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Guido Gasparri

Publications and source records attributed to Guido Gasparri.

5 recordsLinked to original sources
PubMed2006

Galectin-3 and Ki-67 expression in multiglandular parathyroid lesions.

Hyperplastic and neoplastic parathyroid lesions may present overlapping morphologic features, and several markers have been proposed to distinguish benign from malignant growths. Recently, it was reported that galectin-3 is a useful marker of malignancy in uniglandular parathyroid diseases. To investigate galectin-3 and Ki-67 immunoexpression in parathyroid hyperplastic disease, 63 multiglandular lesions (13 primary, 40 secondary, and 10 tertiary hyperplasia cases) were analyzed and compared with 45 control cases of parathyroid adenomas and 24 carcinomas. Our data showed that hyperplastic lesions responsible for primary nonfamilial or tertiary hyperparathyroidism, as well as parathyroid adenomas, were negative for galectin-3, as opposed to carcinomas. In addition, secondary and familial primary hyperplasia cases were surprisingly positive for galectin-3 in approximately two thirds of cases. All hyperplastic lesions (positive or negative for galectin-3) had a low Ki-67 index. Based on these findings, secondary hyperplasia has a low proliferative potential but an unexplained galectin-3 reactivity, which reduces its diagnostic role in differentiating benign from malignant nodules in the context of multiglandular parathyroid diseases.

Adenocarcinoma↗
PubMed2005

Galectin-3 expression in parathyroid carcinoma: immunohistochemical study of 26 cases.

The diagnosis of parathyroid carcinoma (PC) is difficult and based on morphological features that are not totally reliable. Several molecular markers proved useful in the evaluation of PC, but their sensitivity, specificity, or both are rather low. With the aim of identifying a marker of malignancy in parathyroid tumors, we tested the expression of galectin-3 (Gal-3), a lectin expressed in several malignant tumors, including follicular carcinomas (but not adenomas) of the thyroid. Twenty-six PCs and 30 control parathyroid adenomas (PAs) were collected. The PCs had been diagnosed based on capsular/vascular invasion (26/26 cases), extraparathyroid infiltration (16), local recurrence (9), and distant metastases (6). All cases were immunohistochemically tested for Gal-3 and for other markers claimed to be useful in the differential diagnosis of parathyroid neoplasms, namely, Ki67, p27, and bcl2. Gal-3 was expressed by 24 of the PC (92.3%), but only 1 PA (3.3%) (P < .001). All metastasizing PCs were Gal-3-positive. As expected, the Ki67 proliferative index was higher in PCs (mean, 6.7%) than in PAs (1.9%); p27 was down-regulated in 61.5% of PCs and only 33.3% of PAs, whereas bcl2 was strongly positive in most PAs and in 38.5% of PCs. In a suspected PC, the association of Gal-3 with Ki67 (using a cutoff of 6% for the proliferative activity) appeared the best marker combination (sensitivity 96.2%, specificity 90%), and the profile Gal-3-positive/Ki67 >6% was unique to PCs. We conclude that Gal-3 immunostaining is a valuable tool to support a diagnosis of PC in highly proliferating (Ki67 >6%) tumors affecting a single parathyroid gland.

Adenoma↗
PubMed2003

Decreased expression of stem cell factor in esophageal and gastric mucosa after esophagogastric anastomosis for cancer: potential relevance to motility.

BACKGROUND: Esophageal replacement with gastric tube is a well-established reconstruction of the alimentary tract after esophagectomy in cancer patients. The resulting molecular events in the transposed gastric tube and residual esophagus have yet to be investigated. Stem cell factor (SCF) was recently shown to be critical for signaling in gastrointestinal motility. SCF expression is here correlated with changes in mucosal morphology, acid and biliary reflux, and motility in the residual esophagus and gastric tube. METHODS: Thirteen patients surgically resected for squamous esophageal carcinoma with gastric tube replaced by esophagogastric anastomosis underwent upper endoscopy, esophageal manometry, 24-hour pH monitoring, and bile reflux detection. Esophageal and gastric mucosa samples were examined for SCF expression by immunohistochemical and semiquantitative reverse transcriptase-polymerase chain reaction analysis and for SCF serum levels by enzyme-linked immunosorbent assay. RESULTS: All patients showed severe residual esophagus hypoperistalsis and no gastric tube motor activity. The 24-hour pH monitoring was positive in most; 24-hour bile detection was mostly negative. SCF levels in the residual esophageal and gastric tube mucosa were dramatically decreased compared with those of normal subjects. The correlation between SCF and slow-wave activity was positive. CONCLUSIONS: Hypomotility of the residual esophagus and gastric tube seems closely associated with disruption of the SCF/c-kit signaling pathway. However, the absence of notable relations between mucosal changes after chronic exposure to acid, biliary gastric content, and SCF expression indicates that this analysis cannot be considered part of endoscopic follow-up.

Adult↗
PubMed1996

Recurrence in Parathyroid Hyperplasias Owing to Secondary Hyperparathyroidism is Predicted by Morphological Patterns and Proliferative Activity Values.

The histological pattern and the cell proliferative activity (as detected by Ki-67 immunostaining) of a series of 50 parathyroid hyperplasias (PTHs) secondary to renal failure were studied to assess their value in predicting recurrence of hyperparathyrodism (HPT). On account of their clinical evolution, these cases were divided into two groups, recurrent HPT (23 cases) and nonrecurrent HPT (27 cases). A nodular growth pattern (as opposed to diffuse) was the prevalent one and was observed in 20 (74%) cases of now recurrent HPT and in 22 (95.6%) cases of recurrent HPT, a statistically significant difference (p < 0.05). The Ki-67 proliferative fraction was 1 9% in recurrent HPT cases, as compared with 0.81% in nonrecurrent HPT, a difference which was statistically significant (p = 0.001). We conclude that a nodular pattern of growth and an elevated Ki-67 proliferative fraction (>1.5%) in PTH are both associated with a higher risk of recurrence (4.30) of HPT.

Journal Article↗