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PubMedDate not supplied

Premalignant lesions of prostate and their association with nodular hyperplasia and carcinoma prostate.

BACKGROUND: A relatively new development in the arena of prostatic histopathological study is the premalignant proliferative changes in the glandular epithelium, possibly relating to carcinoma. Two major categories have come up, namely prostatic intraepithelial neoplasia (PIN) and atypical adenomatous hyperplasia (AAH). AIMS: The aims of present study were to identify foci of the two putative premalignant conditions viz. PIN and AAH in ducto-acinar lining epithelia of 200 prostatectomy specimens and their association with nodular hyperplasia and adenocarcinoma prostate. MATERIAL AND METHODS: Micro sections from 200 prostatectomy specimens, received in the Department of Pathology, PGIMS, Rohtak, were extensively studied for the presence and association of premalignant conditions. Significant values were obtained by employing Chi-square (chi2) test, with P value < 0.05 as significant. RESULTS: Out of 177 cases of nodular hyperplasia, 53 (29.9%) showed PIN and 38 (20.3%) showed presence of AAH. All 6 cases (100%) of pure carcinoma revealed foci of PIN. Out of the remaining 23 cases of carcinoma with nodular hyperplasia, foci of PIN were observed in 16 cases (94.1%) and AAH in 2 cases (11.7%). High-grade PIN was observed in 20 cases (86.9%) of the total 23 cases of carcinoma, with/without nodular hyperplasia and 20 cases (11.2%) of nodular hyperplasia. Low-grade PIN was observed in 33 cases (18.6%) of nodular hyperplasia and in only 1 case (5.8%) of carcinoma prostate with nodular hyperplasia. CONCLUSION: PIN, especially high-grade type was the most commonly observed premalignant lesion, in cases of adenocarcinoma, thereby suggesting it to be the likely precursor of carcinoma prostate. AAH showed a weaker association with carcinoma.

Adenocarcinoma↗
PubMed2005

[Clinicopathological analysis in cases with glandular and atypical glandular hyperplasia treated with gestagens].

Many of the cases with endometrial adenocarcinoma of the endometrium are proceeded of glandular and atypical glandular hyperplasia with different risk of progression to neoplasia. Two hundred and eighty cases with glandular and atypical glandular hyperplasia were examined in order to assess the risk of their progression into endometrial cancer. The hyperplasias were evaluated separately for their likelihood of progression to cancer in patients treated and not treated with progestogen therapy. In all cases a fractional re-curreting was performed in order to evaluate the stage of the disease. The leading symptom was the vaginal bleeding in 70% of the cases in the postmenopause. Seventy eight percent of the patients were with obesity (BMI > 30 mg/m2), twenty six percent were with exogenous use of estrogens. 4% of the cases with glandular hyperplasia progressed into cancer and in 13% into atypical grandular hyperplasia. 55% of the atypical glandular hyperplasias progressed into cancers. In the cases with progestogen treatment 70% of the cases showed remission confirmed by re-curetting compared with 23% of the cases without hormonal treatment. The grandular hyperplasia without atypia responded to hormonal therapy. In the postmenopausal patients the atypical glandular hyperplasia should be treated with surgery--total hysterectomy.

Adenocarcinoma↗
PubMed2005

Incidence of endometrial carcinoma in patients with endometrial hyperplasia.

OBJECTIVE: The purpose of this retrospective study was to establish the risk of developing endometrial adenocarcinoma in patients diagnosed with endometrial hyperplasia. MATERIAL AND METHODS: The incidence of endometrial hyperplasia and its relation with endometrial adenocarcinoma was evaluated in 1,139 patients who presented with abnormal bleeding between January 2000 and December 2004; D&C was performed in all cases. There were 591 (51.88%) cases of simple endometrial hyperplasia, out of which 110 (18.61% from 51.88%) cases had atypia, 60 (5.26%) cases of complex hyperplasia, out of which 19 (31.66% from 5.26%) had atypia, and the remaining 488 (42.84%) had different forms of mixed hyperplasia. RESULTS: The incidence of endometrial adenocarcinoma was 3.87% in atypical hyperplasia and 0.81% in other forms, and was related only to cases with atypia in which the incidence was 0.61%. CONCLUSIONS: The most indicated measure to prevent endometrial carcinoma in cases with complex endometria hyperplasia with atypia is hysterectomy, while for other forms of hyperplasia, hormonal treatment is used but only under strict control.

Adenocarcinoma↗
PubMed2006

Cell adhesion and apoptosis in ovarian stromal hyperplasia and hyperthecosis.

The aim of our study was to investigate cell adhesion and apoptosis in ovarian stromal hyperplasia and hyperthecosis in reproductive women with and without polycystic ovarian disease. We have studied 104 patients with a histological diagnosis of ovarian stromal hyperthecosis and stromal hyperplasia. Paraffin sections were stained by hematoxylin-eosin, von Gieson and immunohistochemistry for Bcl-2 (anti-apoptotic protein) and E-cadherin (cell adhesion marker). We assessed the number of Bcl-2-positive and E-cadherin-positive cells. The patients were divided into 4 groups: group 1-33 patients with polycystic ovarian disease and coexistent stromal hyperthecosis, group 2-28 patients with polycystic ovarian disease and coexistent stromal hyperplasia, group 3-24 patients with ovarian stromal hyperthecosis, group 4-19 patients with ovarian stromal hyperplasia. Our results suggest that in ovarian stromal hyperthecosis and stromal hyperplasia coexistent with polycystic ovarian disease, E-cadherin-positivity in internal and external theca cells, and granulosa cells is associated with Bcl-2 expression. Therefore, ovarian cells expressing Bcl-2 and maintaining E-cadherin-positivity may be the viable cells that escape the apoptotic process. In ovarian stromal hyperthecosis without polycystic ovarian disease, luteinized stromal cells are potentially resistant to apoptosis as they are positive for Bcl-2. In ovarian stromal hyperplasia without polycystic ovarian disease, hyperplastic stromal cells are potentially susceptible to apoptosis as they are negative for Bcl-2. E-cadherin is negative both in stromal hyperthecosis and hyperplasia suggesting that E-cadherin expression in ovary is limited to granulosa and theca cells only. Described characteristics of cell adhesion and apoptosis may play a role in pathogenesis of ovarian stromal hyperthecosis and stromal hyperplasia with and without polycystic ovarian disease.

Antibodies, Monoclonal↗
PubMed1991

Reduction of smooth muscle hyperplasia in vein grafts in athymic rats.

While developing an animal model of a vascular malformation, we found that two doses of cyclosporin A significantly reduced the smooth muscle cell hyperplasia observed in vein-arterial interposition grafts in Sprague-Dawley rats. Therefore, we hypothesized that T cells may either produce or augment a mitogen for vascular smooth muscle cells. To further investigate this, we quantitated the extent of smooth muscle cell hyperplasia in the vein grafts of athymic nude rats that lack mature, functioning T cells. Male Sprague-Dawley rats (275 to 350 gm) and athymic nude rats were anesthetized, and a segment of the superficial epigastric vein was placed into the transected femoral artery using microsurgical techniques. Sprague-Dawley rats (N = 9) and athymic nude rats (N = 5) undergoing vein grafting received 30 mg/kg cyclosporin A intraperitoneally, intraoperatively and 24 hours later. Sprague-Dawley rats (N = 7) and athymic nude rats (N = 6) that had vein grafts were not treated with cyclosporin A. Animals were killed at either 3 weeks or 6 weeks and histologic sections were taken from the middle of the graft to avoid clamp-induced trauma. At 3 weeks, untreated vein grafts in Sprague-Dawley rats exposed to arterial pressure exhibited a nine-fold increase in smooth muscle hyperplasia compared with the preoperative vein. Treatment of Sprague-Dawley rats with cyclosporin A resulted in a 57% reduction of smooth muscle hyperplasia (p less than 0.05). Vein grafts from athymic nude rats exhibited a 51% reduction in smooth muscle hyperplasia (p less than 0.05). Sprague-Dawley rats killed at 6 weeks revealed a recovery of smooth muscle hyperplasia equivalent to an untreated Sprague-Dawley vein graft at 3 weeks. Inhibition of smooth muscle hyperplasia persisted for 6 weeks in the athymic nude rats. Cyclosporin A administration or T cell deficiency in athymic nude rats decreases the smooth muscle hyperplasia observed in venous grafts exposed to arterial pressure. This finding provides evidence for a possible role of T cells in the regulation of cell growth in the vascular wall.

Animals↗
PubMed1989

[Endometrial hyperplasia in the province of Trieste].

1103 cases of endometrial hyperplasia were diagnosed between January 1, 1978 and December 31, 1987 at the Department of Anatomy and Pathological Histology of the University of Trieste. Of these, 58% were cases of cystic glandular hyperplasia, 38% of adenomatous hyperplasia and 4% of atypical hyperplasia. Subdividing the period examined into two five-year periods, it was found that the rate of incidence of endometrial hyperplasias was more than doubled, this increase having been caused above all by cases of cystic hyperplasia. Distribution by age classes of subjects suffering from different hyperplastic forms suggests that cystic glandular hyperplasia is not a precursor of the adenomatous form, whereas the latter and atypical hyperplasia might constitute a continuous spectrum of potentially precancerous lesions.

Adolescent↗
PubMed1994

Diagnostic histologic criteria of atypical adenomatous hyperplasia and well differentiated adenocarcinoma of the endometrium.

The purpose of the study was to evaluate certain histological features of adenomatous hyperplasia diagnosed in endometrial curretings, that will enable us to distinguish atypical glandular hyperplasia from early well-differentiated adenocarcinoma. The material for this study was composed of 519 endometrial hyperplasias diagnosed in curettings. Of these, 244 were adenomatous hyperplasias, 109 were cystic hyperplasias, 93 mixed types and 73 were atypical hyperplasias. The cases of atypical hyperplasia were subsequently operated on, and among them, 26 proved to be adenocarcinomas. All histological sections of the currettings showing the atypical hyperplasia were re-evaluated to find criteria diagnostic of adenocarcinoma. The authors have considered as diagnostic criteria the stroma infiltration, the mitotic activity, the nuclear atypia, the stratification of nuclei and the presence of necrosis. The stroma infiltration seems to be the most important indication of an adenocarcinoma of the endometrium.

Adenocarcinoma↗
PubMed1994

Juxtaglomerular cell hypertrophy and hyperplasia induced in rhesus monkeys by angiotensin II receptor antagonists.

BACKGROUND: Juxtaglomerular (JG) cell hypertrophy and hyperplasia were investigated in rhesus monkeys given angiotensin II (AII) AT1 receptor antagonists L-158,338 and DUP 753 (MK-0954, losartan). EXPERIMENTAL DESIGN: In 2 initial studies, L-158,338 was given orally at 10, 30, and 90 mg/kg/day for 3 or 14 weeks. To investigate the observed JG hypertrophy and hyperplasia, in a third 5-week experiment L-158,338 was given alone at 90 mg/kg/day, or with physiologic saline supplementation at 25 ml/kg/day, or coadministered with the angiotensin converting enzyme inhibitor enalapril at 10 mg/kg/day. Physiologic saline was given to attempt to suppress renin release through volume expansion and/or sodium retention. Enalapril was given to lower plasma AII levels and observe whether JG cell hypertrophy and hyperplasia were increased or decreased. For comparison, DUP 753 was given at 90 and 300 mg/kg/day. Plasma renin activity and AII concentration were measured in this study. RESULTS: Dose- and time-dependent increases in JG cell hypertrophy and hyperplasia were seen in the 2 initial experiment. In the third experiment, plasma renin activity and AII concentration were increased 3-fold and 6-fold over pretest values by L-158,338 at 90 mg/kg/day for 5 weeks. Saline supplementation had no effect on these parameters but diminished the group mean severity grade for JG hypertrophy and hyperplasia from 1.5 to 1.0. Enalapril coadministration had no effect on plasma renin activity, whereas it blunted the plasma AII increase caused by L-158,338 and increased the group mean grade to 2.5. DUP 753 at 300 mg/kg/day produced similar increases in plasma renin activity and AII concentration but only resulted in grade 1 JG cell hypertrophy and hyperplasia. CONCLUSIONS: L-158,338-induced JG cell hypertrophy and hyperplasia is an exaggerated pharmacologic response that can be modulated by saline supplementation and angiotensin converting enzyme inhibition. These results suggest that decreased renal perfusion or altered sodium homeostasis and plasma AII concentration are important variables that contribute to AT1 receptor blockade to induce JG cell hypertrophy and hyperplasia.

Angiotensin II↗
PubMed1993

[Sleep apnea in hyperplasia of the pharyngeal lymphatic tissue. Polysomnographic studies in children].

BACKGROUND: Hyperplasia of tonsils and adenoids is a common finding in early childhood. Breathing difficulties caused by hyperplastic lymphatic tissue represent an indication for adenoidectomy and tonsillectomy. It was examined, whether a polysomnographic recording is a useful tool to assess the severity of obstructive sleep apnea in children with hyperplasia of tonsils and adenoids. METHODS: In 15 patients (10 boys, 5 girls), 1.0 to 6.6 years of age, with a history of breathing difficulties during sleep a thorough clinical evaluation was performed. Additionally, a polysomnographic recording was carried out, including thoracic and abdominal breathing movements, nasal and buccal thermistor, ECG and transcutaneous blood gases. RESULTS: Before therapy, severe obstructive apnea was demonstrated by polysomnography in all patients. This finding disappeared almost completely after surgery. Hyperplasia of adenoids was diagnosed in 3 patients, hyperplasia of tonsils in 3 patients, hyperplasia of tonsils and adenoids in 8 patients, and other kind of lymphatic hyperplasia in 1 patient. CONCLUSION: Hyperplasia of tonsils and adenoids contributes to the development of sleep-apnea-syndrome in childhood. A polysomnographic recording seems to be a useful tool to describe the severity of obstructive sleep apnea in children with hyperplasia of tonsils and adenoids.

Adenoidectomy↗
PubMed1997

[Hysteroscopic diagnosis and follow-up of adenomatous hyperplasia and therapeutic consequences].

63 cases of adenomatous endometrial hyperplasia (1st-3rd degree) were diagnosed by hysteroscopy and D&C at the Department of Obstetrics and Gynaecology of the University of Greifswald from January 1991 to December 1994. In 40 patients with adenomatous hyperplasia (2nd-3rd degree) a hysterectomy was performed. 23 patients presenting with 1st degree hyperplasia were treated continuously with gestagenes for a period of 6 months. In those cases we performed a repeated diagnostic hysteroscopy and D&C to check the success of hormonal treatment. In 92.5% of tall cases the histological diagnoses of a lower degree adenomatous hyperplasia, cystic glandular hyperplasia or of a normal endometrium were made after hysterectomy. Only in one patient (2.5%) an endometrial carcinoma developed from an adenomatous hyperplasia (3rd degree). There was no progression to observe of adenomatous hyperplasia after hormonal therapy with gestagenes. We conclude that in those cases a hysterectomy has not necessarily to be carried out. However, in adenomatous hyperplasia of 3rd degree hysterectomy has to be the treatment of choice, because there is an increased risk of invasion.

Adenocarcinoma↗
PubMed1976

[ACTH secretion and adrenocortical responsiveness in Cushing's syndrome due to adrenocortical hyperplasia (author's transl)].

A radioimmunoassay for plasma ACTH has been developed utilizing highly purified human ACTH (Li) labelled with 125I by the lactoperoxidase method as a tracer and an ACTH antibody produced by immunization of rabbits with ACTH-Z (Organon). The assay is highly specific, reproducible and sensitive to 20 pg of ACTH per ml. Utilizing this technique, endogenous ACTH secretion, adrenal responsiveness to endogenous ACTH and hypothalamic pituitary adrenal feedback mechanisms have been assessed in normal subjects and in patients with Cushing's syndrome due to adrenocortical hyperplasia and nodular cortical hyperplasia. The potential effect of a negative feedback mechanism on the circadian rhythmicity after SU-4885 administration was assessed by initiating SU-4885 either at 9 p.m. or 8 a.m. In normal subjects, the circadian rhythm of ACTH was persistent and independent of a decrease in cortisol. However, in a single case of Cushing's syndrome due to adrenocortical hyperplasia, the circadian rhythm was different from that of normal subjects, possibly influenced by a negative feedback mechanism when SU-4885 was initiated at 8 a.m. In Cushing's syndrome due to adrenocortical and nodular cortical hyperplasia, a significant correlation was observed between the mean plasma ACTH and urinary 17-OHCS values before and after SU-4885 administration (r=0.743, p less than0.01). A significant correlation was also obtained in normal subjects between plasma ACTH and urinary 17-OHCS values (r=0.889, p less than 0.01). However, there was quantitatively more 17-OHCS excreted in the urine for a given plasma ACTH level in patients with Cushing's syndrome than in normal subjects. To assess the relative biological activity of endogenous and exogenously administered ACTH, the ratio of daily 17-OHCS during SU-4885 administration and Cortrosyn-Z administration was expressed as the Cortrosyn Equivalent Quotient (C.E.Q.). The correlation between plasma ACTH and C.E.Q. was similar and significant for normal subjects and patients with Cushing's syndrome (r=0.670, p less than 0.01). These data suggest that there is hyper-responsiveness of the adrenal glands to endogenous ACTH in Cushing's syndrome due to adrenocortical hyperplasia and nodular cortical hyperplasia and that the adrenal hyperactivity is not engendered by a qualitative change in the ACTH release from the pituitary gland. To assess pituitary suppressibility, dexamethasone was administered 40 days or more later following total adrenalectomy in 9 patients with Cushing's syndrome, 6 with adrenocortical hyperplasia and 3 with nodular cortical hyperplasia. One day after discontinuation of substitution therapy, 2 mg of dexamethasone was administered orally followed on successive days by 4 and 8 mg doses. In each instance, dexamethasone was given at midnight and the plasma ACTH concentration was determined at 9:00 a.m. on the day before and after administration of the dexamethasone. A patient with Addison's disease was studied as a control...

17-Hydroxycorticosteroids↗
PubMed1988

Large acinar atypical hyperplasia and carcinoma of the prostate.

Step-sections of 429 whole prostate glands were studied. Large acinar atypical hyperplasia was graded as mild, moderate, and severe based on the degree of cellular anaplasia. The relationship between atypical hyperplasia and prostatic carcinoma was investigated. There was a strong association between prevalence and grade of atypical hyperplasia and prostatic carcinoma in patients up to 60 years old. Beyond the age of 60 no association was detected. In the younger age groups (36 to 60 years) atypical hyperplasia was found in 86.8% of prostates with carcinoma, but only in 37.9% of benign glands. Corresponding figures for the over-60 age group were 68.8% and 65.1%, respectively. A biologic explanation of the association between atypical hyperplasia and carcinoma in the younger age groups has been proposed. It was suggested that these men with atypical hyperplasia, particularly with severe atypical hyperplasia, have a greater risk for developing prostatic carcinoma.

Adult↗
PubMed2000

Effect of vascular freezing on the histopathology of dissected small vessels in the rat: vascular freezing does induce intimal hyperplasia in arteries and veins.

Intimal hyperplasia is the primary response of a vessel wall after injury. It may be the single most significant factor affecting long-term patency. The purpose of this study was to find out whether freeze injury, inflicted on rat microvessels, would be followed by intimal hyperplasia. Toward this aim, we exposed the superficial femoral vessels in the rat. On one side they were frozen using liquid nitrogen spray. The other side was dissected as the control. Vessel segments, harvested immediately and after 1, 2, 3, and 5 months, were studied light microscopically for the occurrence and content of intimal hyperplasia. In the arteries a considerable intimal hyperplasia was found within a 4-week interval, persisting for at least 5 months, as a result of the freeze injury. In the veins, the intimal hyperplasia was much less marked but was nevertheless demonstrable. These findings are not in agreement with earlier studies, in which freezing of injured rat microarteries with liquid nitrogen spray was followed by complete regeneration of the vessel wall, without intimal hyperplasia taking place. The factors contributing to these differences are discussed. It is concluded that freezing of a vessel wall is followed by intimal hyperplasia, which is part of the normal healing process.

Animals↗
PubMedDate not supplied

On the pathogenesis of focal nodular hyperplasia of the liver.

Fifty-one focal nodular hyperplasia lesions from 36 patients were examined histologically. Serial sections and three-dimensional models were studied in selected cases. Lesions were multiple in 19% of patients. Thirty-four patients were female. One case had 11 focal nodular hyperplasia lesions and 7 hemangiomata in the liver. Three had astrocytoma and one had anomalous pulmonary venous drainage. Morphometric analysis revealed that the lesions were supplied by an anomalous artery larger than expected for the locale in the liver. This artery branched to form a spider-like structure and was usually not accompanied by a portal vein or duct. Each terminal arterial branch supplied a separate nodule 1 mm in diameter; adjacent nodules coalesced to form the focal nodular hyperplasia lesion. The arterial blood appeared to drain directly into the sinusoids of the nodule. We propose that focal nodular hyperplasia is an hyperplastic response of the hepatic parenchyma to a preexisting arterial spider-like malformation. The frequent coexistence of focal nodular hyperplasia with other vascular and neuroendocrine anomalies suggest that the malformations are developmental in origin. The basic requirement for development of hepatic hyperplasia may be greater blood flow to a region compared to the adjacent parenchyma. This requirement appears to be met in the other forms of nodular transformation of the liver, i.e., nodular regenerative hyperplasia and partial nodular transformation.

Adolescent↗
PubMed1994

The prognostic and therapeutic implications of cytologic atypia in patients with endometrial hyperplasia.

From 1970 to 1992, 136 patients with a histologic diagnosis of endometrial hyperplasia underwent total abdominal hysterectomy at the University of Kentucky Medical Center. Slides of the curettage or biopsy specimens were reviewed and classified according to the International Society of Gynecologic Pathologists System as simple or complex endometrial hyperplasia with or without cytologic atypia. Slides of the hysterectomy specimens were likewise reviewed independently and classified according to the same system. Eighty-two patients had a preoperative diagnosis of simple or complex endometrial hyperplasia without atypia. There were no cases of occult endometrial carcinoma in the hysterectomy specimens of these patients. Simple or complex hyperplasia with atypia was present in 54 patients and endometrial adenocarcinoma was observed in 19 of these cases (35%). The International Federation of Gynecology and Obstetrics stage and histologic grade of these patients was as follows: Stage IA grade 1--5; Stage IB grade 1--10; Stage IB grade 2--1; Stage IC grade 1--1; Stage IC grade 2--1; and Stage IIIA grade 2--1. The risk of associated endometrial cancer in patients with atypical hyperplasia was independent of age, diabetes mellitus, hypertension, or the use of exogenous estrogens. All patients with endometrial cancer have been followed for 1-12 years (mean 3.0 years) after therapy and no patient has experienced tumor recurrence. These data suggest that there is a significant risk of endometrial cancer in patients with histologic evidence of atypical endometrial hyperplasia on curettage or biopsy. At the time of surgery, patients with atypical endometrial hyperplasia should have careful inspection of the uterine specimen. Any endometrial tissue suspicious for malignancy should be examined histologically, and if cancer is confirmed, complete surgical staging should be performed.

Adenocarcinoma↗
PubMed1999

The effect of medroxyprogesterone acetate on angiogenesis in complex endometrial hyperplasia.

OBJECTIVE: To evaluate the effect of orally administered medroxyprogesterone acetate upon angiogenesis in the myometrium of patients with complex endometrial hyperplasia. METHODS: Microvessel counts in the myometrium of consecutive patients with complex endometrial hyperplasia, treated with oral medroxyprogesterone acetate prior to hysterectomy (n = 12), were compared with microvessel counts of consecutive control patients with complex endometrial hyperplasia without prehysterectomy medroxyprogesterone acetate treatment (n = 15). All specimens were stained immunohistochemically for factor VIII-related antigen as a sensitive and specific marker for vascular endothelium. Areas with the highest angiogenic intensity, within the myometrium immediately underlying complex endometrial hyperplasia, were selected. Three fields (x400) were selected for each slide, and the mean microvessel count per high-power field was calculated. Statistical analysis included factorial analysis of variance/covariance, and multiple regression analysis with P < 0.05 considered significant throughout. RESULTS: Microvessel counts of uterine specimens of patients with complex endometrial hyperplasia treated with oral medroxyprogesterone acetate were significantly lower than microvessel counts of control patients with complex endometrial hyperplasia without medroxyprogesterone acetate therapy (median 20, range 11-37 versus median 38, range 20-130, respectively, P < 0.001). CONCLUSION: Orally administered medroxyprogesterone acetate has a significant antiangiogenic effect upon myometrium immediately underlying complex endometrial hyperplasia.

Administration, Oral↗
PubMed1999

Endometrial carcinoma associated with hyperplasia--immunohistochemical study of angiogenesis and p53 expression.

OBJECTIVE: To clarify the hypothesis that there are two pathways of endometrial carcinogenesis we compared the frequency of abnormal p53 protein expression and angiogenesis in endometrial carcinomas with and without hyperplasia. METHODS: Specimens obtained from 70 patients with stage I-IV endometrial carcinomas were available for this immunohistochemical study. Immunohistochemical staining for factor VIII-related and p53 antigens was performed using a standard immunoperoxidase technique (Histofine SAB-PO Kit, Nichirei Co., Tokyo, Japan). Microvessels were highlighted by staining endothelial cells for factor VIII-related antigen, and microvessel density (MVD) was counted in a x200 field (0.785 mm2 per field) in the area of most active neovascularization. p53 protein was detected with monoclonal anti-p53 antibodies (clone DO-7, Dako, Santa Barbara, CA). RESULTS: Twenty-six of 73 (37%) patients had hyperplasia in the endometrium adjacent to the carcinoma. Significantly more patients with low MVD (less than 60) had carcinoma with hyperplasia than those with carcinoma without hyperplasia (P = 0.0053). p53 expression was noted in a carcinomatous area in 8 of 26 patients (30. 8%) with hyperplasia compared to 26 of 44 (59.1%) without hyperplasia, and the difference was statistically significant (P = 0. 0220). CONCLUSION: The presence or absence of hyperplasia is a different pathogenesis and important in assessing the biological behavior of endometrial carcinoma, especially concerning angiogenesis and p53 expression.

Adenocarcinoma↗
PubMed1998

Local delivery of a tissue factor antibody reduces early leukocyte infiltration but fails to limit intimal hyperplasia in experimental vein grafts.

BACKGROUND: Tissue Factor-mediated thrombin generation involves the generation of VIIa and Xa and has been implicated in the pathogenesis of intimal hyperplasia. In experimental vein grafts, Tissue Factor protein is increased over the first 3 days and colocalized with CD18-positive leukocytes; this increase in Tissue Factor precedes the development of intimal hyperplasia. This study further evaluates the potential role of Tissue Factor in vein graft intimal hyperplasia by directly inhibiting Tissue Factor protein. METHODS: New Zealand white rabbits underwent interpositional bypass grafting of the common carotid artery using the external jugular vein. Perioperatively, murine anti-rabbit Tissue Factor antibody (109 microg/ml gel, 12,500x IC50 of Tissue Factor activity) was applied to the adventitial surface of the graft, using a pluronic gel (30% soln.). Tissue Factor antibody treated vein grafts were compared to control and empty gel-treated vein grafts. Vein grafts were examined at 3 days to assess CD18-positive leukocyte infiltration and the presence of residual antibody by Western blotting. At 28 days, intimal and medial dimensions were quantified using videomorphometry. RESULTS: At day 3, there was marked reduction in CD18-positive leukocytes in the Tissue Factor antibody versus control vein grafts (6.3 +/- 4.7 vs 20.8 +/- 7.4 per 200x field, P < 0.05). At 28 days, intimal hyperplasia was similar for the control (70 +/- 4 microm, mean +/- SEM), gel (73 +/- 4 microm), and Tissue Factor antibody (75 +/- 4 microm) vein grafts. However, medial thickness (76 +/- 4 microm;, P < 0.05) was significantly increased compared to the gel treated vein graft (61 +/- 5 microm). CONCLUSION: Local delivery of pharmacologic doses of an anti-rabbit Tissue Factor antibody decreased CD18-positive leukocyte infiltration but failed to limit intimal hyperplasia in experimental vein grafts. The results suggest that inhibition of Tissue Factor protein modulates polymorphonuclear leukocyte-endothelial interactions but not in the subsequent development of intimal hyperplasia. It implies that the relationship between the extrinsic coagulation cascade and intimal hyperplasia in vein grafts is complex.

Animals↗