Pseudohyperplastic prostatic adenocarcinoma.
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Adenocarcinoma↗
Biomedical subjects
Z Kaleem
Publications and source records attributed to Z Kaleem.
Allelotype of follicular thyroid carcinomas reveals genetic instability consistent with frequent nondisjunctional chromosomal loss.
Numerous studies aimed at the identification of chromosomal regions that are frequently deleted in specific tumor types have pointed to the location and involvement of specific tumor suppressor genes. Previous studies of loss of heterozygosity (LOH) among thyroid tumors have revealed frequent allelic deletions at a few chromosomal regions. A systematic genome-wide examination of LOH in a substantial number of follicular carcinomas, however, has not been performed previously. We assessed LOH at polymorphic markers from each nonacrocentric autosomal arm in a panel of 28 follicular thyroid carcinoma tumor and normal pairs. In contrast to the results of previous allelotype studies, we found high rates of LOH at multiple chromosomal regions. The highest rate of loss in our study was at 2p (50.0%), and 2q (50.0%), and the mean rate of LOH was 20.4%. Marked genetic instability in a subset of tumors was demonstrated by high fractional allelic loss, which accounted for more than 80% of observed LOH in this study. High fractional allelic loss was significantly associated with oxyphilic features and poor differentiation of these tumors. Our data provide evidence of a prevalent phenotype of nondisjunctional whole chromosomal loss in follicular thyroid carcinomas.
Adenocarcinoma, Follicular↗
Primary pulmonary meningioma. Report of a case and review of the literature.
Extracranial meningiomas are rare outside the head and neck region. We report a case of primary pulmonary meningioma, initially detected as a radiographic incidental finding, occurring in an asymptomatic 45-year-old woman. Light microscopic examination of both cytologic and histologic preparations was typical of a classical meningioma and included such features as intranuclear pseudoinclusions, psammoma bodies, and cellular whorls. Immunohistochemistry demonstrated tumor cell positivity for vimentin and epithelial membrane antigen, as is characteristic of meningioma. Ultrastructural analysis showed interdigitating cell membranes and desmosomes, with no evidence of basal lamina, neurosecretory granules, or microvilli. On short-term follow-up, the patient is well and has no evidence of a cranial or spinal meningioma. The previous 10 cases reported in the literature had similar characteristics, including a tendency toward occurrence in middle age to older women, asymptomatic presentation, peripheral lung location, and morphologic features. Finally, other conditions in the differential diagnosis and possible histogenesis are discussed.
Cell Membrane↗
Allelotype analysis of esophageal adenocarcinomas: evidence for the involvement of sequences on the long arm of chromosome 4.
The incidence of esophageal adenocarcinoma has increased dramatically over the past 20 years. The causes for this change in incidence and the genetic defects that underlie tumorigenesis are unknown. We performed loss of heterozygosity (LOH) studies in esophageal adenocarcinomas in an effort to map the location of tumor suppressor genes involved in the initiation or progression of this cancer. A genome-wide search for LOH was undertaken using microsatellite repeat polymorphisms and a panel of 27 tumor and matched normal DNAs. This is the first report of an allelotype analysis of esophageal adenocarcinomas. We observed frequent loss of sequences on the short arm of chromosome 17 in the region of the TP53 gene. We also identified a region on 4q lost in more than half of the tumors investigated. The high rate of LOH for 4q sequences speaks to the involvement of an as yet unidentified tumor suppressor gene in esophageal adenocarcinoma tumorigenesis.
Adenocarcinoma↗
Mxi1 tumor suppressor gene is not mutated in primary pancreatic adenocarcinoma.
Amplification of the c-myc oncogene occurs in a variety of solid tumors, including pancreatic adenocarcinomas. The MXI1 gene, located at 10q24-q25, may serve to negatively regulate c-myc oncogene activity, and potentially has tumor suppressor function. As such, altered MXI1 function might contribute to tumorigenesis. We examined 40 primary human pancreatic adenocarcinomas for MXI1 mutations. Single-strand conformation variant analysis and direct sequencing of the variants revealed a MXI1 polymorphism in 1 of 40 tumors. No MXI1 mutations were identified. Southern blot analyses did not reveal any gross rearrangements of MXI1. These results suggest that MXI1 is unlikely to play a role in human pancreatic adenocarcinoma tumorigenesis.
Adenocarcinoma↗
Blastic transformation of mantle cell lymphoma.
In contrast to chronic lymphocytic lymphoma and low-grade follicular lymphomas, mantle cell lymphoma, formerly known as intermediate lymphocytic lymphoma, rarely transforms histologically into large cell lymphoma. Because of its rarity, little information is available on the prognostic or therapeutic implications of histologic transformation of mantle cell lymphoma to a "blastic" form. Here we report a case of a 68-year-old man whose mantle cell lymphoma transformed into a high-grade lymphoma with blastic cytology, which was associated with an extremely rapid clinical course. Flow cytometric analysis revealed the immunophenotype of the original lymphoma, which had typical mantle cell morphology, and the subsequent bone marrow aspirate was virtually identical, as was the immunophenotype of the small cells versus the blastic cells in the subsequent specimen. The rapid clinical course in the patient reported here is similar to that of other rare cases reported and suggests that mantle cell lymphoma in blastic transformation appears to be a very aggressive lymphoma with a clinical course similar to that of other low-grade lymphomas in histologic transformation.
Aged↗
The role of indirect antigen recognition in islet xenograft rejection.
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Animals↗
Hyalinizing trabecular adenoma of the thyroid. A report of two cases with cytologic, histologic and immunohistochemical findings.
BACKGROUND: Hyalinizing trabecular adenoma (HTA) is a rare benign thyroid tumor that is easily confused with medullary carcinoma on surgical specimens and with papillary carcinoma on cytologic specimens. CASES: The fine needle aspiration biopsies (FNABs) and surgically resected specimens from two patients with HTA were studied. Nuclear grooves and nuclear pseudoinclusions were identified in both FNABs. Gross examination of the surgical specimens revealed two nodules (0.8 and 0.5 cm in diameter) in one case and a 6-cm nodule in the other. A thin, fibrous capsule surrounded each nodule. A predominant trabecular pattern was observed in the three lesions. Antibodies to thyroglobulin, carcinoembryonic antigen (CEA), epithelial membrane antigen (EMA), vimentin, chromogranin, synaptophysin, neuron-specific enolase, proliferating cell nuclear antigen (PCNA), Ki-67 and p53 were used to stain 10% buffered, formalin-fixed, paraffin-embedded sections of the surgical specimens. No immunostaining was observed with antibodies against calcitonin, synaptophysin, chromogranin, EMA, vimentin or p53. Less than 5% of cells were CEA positive in one case. The Ki-67 index was low and PCNA expression high. CONCLUSION: HTAs occur as solitary or multiple nodules. FNABs of HTAs contain cells with nuclear grooves and nuclear pseudoinclusions but lack psammoma bodies, high cellularity and papillary structures. Immunohistochemistry using anticalcitonin and antithyroglobulin antibodies is helpful in distinguishing these tumors from medullary carcinoma. The low Ki-67 index and absence of p53 immunostaining are consistent with the benign behavior of this tumor. The significance of high PCNA immunostaining is uncertain.
Adenoma↗