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PubMed1997

Antisense oligonucleotide to proto-oncogene c-myb inhibits the formation of intimal hyperplasia in experimental vein grafts.

BACKGROUND: The development of intimal hyperplasia is a major cause of early vein graft failure. The study examines the effects of locally delivered antisense oligonucleotides to the proto-oncogene c-myb on the development of vein graft intimal hyperplasia. METHODS: Common carotid vein bypass grafting procedures were performed on 60 New Zealand White rabbits. Seventeen grafts were controls, 14 had grafts coated with a commercial gel, 17 had grafts coated with gel containing 200 micrograms of an antisense c-myb oligonucleotide, and 6 rabbits each had grafts coated with gel containing one of two control oligonucleotides. Grafts were harvested 28 days after surgery, and sections were taken for dimensional analysis, morphologic evaluation, and vasomotor function. Grafts were also harvested at 1 day for oligonucleotide uptake/localization analysis and at 3 days for c-myb mRNA analysis. RESULTS: Oligonucleotides were uniformly distributed within the media and adventitia by 1 day. A 38% reduction occurred in mean intimal thickness in the vein grafts coated with antisense to c-myb compared with the other groups. No difference in medial thickness was seen among groups. By scanning and transmission electron microscopy all vein grafts showed a confluent endothelium. In contrast to control vein grafts, which did not relax to acetylcholine, most of the gel and all of the gel/oligonucleotide-coated grafts relaxed by more than 40% of precontracted tension. Responses to a panel of contractile agents were unchanged in the treated groups compared with those in the control group. CONCLUSIONS: Locally delivered antisense oligonucleotides to proto-oncogene c-myb significantly reduces intimal hyperplasia with preservation of acetylcholine-mediated endothelium-dependent relaxation in experimental vein grafts. These findings suggest that targeting a common regulatory pathway of vascular smooth muscle mitogenesis can be successful in reducing the early development of intimal hyperplasia.

Acetylcholine↗
PubMed1994

The effect of transluminal endothelial seeding on myointimal hyperplasia following angioplasty.

Myointimal hyperplasia develops as a generalised response to vascular injury, and may cause stenoses in 40% of all peripheral arterial reconstructions. Disruption of the endothelial monolayer is a prerequisite for the development of intimal hyperplasia, and may be the initiating event in this process. This study examined the hypothesis that restenosis following balloon angioplasty may be reduced by rapid restoration of the endothelial monolayer, achieved by endothelial seeding. Bilateral iliac angioplasties were performed in 11 rabbits. A double balloon catheter was used to seed one angioplasty site with autogenous endothelial cells; the contralateral site was sham seeded with culture medium and acted as a control. Arterial patency rates, the degree of intimal hyperplasia (IH/IEL), and the extent of endothelialisation were quantified at 1 (n = 5) and 3 (n = 6) weeks following balloon dilatation. The results suggest that transluminal endothelial seeding may be a therapeutically applicable technique as it decreases myointimal hyperplasia, and increases patency following angioplasty. This study also illustrates the protective effect of the vascular endothelium following arterial injury, and indicates that intensive efforts should be made to preserve the endothelium during vascular reconstruction.

Angioplasty, Balloon↗
PubMedDate not supplied

Hyperplasia versus adenoma in endocrine tissues: are they different?

The traditional view holds that hyperplasia of endocrine glands is secondary to oversecretion of a trophic hormone. However, in most cases, the mechanism underlying this growth is the spontaneous proliferation of benign neoplasias. Pathologists still depend on subtle morphological criteria to delineate and further classify these tumours. Owing to their variable architecture, a bewildering nomenclature has emerged for these tumours, exemplified by the many names applied to the goitrous thyroid gland: hyperplasia, adenomatous goitre, adenomatoid nodules, benign nodular thyroid disease, adenoma, etc. This article reviews the evidence suggesting that: (1) the varied types of benign neogeneration of endocrine tissue, the spectrum of which ranges from 'simple hyperplasia' to 'true adenoma', involve the same process; (2) even clonality of a growing lesion cannot distinguish hyperplasia from neoplasia; and (3) the basic processes in both cases are not different from those that cause benign tumours in other organs.

Adenoma↗
PubMedDate not supplied

Intimal hyperplasia in the distal ulnar artery; Influence of gender and implications for the hypothenar hammer syndrome.

INTRODUCTION: The distal ulnar artery in the hand is subjected to trauma when the hypothenar eminence is used as a hammer. The clinical presentation of arterial obstruction or aneurysm formation at this site with a history of trauma to the hypothenar eminence is termed the hypothenar hammer syndrome (HHS) and is most commonly observed in the right hands of men. Since the trauma-inducing activities associated with the HHS are common, the histopathology of this arterial segment in our autopsy population was evaluated. METHODS: The distal ulnar artery in the hand was examined in 21 randomly selected autopsies. Formalin-fixed paraffin-embedded cross sections of artery were assessed using hematoxylin and eosin (H&E), trichrome and elastic stains as well as immunohistochemistry for CD34 and alpha-smooth muscle actin. RESULTS: Intimal hyperplasia is common at this site in the vasculature. The degree of intimal hyperplasia, as assessed by the intima/media ratio, is significantly greater in the right hands of men than in either their corresponding left hands or in women. None of the arterial segments examined contained foam cells or extracellular lipid deposits indicative of atherosclerosis. CONCLUSIONS: In the injury-prone segment of the distal ulnar artery, intimal hyperplasia is common but is particularly severe in the right hands of men, correlating with the demographics of the HHS. Although, this arterial segment frequently develops intimal hyperplasia, it is resistant to the development of atherosclerosis.

Adult↗
PubMed2002

Atypical complex endometrial hyperplasia treated with the GyneLase system.

A 47-year-old premenopausal, para 1, gravida 1 woman complained of menometrorrhagia. She had no risk factors for endometrial hyperplasia or cancer, and office endometrial biopsy indicated focal, nonatypical endometrial hyperplasia. Seven months later the patient was scheduled for hysteroscopic endometrial resection. Instead she was treated by hysteroscopy, curettage, and the GyneLase system. The curetting indicated atypical, complex endometrial hyperplasia. The woman refused hysterectomy and salpingo-oophorectomy and adjunctive therapy with progesterone. She agreed to close surveillance and further treatment if she had any vaginal bleeding. At 13 months she remains amenorrheic, the endometrial echo is 2 mm, and follicle-stimulating hormone level is 63 IU/L. Based on the patient's amenorrhea and ultrasound uterine measurement, it is tempting to assume that GyneLase treatment may have cured her atypical hyperplasia. However, at this time, we have no evidence to substantiate this assumption.

Curettage↗
PubMed1999

Hysteroscopic resection of endometrial hyperplasia.

STUDY OBJECTIVE: To evaluate the efficacy and safety of hysteroscopic resection of endometrial hyperplasia without atypia. DESIGN: Pilot feasibility study (Canadian Task Force classification II-1). SETTING: Department of gynecology at a general hospital. PATIENTS: Seventy-three women. Intervention. Transcervical hysteroscopic endometrial resection under general or spinal anesthesia. MEASUREMENTS AND MAIN RESULTS: Efficacy of treatment was based on hysteroscopic and histologic regression of endometrial hyperplasia and subjectively assessed uterine bleeding. Safety was evaluated by adverse events. Forty-four cycling women experienced complete remission of uterine bleeding and none had persistence of endometrial hyperplasia during follow-up; four underwent hysterectomy. Atrophic endometrium was present in 24 menopausal women, one of whom underwent hysterectomy. CONCLUSION: Endometrial resection was effective in achieving regression of endometrial hyperplasia and preventing its recurrence. (J Am Assoc Gynecol Laparosc 6(2):151-154, 1999)

Adult↗
PubMed1997

Vein quality influences neointimal hyperplasia in an organ culture model of human saphenous vein.

OBJECTIVES: The severity of pre-existing pathological changes in human saphenous vein (HSV) correlates with the development of vein graft stenosis and graft patency. The aim of this study was to investigate the influence of pre-existing intimal hyperplasia on development of the neointima in vitro, using an organ culture model. MATERIALS AND METHODS: Segments of HSV were harvested during coronary artery bypass surgery. Histology was performed on part of the vein; the remainder was maintained in culture. Pre-existing intimal thickness (PIT) in HSV from day 0 and neointimal thickness (NIT) in cultured HSV were measured using computerised image analysis on histological sections. Day 0 and 14 veins were compared with respect to intimal hyperplasia. RESULTS: Twelve pairs of veins were examined. A mean tissue ATP of 297 nmoles/g wet weight for cultured. HSV confirmed cell viability. Mean PIT was 180 microns (CI: 86-274) and mean NIT was 60 microns (CI: 48-72), with a significant correlation between them using the Spearman Rank test (Rs = 0.72; p = 0.008). CONCLUSIONS: Pre-existing vein quality as measured by PIT correlates with the development of neointimal hyperplasia in culture, adding further support to clinical evidence that poor vein quality predisposes to vein graft stenosis due to an inherent susceptibility to intimal hyperplasia.

Graft Occlusion, Vascular↗
PubMed2003

Myometrial hyperplasia in pediatric, adolescent, and young adult uteri.

OBJECTIVES: To evaluate if myometrial hyperplasia is a congenital variation in myometrial differentiation, or an acquired structural disorder of the myometrium, this study evaluated whether myometrial hyperplasia was present in uteri of children, adolescents, and young adults. METHODS: We studied 19 pediatric/young adult uteri in cases with no clinical history of uterine disease. Random photomicrographs at 100x, taken at 1, 5, and 10 mm beneath the endometrium, were assessed for increased cellularity and nucleus/cell ratio, as compared to normal myometrium in the outer third of the same uterus. RESULTS: Myometrial hyperplasia was generally absent in prepubertal uteri, first appeared in adolescent uteri just beneath the endometrium, and was found at 5 mm depth only after age 18. It decreased with depth beneath the endometrium (P<0.05). CONCLUSIONS: Myometrial hyperplasia is not a congenital anatomic variation in myometrial differentiation, but rather an age-related acquired structural variation. Its relationship to common adolescent symptoms of dysmenorrhea and anovulatory bleeding remains unknown and unexplored.

Adolescent↗
PubMed2005

Monotherapy versus combination drug therapy for the treatment of benign prostatic hyperplasia.

BACKGROUND: Benign prostatic hyperplasia (BPH) is a medical condition occurring in older men (ie, those aged >60 years) resulting from enlargement of the prostate gland. Consequently, affected men may experience bother-some urinary tract symptoms and diminished quality of life. The risk of lower urinary tract symptoms and complications such as acute urinary retention (AUR) may increase if BPH is untreated. Currently, 2 classes of drugs-alpha-adrenergic blockers (alpha-blockers) and 5alpha-reductase inhibitors-are indicated for the treatment of BPH. Although the 2 classes are commonly used in combination, the evidence has frequently not been supportive of this practice. Results from the Medical Therapy of Prostatic Symptoms (MTOPS) trial, the largest and longest clinical trial on this topic to date, revisited the role of combination therapy in the treatment of BPH. OBJECTIVE: This review presents published trials evaluating alpha-blockers or 5alpha-reductase inhibitors used alone or in combination for the treatment of BPH. METHODS: A MEDLINE search was conducted (December 1974 to November 2004) using the MeSH term prostatic hyperplasia limited to the subheading of drug therapy. These results were cross-referenced with the MeSH term combination drug therapy. An additional search was conducted using the MeSH terms finasteride and adrenergic alpha-antagonists limited to adverse effects and therapeutic uses. These results were cross-referenced with prostatic hyperplasia and combination drug therapy. Review articles and meta-analyses were also used. RESULTS: The Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group and the Prospective European Doxazosin and Combination Therapy studies were well-designed trials that failed to support the theory that combination therapy is preferred over alpha-blockers alone. Finasteride was also shown to be no better than placebo for the outcomes of symptom score and peak urinary flow rates. Other trials suggested that combination therapy (which included finasteride) was more effective at reducing symptom scores in men with enlarged prostates at 1 year and that alpha-blockers may be successfully discontinued once patients are stabilized on finasteride. Although it was a prespecified secondary end point, the incidence of surgery or AUR was reduced by 51% using finasteride over placebo. The additive benefit finasteride provides in reducing symptoms, risk of AUR, and invasive surgery was observed within the first year of treatment and correlated with larger prostate sizes (mean [SD], approximately 55 [26] mL). The MTOPS trial further demonstrated a relative risk reduction of 66% in clinical progression rates for the combination-therapy group versus 39% for the doxazosin group compared with placebo (P < 0.001); the doxazosin group was not statistically different from the finasteride monotherapy group. Improvements in symptom scores were greater in the combination-therapy group versus the doxazosin (P = 0.006) and finasteride monotherapy (P < 0.001) groups. CONCLUSION: Based on the literature, combination therapy has been proven to relieve symptoms and delay progression of BPH in men with moderate to severe symptoms and moderately enlarged prostate glands.

5-alpha Reductase Inhibitors↗
PubMed2000

Decreased cannabinoid CB1 receptor mRNA levels and immunoreactivity in pituitary hyperplasia induced by prolonged exposure to estrogens.

Recent studies have demonstrated that cannabinoid CB1 receptor gene expression in the anterior pituitary gland is under the influence of estrogens. Because these receptors have been recently involved in the development of several types of cancer, it would be interesting to examine the changes produced in these receptors by the development of pituitary hyperplasia after a chronic exposure to estrogens. To this end, we measured mRNA levels and immunoreactivity for the CB1 receptor in the anterior pituitary gland of rats implanted with silastic capsules containing diethylstilbestrod (DES), a synthetic estrogen, or empty capsules. Results were as follows. Induction of pituitary hyperplasia with DES produced the expected body weight loss (-38.4%) and increase in pituitary weight (5-fold) and plasma prolactin (PRL) levels (90-fold). In hyperplastic pituitaries, both CB1 receptor mRNA levels and immunoreactivity decreased significantly (-79.4% and -63.2% respectively). Double immuno-labelling studies demonstrated that CB1 receptors colocalized, in hyperplastic pituitaries, with PRL- or luteinizing hormone-containing cells, as they did in normal pituitaries. In summary, estrogen-induced pituitary hyperplastia was associated with a marked reduction in CB1 receptors, despite the fact that these receptors were located, among others, on lactotroph cells which develop hyperplasia during DES exposure. Whether this decrease is involved in the ethiology of pituitary hyperplasia and whether the pharmacological activation of these receptors might affect this process are presently unknown, but this will be subjected of further research.

Animals↗
PubMed1999

Management of focal nodular hyperplasia and hepatocellular adenoma.

Hepatocellular adenoma and focal nodular hyperplasia are two benign hepatic tumors which are mainly detected in healthy young women. Hepatocellular adenoma is an indication for surgery due to the risk of haemorrhage and malignant transformation. By contrast, focal nodular hyperplasia should be managed conservatively. However, precise diagnosis of these benign liver tumors remains difficult and sometimes impossible, despite new imaging techniques. Because of the risk of diagnostic error, resection or large biopsies of presumed liver tumors should be performed in young women (and a fortiori in men and older patients in whom focal nodular hyperplasia is less prevalent) when the diagnosis of focal nodular hyperplasia is not firmly established. The risk of liver surgery in young patients with normal liver parenchyma is, in the opinion of the authors, lower than the risk of a mistaken diagnosis.

Adenoma, Liver Cell↗
PubMed2003

Histopathological study of renal transplant artery stenosis: role of rejection and cold ischaemia time in the pathogenesis of intimal hyperplasia in an arterial allograft.

INTRODUCTION: Intimal hyperplasia of renal allograft arteries is a cause of hypertension and graft loss and the predisposing factors are poorly understood. We performed a histopathological study focusing on cold ischaemia time and immunological factors and their effect on the donor artery. METHODS: Primary renal artery branches were obtained from patients undergoing transplant nephrectomy for chronic rejection. Non-transplant patients undergoing nephrectomy served as controls. Clinical information including immunosuppression and rejection episodes, cold ischaemia time and graft survival were collected from the patients' charts. Collagen, smooth muscle cells, T cells, macrophages, and neutrophils were quantified using immunohistochemistry. The intima to media ratio was also calculated using imaging software. Statistical analysis was performed using linear regression and the Mann-Whitney test with P < 0.05 significant. RESULTS: Nine transplant patients and five controls were included. All transplant patients received maximum immunosuppression according to clinical standards. The median number of acute rejection episodes was 1 (range 0-5). Cold ischaemia time was 24.3 +/- 9.6 h (mean +/- SD). Mean allograft longeviy was 87.4 +/- 72.9 months (mean +/- SD). The intima/media ratio in the transplant group was higher as compared with the control (P = 0.002). The same was true for intima collagen content (P = 0.001) and intima smooth muscle content (P = 0.036). Cold ischaemia time was 19.6 +/- 11.1 h (mean +/- SD) and did not correlate with intima/media ratio. Also the number of rejection episodes did not correlate with the intima/media ratio. CONCLUSION: Intimal hyperplasia in the allograft artery has a multifactorial aetiology. We were not able to establish an association between intimal hyperplasia and acute rejection episodes or length of cold ischaemia time. It appears that immunosuppression does not prevent the development of intimal hyperplasia.

Adult↗
PubMed1997

Controlled local delivery of tetracycline HCl in the treatment of periimplant mucosal hyperplasia and mucositis. A controlled case series.

The purpose of this controlled case series was to assess the adjunctive efficacy of controlled topical tetracycline HCl application in the treatment of infection associated periimplant mucositis or mucosal hyperplasia. Eight patients with at least 2 endosseous implants showing clinical signs of periimplant mucosal hyperplasia or mucositis were enrolled. All implants received supra- and subgingival scaling, with half of the implants receiving adjunctive controlled local delivery of tetracycline HCl (test). Control implants did not receive any other therapy aside from scaling. Clinical parameters were assessed at baseline, 4, and 12 weeks. Scaling plus controlled local delivery of tetracycline HCl markedly reduced periimplant mucosal hyperplasia in 4 of 5 test implants and demonstrated a trend towards a reduction of bleeding on probing scores. Scaling alone had no effect on mucosal hyperplasia in the 2 control implants presenting with this condition nor bleeding on probing scores. In both groups, plaque index scores were slightly reduced at 4 weeks but returned to baseline values at 12 weeks, whereas pocket probing depths, clinical attachment levels, and probing bone levels remained unchanged during the course of the trial. The observed trends suggest that scaling plus controlled local delivery of tetracycline HCl may have beneficial effects. Randomized controlled trials employing a sample size high enough to reach sufficient statistical power are needed to definitively assess the efficacy of controlled local tetracycline HCl delivery on periimplant diseases.

Administration, Topical↗
PubMed2003

The subgingival microflora in phenytoin-induced gingival hyperplasia.

OBJECTIVES: Microbial flora and gingival conditions were compared between a group of patients with phenytoin-induced gingival hyperplasia as a test group, a control group of patients who were administered phenytoin without gingival hyperplasia and a blank group who took no phenytoin and no gingival hyperplasia in mentally retarded patients. MATERIALS AND METHODS: Subgingival plaque samples were collected from a PHT-induced overgrown gingival pocket and microbiological experiments were performed by culture and PCR methods. RESULTS: The predominant genera in total cultivable bacteria from subgingival plaque samples were streptococcus and actinomyces with recovery ranges of 37.6-42.1% and 23.4-25.5% of total bacteria, respectively, in all groups. The test group showed a significantly higher level of obligate Gram-negative rods than the control and blank groups. Black-pigmented obligate anaerobic Gram-negative rods were detected in 10.3% of total cultivable bacteria in the test group. The black-pigmented rods were predominantly Prevotella intermedia in the test group and Prevotella nigrescens in the control and blank groups. Porphyromonas gingivalis and Porphyromonas endodontalis were also detected in the test group with small values. CONCLUSIONS: These results suggested that black-pigmented rods, particularly P. intermedia, could be habitable in the environment of gingival hyperplasia.

Adolescent↗
PubMed1979

Polypoid and papillary epithelial hyperplasia: a potential cause of ductal obstruction in adult polycystic disease.

In experimental models of cystic renal disease, functional studies define conditions that suggest increased resistance to outflow from dilated or cystic nephrons. Morphologically, models exhibit foci of cellular hyperplasia and micropolyp formation along outer medullary collecting tubules. Temporally, cellular proliferation precedes cyst formation. These findings in models have led to a hypothesis that polypoid hyperplasia participates in cyst formation in susceptible kidneys by increasing resistance to the outflow of tubular urine. The present study was undertaken to establish the presence, extent, and distribution of cellular hyperplasia in human adult polycystic kidney disease. Kidneys from four unrelated individuals were studied by light and by transmission and scanning electron microscopy. Foci of hocation of hyperplasia along the nephron were similar to those seen in the models. These findings delineate a heretofore unappreciated morphologic similarity between the models and human disease and add further support to the hypothesis that partial rubular obstruction participates in the pathogenesis of renal cystic disease, whether it be heritable or acquired, in animals and in man.

Animals↗
PubMed1991

Molecular mechanisms of tubulointerstitial hypertrophy and hyperplasia.

Adult kidneys, which are principally composed of tubulointerstitium, do not normally regenerate or expand their working pool of functional cells at a very high rate. Loss of kidney tissue, however, can lead to some compensatory renal enlargement. The catalytic forces initiating such exchanges have not been fully articulated by current experimental endeavors. Increasing evidence, nevertheless, does suggest that factors other than simple changes in renal hemodynamics may be involved in this process. Different cellular elements in the tubulointerstitial microenvironment probably modulate changes in tubular enlargement or size through a complex cytokine network. Autocrine and paracrine stimulation of enlargement by different local growth factors also seem to play a pivotal role. After binding to cellular receptors, these factors activate signal transduction pathways resulting in expression of immediate early genes, which by themselves can synchronize the expression of subsequent genes through the medium of transacting factors. The renal enlargement response can also be modified by endocrine hormones that can activate such genes directly and/or stimulate other adjunctive processes, like receptor expression for the regional binding of growth factors. Furthermore, renal enlargement is under negative feedback of inhibitory factors like TGF beta. It is possible, for example, that special genes exist which are only expressed to arrest enlargement. It has been further suggested that activation of the Na+/H+ antiporter is a common denominator in renal enlargement. Recent findings, however, indicate that the activation of this antiporter is not always necessary, and might rather be a parallel event rather than a key phenomena in tubular enlargement. G0/G1 transition of tubular cells seems to involve similar factors in tubular hypertrophy and hyperplasia. The factors which are responsible for the final determination of the enlargement pattern (hypertrophy vs. proliferation) are unknown. The separation between hypertrophy and hyperplasia, although suggested by striking differences in cellular regulation, may be somewhat artificial, since responses leading to tubular enlargement also exist in circumstances where hyperplasia and hypertrophy are combined events. Recently it has been proposed that growth factors stimulate gluconeogenesis in proximal tubular cells producing hyperplasia, whereas factors inhibiting gluconeogenesis might induce hypertrophy. Whether the common pathway message of this intriguing hypothesis is correct still requires further validation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

E-cadherin alterations in atypical lobular hyperplasia and lobular carcinoma in situ of the breast.

Tumor development from an early lesion through to invasive disease is not a clearly defined progression in the breast. Studies of invasive lobular carcinoma have reported mutations, loss of heterozygosity (LOH) and loss of protein expression in epithelial (E)-cadherin, a protein involved in cell adhesion. Our study examines in situ lobular neoplastic lesions without concurrent invasive carcinoma for E-cadherin gene alterations and protein expression, beta-catenin, alpha-catenin and p120-catenin protein expression, and LOH at the chromosome 16q locus, with the goal of determining the events occurring at the stage of lobular neoplasia. In all, 13 atypical lobular hyperplasia lesions and 13 lobular carcinoma in situ lesions from archived cases were examined. E-cadherin sequence alterations were evaluated using single strand conformation polymorphism and DNA sequencing, and PCR-based LOH analysis was carried out for the 16q locus. Using immunohistochemistry, we assessed protein expression. A total of 23 of 24 lesions evaluated by immunohistochemistry were negative for both E-cadherin and beta-catenin protein expression, and 21 of 23 lesions were negative for alpha-catenin. Cytoplasmic (rather than membrane) localization of p120-catenin was observed in 20 of 21 cases. Lobular carcinoma in situ cases were characterized by mutations; however, atypical lobular hyperplasia cases were not. LOH at 16q was an infrequent event. From our study, we conclude that an altered E-cadherin adhesion complex is an early event affecting atypical lobular hyperplasia as well as lobular carcinoma in situ and occurs prior to progression to invasive disease. However, the loss of protein expression is accompanied by E-cadherin DNA alterations in lobular carcinoma in situ but not in atypical lobular hyperplasia. These cases lacking both protein expression and gene alterations suggest that another mechanism is involved, possibly as early as at the hyperplastic stage, causing silencing of the E-cadherin complex.

Breast Neoplasms↗
PubMed2006

Steroid receptor coactivator AIB1 in endometrial carcinoma, hyperplasia and normal endometrium: Correlation with clinicopathologic parameters and biomarkers.

Members of the p160 steroid receptor cofactor family, including AIB1 (Amplified in Breast Cancer 1) (also known as SRC-3/RAC3/ACTR/pCIP/TRAM-1), are of interest in endometrial carcinoma as they affect the function of estrogen (ER) and progesterone receptors (PR). Since it is feasible that alterations in the expression levels of coregulators can either augment ER activity or reduce the ability of PR to oppose ER action in endometrial cancers, our primary aim was to analyze expression of the AIB1 protein in endometrial carcinoma, carcinoma-associated complex atypical hyperplasia, and carcinoma-associated normal endometrium using immunohistochemistry and tissue microarrays. Expression of AIB1 was compared with other biomarkers and clinicopathologic parameters. We also tested AIB1 expression in non-carcinoma associated hyperplastic, normal secretory and proliferative endometrium to determine baseline AIB1 levels. In endometrial carcinoma, there is a higher expression of AIB1 compared to carcinoma-associated complex atypical hyperplasia (0.007) or carcinoma-associated normal endometrium (<0.001). AIB1 expression correlates with older age (P = 0.003), peri- or postmenopausal status (P = 0.002) and a higher grade of carcinomas (P = 0.04). There were no differences in the expression of additional steroid hormone receptor co-activators (SRC-1 and p300/CBP) and the co-repressor SMRT between histologic categories. AIB1 expression correlated with ER (r = 0.30, P = 0.006). The strongest correlation was between ER and PR-B isoform nuclear expression (r = 0.52, P < 0.0001). AIB1 levels were higher in non-carcinoma associated normal and hyperplastic endometrium compared to carcinoma-associated complex atypical hyperplasia and carcinoma-associated normal endometrium, and were the highest in normal secretory endometrium. In conclusion, high AIB1 expression in endometrial carcinoma is associated with parameters of poor prognosis. We propose that when AIB1 is overexpressed in endometrial carcinoma, ER action is augmented, leading to endometrial hyperplasia and progression to malignancy. Future studies correlating expression with response to hormonal therapy may be beneficial.

Adenocarcinoma↗