTEN is altered in more than 45% of endometrial carcinomas. The aim of this study was to evaluate the value immunohistochemical expression of PTEN in normal, hyperplastic and neoplastic endometrial tissues. Methods: Ninety-two endometrial samples were enrolled in this study. They were classified into normal (n=6), hyperplastic (n=54) and neoplastic (n=32) endometrial tissues. Formalin-fixed and paraffin-embedded tissue blocks were prepared from each specimen. Tissue sections were immunohistochemically stained by anti-PTEN antibodies. Results: In our study; PTEN was strongly expressed in all normal and hyperplastic endometrial tissues without atypia. Staining intensity was decreased in atypical endometrial hyperplasia and endometrial carcinoma (p<0.0001). we also detected an inverse relationship between PTEN expression on one side and tumor grade (p=0.006), stage (p< 0.0001) and myometrial invasion (p=0.001) on the other side. Conclusions: Our study proved that immunohistochemical expression of PTEN is down-regulated in atypical hyperplastic and neoplastic endometrial tissues. Evaluation of PTEN expression can be useful as a screening method to detect the potentially precancerous hyperplastic lesions.

Vascular Pseudoinvasion After Endometrial Ablation.

Vascular pseudoinvasion or displacement of tumor or normal endometrial tissue is a potential pitfall in uterine pathology. The proposed mechanisms of this phenomenon are mostly associated with the uterine manipulator used during minimally invasive hysterectomies. The aim of this report is to describe vascular pseudoinvasion in a still unreported setting, that of a postendometrial ablation hysterectomy, and to provide a summary of studies dealing with artifactual or nonmalignant myometrial vessel involvement by normal or neoplastic endometrial tissue.

A Potential Invasion-Promoting Role for Ezrin in Endometrial Carcinoma

Background:Ezrin is a cell membrane-cytoskeleton linker that is essential to maintain the normal cell shape and the integrity of cell-cell adhesion. Overexpression of ezrin is correlated with poor prognosis in several malignancies. Aim: To evaluate the expression of ezrin in hyperplastic and neoplastic endometrial tissues and to correlate its expression with the clinical and pathological parameters of endometrial carcinoma. Methods: Tissue sections of 66 specimens including 37 endometrial carcinoma, 16 atypical endometrial hyperplasia and 13 benign endometrial hyperplasia were evaluated for ezrin expression by immunohistochemistry. Results: Ezrin expression was detected in all endometrial carcinoma specimens and in 90% of hyperplasia. There was redistribution of ezrin from membranous expression in endometrial hyperplasia to diffuse cytoplasmic expression in endometrial carcinoma (p < 0.0001). Expression of ezrin was significantly higher in atypical compared to benign hyperplasia (p < 0.001) and it was relatively higher in endometrial carcinoma compared to atypical endometrial hyperplasia (p=0.086). Among the carcinoma specimens, expression of ezrin was significantly associated with invasion of myometrium (p=0.001), higher FIGO stage (p=0.008) and the presence of vascular tumor emboli (p=0.001). Muscle-invasive tumor cells expressed significantly higher levels of ezrin compared to non-invasive cells of the same tumor tissue (p < 0.0001). Tumor size, tumor grade and villoglandular morphology did not correlate significantly with ezrin expression. Conclusion: Ezrin was overexpressed in endometrial carcinoma and its expression was associated with the invasive potential of tumor cells.

Balance of glandular and stromal Bcl2/Bax expression in pre-neoplastic and neoplastic endometrial tissues

Balance of glandular and stromal Bcl2/Bax expression in pre-neoplastic and neoplastic endometrial tissues

The Use of microRNAs in the Management of Endometrial Cancer: A Meta-Analysis.

Introduction: Endometrial cancer (EC) is the most important gynecological cancer in terms of incidence. microRNAs (miRs), which are post-transcriptional regulators implicated in a variety of cellular functions including carcinogenesis, are particularly attractive candidates as biomarkers. Indeed, several studies have shown that the miR expression pattern appears to be associated with prognostic factors in EC. Our objective is to review the current knowledge of the role of miRs in carcinogenesis and tumor progression and their association with the prognosis of endometrial cancer. Materials and Method: We performed a literature search for miR expression in EC using MEDLINE, PubMed (the Internet portal of the National Library of Medicine) and The Cochrane Library, Cochrane databases “Cochrane Reviews” and “Clinical Trials” using the following keywords: microRNA, endometrial cancer, prognosis, diagnosis, lymph node, survival, plasma, FFPE (formalin-fixed, paraffin-embedded). The miRs were classified and presented according to their expression levels in cancer tissue in relation to different prognostic factors. Results: Data were collected from 74 original articles and 8 literature reviews which described the expression levels of 261 miRs in ECs, including 133 onco-miRs, 110 miR onco-suppressors, and 18 miRs with discordant functions. The review identified 30 articles studying the expression pattern of miR in neoplastic endometrial tissue compared to benign and/or hyperplastic tissues, 12 articles detailing the expression profile of miRs as a function of lymph node status, and 14 articles that detailed the expression pattern of miRs in endometrial tumor tissue according to overall survival or in the absence of recurrence. Conclusions: The findings presented here suggest that miR analysis merits a role as a prognostic factor in the management of patients with endometrial cancer.

Expression of Bc-l2 in precancerous endometrial lesion and endometrial carcinoma

The oncogene Bcl-2 is known as a unique gene that plays an important role in the carcinogenesis pathway by blocking apoptosis. Aims: To evaluate the expression of Bcl-2 protein in normal, hyperplastic and neoplastic endometrial tissues. Materials and methods: Eighty three cases including 7 cases of normal endometrial changes, 37 cases of endometrial hyperplasia and 39 cases of endometrial adenocarcinoma were enrolled for this study. The expression of Bcl-2, ER and PR was evaluated by immunohistochemistry using streptavidin-biotin technique. Results: Non-malignant endometrial lesions tend to express significantly higher level of Bc-l2 compared to malignant endometrial lesion(p= 0.014). The expression of glandular Bc-l2 was significantly higher in hyperplasia compared to carcinoma(p=0.006).There was no significant association between Bcl-2 expression and tumors` histological type or stage orgrade. There was a correlation between Bcl-2 expression and ER or PR expression in endometrial carcinoma. Conclusions: Bcl-2 expression might represent a key in understanding the progression of endometrial neoplastic lesions.

Effects of pathological assessment of endometrial tissue in fertility-sparing treatment with progestin for endometrial carcinoma of stage I a and complex atypical hyperplasia

To assess the efficacy and pathological change of fertility-sparing treatment with progestin for endometrial carcinoma (EC) of stage I a and complex atypical hyperplasia (CAH) and to observe the prognosis of the treatment. Nine EC patients of stage I a and 21 CAH patients aged under 40 years who desired childbearing and retaining their fertility were enrolled into this study. All patients were given a daily oral high-dose of progestin with duration of treatment ranging from 6 to 9 months. Diagnostic curettage was performed every 3 months as a modality for seeing the histologic change of neoplastic tissues and endometrial tissue. A careful and long- term follow- up is necessary for patients with complete response (CR). During the first period of fertility-sparing management, according to histologic change, 5 EC patients and 18 CAH patients showed CR with no evidence of endometrial adenocarcinoma or hyperplasia, 2 EC patients and 2 CAH patients showed partial response with a regression to complex or simple hyperplasia without atypia, 2 EC patients and 1 CAH patient showed stable disease or progressive disease. Accordingly, a total of 26 patients showed CR (26 of 30 patients). The median time to CR was 6 months (range, 3 to 21 months) of progestin treatment. The median follow-up time was 55.5 months (range, 24 to 104 months) and all patients were alive. During follow-up, among the 26 patients with CR, 3 of 6 EC patients achieved CR recurred disease after a median time interval of 10 months (range, 6 to 51 months), 7 of 20 CAH patients achieved CR had recurrent disease after a median time interval of 12 months (range, 6 to 55 months). Four of 7 CAH with recurrent disease achieved CR to progestin re-treatment. Eight of 26 patients achieved CR continued a further 3 or 6 months of consolidation therapy, 3 of them had recurrent disease, the remaining 18 stopped progesterone treatment after CR and 7 patients had recurrent disease; there was no significant statistical difference between the two groups (P = 1.000). EC patients succeeded in 4 pregnancies, CAH patients succeeded in 10 pregnancies, they gave birth to 16 healthy babies in all. EC of stage I a and CAH had slow progression of symptoms. Progestin treatment in EC of stage I a and CAH patients was effective. A careful and long-term follow-up is required because of the substantial high rate of recurrence. Progestin re-treatment in most patients with recurrent endometrial cancer is effective and safe.

Optimal protocol for PTEN immunostaining; role of analytical and preanalytical variables in PTEN staining in normal and neoplastic endometrial, breast, and prostatic tissues

In some tumors, phosphatase and tensin homolog (PTEN) inactivation may have prognostic importance and predictive value for targeted therapies. Immunohistochemistry (IHC) may be an effective method to demonstrate PTEN loss. It was claimed that PTEN IHC showed poor reproducibility, lack of standardization, and variable effects of preanalytical factors. In this study, we developed an optimal protocol for PTEN IHC, with clone 6H2.1, by checking the relevance of analytical variables in normal tissue and tumors of endometrium, breast, and prostate. Pattern and intensity of cellular staining and background nonspecific staining were quantified and subjected to statistical analysis by linear mixed models. The proposed protocol showed a statistically best performance (P < .05) and included a high target retrieval solution, 1:100 primary antibody dilution (2.925 mg/L), FLEX diluent, and EnVisionFLEX+ detection method, with a sensitivity and specificity of 72.33% and 78.57%, respectively. Staining specificity was confirmed in cell lines and animal models. Endometrial carcinomas with PTEN genetic abnormalities showed statistically lower staining than tumors without alterations (mean histoscores, 34.66 and 119.28, respectively; P = .01). Controlled preanalytical factors (delayed fixation and overfixation) did not show any statistically significant effect on staining with optimal protocol (P > .001). However, there was a trend of significance for decreased staining and fixation under high temperature. Moreover, staining was better in endometrial aspirates than in matched hysterectomy specimens, subjected to less controlled preanalytical variables (mean histoscores, 80 and 40, respectively; P = .002). A scoring system combining intensity of staining and percentage of positive cells was statistically associated with PTEN alterations (P = .01).

Poly(ADP-ribose) polymerase (PARP) and DNA-fragmentation factor (DFF45): Expression and correlation in normal, hyperplastic and neoplastic endometrial tissues

This study evaluated the immunohistochemical expression of poly(ADP-ribose) polymerase (PARP) and DNA fragmentation factor 45 (DFF45) in normal endometria (NE, n=13), non-atypical (NAH, n=22) and atypical hyperplasia (AH, n=14), endometrioid carcinoma (EC, n=34), serous carcinoma (SC, n=10), and clear cell carcinoma (CCC, n=2). With regard to quantity and intensity of positively stained cells, immunostaining was scored as negative, low, and strong. Nuclear PARP immunoreactivity was found in all cases. If present, DFF45 immunoreactivity was detected predominantly in the nucleus and to some extent in the cytoplasm. PARP immunoreactivity increased significantly from NE via NAH to AH ( P=0.0004), and decreased from AH to endometrial carcinomas ( P=0.0054). DFF45 immunoreactivity increased significantly from NE to NAH and to AH ( P=0.0009). No significant differences were calculated between AH and endometrial carcinomas ( P=0.7495). FIGO stages and tumor grades could not be characterized by PARP and DFF45 immunoexpression ( P=1.000 and 0.7383, as well as P=0.3034 and 0.7533, respectively). Pearson correlation revealed significant associations of PARP and DFF45 immunoscores for all diagnostic categories of NE, NAH, AH, EC, and SC/CCC. Immunoexpression of PARP and DFF45 is apparently altered in endometrial carcinomas as compared with non-neoplastic endometrial tissues, indicating impaired mechanisms of apoptosis in the former.

Expression of Aurora kinases A and B in normal, hyperplastic, and malignant human endometrium: Aurora B as a predictor for poor prognosis in endometrial carcinoma

Aurora kinases such as Aurora A and Aurora B are key regulators of mitosis and have been reported to be overexpressed in various malignancies. However, the expression and localization of Aurora kinases in normal and neoplastic endometrial tissues remain undetermined. In the present study, immunohistochemical expression of Aurora A and B was examined in 40 normal, 30 hyperplastic, and 73 malignant endometria. The data were compared with the expression of Ki-67 and patient survivals. The expression of Aurora A and B at protein and messenger RNA levels was also examined using Western blotting and the reverse transcriptase polymerase chain reaction. The expression of Aurora A in normal endometrium was observed mainly in the proliferative phase and was decreased in the secretory phase. The Aurora A expression was significantly increased in carcinomas compared with normal proliferative endometrium; however, there was no correlation of Aurora A expression with Ki-67 expression or patient survival. The expression of Aurora B in normal endometrium was significantly higher in the proliferative phase than in the secretory phase. In endometrial carcinomas, the expression of Aurora B was correlated with Ki-67 expression and was significantly increased in high-grade tumors. In addition, patients with Aurora B-positive carcinoma showed poor prognosis compared with those with Aurora B-negative carcinoma (P = .0135). Accordingly, the present study indicates the aberrant expression of Aurora A and Aurora B in endometrial carcinomas and the clinical importance of Aurora B expression in relationship to patient prognosis.

Expression and intracellular localization of Smad proteins in human endometrial cancer

The aim of our study was to examine expression of Smad proteins i.e., Smad2, Smad3 and Smad4 both as mRNA and protein as well as their intracellular localization in normal (n=13) and neoplastic (n=42) endometrial tissue specimens using RT-PCR and immunological techniques i.e., Western blot and ELISA. Two uncommon female genital tract tumours, rhabdomyosarcoma of uterine of the cervix and uterine carcinosarcoma were also included. No statistically significant differences were found in the mRNA level of the examined Smad proteins between normal and tumour tissue specimens. Smad2 and Smad3 mRNAs were detected both in uterine carcinosarcoma and rhabdomyosarcoma of the uterine cervix. However, significantly lower Smad2 and Smad4 mRNA level was noted when the depth of myometrial invasion was considered (p<0.05). In endometrial cancer as compared to normal endometrium significantly higher levels of Smad2 and Smad3 proteins, both in cytoplasmic (p=0.002; p=0.0001) and nuclear (p=0.016; p=0.0004) fractions were observed. Both in uterine carcinosarcoma and rhabdomyosarcoma of the uterine cervix Smad2, Smad3 and Smad4 proteins were not detected. Moreover, significantly elevated Smad4 protein level in cytoplasmic fraction was stated when tumour grade and depth of myometrial invasion was undertaken (p<0.05). When intracellular distribution of Smads was considered differences between cytoplasmic and nuclear localization in normal and carcinomatous endometrium was stated. In endometrial cancer decreased number of cases with Smad3 and increased number of cases with Smad4 located in nuclear fraction was found. In conclusion, the disturbances in Smad protein expression and/or differences in their intracellular distribution suggest, that TGF-beta signaling pathway via Smads may be deregulated in endometrial carcinomas.

Thrombospondin-1 and -2 messenger RNA expression in normal and neoplastic endometrial tissues: correlation with angiogenesis and prognosis.

The role of thrombospondin (TSP) in tumor angiogenesis and progression remains controversial. The expression of TSP-1 and TSP-2 mRNAs was assessed. Furthermore, TSP association with clinicopathological features, including microvessel count, regarding prognostic significance was examined. Expression of TSP-1 and TSP-2 were assessed by reverse transcriptase-polymerase chain reaction in 18 normal endometrium and 55 endometrial cancer samples. Microvessel counts were determined by immunostaining for factor VIII-related antigen in endometrial cancer specimens. TSP-1 expression of secretory phase endometrium was markedly higher than that of proliferative phase endometrium (p=0.047). Expression of TSP-1 and TSP-2 was detected in 33 (60.0%) and 15 cases (27.3%), respectively, of 55 endometrial cancer samples. TSP-1 expression was significantly higher in tumors recovered from elderly women (p=0.009). TSP-2 expression was significantly higher in malignancies exhibiting cervical and lymph-vascular space involvement (p=0.029 and p=0.009, respectively). Although not statistically significant, microvessel counts were higher in cases displaying increased TSP-1 expression. The microvessel count in patients with TSP-2 expression was markedly higher than that observed in patients lacking TSP-2 expression (p=0.026). Subjects demonstrating TSP-2 mRNA expression displayed significantly poorer prognosis than those lacking TSP-2 mRNA expression (p=0.016). There was no association between TSP-1 mRNA expression and patient outcome. Our findings provide evidence that elevated TSP expression may be associated with an angiogenic phenotype in endometrial cancer. In addition, TSP-2 expression is a marker for poor prognosis in this disease.

Expression of Complement Regulatory Proteins—CD 35, CD 46, CD 55, and CD 59—in Benign and Malignant Endometrial Tissue

Objective.Complement system plays an important role in host defense mechanisms against microorganisms and tumor cells. To protect themselves from autologous complement-mediated damage, normal host tissues express cell membrane-associated complement regulatory proteins (CRPs). To investigate whether neoplastic endometrial tissues overexpress these proteins to escape complement damage, we examined the distribution of complement receptor type 1 (CR1, CD35), membrane cofactor protein (MCP, CD46), decay-accelerating factor (DAF, CD55), and protectin (MACIF, CD59) on frozen endometrial tissue samples.Methods. A total of 54 endometrial tissue samples were collected. Cryosections were obtained of 31 benign and 23 malignant tissue specimens. Tissue sections were stained by immunohistochemical staining procedure using specific antibodies and employing the avidin–biotin technique. Quantitation of the protein content of these CRPs was determined using the Samba 4000 image analysis system.Results. For all four of the CRPs studied, a statistically significant difference in protein expression between the benign and malignant endometrial tissue specimens (P < 0.0001) was observed.Conclusions. Overexpression of all the CRPs studied (CD35, CD46, CD55, CD59) was observed in the malignant as compared with the benign endometrial tissues. The upregulation of these CRPs may promote resistance of the endometrial malignant tissue to complement-mediated damage, thereby allowing the tumor cells to escape from cytolysis and thus promoting carcinogenesis.

Expression of nm23 in Normal, Hyperplastic and Neoplastic Endometrial Tissues

This study evaluated the expression of nm23 in curettage specimens from 63 cases of normal, hyperplastic and neoplastic endometrial tissues by immunohistochemistry. The histological diagnoses were as follows: normal proliferative (N = 5) or secretory (N = 5), simple hyperplasia (N = 11), complex hyperplasia (N = 9), atypical hyperplasia (N = 8) and adenocarcinoma (N = 25), consisting of endometrioid adenocarcinoma (N = 15), clear cell (N = 7) and serous papillary adenocarcinoma (N = 3). There was no immunostaining for nm23 protein in the 10 cases of normal endometria and in the 28 cases of endometrial hyperplasia. In contrast, 52% of the adenocarcinomas displayed a cytoplasmic staining pattern which was moderate to strong. This difference was statistically significant (p < 0.0001, chi-square test). nm23 expression in curettage specimens had no predictive value for determining the FIGO stage in the hysterectomy specimens (p = 0.2709, chi-square test). No significant difference for nm23 immunoreactivity was found between the histologic subtypes of endometrial adenocarcinoma (endometrioid versus serous papillary and clear cell, p = 0.1413, chi-square test). In this study, there was no immunostaining of normal endometria or of endometrial hyperplasia (including atypical endometrial hyperplasia) to support the hypothesis that expression of the nm23 gene product is related to the development of endometrial adenocarcinoma. In contrast, nm23 expression was upregulated in many cases of endometrial adenocarcinomas irrespective of the histologic subtype.

Expression of messenger RNAs for metalloproteinases 2 and 9, type IV collagen, and laminin in nonneoplastic and neoplastic endometrium

In this study, we analyzed the messenger RNA (mRNA) synthesis of matrix metalloproteinases (MMPs) 2 and 9, and their main substrates laminin and type IV collagen by in situ hybridization in nonneoplastic, hyperplastic, and neoplastic endometrial tissues. In nonneoplastic endometrium stromal synthesis of MMP2, laminin and type IV collagen messenger RNA (mRNA) could be detected throughout the cycle. Their synthesis was strongest in the late secretory and decidualized endometrium. In epithelial cells, only laminin mRNA synthesis was observed. MMP9 mRNA was expressed in only stromal and epithelial cells of the decidualized endometrium. In hyperplastic and neoplastic endometrium, the expression of MMP2, MMP9, laminin, and type IV collagen mRNA was variably present in stromal cells, whereas epithelial cells expressed only laminin mRNA, except for one case of a grade III carcinoma, which also showed signals for MMP2 and MMP9 mRNAs in the carcinoma cells. The presence of MMP2, laminin, and IV collagen mRNA in normal endometrium reflects their importance in the tissue response and matrix remodeling during the proliferative and secretory phases of the menstrual cycle. Their mRNA synthesis follows a similar pattern, suggesting that it is associated with hormonal changes during the menstrual cycle. According to the results, MMP9 does not participate in tissue remodeling during the secretory or proliferative phases, but like MMP2, it is found in the neoplastic endometrial stroma, suggesting that it contributes to the invasion of malignant endometrial cells.

Immunohistochemical Localization of Blood Group Substances in Normal and Neoplastic Endometrial Tissues &amp;ndash; With Special Reference to Type 1 Core Chain Expression

Immunohistochemical stainings were performed to observe the expression of the blood group antigens (A, B, H, Lewisa, Lewisb) and lactoseries type 1 core chain in normal and neoplastic endometrial tissues using a panel of monoclonal antibodies. The results indicated that normal endometrium mostly lacked the expression of these sugar structures. In endometrial carcinoma, the expression of H, Lewisa, Lewisb was evident and type 1 core chain was observed only after neuraminidase pretreatment. These data indicated that type 1 core chains were newly synthesized according to malignant transformations in endometrial tissues and they were partially fucosylated and partially sialylated.

Immunohistochemical Reactivity of Antikeratan Sulfate Monoclonal Antibody 5D4 to Various Conditions of Human Endometrial Tissues and Its Application as a Useful Marker for Identifying Endometrial Epithelia

Immunohistochemical staining was performed on normal, endometriotic, neoplastic endometrial tissues and various epithelial tissues of other organs using a monoclonal antibody, 5D4, which was raised originally against skeletal and corneal keratan sulfate. The results showed that this antibody exhibited strong and consistent reactivity to glandular epithelia found in normal and endometriotic tissues. In endometrial carcinomas, moderate reactivity was noted in well- to moderately differentiated adenocarcinoma. Other epithelial tissues examined showed almost no or faint reactivities. These results suggested that 5D4 would be a useful tool for identifying the endometrial glandular epithelia in histochemical studies.

Estrone Sulfatase Activity in Normal and Neoplastic Endometrial Tissues of Human Uterus

Estrone sulfatase activity was measured in normal and neoplastic endometrial tissues of human uterus. The tissue homogenates were incubated in air with [3H] estrone sulfate (E1-S, 20 microM) at 37 degrees C for 30 min. After the enzyme reaction was terminated with ethyl ether, the ethyl ether extract was purified by thin-layer chromatography. The apparent Km of sulfatase was 3.0 microM, and the maximum velocity was 14.7 nmol/h/mg protein. Estrone sulfatase activity in endometrial tissues was detected throughout the menstrual cycle with no significant change. Moreover, estrone sulfatase activity in endometrial cells was not stimulated by the addition of progestogen. The enzyme activity in cancer tissue was significantly higher than in normal tissue. Thus we concluded that this enzyme may play a role in regulating the estrogen action by sifting the intracellular equilibrium between free estrogens and estrogen sulfates. We also concluded that in the endometrial cancer tissue, sulfatase appears to act on local production of estrone.

Detection of chromogranin in argyrophil cells of endometrial carcinoma

Normal and neoplastic endometrial tissues were examined immunohistochemically for chromogranin which was shown to be a specific marker for neuroendocrine cells. All 20 normal endometriums and 20 endometrial carcinomas without argyrophilia were chromogranin negative. Endometrial carcinomas with argyrophilia tested were composed of three groups; 10 with type I argyrophil cells, 20 with type II argyrophil cells, and 10 with both type I and II argyrophil cells. Type I argyrophil cells of 20 endometrial carcinomas were all chromogranin positive. Chromogranin immunoreactivity was also intimately correlated with the Grimelius reactivity in type II argyrophil cells of 19 endometrial carcinomas, 13 with only type II argyrophil cells and 6 with mixed type of argyrophil cells. Chromogranin was absent in type II argyrophil cells of 11 endometrial carcinomas, 7 with type II argyrophil cells and 4 with mixed type of argyrophil cells. Chromogranin negativity was related to the disappearance of argyrophilia after diastase digestion in 5 of these 11 tumors, and also partly to mucinous substances in the remaining 6 tumors. In conclusion, the results obtained suggest that some of type II argyrophil cells are neuroendocrine in nature as well as type I argyrophil cells.

Peanut-agglutinin (PNA) binding in normal and neoplastic endometrial tissue and in cell cultures of endometrial carcinomas

Peanut-agglutinin (PNA) binding in normal and neoplastic endometrial tissue and in cell cultures of endometrial carcinomas