Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Tissue microdissection”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed2001

Mass spectrometry meets chip technology: a new proteomic tool in cancer research?

DNA chip technologies are the most exiting genomic tools, which were developed within the last few years. It is, however, evident that knowledge of the gene sequence or the quantity of gene expression is not sufficient to predict the biological nature and function of a protein. This can be particularly important in cancer research where post-translational modifications of a protein can specifically contribute to the disease. To address this problem, several proteomic tools have been developed. Currently the most widely used proteomic tool is two-dimensional protein gel electrophoresis (2-DE), which can display protein expression patterns to a high degree of resolution. As an alternative to 2-DE, a preliminary study using a new technique was employed to generate protein expression patterns from whole tissue extracts. Surface-enhanced laser desorption/ionization (SELDI) allows the retention of proteins on a solid-phase chromatographic surface (ProteinChip Array) with direct detection of retained proteins by time of flight-mass spectrometry (TOF-MS). Using this system, we analyzed eight cases of renal cell carcinoma (RCC) including normal, peripheral and central tumor tissue as well as four microdissected cases of cervical intraepithelial neoplasia (CIN) and three microdissected cases of cervix uteri carcinoma. Differentially expressed proteins were found by comparing the protein expression patterns generated using SELDI-based TOF-MS of tumor tissue with normal and neoplastic tissue, respectively. By applying this fast and powerful ProteinChip array technology it becomes possible to investigate complex changes at the protein level in cancer associated with tumor development and progression.

Carcinoma, Renal Cell↗
PubMed2006

Detection of non-maternal components of gestational choriocarcinoma by PCR-based microsatellite DNA assay.

OBJECTIVE: Gestational and non-gestational choriocarcinomas have distinctly different tissues of origin, parental genotypes, natural histories, and responses to therapy. Our objective was to develop a convenient, fast, and reliable assay that would, using only patient tissue, allow separation of gestational from non-gestational choriocarcinomas. METHOD: Benign and malignant tissues, preserved in paraffin blocks and separated by microdissection, were examined using a commercial PCR-based tissue identity assay (ABI AmpFlSTR Profiler Plus Kit and ABI 377 DNA sequencer) to detect genetic profiles of 9 microsatellite markers, along with X and Y chromosome markers. Cases included 6 choriocarcinomas. Controls included eight non-germ cell reproductive tract tumors and two hydatidiform moles. RESULTS: The microsatellite markers identified the five choriocarcinomas diagnosed on clinical and histological grounds as gestational, to be of genetically non-maternal (androgenic) origin. The neoplasm previously classified as a non-gestational choriocarcinoma was demonstrated to be of maternal origin, as were the non-germ cell reproductive tract tumors. Samples from hydatidiform moles contained either androgenic markers only or a mix of maternal and androgenic markers, as previously seen in complete and partial moles, respectively. CONCLUSION: A commercially available microsatellite DNA diagnostic assay is a quick and convenient way to discriminate between gestational and non-gestational choriocarcinoma.

Alleles↗
PubMed2003

Genotypic analysis of primary and metastatic cutaneous melanoma.

Microdissection genotyping was performed on 16 cases of melanoma, including two cutaneous and one lymph node metastases. Three benign nevi were used as controls. Where possible, tumor was microdissected at several sites. Genotyping involved assessment of loss of heterozygosity [LOH]), which was accomplished using a panel of nine polymorphic tetranucleotide microsatellites. Polymerase chain reaction was performed on the normal tissue sample to establish microsatellite heterozygous status. Informative markers were then tested on microdissected lesional tissue and scored for the presence and extent of allelic imbalance (AI). Microsatellite informativeness varied from 33% to 66%. Benign nevi were without AI. All invasive melanomas manifested acquired allelic loss, which involved 75% or 100% of the markers shown to be informative for each subject. Eleven of 13 (84%) primary melanomas demonstrated intratumoral heterogeneity of AI consistent with development of tumor subclones with differing genotypic profiles within thin as well as thick melanomas. Although a consistent pattern did not emerge among the markers, LOH of 9p21 (D9S254) occurred in 60% (9/15) of the cases followed by 40% of cases displaying LOH of 1p34, p53, 10q (MXI1), and 10q23 (D10S520) and 25% with 5q21 (D5S 592) abnormalities. A third of the cases including the metastatic foci demonstrated two different patterns of AI affecting alternative alleles of the same genomic marker within different parts of the melanoma. Two melanomas in situ did not display LOH of any markers in the informative cases although the in situ component in the invasive tumors had allelic losses that were in part similar to the invasive areas. The results of this study support the expanded use of microdissection genotyping and explore other markers to define the unique mutational profile for malignant melanoma that may complement other histologic characteristics of melanoma.

Alleles↗
PubMed2000

Analysis of segmental renal gene expression by laser capture microdissection.

UNLABELLED: Analysis of segmental renal gene expression by laser capture microdissection. BACKGROUND: The study of normal renal physiology has been greatly aided by microdissection techniques that have delineated the exceptional functional and cellular heterogeneity both along the nephron and between different nephron populations. These techniques are not widely used to study renal injury as microdissection is difficult because of tissue necrosis or fibrosis. We developed a procedure to detect specific gene expression in specific locations of the kidney in histologic sections. METHODS: The anatomic specificity of laser capture microdissection (LCM) was employed with the sensitivity of reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: LCM/RT-PCR detected mRNA for podoplanin in 2% of a single glomerulus, rat basic amino acid transporter in 6% of a single cross-section of proximal straight tubule, and renin in eight proximal convoluted tubule cross-sections. LCM/RT-PCR could isolate pure populations of proximal convoluted tubules, proximal straight tubules, and thick ascending limbs from renal histologic sections, although pure collecting ducts could not be isolated. LCM/RT-PCR localized ischemia-reperfusion-induced induction of KC/interleukin-8 primarily to the medullary thick ascending limb, and detected transforming growth factor-beta (TGF-beta) mRNA in glomeruli of a patient with membranous glomerulonephropathy. CONCLUSIONS: When used with an appropriate laser spot size, LCM/RT-PCR can measure gene expression in glomeruli or specific parts of the nephron and can study alterations in steady-state mRNA levels in animal models of renal disease. The applications, limitations, and refinements of this approach are discussed.

Animals↗
PubMed2003

PCR-based quantification of amplified RNA from laser microdissected mouse liver samples.

New molecular methods such as quantitative reverse transcription-polymerase chain reaction (RT-PCR) and microarray gene expression analysis have been established recently to quantify gene expression in tissue samples. Such methods, although highly sensitive, require RNA quantities of at least several micrograms. These amounts are not available in many experiments concerning microdissected embryonic or regenerating structures. We combined laser-assisted tissue preparation, RNA amplification, and quantitative RT-PCR to estimate both accuracy and linearity of gene expression in small tissue samples. Our results show that mRNA isolated from laser-microdissected fetal liver tissue or regenerative nodules, which originated from EGFP-marked transplanted fetal cells, can be significantly increased with the amplification protocol. The quantitative expression ratio of the genes albumin and GAPDH was conserved after one and two rounds of amplification compared to nonamplified material. Furthermore, genes expressed at low levels such as the transcription factor C/EBPbeta become detectable after two rounds of amplification in small microdissected tissue samples.

Albumins↗
PubMed2005

Molecular analysis of primary and recurrent giant cell tumors of bone.

The status of microsatellite markers located on chromosomes 1p36, 3p25, 5q23, 9p22, 10q23, 10q24, 17p13, and 19q12 was used to determine loss of heterozygosity (LOH) in primary giant cell tumors (GCT) of bone in 12 patients. The cases included primary, locally recurrent, and metastatic GCT; three tumors were classified as malignant GCT, based on their morphological features. Microdissection was performed on 24 paraffin-embedded tissue samples. An average of three separate topographic sites were microdissected from each tumor. Case selection in each instance was based on the availability of paired samples of tumor in primary GCTs and their corresponding recurrences, and the presence of normal tissue. The number of cases studied is too small for statistical studies, and thus the analysis is descriptive. All cases were informative for >80% of the markers used. Both primary GCTs and local recurrences and lung metastases displayed LOH of three or more markers, and intratumoral heterogeneity was frequent. Fractional allelic losses (FAL) were not different in recurrent and nonrecurrent GCT. FAL was greatest (>30%) in the metastatic group of GCT. Allelic losses of 1p, 9q, and 19q regions were frequent in all groups. LOH of 17p (in proximity to the p53 locus) and 9p occurred exclusively in the pulmonary metastases from GCT. LOH of 9q and 19q was present in primary as well as recurrent GCTs and in one malignant GCT. Involvement of 1p (including MYCL) and 9q regions has not been previously reported in GCT of bone. The pattern of LOH evident in the 17 markers used in the present study suggests that GCT with malignant features may follow an evolutionary pathway similar to the usual primary GCT of bone.

Adolescent↗
PubMed2005

Peptide patterns of laser dissected human trophoblasts analyzed by matrix-assisted laser desorption/ionisation-time of flight mass spectrometry.

This study describes the first promising steps in the comparison of peptide patterns of laser capture microdissected trophoblast cells obtained from frozen tissue sections in relative low numbers, approximately 125 cells. Trophoblasts were collected by laser capture microdissection from a terme human placenta and dissolved in detergents, sonified, and digested with trypsin. The resulting peptide mixtures were directly analyzed by matrix-assisted laser desorption/ionisation-time of flight mass spectrometry. Using this approach specific peptide patterns that consist on average of approximately 35 peptide peaks for trophoblast cells, and surrounding villous stroma cells could be obtained. From the results it was concluded that trophoblast and surrounding villous stroma cells show exclusive discriminating peptide patterns. In the future this method is potentially suitable for finding specific peptides and identification of proteins that are related to the pathogenesis of trophoblast pregnancy diseases such as preeclampsia.

Detergents↗
PubMed2004

Less DeltamtDNA4977 than normal in various types of tumors suggests that cancer cells are essentially free of this mutation.

Levels of mtDNA(4977) deletions (DeltamtDNA(4977)) have been found to be lower in tumors than in adjacent non-tumoral tissues. In 87 cancer patients, DeltamtDNA(4977) was detected by multiplex polymerase chain reaction (PCR) amplification in 43 (49%) of the tumors and in 74 (85%) of the samples of non-tumoral tissues that were adjacent to the tumors. DeltamtDNA(4977) deletions were detected in 24% of the breast tumors, 52% of the colorectal tumors, 79% of the gastric tumors, and 40% of the head and neck tumors as compared with 77, 83, 100, and 90% of the adjacent respective non-tumoral tissues at the same DNA template dilution. Based on limiting dilution PCR of 16 tumors and their adjacent non-tumoral tissues, it was found that the amount of DeltamtDNA(4977) was 10- to 100-fold lower in the tumor than in the respective control non-tumoral tissues. Real-time PCR experiments were performed to quantify the number of DeltamtDNA(4977) deletions per cell, by determining the mitochondrial-to-nuclear DNA ratio. In all of the cases of breast, colorectal, gastric, and head and neck cancer the proportion of DeltamtDNA(4977) in tumors was lower than that of the respective non-tumoral tissue. Traces of DeltamtDNA(4977) in tumors were apparently due to contamination of tumor tissue with surrounding non-tumoral tissue, as evidenced by tumor microdissection and in situ PCR techniques, suggesting that tumors are essentially free of this mutation. Although the metabolic effect of DeltamtDNA(4977) may be minimal in normal (non-tumor) tissue, in tissue under stress, such as in tumors, even low levels of DeltamtDNA(4977) deletions may be intolerable.

Breast Neoplasms↗
PubMed1998

Utility of microdissection and polymerase chain reaction for the detection of immunoglobulin gene rearrangement and translocation in primary intraocular lymphoma.

OBJECTIVE: Primary intraocular lymphoma, a non-Hodgkin's lymphoma, is a primary central nervous system lymphoma (PCNSL). Diagnosis is usually made by identifying malignant, large B lymphocytes in the vitreous, eye, brain, and cerebral spinal fluid; however, these cells are few, friable, and difficult to recognize. Recently, clonal heavy chain immunoglobulin (IgH) gene rearrangement and bcl-2 gene translocation have been reported in systemic B-cell lymphoma and are used for the detection of malignant cells and in making a diagnosis. The authors investigated the molecular changes in three eyes and a chorioretinal biopsy specimen of four patients with PCNSL. DESIGN: Human tissue study. MATERIALS: Five ocular specimens of PCNSL were collected. INTERVENTION: The first patient had a diagnostic enucleation of the left eye. The second patient underwent diagnostic chorioretinal biopsy. In the third case, a pair of autopsied eyes with reactive lymphoplasmacytic infiltrates of a patient with acquired immune deficiency syndrome (AIDS) were studied. In the fourth case, an enucleated eye of a patient with AIDS-associated lymphoma was sampled. MAIN OUTCOME MEASURES: The bcl-2 and IgH genes of the lymphoma cells from routine, paraffin-embedded, formaldehyde-fixed, or frozen histologic tissue sections were analyzed using microdissection and polymerase chain reaction (PCR) technique. RESULTS: Lymphoma cells obtained from the above four cases showed IgH rearrangement gene in the third framework of the VH region. Bcl-2-associated translocation also was detected in three cases (cases 1, 2, and 4). CONCLUSION: Rearrangement of the IgH gene can serve as a molecular marker for PCNSL. Microdissection allows for procurement and analysis of specific, selected, minute cell populations that are obtained from histologic sections of the complex, heterogeneous tissue. Translocation of IgH and bcl-2, the apoptotic "survival" signal and proto-oncogene, could contribute to the pathogenesis of PCNSL. The combination of microdissection and PCR is a powerful tool for studies of small lesions and cell populations and for understanding disease mechanisms.

Adult↗
PubMed2003

Mutational analysis of the androgen receptor using laser capture microdissection and direct sequencing.

Molecular analysis of prostate cancer specimens is complicated by tumor heterogeneity and admixture of malignant cells with benign epithelium, stroma and inflammatory cells. Laser Capture Microdissection allows procurement of selected groups of cells from specific areas of tissue sections. We have used Laser Capture Microdissection to obtain pure samples of malignant prostate epithelial cells from frozen radical prostatectomy specimens. Methods for DNA extraction, androgen receptor amplification and exon sequencing have been optimized. These methods should be adaptable for molecular analysis of DNA, RNA and protein from other complex tissues.

DNA Mutational Analysis↗
PubMed1998

Tubular localization and tissue distribution of peptide transporters in rat kidney.

PURPOSE: To define the tubular localization and tissue distribution of PEPT1 (low-affinity, high-capacity transporter) and PEPT2 (high-affinity, low-capacity transporter) in rat kidney. METHODS: mRNA expression of PEPT1 and PEPT2 was assessed with reverse transcription-polymerase chain reaction (RT-PCR) methods using cDNA prepared from microdissected nephron segments in rat. Tissue localization of rat renal PEPT1 and PEPT2 mRNA was further assessed by in situ hybridization with radiolabeled probes. RESULTS: RT-PCR analysis of microdissected segments from rat nephron showed that both PEPT1 and PEPT2 are confined to a proximal tubule. While PEPT1 is specific for early regions of the proximal tubule (pars convoluta), PEPT2 is overwhelmingly but not exclusively expressed in latter regions of the proximal tubule (pars recta). All other segments along the nephron were negative for PEPT1 or PEPT2 mRNA transcripts. These finding were supported by in situ hybridization results in which PEPT1 was selectively expressed in kidney cortex and PEPT2 in the outer stripe of outer medulla. CONCLUSIONS: Contrary to current opinion, the data suggest that peptides are handles in a sequential manner in proximal regions of the nephron, first by the low-affinity, high-capacity transport system and second by the high-affinity, low-capacity transport system.

Animals↗
PubMed2005

Leiomyosarcoma and malignant fibrous histiocytoma share similar allelic imbalance pattern at 9p.

Formalin-fixed, paraffin-embedded tissue from 45 soft tissue sarcomas was analysed for allelic imbalance/loss of heterozygosity (AI/LOH) of chromosome 9. The specimens consisted of 17 cases of soft tissue leiomyosarcoma (LMS), 4 cases of cutaneous LMS, 22 cases of conventional malignant fibrous histiocytoma (MFH) and 2 cases of angiomatoid fibrous histiocytoma. All cases were categorised morphologically and immunohistochemically. DNA was microdissected from normal and neoplastic tissues. AI/LOH was performed using six microsatellite markers on the 9p region. The frequency of allelic imbalance at different loci on chromosome 9p was analysed in LMS and MFH and then compared with values previously examined in synovial sarcoma and malignant peripheral nerve sheath tumour. Although AI/LOH and microsatellite instability (MSI) were more frequent in MFH, LMS and MFH groups showed similar patterns of allelic imbalance at the 9p region. Alterations of chromosome 9p have been reported in many cell lines and tumours including LMS and MFH. 9p21 region encodes p16(INK4A) and p15(INK4B). Allelic imbalance observed at 9p 21 in this study suggests that alterations of the negative cell cycle regulators may be an important step in the pathogenesis of MFH and LMS. However, the most frequent allelic imbalance was observed at 9p24 at D9S230. Alterations of this locus were very rare in synovial sarcoma and malignant peripheral nerve sheath tumours and were absent in cutaneous LMS and angiomatoid fibrous histiocytoma. This locus may point to the existence of a genetically altered tumour suppressor gene involved in the pathogenesis of LMS and MFH. Our results support the hypothesis that MFHs may represent a morphological pathway in tumour progression of LMSs.

Allelic Imbalance↗
PubMed2000

Clonal analysis of micronodules in virus C-induced liver cirrhosis using laser capture microdissection (LCM) and HUMARA assay.

Most hepatocellular carcinomas (HCC) arise from malignant transformation of regenerative cirrhotic nodules. Because HCC has a very poor prognosis, detection of these premalignant lesions may improve the management of patients with cirrhosis. In this regard, clonal analysis of liver micronodules should be of particular interest in order to differentiate polyclonal regenerative micronodules from monoclonal neoplastic potentially malignant micronodules. To address this issue, 112 micronodules from 15 cases of explanted liver cirrhosis were carefully microdissected from paraffin-embedded tissue using a laser capture microscopy system. Clonal analysis was performed by analyzing X-chromosome inactivation, as indicated by the methylation status of the human androgen receptor gene (HUMARA). For each microdissected micronodule, a large set of pathological features was evaluated and correlated with their clonal status. Clonal analysis showed that 57 micronodules (51%) were monoclonal and 55 (49%) were polyclonal. Prevalence of monoclonal nodules ranged from 25% to 71% according to cases. In all cases, mono- and polyclonal nodules were randomly distributed in the cirrhotic liver. Although the clonal status was not significantly affected by the presence or absence of macronodules in the adjacent liver, size of monoclonal micronodules was significantly larger than size of polyclonal micronodules (mean size of the monoclonal nodules: 3 + 0.1 mm vs mean size of the polyclonal nodules: 2.5 +/- 0.1 mm, p = 0.007). Among the elementary pathological features evaluated, only the presence of iron overload was correlated with a monoclonal status (p = 0.04). In conclusion, clonal analysis of liver cirrhosis shows that 51% of micronodules are monoclonal lesions, supporting the notion that liver cirrhosis is a multineoplastic lesion. Because monoclonality is a marker of neoplasia, cirrhosis with accumulation of monoclonal nodules may be carefully followed, and monoclonal nodules should be screened for additional markers to assess their biological behavior.

Adult↗
PubMed1976

LH- and FSH-stimulating of adenylate cyclase in seminiferous tubules from young rats: functional FSH and LH receptors unmasked by homogenization.

LH- and FSH-sensitive adenylate cyclase activity was present in homogenates of whole testis tissue as well as in microdissected seminiferous tubules derived from young rats. In homogenates of seminiferous tubules a single adenylate cyclase appears to interact with both LH and FSH through separate hormone-specific receptors. Disruption of testis tissue by homogenization exposes functional FSH and LH receptors which are inaccessible to the hormones in intact cell preparations. These results indicate that in certain seminiferous tubule cell types only a fraction of the total functional receptors present is accessible to the cell surface for interaction with hormone.

Adenylyl Cyclases↗
PubMed2002

Cysteine-rich secretory protein-3: a potential biomarker for prostate cancer.

Electronic profiling of publicly available expressed sequence tag databases identified a gene, cysteine-rich secretoryprotein-3 (CRISP-3), that is up-regulated in prostate cancer, and of which the expression is relatively prostate-specific. The objective of this study was to examine the potential of CRISP-3 as a biomarker for prostate cancer. In transient transfection studies, CRISP-3 was found to be a secretory protein. Using a multiple tissue dot blot experiment, CRISP-3 transcript was identified in a limited number of human tissues including the prostate. In situ hybridization experiments indicated that CRISP-3 mRNA is epithelial-specific and is up-regulated in prostate adenocarcinoma compared with benign prostate tissue. CRISP-3 mRNA overexpression in cancer was confirmed using quantitative real-time reverse-transcription-PCR using benign prostatic epithelia and adenocarcinoma (in 5 of 5 cases) isolated by laser capture microdissection, as well as bulk tissues (in 20 of 23 cases) from surgically resected human prostates. These findings suggest that CRISP-3 is a potential biomarker for prostate cancer.

Adenocarcinoma↗
PubMed2006

Gene expression signatures of morphologically normal breast tissue identify basal-like tumors.

INTRODUCTION: The role of the cellular microenvironment in breast tumorigenesis has become an important research area. However, little is known about gene expression in histologically normal tissue adjacent to breast tumor, if this is influenced by the tumor, and how this compares with non-tumor-bearing breast tissue. METHODS: To address this, we have generated gene expression profiles of morphologically normal epithelial and stromal tissue, isolated using laser capture microdissection, from patients with breast cancer or undergoing breast reduction mammoplasty (n = 44). RESULTS: Based on this data, we determined that morphologically normal epithelium and stroma exhibited distinct expression profiles, but molecular signatures that distinguished breast reduction tissue from tumor-adjacent normal tissue were absent. Stroma isolated from morphologically normal ducts adjacent to tumor tissue contained two distinct expression profiles that correlated with stromal cellularity, and shared similarities with soft tissue tumors with favorable outcome. Adjacent normal epithelium and stroma from breast cancer patients showed no significant association between expression profiles and standard clinical characteristics, but did cluster ER/PR/HER2-negative breast cancers with basal-like subtype expression profiles with poor prognosis. CONCLUSION: Our data reveal that morphologically normal tissue adjacent to breast carcinomas has not undergone significant gene expression changes when compared to breast reduction tissue, and provide an important gene expression dataset for comparative studies of tumor expression profiles.

Adult↗
PubMed2005

Loss of heterozygosity in multistage carcinogenesis of esophageal carcinoma at high-incidence area in Henan Province, China.

AIM: Microsatellites are the repeated DNA sequences scattered widely within the genomes and closely linked with many important genes. This study was designed to characterize the changes of microsatellite DNA loss of heterozygosity (LOH) in esophageal carcinogenesis. METHODS: Allelic deletions in 32 cases of matched precancerous, cancerous and normal tissues were examined by syringe microdissection under an anatomic microscope and microsatellite polymorphism analysis using 15 polymorphic markers on chromosomes 3p, 5q, 6p, 9p, 13q, 17p, 17q and 18q. RESULTS: Microsatellite DNA LOH was observed in precancerous and cancerous tissues, except D9S1752. The rate of LOH increased remarkably with the lesions progressed from basal cell hyperplasia (BCH) to squamous cell carcinoma (SCC) (P<0.05). Three markers, D9S171, D13S260 and TP53, showed the highest incidence of LOH (>60%). LOH loci were different in precancerous and cancerous tissues. LOH in D3S1234 and TP53 was the common event in different lesions from the same patients. CONCLUSION: Microsatellite DNA LOH occurs in early stage of human esophageal carcinogenesis, even in BCH. With the lesion progressed, gene instability increases, the accumulation of this change may be one of the important mechanisms driving precancerous lesions to cancer.

Adult↗
PubMed2006

Aberrant expression of deoxyribonucleic acid methyltransferases DNMT1, DNMT3A, and DNMT3B in women with endometriosis.

OBJECTIVE: Since endometriosis is a persistent disease with substantial gene dysregulation, there must be cellular memory of some sort that constitutes a unique cell identity for endometriotic cells. Epigenetic regulation, especially through DNA methylation, is a flexible, yet stable, mechanism for maintaining such a cellular memory. The aim of this study was to determine gene expression levels of DNMT1, DNMT3A, and DNMT3B, the three genes coding for DNA methyltransferases that are responsible for methylation. DESIGN: Cross-sectional measurements of gene expression levels of DNMT1, DNMT3A, and DNMT3B on endometriotic tissue. SETTING: Academic. PATIENT(S): Seventeen patients with laparoscopically confirmed endometriosis and 8 healthy women who underwent tubal sterilization who were free of endometriosis were recruited for the study. INTERVENTION(S): Epithelial cells were harvested from tissue samples by laser capture microdissection and messenger RNA abundance was measured by quantitative real-time reverse transcription-polymerase chain reaction. MAIN OUTCOME MEASURE(S): The expression levels of these genes in epithelial cells from 13 ectopic endometrial tissue samples, 10 eutopic endometrial tissue samples taken from women with endometriosis, and 8 normal endometrial tissue samples from women without endometriosis. RESULT(S): The genes DNMT1, DNMT3A, and DNMT3B were over-expressed in the ectopic endometrium as compared with normal control subjects or the eutopic endometrium of women with endometriosis, and their expression levels were correlated positively with each other. CONCLUSION(S): The aberrant expression of these genes suggests that aberrant methylation may be rampant in endometriosis. This also provides a strong piece of evidence that endometriosis ultimately may be an epigenetic disease.

Adult↗