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A G Naccarato

Publications and source records attributed to A G Naccarato.

At least 19 recordsLinked to original sources
PubMed2000

Gender and age-related variation in adenylyl cyclase activity in the human prefrontal cortex, hippocampus and dorsal raphe nuclei.

The influence of gender and age on adenylyl cyclase activity was investigated, through a Dowex-alumina double step chromatographic procedure, in the prefrontal cortex, hippocampus and dorsal raphe nuclei obtained from autopsy cadavers. Results showed that forskolin-stimulated enzyme activity in raphe nuclei was greater in men than in women; a region-dependent rank order of basal, forskolin-induced adenylyl cyclase activity and percentage forskolin-stimulation was observed in women only. Lastly, basal values correlated positively with forskolin-stimulated adenylyl cyclase activity in all areas except the prefrontal cortex of the male subjects. Positive significant correlations were also found between both forskolin-stimulated enzyme activity and percentage forskolin stimulation and aging in the prefrontal cortex. Overall, the findings suggest that sex and/or age-related differences in brain adenylyl cyclase vary from one cerebral region to the other.

Adenylyl Cyclases↗
PubMed2000

Bio-morphological events in the development of the human female mammary gland from fetal age to puberty.

Bio-morphological understanding of the developing human mammary glands may clarify some aspects of breast pathology, including cancer. In particular, some epidemiological data suggests that during fetal growth an altered intrauterine hormonal status, especially a change in estrogen status, could predispose to carcinogenesis. In an attempt to achieve new information on early breast growth, a series of developing human breasts have been analyzed, namely: 4 fetal breasts (28-32 weeks of gestational age), 7 infant breasts (7 h to 2 years) and 1 puberal breast (12 years). In addition to the morphological features, we studied the immunohistochemical expression of some markers involved in morphogenesis, such as MIB-1 for cell proliferation, bcl-2 for apoptosis control, CD34 for vasculogenesis, estrogen (ER) and progesterone (PR) receptors for hormonal profile, and smooth-muscle actin for myoepithelial differentiation. The results were as follows: (a) lobules, absent between 28 weeks and 2 days, were well evident at 2 years of age and at puberty; (b) myoepithelial cells appeared from 28 weeks onward and persisted later with no modification in quantity and distribution; (c) epithelial cell proliferation was constantly low; (d) in all breasts inner epithelial cells showed diffuse bcl-2 positivity, while basal myoepithelial-like cells were generally negative; (e) all breasts were well vascularized with two different patterns: periductal vascularization (PDV) and interductal vascularization (IDV), IDV being always present, whereas PDV was found only in infant breasts; (f) ER and PR were almost absent in fetal and infant breasts, while their expression was high in the epithelial cells of the puberal breast; (g) stromal cells had no hormonal receptors and were heterogeneous for proliferation and bcl-2 expression. Interestingly, two fetal breasts showed high proliferation and high ER expression, respectively, in their epithelial compartment. This could be the expression of an altered hormonal environment in utero, representing a basis for possible subsequent cancer initiation.

Antigens, CD34↗
PubMed2000

Lack of stereoselectivity of 8-hydroxy-2(di-N-propylamino)tetralin-mediated inhibition of forskolin-stimulated adenylyl cyclase activity in human pre- and post-synaptic brain regions.

The stereoselectivity of the serotonin1A (5-HT1A) receptor compound 8-hydroxy-2(di-N-propylamino)tetralin (8-OH-DPAT) on forskolin-stimulated adenylyl cyclase activity was investigated in membranes from human 5-HT pre-synaptic (raphe nuclei) and post-synaptic (hippocampus and prefrontal cortex) regions of autopsy brains. After sample incubation with agonists and antagonists, results showed that both the racemic mixture of 8-OH-DPAT or its (+) and (-) enantiomers behaved as full agonists in the tested brain regions. Enantiomer potency (EC50, nM) and efficacy (percentage of maximal inhibition, %) values were similar in all regions under investigation. However, some inter and intra-region variations in racemic 8-OH-DPAT potency and efficacy have been observed. In particular, the potency of racemic 8-OH-DPAT was higher in the prefrontal cortex and raphe nuclei than in the hippocampus, where it was in fact lower than either single enantiomers. Agonist effects were competitively reversed by 5-HT1A antagonists, although once again a different profile was revealed in the hippocampus. The data underscores the lack of stereospecificity of 8-OH-DPAT-mediated inhibition of adenylyl cyclase activity in either pre- or post-synaptic human brain regions. Moreover, such results have significant implication, as they support the notion that human 5-HT1A receptors might vary from one brain region to the other.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2000

Parathyroid expression of calcium-sensing receptor protein and in vivo parathyroid hormone-Ca(2+) set-point in patients with primary hyperparathyroidism.

A reduced expression of calcium-sensing receptor (CaR) messenger ribonucleic acid and protein accompanied by abnormalities in parathyroid cell proliferation and PTH secretion are present in primary hyperparathyroidism. We studied the expression of CaR protein by immunohistochemistry in 36 sporadic parathyroid adenomas and investigated the relationship between CaR expression and several preoperative clinical parameters, including the set-point of Ca(2+)-regulated PTH secretion (measured in vivo). The adenomas were classified in 4 categories according to the intensity of immunohistochemical staining: 5 (14%) showed a CaR staining intensity similar to that of normal parathyroid ( ), 10 (27%) showed moderate staining (++), 16 (45%) showed weak staining (+), and 5 (14%) were negative (-). The intensity of CaR staining was not related to preoperative serum Ca(2+), PTH levels or adenoma volume. Twenty-nine patients underwent preoperatively the calcium infusion test to evaluate the PTH-Ca(2+) set-point. Individual values of PTH-Ca(2+) set-point ranged from 1.38-1.93 mmol/L and were significantly correlated with basal Ca(2+) levels (r = 0.96; P: = 0. 0001) and adenoma volume (r = 0.5; P: = 0.01). The mean PTH-Ca(2+) set-point values were significantly different in the 4 groups of patients classified according to immunohistochemical staining intensity of their adenoma (P: = 0.025; F = 3.78); the mean PTH-Ca(2+) set-point was significantly higher in the groups classified as negative than in those classified as weak or moderate. No correlation was observed between the PTH-Ca(2+) set-point and basal PTH levels or between the percent maximal PTH inhibition and adenoma volume and basal PTH or Ca(2+) levels. In summary, our data suggest that there is a relationship between apparent CaR protein expression and PTH-Ca(2+) set-point abnormality, suggesting that a reduced receptor content might have an important role in the pathogenesis of primary hyperparathyroidism.

Adenoma↗
PubMed2000

Activating thyrotropin receptor mutations are present in nonadenomatous hyperfunctioning nodules of toxic or autonomous multinodular goiter.

Toxic multinodular goiter, a heterogeneous disease producing hyperthyroidism, is frequently found in iodine-deficient areas. The pathogenesis of this common clinical entity is still unclear. The aim of the present study was to search for activating TSH receptor (TSHr) or Gs alpha mutations in areas of toxic or functionally autonomous multinodular goiters that appeared hyperfunctioning at thyroid scintiscan but did not clearly correspond to definite nodules at physical or ultrasonographic examination. Surgical tissue specimens from nine patients were carefully dissected, matching thyroid scintiscan and thyroid ultrasonography, to isolate hyperfunctioning and nonfunctioning areas even if they did not correspond to well-defined nodules. TSHr and Gs alpha mutations were searched for by direct sequencing after PCR amplification of genomic DNA. Only 2 adenomas were identified at microscopic examination, whereas the remaining 18 hyperfunctioning areas corresponded to hyperplastic nodules containing multiple aggregates of micromacrofollicules not surrounded by a capsule. Activating TSHr mutations were detected in 14 of these 20 hyperfunctioning areas, whereas no mutation was identified in nonfunctioning nodules or areas contained in the same gland. No Gs alpha mutation was found. In conclusion, activating TSHr mutations are present in the majority of nonadenomatous hyperfunctioning nodules scattered throughout the gland in patients with toxic or functionally autonomous multinodular goiter.

Adenoma↗
PubMed1999

Effects of postmortem delay on serotonin and (+)8-OH-DPAT-mediated inhibition of adenylyl cyclase activity in rat and human brain tissues.

The reproducibility of serotonin (5-HT) and (+)8-OH-DPAT-mediated inhibition of adenylyl cyclase activity was assessed in membranes, stimulated by forskolin, of rat frontal cortex postmortem as well as of human fronto-cortical, hippocampal and dorsal raphe tissues obtained from autopsy brains. The results revealed that differences between basal and forskolin-stimulated enzyme activities were still significant after 48 h postmortem in rat cortex and in all human brain regions up to 46 h after death. However, a decrease of about 17 and 26% in forskolin-stimulated adenylyl cyclase activity was observed at 24 and 48 h, respectively, in rat cortex. 5-HT and the 5-HT1A receptor agonist, (+)8-hydroxy-2(di-N-propylamino)tetraline (8-OH-DPAT), were able to inhibit forskolin-stimulated adenylyl cyclase activity in a dose-dependent manner for 48 h after death in rat and human brain. In rat cortex, both 5-HT and (+)8-OH-DPAT potencies (EC50, nM) and efficacies (percent of maximum inhibition capacity, %) varied significantly with postmortem delay. Conversely, in human tissues, postmortem delay and subject age did not modify agonist potencies and efficacies. Furthermore, a regionality of 5-HT potency and efficacy was revealed in the human brain. 5-HT was equally potent in cortex and raphe nuclei, while being more potent but less effective in hippocampus. (+)8-OH-DPAT was more active in hippocampus and raphe nuclei than in cortex. (+)8-OH-DPAT behaved as an agonist in all areas, as its efficacy was similar or greater than those obtained with 5-HT. The (+)8-OH-DPAT dose-response curve was completely reversed by 5-HT1A receptor antagonists in rat cortex and all human brain areas. In conclusion, we suggest here that differences between rat and human brain might exist at the level of postmortem degradation of 5-HT-sensitive adenylyl cyclase activity. In human brain, 5-HT1A receptor-mediated inhibition of adenylyl cyclase seems to be reproducible, suggesting that reliable experiments can be carried out on postmortem specimens from patients with neuropsychiatric disorders.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1999

Different proliferative patterns characterize different preinvasive breast lesions.

The study of cell-cycle associated proteins Ki-67/MIB-1, bcl-2 and p53 could clarify some features regarding the early phases of neoplastic progression in the breast. An extensive immunohistochemical study was carried out of the expression of these markers in all kinds of preinvasive breast lesions and their collateral normal parenchyma, a type of analysis not previously reported. The specimens were 35 florid ductal hyperplasias (FDHs), 8 atypical ductal hyperplasias (ADHs), 12 well-differentiated intraductal carcinomas (WDICs), 20 intermediately differentiated intraductal carcinomas (IDICs), 14 poorly differentiated intraductal carcinomas (PDICs), 12 atypical lobular hyperplasias (ALHs), 12 type-A lobular carcinomas in situ (LCIS), 150 normal small-size ducts and 365 lobules. All FDHs, ADHs, WDICs, and lobular lesions showed low proliferation (Ki-67/MIB-1), bcl-2 positivity, and p53 negativity; all PDICs expressed high proliferation, while 85 per cent and 7 per cent were p53 and bcl-2 positive respectively; IDICs showed high proliferation (50 per cent), bcl-2 expression (70 per cent), and p53 positivity (30 per cent), but no correlation between the expression of these markers was observed. Independent of the type of collateral lesion and age of the patient, 90 per cent and 10 per cent of small ducts/lobules showed low and high proliferation and diffuse and low bcl-2 expression respectively; no p53 positivity was observed. The modulation of cell proliferation and apoptosis control in ductal lesions could be the expression of a progression from hyperplasia/WDIC to PDIC, in which IDICs represent the link, owing to their immunoprofile. An alternative purely speculative hypothesis is that the different immunoprofile of the preinvasive lesions reflects their different origin in normal breast parenchyma. Low proliferative or bcl-2 positive lobules could be the site of origin of the lesions maintaining this phenotype, namely FDHs, ADHs, WDICs and lobular lesions, while highly proliferative or bcl-2 negative lobules could be the site in which PDICs develop. Consequently, preinvasive breast lesions could express a different regulation of apoptosis control and proliferative activity from the very beginning, rather than a modulation during neoplastic progression.

Adult↗
PubMed1999

Functioning and nonfunctioning thyroid adenomas involve different molecular pathogenetic mechanisms.

The molecular biology of follicular cell growth in thyroid nodules is still poorly understood. Because gain-of-function (activating) mutations of the thyroid-stimulating hormone receptor (TShR) and/or Gs alpha genes may confer TSh-independent growth advantage to neoplastic thyroid cells, we searched for somatic mutations of these genes in a series of hyperfunctioning and nonfunctioning follicular thyroid adenomas specifically selected for their homogeneous gross anatomy (single nodule in an otherwise normal thyroid gland). TShR gene mutations were identified by direct sequencing of exons 9 and 10 of the TShR gene in genomic DNA obtained from surgical specimens. Codons 201 and 227 of the Gs alpha gene were also analyzed. At histology, all hyperfunctioning nodules and 13 of 15 nonfunctioning nodules were diagnosed as follicular adenomas. Two nonfunctioning thyroid nodules, although showing a prevalent microfollicular pattern of growth, had histological features indicating malignant transformation (a minimally invasive follicular carcinoma and a focal papillary carcinoma). Activating mutations of the TShR gene were found in 12 of 15 hyperfunctioning follicular thyroid adenomas. In one hyperfunctioning adenoma, which was negative for TShR mutations, a mutation in codon 227 of the Gs alpha gene was identified. At variance with hyperfunctioning thyroid adenomas, no mutation of the TShR or Gs alpha genes was detected in nonfunctioning thyroid nodules. In conclusion, our findings clearly define a different molecular pathogenetic mechanism in hyperfunctioning and nonfunctioning follicular thyroid adenomas. Activation of the cAMP cascade, which leads to proliferation but maintains differentiation of follicular thyroid cells, typically occurs in hyperfunctioning thyroid adenomas. Oncogenes other than the TShR and Gs alpha genes are probably involved in nonfunctioning follicular adenomas.

Adenoma↗
PubMed1998

Bcl-2, p53 and MIB-1 expression in normal and neoplastic parathyroid tissues.

An altered control of the mechanisms involved in cell proliferation and programmed cell death (apoptosis) might play an important role in parathyroid tumorigenesis. We evaluated by immunohistochemistry the expression of bcl-2 and p53 proteins, as markers of apoptosis control, and MIB-1, as marker of cell proliferation, in a series of normal and neoplastic parathyroid tissues. The specimens were 33 normal parathyroids, 43 parathyroid adenomas and 3 parathyroid carcinomas. Results were scored as positive when more than 1% of cells were stained for MIB-1 and p53, and more than 10% for bcl-2. All normal parathyroids showed numerous bcl-2 positive cells (> or = 80%), low proliferation rate (MIB-1) and no p53 protein expression. Twenty-four (55%) adenomas were bcl-2 positive; in 16 of these the number of positive cells was high (> 50%) and immunoreactivity was diffusely distributed within the adenoma; 8 cases showed a zonal staining pattern, in which groups of stained cells were surrounded by negative cells. Nineteen adenomas (45%) and all carcinomas were bcl-2 negative. A high proliferative rate (MIB-1) was found in all carcinomas and 4 adenomas (9%); all MIB-1 positive adenomas were bcl-2 negative. p53 was negative in all specimens. No significant differences in serum calcium and intact PTH levels nor in tumor size were found between bcl-2 negative and bcl-2-positive and MIB-1-positive and MIB-1-negative adenomas. An inverse, but not statistically significant (p = 0.06) correlation was observed between the percentage of bcl-2 positive cells and serum calcium level in parathyroid adenomas. In conclusion, parathyroid adenomas are a heterogeneous group of lesions in which the pattern of bcl-2 and MIB-1 protein expression ranges between that of normal parathyroid (bcl-2 positivity and MIB-1 negativity) and that of parathyroid carcinoma (bcl-2 negativity and MIB-1 positivity). The question of whether the finding of the MIB-1 positive-bcl-2 negative phenotype identifies a subgroup of clinically more aggressive adenomas remains to be established.

Adenoma↗
PubMed1998

Spectrum of GCDFP-15 expression in human fetal and adult normal tissues.

GCDFP-15, a glycoprotein identified in the cyst fluid of cystic breast disease, is considered to be a marker of apocrine differentiation. Studies on GCDFP-15 localization in adult normal tissues are lacking, and no information on GCDFP-15 expression during fetal development has been reported. We investigated GCDFP-15 expression in a large series of formalin-fixed, paraffin-embedded normal human adult and fetal tissues using the monoclonal antibody BRST-2. In normal adult tissues GCDFP-15 expression was found in all apocrine, lacrimal, ceruminous and Moll's glands and in numerous serous cells of the submandibular, sublingual and minor salivary glands. The serous cells of nasal and bronchial glands were also positive; parotid and laryngeal glands showed rare immunoreactive cells. GCDFP-15-positive cells were observed in all cutaneous eccrine glands from different body sites. In fetal tissues immunoreactivity was observed in numerous acinous cells of all tracheal, bronchial and submandibular salivary glands. GCDFP-15 positivity was identified in numerous cells of all axillary sweat glands and in rare cells of some sweat glands of the thorax, abdomen, back, leg and arm. In both apocrine and nonapocrine glands GCDFP-15 was always localized in the secretory component. These data suggest that GCDFP-15 is a glandular differentiation marker associated with apocrine secretion; that it is expressed in glands that have phylogenetic origins in common with apocrine glands (submandibular salivary and submucosal bronchial glands); and that eccrine cutaneous glands express GCDFP-15 and thus might be referred to as mixed apocrine-eccrine glands. GCDFP-15 is expressed during fetal development and may represent a common marker of embryologically linked glandular structures.

Adult↗
PubMed1998

Primary chemotherapy in locally advanced breast cancer (LABC): effects on tumour proliferative activity, bcl-2 expression and the relationship between tumour regression and biological markers.

The rate of tumour cell proliferation evaluated by the [3H]-thymidine labelling index ([3H]-dT-LI) is known to be an independent prognostic factor in patients with operable breast cancer and significantly predicts the response to chemotherapy in patients with advanced disease. In locally advanced breast cancer (LABG), we examined whether chemotherapy induced modifications in [3H]-dt-LI, and bcl-2 expression and their relationship with tumour regression and prognosis. 70 LABC patients received three courses of primary chemotherapy (FEC: 5-fluorouracil 600 mg/m2, epidoxorubicin 60 mg/m2, cyclophosphamide 600 mg/m2, followed by surgery and subsequent adjuvant chemotherapy consisting of three courses of FEC alternated with three courses of CMF (cyclophosphamide 600 mg/m2, methotrexate 40 mg/m2, 5-fluorouracil 600 mg/m2). Tumour biological markers were evaluated on diagnostic biopsy, before primary chemotherapy and at surgery. Tumour cell proliferation was determined by [3H]-dT-LI, whilst bcl-2 expression was examined by immunohistochemical staining. The overall response rate to primary FEC was 74.3% (95% confidence interval 57.6-83.2%). The response rate correlated with high [3H]-dT-LI: 88% (29/33) of patients with high [3H]-dT-LI achieved an objective response compared with 62% (23/37) of patients with low [3H]-dT-LI (P = 0.014). The 3 patients achieving a pathological complete response after induction treatment had high proliferative tumours. The highest 2-year relapse free survival (66.6%) was observed in patients with low [3H]-dT-LI after primary chemotherapy. The median bcl-2 expression values before and after primary chemotherapy were 0% (range 0-80) and 30% (range 0-90), respectively (P = 0.03). Our data indicate that primary chemotherapy can modulate tumour cell kinetics and apoptosis-related genes. Pretreatment proliferative activity correlated with tumour response, whilst post-treatment [3H]-dT-LI correlated with relapse free survival.

Adult↗
PubMed1998

Preoperative localization of suspicious parathyroid adenomas by assay of parathyroid hormone in needle aspirates.

OBJECTIVE: To determine the usefulness of parathyroid hormone (PTH) measurement in needle aspirates of a suspicious neck mass to confirm its parathyroid nature in patients with primary hyperparathyroidism. METHODS: Thirty-three patients with surgically proved primary hyperparathyroidism were submitted to neck ultrasound (US), parathyroid scintigraphy, and assay of PTH in the aspirate (PTHa) of the suspicious cervical mass. RESULTS: Based on the results of neck US and parathyroid scintigraphy, patients were divided into two groups. Group 1: 16 patients (seven with nodular goiter) with concordant positive US and scintigraphic results. In all but one patient, PTHa was detectable and often markedly elevated (> 1000 pg in 12 patients, between 292 pg and 803 pg in three patients and 53 pg in one patient). The patient with undetectable PTHa had a small lower left parathyroid adenoma (8x8x10 mm). Group 2: 17 patients (12 with nodular goiter) with discordant US and scintigraphic results. PTHa established the parathyroid nature of the mass in 13 cases (> 1000 pg in 8 patients, between 501 pg and 953 pg in three patients and 90 and 79 pg in two patients): 11 of these had a suspected lesion by US examination but the scintigraphy results were negative; two had a mass that gave positive scintigraphy results but was of uncertain origin according to US: in both cases an intrathyroidal parathyroid adenoma was found. PTHa was undetectable in four cases (three with nodular goiter): all of these had equivocal US results, and three had positive scans and one a negative scan. CONCLUSIONS: Assay of PTHa is a simple method and should be useful for confirming the parathyroid nature of a cervical mass in patients with discordant or non-diagnostic US and scintigraphic results.

Adenoma↗
PubMed1998

[Visceral pleura lipoma: a previously undescribed localization and review of the literature on pleural lipomas].

Pleural lipomas are rare, often asymptomatic tumours arising from the parietal pleura. Whereas radiographic signs of pleural lipomas are aspecific, computed tomography and magnetic resonance imaging permit accurate preoperative diagnosis. We describe the clinical-pathologic features of the first case of lipoma arising from the visceral pleura, accidentally discovered in a woman during removal of chest schwannoma. A review of literature concerning pleural lipomas is also presented.

Female↗
PubMed1997

Apparent absence of aging and gender effects on serotonin 1A receptors in human neocortex and hippocampus.

The effects of gender, aging and gender x age on the binding of the 5-HT1A receptor high-affinity agonist [3H]8-hydroxy-2(di-N-propylamino)tetralin ([3H]8-OH-DPAT), were evaluated and compared in tissues of human prefrontal, temporal, parietal, occipital cortex and hippocampus obtained from 21 autopsy subjects. The results revealed no variation with age or gender in either the [3H]8-OH-DPAT maximum binding capacity (Bmax) or dissociation constant (Kd) values. On the other hand, when separate correlations to subject ages were performed for men and women, aging effects on [3H]8-OH-DPAT Bmax and Kd were detected: in men, a significant age-dependent decrease in Kd values was observed in the occipital cortex; in women, the Bmax significantly decreased with aging in the parietal cortex and hippocampus, while increasing in occipito-cortical membranes. Overall, the present study reveals that, although neither gender nor aging 'per se' seem to modify the 5-HT1A receptor binding, gender may reveal region-specific aging effects, i.e. on receptor affinity in men and receptor density in women. Such findings should stimulate further investigation on the hypothesized existence of gender x age-related cross-connections between serotonergic system and hypothalamus-pituitary-gonadal circuits.

Adult↗
PubMed1997

The spectrum of 67-kD laminin receptor expression in breast carcinoma progression.

Laminin is a glycoprotein of the basement membrane (BM), involved in a variety of normal and pathological cellular events including tumour invasion and metastasis. Cells bind laminin through different types of receptor. The 67-kD laminin receptor (67LR) is a cell-surface protein which binds laminin with high affinity. 67LR expression has been shown to increase in neoplastic cells, compared with normal tissues, and 67LR seems to play an important role during the first steps of neoplastic progression. In this study, 67LR expression was analysed during the morphological phases of breast cancer progression from normal tissue to invasive carcinoma. A total of 506 formalin-fixed, paraffin-embedded normal breast structures and lesions were stained by immunohistochemistry usign the MLuC5 monoclonal antibody, which is specific for 67LR. The results show that in normal breast and in any kind of breast lesion, myoepithelial and endothelial cells express 67LR. While 67LR is not seen in the epithelium of normal breast, cysts, adenosis, and benign tumours, it is expressed in the epithelial cells of several hyperplasias and carcinomas in situ, both ductal and lobular, as well as in all invasive carcinomas. The 67LR-positive cell subpopulation expands from hyperplastic lesions to invasive carcinoma, suggesting that 67LR could be related to the induction and progression of breast cancer.

Breast↗
PubMed1997

Usefulness of echo-color Doppler in differentiating parathyroid lesions from other cervical masses.

The aim of our study was to clarify possible differential color Doppler US features between parathyroid lesions and other cervical masses. A total of 56 parathyroid lesions in 54 patients with primary hyperparathyroidism were preoperatively examined with color Doppler sonography. Color Doppler flow patterns were compared with those of 72 thyroid nodules and 20 cervical lymph nodes. In 38 parathyroid lesions a correlation between color Doppler patterns and size, location, and pathological findings was performed. Color Doppler sonography showed five vascular distribution patterns: pattern I, absence of flow; pattern II, focal peripheral flow ("vascular pole") with arterial Doppler spectrum; pattern III, peripheral flow; pattern IV, internal flow ("parenchymal pattern"); pattern V, peripheral and intranodular flow. Pattern I was not specific for any cervical lesion considered. Conversely, pattern IV was observed solely in parathyroid lesions, and pattern II was observed in only one nonparathyroid lesion (thyroid nodule). Mixed pattern (pattern V) was observed solely in thyroid nodules. In addition, pattern III was a characteristic finding of thyroid nodules and was observed in only one parathyroid lesion. Color Doppler patterns of the parathyroid masses did not correlate with the size of the lesion or pathological findings, but only with the location of the gland. Our study showed that color Doppler assessment of parathyroid lesions is a useful integration of gray-scale US and may be helpful in distinguishing parathyroid lesions from other cervical masses.

Adenoma↗
PubMed1997

Apocrine epithelium of the breast: does it result from metaplasia?

Benign and malignant breast lesions may show an apocrine epithelium considered to be the result of metaplasia. In an attempt to clarify the histogenesis of the breast apocrine epithelium we searched for the presence of apocrine cells or cells with apocrine differentiation during human breast development. We analysed 10 autopsy specimens of female breasts from fetuses between 28 and 40 weeks of gestational age and tissue from 6 normal breasts, obtained after breast reduction in nulliparous young women between 22 and 28 years of age. Formalin-fixed, paraffin-embedded sections were stained with haematoxylin-eosin, PAS-diastase and a monoclonal antibody (BRST-2) anti-GCDFP-15, which is a specific apocrine marker. A 40-week fetal breast was analysed by electron microscopy. No cells with histological and ultrastructural apocrine features were found in the ducts of fetal breasts. All fetal breasts showed some ducts with sparse GCDFP-15-immunoreactive cells; the number of these cells increased with gestational age. PAS-diastase was negative. No cells with apocrine morphology were found in ducts and lobules of normal adult breasts. Scattered GCDFP-15-positive luminal epithelial cells and rare PAS-diastase-positive cells were observed in some lobules of all adult breasts. Cells with biochemical characteristics (GCDFP-15 expression) of apocrine differentiation are evident during human fetal breast development and persist in adult mammary glands. Unknown stimuli may induce these cells to take on an apocrine morphology. Apocrine epithelium of the breast may be a normal process of differentiation rather than metaplasia. We suggest the term "apocrine differentiation precursor cells" for GCDFP-15-positive breast epithelial cells with no apocrine morphology.

Adult↗