Local endoscopic removal of duodenal carcinoid tumors.

A swift and aggressive diagnostic and therapeutic approach is advisable when managing submucosal or polypoid lesions in the duodenum, since it is not possible to distinguish small, benign, and unremarkable duodenal growths macroscopically from malignant tumors such as carcinoids. This paper presents a systematic review of the published literature listed in Medline, focusing on the results after endoscopic treatment of duodenal carcinoids during the last 15 years; on the biological behavior of duodenal carcinoids; and on the endoscopic appearance of duodenal carcinoids. Endoscopic ultrasonography (EUS) is extremely useful in the diagnostic and preoperative work-up. The results indicate that endoscopic removal of duodenal carcinoids smaller than 1 cm that are located outside the periampullary region, with no EUS signs of invasion of the muscularis propria, is a safe, patient-friendly, adequate, and effective treatment.

Parasympathetic non-adrenergic, non-cholinergic-induced protein synthesis and mitogenic activity in rat parotid glands.

Electrical stimulation of the parasympathetic auriculo-temporal nerve (40 Hz, 30 min), in the anaesthetized rat under - and -adrenoceptor blockade, increased [3H]thymidine and [3H]leucine uptake into the parotid glands by 80 and 263 %, respectively. The increase in response to parasympathetic stimulation was almost the same ([3H]thymidine 82 % and [3H]leucine 283 %) when atropine (2 mg kg-1 I.P. or I.V.) was included in the pretreatment. Neither intravenous infusion of vasoactive intestinal peptide (0.5-20 mg kg-1 min-1, 30 min) nor of bethanechol (10 mg kg-1 min-1, 30 min), under adrenoceptor blockade, increased the uptake of [3H]thymidine into the glands. However, these drugs increased [3H]leucine uptake, and in combination they interacted positively. Whereas vasoactive intestinal peptide is likely to be involved in the parasympathetic nerve-evoked protein synthesis, the nature of the non-adrenergic, non-cholinergic component(s) involved in the mitogenic response is presently unknown.

Adipose tissue distribution in postmenopausal women with adenomatous hyperplasia of the endometrium.

OBJECTIVE: To investigate body fat distribution in postmenopausal women with adenomatous and atypical hyperplasia of the endometrium. METHODS: A prospective population-based case control study was performed in a health care county in Sweden. General obesity, as reflected by body mass index (BMI), and adipose tissue distribution, expressed as waist to hip circumference ratio (WHR), were evaluated in a cohort of 367 postmenopausal women who underwent dilatation and curettage because of uterine bleeding. The study group consisted of 29 women with adenomatous or atypical hyperplasia of the endometrium. The controls consisted of 49 age-matched postmenopausal women randomly selected from the computerized population register of the same region. RESULTS: The frequency of endometrial adenomatous and atypical hyperplasia in postmenopausal women with bleeding was 7.2%. In the total population of postmenopausal women the incidence of these endometrial lesions was 44 per 100,000 per year. Body weight (P = 0.039), BMI (P = 0.007), and WHR (P = 0.022) were higher in postmenopausal women with endometrial adenomatous and atypical hyperplasia than in controls. In multivariate analysis only BMI remained statistically associated with adenomatous hyperplasia (P = 0.012). CONCLUSIONS: General obesity, but neither upper nor lower body fat distribution, was characteristic of postmenopausal women with adenomatous and atypical hyperplasia of the endometrium. Overall obesity is a risk factor for these endometrial precancerous lesions, as it is also claimed to be for endometrial cancer.

Vascular protein leakage in the rat parotid gland elicited by reflex stimulation, parasympathetic nerve stimulation and administration of neuropeptides.

Evans blue accumulated in parotid glands of conscious rats in response to feeding (over 60 min), in the absence of atropine and adrenoceptor antagonists and in their presence, and after pretreatment with the sensory neurotoxin capsaicin. Stimulation of the auriculo-temporal nerve (40 Hz, 10 or 20 min), without and with the blockers, caused Evans blue to accumulate. A periglandular oedema also contained the dye. Administration (i.v.) of neurokinin A accumulated Evans blue, while substance P, vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating peptide (PACAP), calcitonin gene-related peptide (CGRP) and pilocarpine lacked effect. Pilocarpine enhanced the action of neurokinin A and, furthermore, substance P combined with either VIP, PACAP or CGRP resulted in accumulation of Evans blue. In the sublingual + submandibular glands, Evans blue increased in response to neurokinin A and pilocarpine; furthermore, substance P and VIP, and substance P and CGRP, interacted positively. Bradykinin lacked effect in the glands. Comparisons were made with the urinary bladder. Accumulation of Evans blue reflects plasma protein extravasation. In salivary glands, the phenomenon occurred during feeding and was independent on intact sensory innervation; instead, the parasympathetic innervation containing the neuropeptides was in focus. In the clinic, the present findings may have implications for the aetiology of gland swelling and pain.

Benign epithelioid schwannoma.

Benign schwannoma (neurilemoma) has various morphologic patterns that may cause problems in differential diagnosis. Although an epithelioid variant of malignant schwannoma simulating carcinoma and melanoma is well recognized, a benign counterpart has not yet been defined. In the current study, we describe five cases of benign epithelioid schwannoma that were in the subcutis (four cases) and the neck of the urinary bladder (one case). The tumors occurred in adults 28-73 years of age, were 1-4.5 cm in diameter, were well circumscribed and cellular, and were composed of epithelioid cells arranged in cords and nests. The benign nature of the lesions was evident by a constellation of features, including small size, sharp circumscription, bland morphology, low proliferative activity (four of five had < or =1% Ki67 immunostaining), and a benign clinical course after either marginal or intralesional excision. All cases had some features of classic schwannoma light microscopically and a high degree of Schwann cell differentiation both ultrastructurally and immunohistochemically. The recognition of benign epithelioid schwannoma is important because it may be misinterpreted as a malignant neuroectodermal, mesenchymal, epithelioid, or melanocytic tumor.

Cytogenetics of parametrial leiomyoma.

The cytogenetical findings from a parametrial leiomyoma are presented. The results, together with those of five previously presented cases, show obvious differences when compared to the chromosomal findings in uterine myomas. Ontogenic factors are proposed to be causative for the cytogenetical differences.

Molecular analysis of uterine leiomyomas using the probes D7S13(7q) and HSPA2(14q).

Human uterine leiomyomas, mostly cytogenetically characterized, were analyzed by Southern blotting. The region 7q22.3-q31.2 was analyzed in 54 leiomyomas using the polymorphic probe D7S13. The region 14q22-24 was investigated in 25 leiomyomas with the probe HSPA2. No evidence of rearrangement or amplification of these DNA-regions was observed. Nor was any loss of polymorphism for the probe D7S13 seen. These, and earlier negative results, motivate further molecular investigation to understand the mechanisms reflected by recurrent chromosome aberrations in myomas.

Histopathological findings in women with postmenopausal bleeding.

OBJECTIVE: To investigate endometrial histopathology in a geographically defined population of women presenting with postmenopausal bleeding. DESIGN: Prospective study with collection of data during an 18-month period. SETTING: The health care county of Skaraborg, Sweden. SUBJECTS: Dilatation and curettage using general anaesthesia was performed on 457 postmenopausal women suffering from uterine bleeding. Women using hormone replacement therapy for climacteric complaints were not included in the investigation. MAIN OUTCOME MEASURES: The frequency of bleeding was correlated to endometrial histopathology, and in relevant cases to pathological conditions in cervix and ovaries in a defined population of postmenopausal women. RESULTS: The incidence of postmenopausal bleeding decreased with increasing age while the probability of cancer as the underlying cause increased. The peak incidence of endometrial carcinoma was found in women between 65 and 69 years of age. Endometrial histopathology showed: atrophy (50%); proliferation (4%); secretion (1%); polyps (9%); different degrees of hyperplasia (10%); adenocarcinoma (8%); not representative (14%); other disorders (3%). In six women a squamous carcinoma of the cervix was found, and eight proved to have ovarian tumours. CONCLUSIONS: The histopathological finding of endometrial adenomatous hyperplasia or cancer in about 15% of the postmenopausal women with bleeding justifies a thorough examination. The probability of cancer as the underlying cause increased with age. The endometrium was atrophic in 50%. Eight women had ovarian tumours. These findings may imply that transvaginal ultrasound examination should be included in the evaluation of postmenopausal bleeding as occasionally endometrial biopsies of atrophic endometrium could be avoided and ovarian pathology detected.

Cytogenetical observations and hormone receptor expression in five extra-uterine leiomyomas.

The chromosomes were studied by an in vitro technique in four parametrial and one gastric leiomyomas. The findings in parametrial myomas (the present four cases and one published earlier) differed from the observations in uterine cases by the absence of normal stemlines and the absence of 1p,6p and 7q changes. As has been shown earlier for intraocular melanomas, the location within an organ or organ system could be the explanation for the chromosomal differences. The scanty data for leiomyomas in the digestive tract (the present case and two in the literature) suggest evolutionary patterns different from those in myomas in the genital tract. The reasons for this are unknown but differences in hormonal sensitivity, as reflected by estrogen and progesterone receptor expression, might at least be a contributory factory.

Aggressive angiomyxoma of the vulva: an unusual, deceptive and recurrence-prone tumour with evidence of estrogen receptor expression. Case report.

Positive staining for estrogen receptors is reported in a new case of aggressive angiomyxoma of the vulva. Clinical, light- and electron microscopic features as well as immunohistochemical reactions in this case are compared with the 28 earlier published cases, and the main differential diagnosis, angiomyofibroblastoma of the vulva, is discussed.

A study on the oncogenes gli, fos, jun and met in human uterine leiomyomas.

122 human uterine leiomyomas, representing the main chromosomal aberrations seen in these tumours, were analyzed by Southern blotting. Probes for the four oncogenes, gli, fos, jun, and met, all localized in or close to the chromosomal breakpoints in leiomyomas, were used. In only one single leiomyoma, with a 7p+q- marker, was there evidence of rearrangement of one of the oncogenes, namely met.

Benign parotid oncocytoma with the chromosomal abnormality trisomy 7.

This report concerns the first cytogenetical study of a benign salivary gland oncocytoma. The cultured tumor was studied in five consecutive preparations. The first three were dominated by cells with a normal karyotype. In the two subsequent preparations a hyperdiploid stemline characterized by trisomy 7 had taken over. Trisomy 7 has previously been observed in a number of different, benign, premalignant and malignant conditions. We interpreted trisomy 7 in the salivary gland oncocytoma, as in these other conditions, to be a neoplasia-related, probably primary, gross chromosomal change and not an expression of aging or comparable events in normal cells.

Cytogenetics of multiple uterine leiomyomas, parametrial leiomyoma and disseminated peritoneal leiomyomatosis.

Using banding techniques the chromosomes were studied in 15 leiomyomas. The material comprised nine uterine myomas from one patient, one parametrial leiomyoma from a second patient and five tumors from a third patient with disseminated peritoneal leiomyomatosis. The results were considered together with pooled data from the literature. From this it could be concluded that: (1) each leiomyoma was the product of a separate clonal development; (2) different leiomyomas from the same patient sometimes showed an identical abnormal stemline (possibly because of etiological influences); (3) uterine and extra-uterine leiomyomas seemed to follow similar evolutionary pathways in their chromosomal progression.

Chromosomal patterns in human benign uterine leiomyomas.

Chromosomal observations by banding technique in 18 short-term cultured human uterine leiomyomas are reported. Half of the tumors had a primary or secondary abnormal stemline. They were usually characterized only by structural changes, in particular reciprocal translocations or insertions. Reviewing already published cases together with the new material confirmed that the aberrations in abnormal stemlines predominantly affected chromosomes 1, 2, 6, 7, 12, 14, and X. In these chromosomes the regions 1p36, 2p24, 6p12-21, 7q21-31, 12q13-15, 14q22-24, and the short arm of the X chromosome were preferentially affected. As in two other thoroughly studied human benign tumors, the pleomorphic adenoma and the meningioma, the very specific but sometimes complex chromosomal aberrations in leiomyomas could well be events of primary evolutionary importance. Likewise, in cases with a normal stemline, it is possible that comparable changes in the corresponding specific chromosomal regions have occurred at a submicroscopic level. Ascertaining this possibility, as well as the role of the aberrations with regard to the benign nature of the tumors, must be the focus of future analysis using molecular techniques.

Ependymoma of the ovary. A clinico-pathologic, ultrastructural and immunohistochemical investigation. A case report.

A case of primary malignant ovarian ependymoma is described. The course of the tumor disease was extremely prolonged with a 50 year history. The diagnosis is supported by immunohistochemical and ultrastructural evidence of ependymal differentiation. The histogenesis and the origin from a possible preexisting ovarian teratoma are discussed.

Cytogenetic observations in a human gastric leiomyosarcoma.

The chromosomes of a human gastric leiomyosarcoma were studied in preparations from short-term cultures. The tumor had a triploid-near-triploid modal population characterized by extensive numerical and structural changes. Of these deviations, del(1)(p12-13), monosomy 14, and underrepresentation of chromosomes 18 and 22 were abnormalities in common with two of the three previously studied leiomyosarcomas of the small bowel.

Similar chromosomal evolution in a uterine stromomyosarcoma and in one of two leiomyomas from the same patient.

The chromosomes from three uterine tumours found in the same patient, two benign leiomyomas (L22 and L23) and a low-grade stroma cell sarcoma with leiomyomatous differentiation (L24), were studied by banding technique. L23 had an abnormal stemline distinguished by triosomy 12. The sarcoma showed a stemline with the same 7q-marker as L23 plus a marker del (12)(q13-24). A comparison with cytogenetically studied myomas collected from the literature showed (1) that there are at least three different recurrent, primary, gross chromosomal changes, viz. t(12;14)(q14-15;q23-24), t(1;2)(p36;p24) and del(7)(q22-31) and that there exist at least five further types of primary chromosomal deviations. The sarcoma showed aberrations identical or closely related to the recurrent structural deviations in myomas. These observations indicate a similar evolutionary pattern in benign and malignant leiomyomatous tumours.