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A Berchuck

Publications and source records attributed to A Berchuck.

At least 55 records · Page 3Linked to original sources
PubMed1997

Relationship between lifetime ovulatory cycles and overexpression of mutant p53 in epithelial ovarian cancer.

BACKGROUND: Several lines of evidence have suggested a relationship between a woman's number of ovulatory cycles and the development of ovarian epithelial cancer. Repair of the ovarian surface after ovulation requires cellular proliferation, and spontaneous mutations arising during the DNA synthesis that accompanies this proliferation may play a role in carcinogenesis. PURPOSE: We conducted a molecular epidemiologic study to test the hypothesis that a greater number of ovulatory cycles increases the risk of ovarian cancer by inducing proliferation-associated DNA damage. In particular, we examined the association between the lifetime number of ovulatory cycles and mutation of the p53 tumor-suppressor gene (also known as TP53) in ovarian tumors. METHODS: Case-case and case-control analyses involving participants in the Cancer and Steroid Hormone study were used to examine the association between p53 gene mutation in ovarian tumors and the lifetime number of ovulatory cycles. The women in our study were 20-54 years of age and included 197 case patients with invasive ovarian epithelial cancer and 3363 control subjects. Mutation of the p53 gene was indicated by overexpression of p53 protein (i.e., cellular accumulation of mutant p53 protein) in paraffin-embedded ovarian cancer tissue blocks; the mutant protein was detected by means of standard immunohistochemical techniques. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by employing multivariate analyses, with the use of logistic regression. Reported P values are two-sided. RESULTS: Women whose cancers overexpressed p53 protein (p53 positive) had a greater mean number of lifetime ovulatory cycles (388 +/- 77.4 cycles [mean +/- standard deviation]) than women whose cancers did not overexpress p53 protein (p53 negative) (342 +/- 119.0 cycles) (P = .0025). Furthermore, women with p53-positive tumors were more likely to have had moderate (i.e., 235-375) or high (i.e., 376-533) numbers of ovulatory cycles than women with p53-negative tumors (age-adjusted ORs = 7.0 [95% CI = 1.6-30.5] and 7.7 [95% CI = 1.4-41.2], respectively) (< or = 234 cycles was the referent category). After controlling for age, menopausal status, and nulliparity, women with p53-positive tumors were found to be significantly more likely to have had moderate or high numbers of ovulatory cycles than control subjects (ORs = 4.3 [95% CI = 1.4-13.0] and 9.1 [95% CI = 2.7-30.9], respectively); the corresponding ORs for women with p53-negative tumors compared with control subjects were 0.6 (95% CI = 0.3-1.4) and 1.3 (95% CI = 0.5-3.2), respectively. CONCLUSIONS AND IMPLICATIONS: A higher number of ovulatory cycles may be associated with increased amounts of proliferation-associated DNA damage and increased risk of developing p53-positive but not p53-negative epithelial ovarian cancer. Our results are consistent with more than one developmental pathway in the pathogenesis of this type of cancer.

Adult↗
PubMed1997

Prognostic value of MIB-1 in advanced ovarian carcinoma as determined using automated immunohistochemistry and quantitative image analysis.

BACKGROUND AND OBJECTIVES: The monoclonal antibody MIB-1 is an immunohistochemical marker reacting most strongly with cells in late S phase, G2, and M portions of the cell cycle. This antibody, reactive in formalin-fixed, paraffin-embedded tissue, allows the quantitation of a proliferation index (PI) in both current clinical cases and archival material using a computerized image analyzer (CIA). METHODS: Since many laboratories make use of automated immunohistochemistry (AIH), this study was performed to explore the technical feasibility of using AIH (Ventana ES 320) in combination with CIA (CAS 200) to evaluate MIB-1 PI as a prognostic marker as assessed by overall survival in 50 archival (formalin-fixed, paraffin-embedded), advanced stage primary ovarian carcinomas. RESULTS: Exploratory methods confirmed that 15% was a cutpoint that could dichotomize these 50 patients into two prognostic groups based on overall survival. The median survival of patients whose carcinoma had a high MIB-1 expression (> or = 15%) was 16 months compared with 30 months in the patients whose tumors demonstrated low MIB-1 expression (< 15%, P = 0.01). After adjustment for age, MIB-1 retained its prognostic significance (P = 0.02). Patients 60 years and older had shorter survival than younger patients (P = 0.06), but these two groups did not differ with respect to PI (P = 0.76). Those patients with a negative second look laparotomy had a longer median survival of 70 months compared with 18.5 months in patients with a positive second look (P < 0.001); the median PIs were 17% and 27%, respectively (P = 0.36). There were no significant relationships between clinical stage, nuclear grade, DNA ploidy, p53, and either survival or PI. CONCLUSIONS: In this study, we concluded that the combination of AIH and CIA yielded a reliable quantitation of MIB-1 proliferative index and that this proliferative marker had prognostic significance in late stage ovarian carcinoma. Further studies in a larger group of patients are needed to confirm the relationship between proliferation index and other known clinicopathologic and genetic variables.

Antibodies, Monoclonal↗
PubMed1997

Analysis of genetic alterations in uterine leiomyomas and leiomyosarcomas by comparative genomic hybridization.

Uterine leiomyomas are the most prevalent tumor type in women of reproductive age and are the most common reason for hysterectomies. Although uterine leiomyomas are considered to be benign, they are a major public health concern for women. In contrast, leiomyosarcomas are rare but highly malignant uterine tumors. They may arise in uteri with preexisting leiomyomas and histologically sometimes resemble leiomyomas, thus causing controversy about whether leiomyosarcomas arise within leiomyomas. In this study, we used comparative genomic hybridization (CGH) to identify genetic alterations unique to each tumor type and alterations that are common between the two tumors. We analyzed 14 cases of uterine leiomyomas and eight cases of uterine leiomyosarcomas. Only two of the 14 leiomyomas exhibited genetic alterations, and those were restricted to gains on chromosomes 14 and 19 and losses on chromosomes 1 and 4. In addition, 68 leiomyomas were examined for loss of heterozygosity on chromosomes 1 and 4, and only three tumors exhibited any losses. In contrast, all eight leiomyosarcomas showed gains and losses of DNA by CGH, and in many cases multiple changes were observed. The most commonly observed genetic aberration, occurring in five tumors, was gains on both arms of chromosome 1, suggesting that this chromosome contains loci involved in the development of leiomyosarcoma. Our results do not provide evidence for the progression from benign leiomyoma to malignant leiomyosarcoma. Moreover, the large number of random chromosomal alterations in the leiomyosarcomas suggests that increased genetic instability plays a role in the formation of these tumors.

Chromosome Aberrations↗
PubMed1997

Racial disparity in overexpression of the p53 tumor suppressor gene in stage I endometrial cancer.

OBJECTIVE: This study was conducted to determine whether overexpression of the p53 tumor suppressor gene is associated with poor outcome in early-stage endometrial cancers and whether a racial difference in the frequency of p53 overexpression contributes to the observed racial disparity in survival rates. STUDY DESIGN: Immunostaining for the p53 gene was performed in 164 women with stage I endometrial adenocarcinomas. RESULTS: Overexpression of mutant p53 protein was seen in 28 out of 164 (17%) cases and was associated with a poor histologic grade (p = 0.003) and a nonendometrioid histologic appearance (p = 0.06). Overexpression also was three times more frequent in blacks (15 out of 44, 34%) than in whites (13 out of 117, 11%) (p = 0.003). Recurrent disease developed in 15 out of 164 (9%) cases and was more than twice as frequent in cases when the p53 gene was overexpressed (5 out of 28, 18%) than in cases with normal expression (10 out of 136, 7%). Recurrent disease was seen in 6 out of 44 (14%) blacks compared to 9 out of 117 (8%) whites. CONCLUSIONS: These data support the hypothesis that differences in the frequency of alteration of the p53 tumor suppressor gene contribute to the racial disparity in endometrial cancer survival.

Adenocarcinoma↗
PubMed1997

Signet-ring cell carcinoma of the endometrium: a primary tumor masquerading as a metastasis.

Extragenital metastases to the endometrium are unusual, but several histologic features have been suggested as highly suggestive or even pathognomonic for this diagnosis. We report an endometrial carcinoma with a prominent signet-ring cell morphology and a diffusely permeative pattern of infiltration, features that have been reported as indicating an extragenital metastasis. To the best of our knowledge, this is the first reported case of a signet-ring cell carcinoma of the endometrium. Gynecological pathologists should be aware of this entity because of its potential primary of metastatic signet-ring carcinoma to be endometrium.

Aged↗
PubMed1997

Dideoxy fingerprinting assay for BRCA1 mutation analysis.

Since the isolation of BRCA1, the familial breast/ovarian cancer predisposition gene, much effort has been invested in characterizing the mutation spectrum. The large size of the gene and the wide distribution of its more than 100 mutations has increased the challenge of this endeavor such that traditional mutation detection techniques are inadequate. We examined the sensitivity of dideoxy fingerprinting (DDF), which combine a Sanger sequencing reaction with multiple-fragment single-strand conformation analysis (SSCA), as a mutation detection technique to screen BRCA1. Here we describe the technique and compare its sensitivity with that of SSCA in detecting 21 previously described BRCA1 sequence variants. All the variants were detected by DDF, but only 17 of 21 (81%) were observed by SSCA under standard conditions. Three of four alterations missed by SSCA were base substitutions. As a BRCA1 mutation detection technique, DDF was more sensitive than SSCA and may prove to be a useful research tool in defining the mutation spectrum within this and other genes.

Breast Neoplasms↗
PubMed1997

Loss of heterozygosity at chromosome segment Xq25-26.1 in advanced human ovarian carcinomas.

To determine whether a tumor suppressor gene of importance to epithelial ovarian cancer resides on the X chromosome, we examined loss of heterozygosity (LOH) in 123 epithelial ovarian cancer cases. In 54 such cases, we examined LOH at 26 loci on the human X chromosome. In eight cases, we examined LOH in 14 loci and in 61 cases we examined LOH in 13 loci. Matched DNA samples from tumors and corresponding normal tissues were analyzed by polymerase chain reaction (PCR) amplification of microsatellite markers. Frequent losses were found in epithelial carcinomas at the Xq25-26.l region, including DXS1206 (34.5% loss in informative cases), DXS1047 (27.7%), HPRT (24.1%), and DXS1062 (33.3%). The minimum overlapping region of LOH was approximately 5 megabases (Mb), flanked by DXS1206 (Xq25) and HPRT (Xq26.1). The methylation status of the remaining allele of the androgen receptor gene in the tumors exhibiting LOH at the Xq25-26.1 region suggested that the loss was exclusively in the inactive X chromosome. We next determined whether a significant relationship exists between Xq LOH and other parameters, including histologic grade and/or clinical stage of the tumors and LOH at TP53. The Xq LOH had a significant association with grade 2 to 3 tumors at stages II to IV. Sixteen of 18 cases that showed Xq LOH revealed LOH at the TP53 locus, and 45% of tumors exhibiting LOH at TP53 showed Xq LOH. These results suggest that there may be a tumor suppressor gene or genes which escape inactivation of the X chromosome at Xq25-26.1, and that the loss of the gene(s) at Xq25-26.1 is frequently accompanied by loss of the TP53 or loss of another gene on chromosome 17. These losses may contribute to the progression from a well-differentiated to a more poorly differentiated state or to metastatic aggressiveness.

Carcinoma↗
PubMed1996

Clinical and pathological features of ovarian cancer in women with germ-line mutations of BRCA1.

BACKGROUND: We tested the hypothesis that ovarian cancers associated with germ-line mutations of BRCA1 have distinct clinical and pathological features as compared with sporadic ovarian cancers. METHODS: We reviewed clinical and pathological data on patients with primary epithelial ovarian cancer found to have germ-line mutations of BRCA1. Survival among patients with advanced-stage cancer and such mutations was compared with that in control patients matched stage, grade, and histologic subtype of the tumors. A combination of single-strand conformation and sequencing analyses was used to examine the 22 coding exons and intronic splice-donor and splice-acceptor regions of BRCA1 for mutations in pathological specimens. Alternatively, some patients were known to be obligate carriers of the mutant BRCA1 gene because of their parental relationships with documented mutant-gene carriers. RESULTS: We identified 53 patients with germ-line mutations of BRCA1. The average age at diagnosis was 48 years (range, 28 to 78). Histologic examination in 43 of the 53 patients showed serous adenocarcinoma. Thirty-seven tumors were of grade 3, 11 were of grade 2, 2 were of grade 1, and 3 were of low malignant potential. In 38 patients, the tumors were of stage III; 9 patients (including those with tumors of low malignant potential) had stage I disease, 5 had stage IV, and 1 had stage II. As of June 1996, with a median follow-up among survivors of 71 months from diagnosis, 20 patients had died of ovarian cancer, 27 had no evidence of the disease, 4 were alive with the disease, and 2 had died of other diseases. Actuarial median survival for the 43 patients with and advanced-stage disease was 77 months, as compared with 29 months for the matched controls (P<0.001). CONCLUSIONS: As compared with sporadic ovarian cancers, cancers associated with BRCA1 mutation appear to have a significantly more favorable clinical course.

Actuarial Analysis↗
PubMed1996

Cell cycle control of BRCA2.

Identifying the conditions and kinetics of the induction of BRCA2 gene expression may implicate roles for the function of the tumor suppressor gene. In this study, expression of BRCA2 mRNA is shown to be regulated by the cell cycle and associated with proliferation in normal and tumor-derived breast epithelial cells. Cells arrested in G(0) or early G1 contained low levels of BRCA2 mRNA. After release into a proliferating state, cells produced maximum levels of BRCA2 mRNA in late G1 and the S-phase. Similar cell cycle control of BRCA2 was observed in fractions of exponentially growing cells isolated by centrifugal elutriation. Expression of BRCA2 was shown to be independent of bulk DNA synthesis. In addition, the kinetics of BRCA2 mRNA up-regulation appeared to be similar to those of BRCA1, suggesting that the two genes could be commonly controlled. These results imply that these two tumor suppressor genes are utilized during growth and may have a protective role in cellular proliferation.

Adult↗
PubMed1996

Mutational analysis of the p21/WAF1/CIP1/SDI1 coding region in human tumor cell lines.

p21/WAF1/CIP1/SDI1 is an important cell-cycle mediator with tumor suppressor gene capabilities, and its inactivation could potentially lead to tumor progression. Because tumor suppressor genes are commonly inactivated by somatic and germline mutations, we analyzed a variety of human tumor cell lines for p21 mutations. We used single-strand conformational analysis and direct sequencing to identify possible mutations in the p21 coding region. Two base-alterations were observed in 41 immortalized human tumor cell lines. A previously reported polymorphism that results in a serine-to-arginine amino-acid substitution at codon 31 was found in 24% (10 of 41) of the tumor cell lines but was also found in 10% (six of 62) of normal parental DNAs tested and 7% (three of 43) of normal DNAs from patients with primary endometrial tumors. Another nucleotide substitution found at codon 80 resulted in the replacement of threonine with methionine. Codon 80 changes were found in 7% (three of 41) of the tumor cell lines (all endometrial) and in 2% (one of 62) of the normal parental DNAs. This change was not found in any of the primary endometrial tumors examined. The biological activity of these base changes was analyzed by using in vitro cyclin-dependent kinase 2-cyclin A kinase assays and calcium phosphate transfections. We observed that wild-type p21 and the p21 variants had similar growth-inhibitory abilities. Thus, our results suggest that mutation of the p21 gene is not prevalent in human tumor cell lines and is not a probable mechanism of inactivation of this gene.

Base Sequence↗
PubMed1996

Microsomal epoxide hydrolase polymorphism as a risk factor for ovarian cancer.

Microsomal epoxide hydrolase (EPHX) is one of many enzymes involved in the metabolism of endogenous and exogenous toxicants. Polymorphic forms of the human EPHX gene have been described that vary in enzymatic activity, and one, Tyr113His, has been associated with hepatocellular carcinoma susceptibility. We demonstrated that EPHX was highly expressed in the human ovary, and investigated whether specific EPHX genotypes are associated with ovarian cancer susceptibility. Seventy-three Caucasian patients with ovarian cancer and 75 Caucasian-female controls without cancer were genotyped for the Tyr113His polymorphism by a polymerase chain reaction-restriction fragment length polymorphism assay. The frequency of the homozygous high-activity genotype was 41% in the control population and 64% in the ovarian cancer patients. The odds ratio for ovarian cancer with this genotype was 2.6 (95% confidence interval 1.3, 5.0; P < 0.01). The increased ovarian cancer risk associated with the high-activity genotype could reflect differences in metabolic activation of endogenous or exogenous carcinogens.

Blotting, Northern↗
PubMed1996

A phase I/II study of high-dose cyclophosphamide, cisplatin, and thioTEPA followed by autologous bone marrow and granulocyte colony-stimulating factor-primed peripheral-blood progenitor cells in patients with advanced malignancies.

The purpose of the present study was to determine the maximally tolerated dose of thioTEPA given with fixed high-dose cyclophosphamide (CPA) and cisplatin (cDDP) followed by autologous bone marrow (ABM) with or without granulocyte colony-stimulating factor (G-CSF)-primed peripheral-blood progenitor cells (PBPCs) in patients with advanced malignancies. Patients were required to have histologically documented malignancies and adequate renal, hepatic, pulmonary, and cardiac function. CPA was given at 1,875 mg/m2 per day as a 1-h i.v. infusion for 3 consecutive days, and cDDP was given at 55 mg/m2 per day as a 24-h continuous i.v infusion over 3 days concurrently with CPA. ThioTEPA was given once as a 1-h i.v. infusion (300-900 mg/m2) either following (the first 13 patients) or prior to CPA and cDDP. In all, 31 patients received PBPCs. A total of 46 patients were treated. There were 6 deaths among the 15 patients who did not receive PBPCs (13 received thioTEPA following CPA and cDDP). Among the other 31 patients who received PBPCs (all of whom also received thioTEPA prior to CPA and cDDP), there were 4 deaths, all involving patients with refractory ovarian carcinoma. The main toxicities were mucositis, esophagitis, hepatotoxicity, and nephrotoxicity. The median time required to achieve an absolute neutrophil count of 500 microliter was 10 days (range, 9-12 days) for those who received PBPCs and 15 days (range, 15-34 days) for those who did not receive PBPCs. Altogether, 47% of the major organ toxicities (grades 3 and 4 renal, hepatic, and cardiac toxicities) occurred among the 15 patients who did not receive PBPCs, although these patients received thioTEPA at the lowest 2 dose levels. There were 3 complete responses and 22 partial responses among 35 evaluable patients (overall response rate, 71%), with the median duration of response being 3.5 months (range, 2-17 months). The maximally tolerated dose of thioTEPA was 600 mg/m2 given as a 1-h i.v. infusion on the day prior to CPA and cDDP administration, The combination of high-dose CPA, cDDP, and thioTEPA is a well-tolerated regimen when thioTEPA is given prior to CPA and cDDP and when the combination also includes PBPCs in addition to ABM. This regimen is active in a variety of malignancies.

Adult↗
PubMed1996

An inevitable dilemma: prenatal testing for mutations in the BRCA1 breast-ovarian cancer susceptibility gene.

The BRCA1 breast-ovarian cancer susceptibility gene was identified recently. Germline mutations in BRCA1 may be responsible for as many as 5% of breast and ovarian cancers. Inherited alterations confer up to a 94% risk of developing breast and/or ovarian cancer by age 70. With the discovery of BRCA1, there will be a heavy demand for genetic testing. Because of the large size of the gene and the distribution of reported mutations, scientists face considerable technical problems in developing widely available screening tests; clinicians will face even greater ethical problems in applying them. In the context of research programs, women with BRCA1 mutations are already being identified, and their physicians are confronted with a number of complex medical, ethical, legal, and social issues. Obstetricians will be faced with counseling parents regarding prenatal testing for specific BRCA1 mutations. Although it is difficult to formulate straightforward guidelines regarding prenatal BRCA1 testing, clinicians and health care providers must be familiar with the nuances of the debate so that these issues can be discussed wisely with patients. As with many ethically challenging problems in medicine, individual clinicians and their patients will have to work together to determine the course of action with which they are most comfortable. Although elective termination of a pregnancy with a germline mutation in BRCA1 is an option, experience with other adult-onset diseases suggests that only a minority of parents will choose this option.

BRCA1 Protein↗
PubMed1996

p53 overexpression in advanced-stage endometrial adenocarcinoma.

OBJECTIVES: Mutation and overexpression of the p53 tumor suppressor gene in endometrial cancers are associated with advanced stage and poor survival. We sought to determine whether p53 overexpression is an independent variable predictive of poor prognosis in advanced endometrial adenocarcinomas. STUDY DESIGN: Immunohistochemical evaluation was used to examine p53 expression in paraffin blocks from 179 endometrial adenocarcinomas. RESULTS: p53 overexpression was seen in 35% of cancers and was associated with higher stage (p = 0.004), black race (p < 0.001), higher grade (p = 0.02), lack of hormone replacement (p = 0.04), and older age (p = 0.05). In addition to a higher frequency of p53 overexpression (57% vs 26%), black women had a lower survival rate than white women (p = 0.001), but overexpression was associated with poor survival in both races. After we corrected for hormone use, multivariate analysis revealed that older age (p < 0.001), higher stage (p < 0.001), higher grade (p = 0.01), and p53 overexpression (p = 0.04) were predictive of poor survival. CONCLUSIONS: Overexpression of p53 in advanced-stage endometrial cancers is an independent variable that is associated with poor survival, occurs more frequently in black women, and may contribute to the racial disparity in survival.

Adenocarcinoma↗
PubMed1996

Preoperative evaluation of macrophage colony-stimulating factor levels in patients with endometrial cancer.

OBJECTIVE: Our purpose was to examine the relationship between preoperative serum levels of macrophage colony-stimulating factor, alone and in combination with CA 125, and the presence of prognostic clinicopathologic factors and subclinical metastases in women with endometrial cancer. STUDY DESIGN: Ninety-two women who underwent primary exploration for endometrial adenocarcinoma had preoperative serum samples evaluated for macrophage colony-stimulating factor and CA 125 levels. Multivariate analysis was used to determine the associations of surgicopathologic findings with macrophage colony-stimulating factor and CA 125 levels. Logistic regression analysis was used to identify factors associated with the risk of extrauterine disease. The association of macrophage colony-stimulating factor and CA 125 levels with stage, grade, and depth of myometrial invasion and histologic characteristics were analyzed with Fisher's two-tailed exact test. RESULTS: Elevated levels of macrophage colony-stimulating factor were not associated with depth of myometrial invasion, histologic grade, or histologic cell type; however, advanced stage (p = 0.02) and the presence of lymph node metastases (p = 0.04) were associated with elevated levels. Sensitivity and specificity of macrophage colony-stimulating factor for predicting extrauterine disease were 42% and 89%, respectively. If either an elevated macrophage colony-stimulating factor or an elevated CA 125 level was used to predict extrauterine disease, the sensitivity was increased to 67% but the specificity was decreased to 78%. Macrophage colony-stimulating factor elevations predicted lymph node metastases with a sensitivity of 50% and a specificity of 86%. A multivariate regression model showed CA 125 to be the most significant predictor of extrauterine disease; macrophage colony-stimulating factor also contributed prognostic information (p = 0.02). The sensitivity and specificity of the multivariate model for predicting extrauterine disease were 75% and 73%, respectively. CONCLUSION: Macrophage colony-stimulating factor and CA 125 are neither sensitive nor specific enough to be used as predictors of the presence or absence of extrauterine disease in patients with endometrial cancer.

Adenocarcinoma↗
PubMed1996

Expression of the 67-kD laminin receptor, galectin-1, and galectin-3 in advanced human uterine adenocarcinoma.

Alterations of tumor cell interactions with laminin, a basement membrane glycoprotein, are consistent features of the invasive and metastatic phenotype. Qualitative and quantitative changes in the expression of cell surface laminin-binding proteins have been correlated with the ability of cancer cells to cross basement membranes during the metastatic cascade. Such phenotypic modifications are usually associated with poor prognosis. In this study, the authors examined the possibility that expression of three laminin-binding proteins, the 67-kD laminin receptor (67LR), galectin-1, and galectin-3, is altered in human endometrial cancer in a fashion similar to that reported in other carcinomas, such as breast, colon, and ovarian cancer. Twenty advanced uterine adenocarcinomas were analyzed for expression of these three molecules using immunoperoxidase staining and specific antibodies. The authors found a significant increase in the expression of the 67LR and galectin-1 in cancer cells compared with normal adjacent endometrium (P = .0004 and .0022, respectively). As observed in other carcinomas, a significant down-regulation of galectin-3 expression was found in endometrial cancer cells compared with normal mucosa (P = .02). In the galectin-3 positive tumors, galectin-3 was detected in the cytoplasm and/or nucleus of cancer cells. Interestingly, tumors in which galectin-3 was detected only in the cytoplasm were characterized by deeper invasion of the myometrium than lesions where galectin-3 was found both in nucleus and cytoplasm (P = .02). This study shows an alteration of nonintegrin laminin-binding protein expression in advanced human endometrial cancer. Further studies on larger populations should determine the prognostic value of the detection of these laminin-binding proteins in endometrial carcinoma. Inverse modulation of the 67LR and galectin-3 appears to be a phenotypical feature of invasive carcinoma.

Adenocarcinoma↗