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Laurentia Nodit

Publications and source records attributed to Laurentia Nodit.

11 recordsLinked to original sources
PubMed2006

Endoscopic ultrasound-guided fine needle aspirate microsatellite loss analysis and pancreatic endocrine tumor outcome.

BACKGROUND & AIMS: The clinical course of pancreatic endocrine tumor (PET) varies depending on tumor aggressiveness, disease extent, and possibly accumulated molecular alterations. Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) results, although accurate in diagnosing PET, correlate poorly with PET outcome. The role of detecting key molecular abnormalities in predicting PET behavior and clinical outcome from EUS-FNA material remains unknown. METHODS: Patients with confirmed PET who underwent EUS-FNA during a 32-month period were included. Patient demographics and clinical data were recorded and follow-up information was obtained by contacting their physician to evaluate disease progression. Representative tumor cells were microdissected from the FNA material. DNA was harvested and amplified, targeting a panel of 17 polymorphic microsatellite markers on chromosomes 1p, 3p, 5q, 9p, 10q, 11q, 17p, 17q, 21q, and 22q. The polymerase chain reaction products were subjected to fluorescent capillary gel electrophoresis to detect microsatellite loss. The fractional allelic loss (FAL) was calculated. RESULTS: Twenty-five patients were studied. Thirteen were classified histologically as benign PET limited to the pancreas and 12 as malignant PET (invasive or metastatic). The mean FAL in the benign and malignant PET was 0.03 and 0.37 (P<.0001), respectively. In addition, the mean FAL was significantly greater in those with disease progression as compared with patients with stable disease (0.45 vs 0.09 respectively, P<.0001). CONCLUSIONS: Microsatellite loss analysis of EUS-FNA material from PET can be performed reliably and an FAL value of more than 0.2 is associated with disease progression. This technique may have value in the preoperative assessment and risk stratification of patients with PET.

Adult↗
PubMed2006

Endoscopic ultrasound fine needle aspirate DNA analysis to differentiate malignant and benign pancreatic masses.

OBJECTIVES: Accurate diagnosis of malignant and benign pancreatic masses can be challenging, potentially delaying treatment for cancer and subjecting patients with benign disease to unnecessary surgery. Endoscopic ultrasound fine needle aspirate (EUS-FNA) of pancreatic masses remains inconclusive in a subset of patients. The role of EUS-FNA molecular analysis in this context is studied. METHODS: Patients with benign pancreatic masses (6 cases, 4 autoimmune pancreatitis, 2 focal chronic pancreatitis) and malignant pancreatic masses (15) with inconclusive cytology (5 cases) and positive cytology (10 controls) were selected. All cases had definitive pathology. Representative cells were microdissected from each EUS-FNA sample and subjected to PCR for analysis of 16 microsatellite allele loss markers situated at 1p, 3p, 5q, 9p, 9q, 10q, 17p, 17q, 21q, and 22q. Loss of heterozygosity analysis used fluorescent capillary electrophoresis for quantitative determination of allelic imbalance. k-ras-2 point mutation analysis was also performed. Mean fractional mutation rate (FMR) was calculated and compared for each group. RESULTS: All malignant cases carried multiple mutations (FMR 0.50), regardless of positive cytology (FMR 0.52) or suspicious cytology (FMR 0.47) (p = NS). Five of the 6 benign cases carried no mutations whereas 1 case of autoimmune pancreatitis and coexisting PanIN lesions exhibited a k-ras mutation (FMR 0.01). The mean FMR for the malignant and benign samples was significantly different (p < 0.0001). CONCLUSIONS: Broad panel microsatellite loss and k-ras point mutation analysis can be reliably performed on EUS-FNA samples from pancreatic masses and improves the diagnostic accuracy. Furthermore, it accurately differentiates between malignant and benign pancreatic masses.

Adult↗
PubMed2005

Identification of lymphatic endothelium in pediatric vascular tumors and malformations.

The distinction between lymphatic and other vascular vessels on microscopic sections is a challenging task. D2-40, a novel antibody, has been reported to be selective for lymphatic endothelium. We studied the specificity and sensitivity of D2-40 in pediatric vascular tumors and malformations. Fourteen lymphatic and 11 vascular lesions were randomly selected and stained with D2-40 and CD31 antibodies. The lymphatic lesions included 6 lymphatic malformations, 5 cystic hygromas (macrocystic lymphatic malformation), 2 lymphovenous malformations, and 1 lymphangioma, and the vascular lesions comprised 3 infantile hemangiomas, 3 Kaposiform hemangioendotheliomas, 2 tufted angiomas, 1 pyogenic granuloma, 1 arteriovenous, and 1 venulocapillary malformations. The staining patterns of the vascular channels were compared. In all lesions D2-40 labeled only the endothelium of thin-walled vascular channels morphologically consistent with lymphatic vessels (25 of 25). No staining of the vascular lesions (0 of 11) or of arteries and veins (0 of 25) was observed. All lymphatic lesions had D2-40-positive vessels; however, the percentage of vessels that stained varied. Five lymphatic lesions showed more than 75% D2-40-positive channels, 5 lesions had approximately 50%, and 4 cases showed fewer than 25% D2-40-positive channels. There was a tendency of more consistent D2-40 staining of small versus large lymphatic channels. CD31 constantly labeled arteries, veins, capillaries, and lymphatics in all lesions and all endothelial cells in the vascular lesions. D2-40 is a very specific antibody for lymphatic endothelium, with variable sensitivity. CD31 more reliably identifies lymphatic endothelium. Currently, D2-40 appears to be a good marker to identify lymphatic vessels in pediatric vascular tumors and malformations.

Adolescent↗
PubMed2005

Improving the quality of cytology diagnosis: root cause analysis for errors in bronchial washing and brushing specimens.

Detailed root cause analysis to determine causes of pulmonary cytology errors has not been used to design specific practice changes. We performed root cause analysis of all false-negative bronchial brushing and washing specimen errors (n = 32) detected by the cytologic-histologic correlation process in 2002. Medical records and all slides were reviewed. Based on the correlation process, 10 errors were interpretive, 16 sampling, and 6 combined interpretive/sampling. Root cause analysis showed that the lesion was not accessible in 8 cases and tumor was readily identified on the slides in only 1 case. In 11 cases, the malignant cells were few and not recognized, and in 13 cases, obscuring artifacts (eg, cellular crushing and air drying) limited interpretation. Sampling issues had a major role in the misdiagnosis in 31 cases (97%), and recommendations for error reduction include immediate interpretation and the use of transmucosal fine-needle aspiration.

Bronchoalveolar Lavage Fluid↗
PubMed2004

Transient posttransplant graft-versus-host lymphadenopathy.

There is sparse information in humans on graft-versus-host (GVH) lymphadenopathy. A 15-month-old male received a liver and small bowel transplant for short bowel after gastroschisis. At 21 days he developed a GVH-like skin rash. Flow cytometry demonstrated 16.1% circulating donor cells. Polymerase chain reaction for Epstein-Barr virus was negative. Two months later, the rash recurred with diffuse lymphadenopathy. Lymph node biopsy showed effaced architecture without visible follicles, large numbers of CD79a(+) immunoblasts interspersed with smaller CD3(+) and CD8(+) cells, and prominent dendritic cell hyperplasia. Human herpes virus 8, cytomegalovirus, and EBER-1 probes were negative, as was polymerase chain reaction for human herpes virus 6. Allograft intestinal biopsies on days 10 and 24 had a similar infiltrate. The features appeared to be those of lymphocytes trafficking between the graft and host with a mixed lymphocyte reaction in situ, a GVH-type reaction without tissue damage. The reaction was self-limiting in the intestinal graft, and the lymphadenopathy resolved with some decrease in immunosupression. Circulating donor cells fell to 2.5% by day 62, and the child has been rejection free on low-dose immunosuppression.

Diagnosis, Differential↗
PubMed2004

Allelic loss of tumor suppressor genes in ameloblastic tumors.

Ameloblastoma is an odontogenic tumor with a variety of histologic appearances and an unpredictable biologic behavior. Little is known about allelic losses of tumor suppressor genes in ameloblastomas. This study surveyed DNA damage in ameloblastomas and correlated this with histologic sub-type and clinical outcome. There were 12 ameloblastomas (two peripheral, eight solid, and two unicystic) and three ameloblastic carcinoma studied for loss of heterozygosity of tumor suppressor genes on chromosomes 1p, 3p, 9p,10q, and 17p (L-myc, hOGG1, p16, pten, and p53). The frequency of allelic loss and the intratumoral heterogeneity were calculated. L-myc (71% frequency of allelic loss) and pten (62% frequency of allelic loss) had the most frequent allelic losses. Overall frequency of allelic loss and intratumoral heterogeneity were higher in mandibular and in unicystic tumors and lower in tumors that recurred/metastasized. The rate of allelic loss in the three carcinomas was similar to that seen in benign tumors. The frequency of allelic loss and intratumoral heterogeneity did not correlate with age, gender, histologic subtype, or prognosis. Since tumors that behaved aggressively did not harbor more allelic losses, it is likely that DNA damage in ameloblastomas and ameloblastic carcinomas is sporadic and cumulative. We conclude that other genetic or epigenetic mechanisms may be responsible for malignant behavior in ameloblastic carcinomas.

Adult↗
PubMed2003

Indolent mantle cell lymphoma with nodal involvement and mutated immunoglobulin heavy chain genes.

Mantle cell lymphoma (MCL) is typically considered an aggressive but incurable neoplasm composed of cyclin D1+ monoclonal B-cells with a t(11;14)(q13;q32) and usually unmutated immunoglobulin (Ig) genes. Although it has been suggested that a more indolent leukemic disorder exists with the same phenotype and genotype but with mutated Ig genes, others have considered these cases to be variants of chronic lymphocytic leukemia. We present a case of an indolent MCL that was documented with cyclin D1 expression in a lymph node biopsy performed more than 12 years ago. The patient has peripheral blood involvement with a lymphocyte count in the reference range, variable thrombocytopenia, and minimal adenopathy but is otherwise well, never having received any antineoplastic therapy. Study of peripheral blood samples from 2002 revealed a CD5-variable B-cell monoclonal proliferation with a t(11;14)(q13;q32) plus other karyotypic abnormalities, positive fluorescence in situ hybridization studies for the CCND1/IgH translocation, and clonal Ig gene rearrangement with mutated Ig genes (95.7% homology to VH 4-31). The subtle but diagnostic lymph node biopsy in this case helps to further support that an indolent t(11;14) monoclonal lymphocytosis with mutated Ig genes can represent an MCL variant rather than chronic lymphocytic leukemia.

Adult↗