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PubMed1998

Adenoid basal epitheliomas of the uterine cervix: a reevaluation of distinctive cervical basaloid lesions currently classified as adenoid basal carcinoma and adenoid basal hyperplasia.

A series of 12 adenoid basal carcinomas and three adenoid basal hyperplasias of the cervix were analyzed. The ages of the patients with adenoid basal carcinoma ranged from 30 to 91 years with a mean of 71 years. Pap smear results for 11 of 12 (92%) were abnormal. Almost all patients were asymptomatic. None had a gross cervical tumor. All tumors had typical histologic features of adenoid basal carcinoma, with various degrees of squamous differentiation. Depth of tumor invasion ranged from 2 mm to 10 mm (mean, 4.3 mm; median, 3.7 mm), exceeding 3 mm in six tumors (50%). Tumor volume was >500 mm3 in four tumors (33%). An associated neoplastic squamous lesion was present in 92% of patients, including high-grade cervical intraepithelial neoplasia in 10 cases and microinvasive squamous cell carcinoma in one. Treatment was predominantly surgical, usually after some form of cervical conization; conization alone was performed in three patients. Lymph nodes were removed in five patients; none of 104 nodes had metastases. No recurrence of tumor developed in any patient. Nine patients were alive without disease after 4 to 82 months (mean, 30 months), and three died without disease after 24, 63, and 87 months. The three patients with adenoid basal hyperplasia also were asymptomatic and did not have a gross cervical lesion. Pap smear results for two patients were abnormal. The adenoid basal hyperplasias were incidental, very superficial lesions that resembled small adenoid basal carcinomas. Generally, they were attached to the squamous or endocervical mucosal epithelium; all were less than 0.5 mm in depth. Treatment was hysterectomy in one patient and conization in two. Follow-up was short but uneventful. Our findings, together with those previously reported, indicate (1) adenoid basal carcinoma with typical histologic features is not a malignant neoplasm in that it typically presents in asymptomatic women, usually is discovered after an abnormal Pap smear result due to cervical intraepithelial neoplasia, does not produce a grossly visible lesion, has never metastasized to regional lymph nodes or elsewhere, and has never itself caused death; (2) rare, histologically atypical tumors with distinctly malignant features should not be regarded as adenoid basal carcinoma; and (3) adenoid basal hyperplasia probably is a small adenoid basal carcinoma. We propose the term "adenoid basal epithelioma" to replace adenoid basal carcinoma and adenoid basal hyperplasia, because it better describes the clinicopathologic features of these distinctive lesions and their excellent prognosis and may reduce the likelihood of unnecessarily aggressive treatment.

Adult↗
PubMed1999

Parathyroid hyperplasia, adenomas, and carcinomas: differential expression of p27Kip1 protein.

The histologic spectrum of proliferative parathyroid lesions (hyperplasia, adenoma, and carcinoma) often overlap, and differentiation between these lesions may at times be difficult. p27kip1 (p27) is a cyclin-dependent kinase inhibitor that helps regulate the transition from the G1 to the S phase of the cell cycle. Significantly higher levels of p27 expression have been detected in some normal tissues than in their neoplastic counterparts. The authors analyzed a series of parathyroid lesions to determine if expression of this cell cycle protein may be useful in distinguishing between parathyroid hyperplasia, adenomas, and carcinomas. Formalin-fixed paraffin-embedded tissues from randomly selected patients (22 histologically normal parathyroid glands, 33 cases of hyperplasia, 43 adenomas, and 17 carcinomas) were analyzed for expression of p27 by immunostaining. All cases were also immunostained for Ki67 with antibody MIB-1. The distribution of immunoreactivity was analyzed by quantifying the percentage of positive nuclei that was expressed as the labeling index (LI). In situ hybridization (ISH) for p27 mRNA was done using a cRNA probe with 30 of these cases. Normal parathyroid glands had the highest p27 LI (89.6 +/- 1.4), followed by hyperplasia (69.6 +/- 7.5), adenomas (56.8 +/- 3.4), and carcinomas (13.9 +/- 2.6). ISH showed no differences in p27 mRNA, indicating that the expression of the p27 gene was controlled at a posttranslational level in parathyroid tissues. Ki67 expression was significantly higher in carcinomas (LI = 8.4 +/- 1.9) than in adenomas (LI = 2.7 +/- 0.2) and hyperplasia (LI = 3.3 +/- 0.4). These results suggest that both p27 and Ki67 may be helpful in the diagnosis of histologically difficult parathyroid lesions.

Adenoma↗
PubMed2001

Prospective multicenter evaluation of the morphometric D-score for prediction of the outcome of endometrial hyperplasias.

Prospective multicenter evaluation of the WHO classification and the morphometric D-score to predict endometrial hyperplasia cancer progression. In 132 endometrial hyperplasias WHO classification was performed by two experienced gynecologic pathologists. The D-score was assessed blindly by technicians in a routine diagnostic setting. Development of endometrial carcinoma during a 1-10-year follow-up was used as the end point. Eleven of 132 patients (8%), 10 of 61 (16%) atypical hyperplasias, and 1 of 71 (1%) nonatypical hyperplasias developed cancer. Twenty-six curettings had a D-score < or = 0 ("unfavorable" or endometrial intraepithelial neoplasia) of which 10 (38%) developed cancer. None of the 86 cases with a D-score > 1 ("favorable") and one of the 20 (5%) cases with 0 < D-score < or = 1 ("uncertain") developed cancer. Sensitivity of the D-score was 100%, specificity 82%, the positive and negative predictive values were 38% and 100%, respectively. These values are similar to those in three prior retrospective D-score studies but higher than the WHO values (which are 91%, 58%, 16%, and 99%, respectively). The D-score in endometrial hyperplasias is a more sensitive and specific marker for cancer prediction than the WHO classification, can be assessed in a routine clinical setting on standard hematoxylin and eosin sections (15-30 minutes per case), and is highly reproducible and cost-effective (U.S. $50 per case).

Adult↗
PubMed1982

Antiplatelet therapy reduces aortic intimal hyperplasia distal to small diameter vascular prostheses (PTFE) in nonhuman primates.

While the use of prosthetic grafts in small diameter arterial reconstruction is required when suitable autogenous graft material is unavailable, late occlusion of prosthetic grafts caused by proliferative lesions has been described. This study evaluated the suitability of 3-mm (ID) microporous polytetrafluoroethylene (PTFE) Gore-Tex grafts inserted in the abdominal aorta of eight nonhuman primates (Macaca fascicularis), and the effects of prolonged antiplatelet treatment on both graft patency and the development of intimal hyperplasia in the adjacent vasculature. Four monkeys received antiplatelet medication consisting of aspirin (163 mg twice daily) and dipyridamole (25 mg twice daily). When killed at four months following graft insertion, all four grafts in the antiplatelet medicated group were patent, while in the control group, only two of four grafts were patent. Histologic examination and quantitative photogravitometric evaluation of the degree of luminal narrowing were performed on all grafts and the adjacent vasculature. These studies revealed that while all graft and aortic segments showed varying amounts of intimal thickening, occlusions in the control animals were related to intimal hyperplasia in the host aorta at the site of the distal anastomosis. Intimal hyperplasia in all aortic segments examined distal to the graft was significantly reduced by antiplatelet therapy. Electronmicroscopy showed that smooth muscle cells were the predominant cells of the intimal thickening of the aorta (intimal hyperplasia), and that proliferation of these cells did not extend into the graft itself. The predominant cell population of the intimal thickening of the graft were of the myofibroblast type (neointimal hyperplasis). The luminal surface of the graft was lined with cells that had some but not all of the characteristics of mature endothelial cells. In vitro studies confirmed global interference with platelet function and arachidonic acid metabolism in medicated animals. Medication inhibited platelet cyclo-oxygenase without affecting platelet lipoxygenase, thromboxane synthetase, or prostacyclin-like activity in undisturbed arteries. This study shows that severe intimal hyperplasia develops rapidly in the recipient vessel adjacent to small diameter Gore-Tex grafts, and that the severity of the response is reduced by antiplatelet agents. Histologic examination revealed that the intimal thickening in the graft and the adjacent aortic segments were composed of cells that were not morphologically identical, suggesting two separate aetiologies and the possible need to use different approaches in their prevention.

Animals↗
PubMed1990

Reduction of intimal hyperplasia and enhanced reactivity of experimental vein bypass grafts with verapamil treatment.

Recent studies have shown that calcium antagonists exert an antiatherogenic effect in animals fed cholesterol. Vein graft intimal hyperplasia is believed to be an early event in atherosclerotic lesion formation, which is a significant cause of graft failure. Altered vasoreactivity has also been postulated in the etiology of vein graft failure. Therefore this study examined the effect of verapamil treatment on the development of intimal hyperplasia and the vasoreactivity of experimental vein bypass grafts. The right external jugular vein was grafted into the right carotid artery of 30 male New Zealand white rabbits fed normal rabbit chow. The left external jugular vein was used as the control vein. Fifteen animals received verapamil (1.25 mg/day for 28 days) via the femoral vein by means of an osmotic pump. In 15 control animals the pump contained saline. Plasma verapamil concentration was 50.9 +/- 13.2 ng/mL (x +/- SEM), a dose that showed no effect on either blood pressure, total serum cholesterol, or in vitro platelet aggregation to ADP. Fourteen of fifteen grafts were patent in each group, for a patency rate of 93%. Histologic examination using computer morphometry showed significant reduction of intimal hyperplasia at the proximal, middle, and distal graft segments (p less than 0.05). In addition in vitro isometric tension studies of the vein grafts and control veins showed that verapamil causes enhanced reactivity of both vein grafts and control veins in response to norepinephrine and histamine (p less than 0.05). Reactivity of vein grafts to serotonin was unaltered. While none of the normal veins in the control group responded to serotonin, normal veins treated with verapamil contracted readily in response to serotonin. Endothelial-dependent relaxation to acetylcholine was absent in both control and verapamil-treated vein grafts, while normal veins from both groups responded to the same extent to acetylcholine. Because we could not demonstrate any difference in platelet or endothelium function between untreated and verapamil-treated animals, we examined the direct effect of verapamil on smooth muscle. Verapamil significantly inhibited [3H]-thymidine incorporation into DNA in vascular smooth muscle cells in culture in a dose-dependent manner. Verapamil treatment significantly reduces intimal hyperplasia in experimental vein grafts and inhibits smooth muscle cell proliferation in culture. Furthermore the enhanced reactivity to norepinephrine and histamine in the verapamil-treated vessels has no detrimental effect on the patency rate at 4 weeks. Thus by inhibiting intimal hyperplasia, calcium antagonists may improve the long-term patency of vein bypass grafts.

Animals↗
PubMed1990

Gallium-67 scan for distinguishing follicular hyperplasia from other AIDS-associated diseases in lymph nodes.

We have studied gallium-67 citrate scan (Ga-67) in the diagnosis of lymphadenopathy in patients with HIV-associated symptoms. Thirty HIV-infected patients with lymphadenopathy, fever and/or weight loss were evaluated with Ga-67. Lymph-node biopsy and/or needle aspirations were done in all patients. Twelve of 17 patients with grade 2 or 3 Ga-67 (uptake equal to or greater than that in the liver) had mycobacteriosis, three had lymphoma, one had Kaposi's sarcoma plus Castleman's disease and one had follicular hyperplasia. The three patients with grade 1 Ga-67 (uptake greater than that in soft tissue but less than that in the liver) had follicular hyperplasia. Of the 10 patients with grade 0 Ga-67 (less than or equal to that in soft tissue), nine had follicular hyperplasia and one had Kaposi's sarcoma. Sixteen of 17 patients with grade 2 or 3 Ga-67 versus one of 13 with Ga-67 grade 1 or 0 had diseases other than follicular hyperplasia (P less than 0.0001). Ga-67 may be a practical diagnostic tool in HIV-infected patients with lymphadenopathy and constitutional symptoms. A grade 1 or 0 Ga-67 suggests the presence of follicular hyperplasia, and lymph-node biopsy may be avoided unless Kaposi's sarcoma is suspected.

Adult↗
PubMed1997

Comparison of the reproducibility of the WHO classifications of 1975 and 1994 of endometrial hyperplasia.

In a blinded, randomized design, six histopathologists with an interest in gynecological pathology examined the inter- and intraobserver variation of the histopathological diagnosis of endometrial hyperplasia according to the World Health Organization (WHO) classification of 1975 and the new WHO classification of 1994. On four occasions, the pathologists assessed hematoxylin/eosin-stained slides from 128 cases originally diagnosed and coded in the Snomed system as endometrial hyperplasia. In the first and third rounds, the slides were classified according to the 1975 classification and in the second and fourth rounds according to the 1994 classification. The overall interobserver agreement in the two rounds where the 1975 classification was used was 0.47 and 0.51, and the kappa values 0.24 [95% confidence interval (CI) 0.21-0.27] and 0.30 (95% CI 0.27-0.33). The overall interobserver agreement in the two rounds using the 1994 classification was 0.45 and 0.41 and the kappa values 0.25 (95% CI 0.23-0.28) and 0.20 (95% CI 0.17-0.22). Reducing the classification to two categories with clinical significance (atypical endometrial hyperplasia versus others in the 1975 classification, and atypical endometrial hyperplasia, complex versus others in the 1994 classification) increased the overall agreement of the 1975 classification in both rounds to 0.91 and of the 1994 classification to 0.92 and 0.90. The kappa values increased to 0.54 (95% CI 0.49-0.58) and 0.49 (95% CI 0.45-0.54) in the 1975 classification and to 0.59 (95% CI 0.54-0.63) and 0.42 (95% CI 0.37-0.46) in the 1994 classification. The intraobserver overall agreement for the 1975 classification ranged from 0.80 to 0.55 and the kappa values from 0.70 (95% CI 0.58-0.81) to 0.28 (95% CI 0.17-0.39). The intraobserver overall agreement for the 1994 classification ranged from 0.71 to 0.46 and the kappa values from 0.60 (95% CI 0.51-0.70) to 0.20 (95% CI 0.09-0.30). It is concluded that there is considerable inter- and intraobserver variation using both the 1975 and the 1994 classifications of endometrial hyperplasia. We propose that there is need for a specification and for a simplification of the classification.

Double-Blind Method↗
PubMed2001

Locally invasive tumors arising from hyperplasia of the retinal pigment epithelium.

PURPOSE: Focal hyperplasia of the retinal pigment epithelium (RPE) is a common fundus condition that is generally stationary, with little or no tendency to enlarge or spawn neoplasms. The purpose of this report is to describe the unusual clinical features of two similar cases in which a nodular tumor of the RPE was documented to arise from a small focus of hyperplasia of the RPE. METHODS: Clinical and cytopathologic observations of two patients. RESULTS: Both patients were observed for approximately 25 years with an unusual progressive fundus tumor that originally arose from a small, flat, irregular focus of hyperplasia of the RPE. The originally observed pigmented lesion was attributed to toxoplasmosis in one patient and laser treatment for central serous chorioretinopathy in the other. In both patients, the tumor enlarged, invaded through the full-thickness sensory retina, and produced a characteristic retinal perforation with apposition of the mass to the vitreous. In both instances, fine-needle aspiration biopsy showed scant pigmented cells, but a definite diagnosis was not made. However, clinical observations in both patients suggested that these tumors were acquired neoplasms that arose from small foci of hyperplasia of the RPE. CONCLUSION: Focal hyperplasia of the RPE can give rise to unusual invasive tumors that invade and replace the overlying sensory retina. These tumors have unique clinical features that differentiate them from uveal melanoma and other pigmented fundus lesions.

Adult↗
PubMed2003

Aetiology and pathogenesis of benign prostatic hyperplasia.

PURPOSE OF REVIEW: Prostatic hyperplasia predominantly involves the stromal compartment of the gland and affects more than 70% of men of 70 years or older with or without obstructive symptoms of benign prostatic hyperplasia. A consensus view is emerging concerning the factors and control systems that modulate cell proliferation and connective tissue biology in the prostate. The purpose of this review is to discuss some of the recent work contributing to the latter in the context of the aetiology of benign prostatic hyperplasia. RECENT FINDINGS: Studies over the last 3-5 years have identified transforming growth factor beta, fibroblast growth factor and insulin-like growth factor family members as key regulators of cell proliferation and extracellular matrix turnover with interrelated activities. Recently, oestrogens, adrenergic signalling and inflammatory processes have been shown to impact and potentially perturb the balance between the activities of the above factors. These agents are all subject to alteration with age and as such are candidates for potential triggers of the initiation of stromal hyperplasia. SUMMARY: The current model for the control and dysregulation of prostatic stromal growth is discussed in relation to the pathogenesis of benign prostatic hyperplasia and future directions for research.

Age Factors↗
PubMed2003

New innovative therapies for benign prostatic hyperplasia: any advance?

PURPOSE OF REVIEW: Benign prostatic hyperplasia is the most common human neoplasm and it is the most frequent tumour requiring surgical treatment in men. Not surprisingly, interest centres on either understanding of prostatic growth during ageing or on various medical or interventional treatments. RECENT FINDINGS: Recent publications describe the interaction of various 5alpha-reductase inhibitors on the two 5alpha-reductase isoforms type 1 and 2, giving a potential new insight into the pathogenesis of benign prostatic hyperplasia. Likewise, chronic inflammation increases growth patterns of fibromuscular tissue in benign prostatic hyperplasia similar to wound healing, and a paracrine loop for chronic inflammation with overexpression of interleukin could be identified. This could be of particular importance in the further understanding of prostatic enlargement. Herbal drug treatment for lower urinary tract symptoms seems to be more effective than previously thought. According to recent publications the effectiveness is well beyond placebo effects. Likewise, alpha-blockers play an important role in treatment of lower urinary tract symptoms with alpha-1 adrenoreceptor antagonists preventing cell proliferation and apoptotic imbalances in prostatic tissue. The effect of alpha-blockers, however, may be limited by severe bladder outlet obstruction with patients at increased risk of treatment failure. Laser prostatectomy and microwave thermotherapy are under consideration as alternative treatments of benign prostatic hyperplasia. The efficacy of urodynamically proven de-obstruction as compared with transurethral resection of the prostate needs to be evaluated. Newer alternative treatments like ethanol installation or bipolar plasma kinetic vaporization have been described, but long-term results and larger patients cohort are still lacking. SUMMARY: New insights into prostatic growth and pathogenesis of benign prostatic hyperplasia are presented. Medical treatment and interventional therapies are evaluated for their safety and efficacy. Only a few new therapeutical options, however, have been published during this review period.

Adrenergic alpha-Antagonists↗
PubMed2004

Benign prostatic hyperplasia progression and its impact on treatment.

PURPOSE OF REVIEW: Management of men with benign prostatic hyperplasia should reduce the lifetime risk of acute urinary retention and the need for benign prostatic hyperplasia-related surgery. A number of recent studies demonstrate that 5alpha-reductase inhibitors are unique in providing a long-term combination of improvements in symptoms and flow, and reductions in the risks of acute urinary retention and surgical intervention. RECENT FINDINGS: The 5alpha-reductase inhibitor finasteride was shown to reduce the risk of retention and surgery in men with large prostate volumes and/or high PSA. Recent studies have examined the role of adding an alpha1-blocker to 5alpha-reductase inhibitor in short- or long-term combination. The Medical Therapy of Prostatic Symptoms study randomised 3,047 men with benign prostatic hyperplasia to treatment with a 5alpha-reductase inhibitor (finasteride), an alpha1 blocker (doxazosin), a combination of both, or placebo. Only treatment arms containing 5alpha-reductase inhibitor therapy were associated with longer-term significant reductions in the risk of acute urinary retention and invasive therapy for benign prostatic hyperplasia. Three randomised, two-year, placebo-controlled studies have assessed the clinical relevance of the >93% DHT suppression provided by dutasteride. Dutasteride was also associated with a reduction in the risk of acute urinary retention of 57%, and a reduction of 48% in the risk of surgical intervention compared with placebo after 2 years. SUMMARY: Short-term combination of 5alpha-reductase inhibitor and alpha-blockade are optimal in providing symptomatic improvement among patients who require symptom relief, while enabling the initiation of 5alpha-reductase inhibitor therapy to reduce the risk of subsequent acute urinary retention or benign prostatic hyperplasia-related surgery in men who are at greater risk of disease progression.

Adrenergic alpha-Antagonists↗
PubMed1995

Antral G-cell hyperplasia: a vanishing disease?

The diagnosis and management of antral gastrin-(G-) cell hyperplasia was a major topic of interest in the 1970s. Following the discovery of Helicobacter pylori in the 1980s, little attention was paid to this condition until it was shown that H. pylori infection was associated with hypergastrinaemia and that eradication of the organism returned the gastrin level to normal. Recent reports have examined the relationship between H. pylori and antral G-cell hyperplasia. H. pylori infection is present in about 50% of cases of antral G-cell hyperplasia and, importantly, eradication of the organism normalizes not only the gastrin level but also the antral G-cell count. Eradication treatment should be the therapy of choice. It is also of interest that H. pylori-negative antral G-cell hyperplasia or hyperfunction does exist. The historical aspects, the relationship between antral G-cell hyperplasia and H. pylori and recent case reports are reviewed.

Animals↗
PubMed2006

Estrogen replacement effectively improves the accelerated intimal hyperplasia following balloon injury of carotid artery in the ovariectomized rats.

Present experiments were designed to investigate the effects of ovariectomy (OVX) and estrogen replacement (ER) on neointimal formation after balloon injury of the rat carotid artery. Young adult female rats were divided into 3 groups of sham operation (control), ovariectomy, and ovariectomy plus estrogen replacement. Estrogen replacement was initiated by implanting a sustained release pellet containing water-soluble 17beta-estradiol 1 week after the ovariectomy. Carotid arteries were harvested 2 weeks after the balloon injury for determinations. The balloon injury caused intimal hyperplasia, which was accompanied by the impaired endothelium-dependent relaxation and cyclic GMP production, and accumulation of asymmetric dimethylarginine (ADMA) as an endogenous NOS inhibitor. Bilateral ovariectomy accelerated the intimal hyperplasia. The acceleration was accompanied by the enhanced impairment of NO production, attenuated reendothelialization, and enhanced accumulation of ADMA. The estrogen replacement improved the accelerated intimal hyperplasia with concomitant improvement of the impaired NO production and accumulated asymmetric dimethylarginine, and facilitated reendothelialization. These results suggests that the enhanced impairment of NO production, which possibly results from the accumulated asymmetric dimethylarginine and lack of reendothelialization, may contribute to the acceleration of intimal hyperplasia by ovariectomy and that estrogen replacement effectively improves the intimal hyperplasia by restoring the impaired NO production through reducing endogenous NOS inhibitor and facilitating reendothelialization.

Animals↗
PubMed2006

Celiac disease associated with nodular regenerative hyperplasia, pulmonary abnormalities, and IgA anticardiolipin antibodies.

The association of nodular regenerative hyperplasia with celiac disease is not as well established as it is with hepatopulmonary syndrome and portopulmonary hypertension. IgA anticardiolipin antibodies were reported recently in celiac patients with nodular regenerative hyperplasia. The subject of this study was the description of pulmonary abnormalities and IgA anticardiolipin antibodies in celiac patients with noncirrhotic portal hypertension. Five patients with portal hypertension were investigated to diagnose its etiology. Celiac disease was diagnosed by means of autoantibody reactivity and duodenal biopsies. Liver histology revealed nodular regenerative hyperplasia in four patients and suggested its presence in 1 case. Two cyanotic patients had severe hypoxemia with a confirmed diagnosis of hepatopulmonary syndrome. Another case exhibited features of hepatopulmonary syndrome with increased levels of arterial pulmonary pressure. The remaining 2 cases had slight abnormalities of arterial oxygenation. Three patients had reactivity to IgA anticardiolipin antibodies. The concomitance of celiac disease and nodular regenerative hyperplasia, two infrequent conditions, raises suspicion of there being a nonfortuitous coincidence. Pulmonary abnormalities, and especially hepatopulmonary syndrome, are described for the first time in association with celiac disease and nodular regenerative hyperplasia.

Adolescent↗
PubMed2005

Gastric foveolar metaplasia with dysplastic changes in Brunner gland hyperplasia: possible precursor lesions for Brunner gland adenocarcinoma.

Cases of adenocarcinomas developed in Brunner gland hyperplasia (BGH) have been sporadically reported. Herein, we report the morphologic spectrum of hyperplastic changes culminating into dysplasia and carcinoma in 722 cases of BGH listed in our files. Fifteen of these cases showed dysplastic changes, with 8 graded as low-grade dysplasia, 5 as high-grade dysplasia, 11 as atypical hyperplasia, and 2 as invasive carcinoma, although each frequently coexisted in the same tumor. In two carcinomas, one had high-grade dysplasia in the mucosa, and another had only atypical hyperplasia. Interestingly, hyperplastic glands around dysplastic foci were associated with gastric foveolar metaplasia and papillary configuration in 13 cases, 11 of which showed a gradual increase in nuclear atypism in the transition from metaplastic to dysplastic glands. All of the metaplastic gastric glands showed diffuse and strong immunopositivity for gastric foveolar mucin (MUC5AC). Immunohistochemical profiles also supported the concept of a continuous spectrum in carcinogenesis from gastric foveolar hyperplasia through atypical hyperplasia or dysplasia and eventually to frank adenocarcinoma. The results of our study suggest, therefore, that dysplastic and/or carcinomatous change does occur in BGH, that they form the continuous morphologic spectrum, and that papillary foveolar metaplasia may be a precursor lesion in the process of carcinogenesis with a background of BGH.

Adenocarcinoma↗
PubMed2005

Immunohistochemical detection of human telomerase reverse transcriptase (hTERT), topoisomerase IIalpha expression, and apoptosis in endometrial adenocarcinoma and atypical hyperplasia.

This study evaluated the immunohistochemical expression of human telomerase reverse transcriptase (hTERT) in endometrial carcinoma and atypical endometrial hyperplasia, and related it to the expression of topoisomerase (TP)IIalpha (a proliferation associated enzyme); apoptosis as determined by the frequency of apoptotic bodies (ABI); mitotic counts; and other clinicopathologic variables. Immunoreactivity for hTERT and TPIIalpha as well as ABI were assessed in 57 endometrial samples (12 atypical hyperplasias, 33 endometrioid carcinomas, 12 serous/clear cell carcinomas). hTERT immunoreactivity, TPIIalpha labeling indices (LI), ABI, and ratios of the indices (ABI/TPIIalpha LI) increased from atypical hyperplasias to endometrioid carcinomas to serous/clear cell carcinomas (p < 0.0001 for each variable). hTERT expression increased with ABI (p < 0.0001), TPIIalpha LI (p = 0.0019), ABI/TPIIalpha ratios (p < 0.0001), and grade (p = 0.0005), but not with FIGO stage (p = 0.2775). TPIIalpha LI, ABI, and ratios were related to high grade (p = 0.0001 for each variable), but not with FIGO stage (p = 0.7362, p = 0.7554, and p = 0.7405, respectively). TPIIalpha LI and ABI were significantly correlated in atypical hyperplasias (p = 0.0004), endometrioid carcinomas (p < 0.0001), and serous/clear cell carcinomas (p = 0.024). Immunostaining levels for hTERT were similar in atypical hyperplasias and grade 1 endometrioid carcinomas (p = 0.1956). These results suggest that hTERT expression is closely related to proliferation, apoptosis, and high grade in endometrial carcinomas, reflecting cell cycle deregulation in endometrial carcinogenesis.

Adenocarcinoma↗
PubMed2004

Reduction of tissue hyperplasia with a rhenium-188 mercaptoacetyltriglycine-3-filled balloon: preliminary study in a canine urethral model.

PURPOSE: To evaluate the efficacy of beta-radiation therapy with rhenium-188 mercaptoacetyltriglycine-3 (MAG(3))-filled balloons to reduce tissue hyperplasia secondary to stent placement in 18 canine urethras. MATERIALS AND METHODS: Eight dogs were treated with 188-Re MAG(3)-filled balloon dilation immediately after stent placement and were killed 4 weeks later (group I, n = 4) or 8 weeks later (group II, n = 4). Five dogs were treated with 188-Re MAG(3)-filled balloon dilation 2 weeks after stent placement and were killed 4 weeks after stent placement (group III). The remaining five dogs were treated with conventional balloon dilation immediately after stent placement and were killed 4 weeks later; these animals formed the control group (group IV). Retrograde urethrography (RUG) was performed during follow-up and three histologic parameters were investigated: the number of epithelial layers, papillary projection thickness, and degree of submucosal inflammatory cell infiltration. The areas inside and outside the ends of the stents were evaluated in each case after animal sacrifice. After testing statistical significance of data for RUG and histologic findings in the four study groups, the Mann-Whitney U test was used to compare groups I and II to determine delayed effects of irradiation, groups I and III to determine benefits of delayed irradiation, groups I and IV to determine efficacy of immediate irradiation for reducing tissue hyperplasia, and groups III and IV to determine efficacy of delayed irradiation for reducing tissue hyperplasia. RESULTS: There were no significant differences in the four study groups on RUG before animal sacrifice. Between groups I and II, group II showed significantly lower mean values in five of six histologic comparisons. Between groups I and III, group III showed significantly lower mean values in only papillary projection thickness inside the stent ends. Between groups I and IV, group I showed significantly lower mean values in all three histologic parameters outside the stent ends. Between groups III and IV, group III showed significantly lower mean values in only two histologic parameters (papillary projection thickness in the in-stent area and inflammatory cell infiltration outside the stent edges). CONCLUSION: beta-Irradiation with use of a 188-Re MAG(3)-filled balloon shows the potential to reduce tissue hyperplasia secondary to stent placement in a canine urethral model. Treatment with 188-Re MAG(3)-filled balloons at the time of stent placement shows not only favorable outcomes for reducing tissue hyperplasia but also improved delayed effects until 8 weeks.

Animals↗
PubMed2004

Estrogen enhancement of androgen-responsive gene expression in hormone-induced hyperplasia in the ventral prostate of F344 rats.

It has been postulated that, in addition to the crucial role of androgens, estrogens may be involved in development of prostate hyperplasia and cancer. In rats, combined administration of estrogen and androgen synergistically increases ventral prostate weight, and continued treatment results in the development of glandular hyperplasia. Prostate adenocarcinoma can be induced by chemical carcinogens in rats, and estrogen given together with an androgen generally shortens the latent period or increases the incidence and/or multiplicity of carcinomas. However, the mechanisms responsible for these synergistic effects of estrogen and androgen are poorly understood. In the present study, we examined the combined effects of 17beta-estradiol (E2) and testosterone (T) on gene expression in an early stage of prostate hyperplasia in an F344 rat model. ERalpha expression, which has been suggested to contribute to development of prostatic hyperplasia, was increased by the combined treatment with T and E2, while it was suppressed by T alone. Expression levels of two androgen-responsive genes, probasin and kallikrein S3, were increased in the ventral prostate of rats treated with T plus E2 for 4 weeks in a dose-dependent manner, while short-term treatment did not alter the expression. These results suggested that enhancing effects of E2 on transcription of androgen-responsive genes, as well as an increased level of ERalpha may play roles in the synergistic effects of E2 on T-induced prostate hyperplasia.

Androgen-Binding Protein↗