Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
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Biography Historical Article
A brief history of the pathology of the gonads.
Our understanding of gonadal pathology has reached its current state as a result of the contributions of numerous outstanding investigators. Knowledge of testicular tumor pathology dates back to the great British workers Percival Pott and Sir Astley Cooper but the single greatest early stride was made with the description in 1906 by the French urologist Maurice Chevassu of the seminoma. The seminal 1946 paper of Nathan B Friedman and Robert A Moore, which segregated out as a distinct entity embryonal carcinoma, is, however, the foundation for the current classification of testicular tumors. ⋯ His many original observations have touched upon virtually all categories of ovarian tumor pathology. His second series fascicle 'Tumors of the Ovaries and Maldeveloped Gonads' utilized the WHO classification and presented a lucid elaboration of his by then vast experience with ovarian tumors. All the above have left a rich legacy which those who follow in their path will be challenged to equal.
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Comparative Study
Pulmonary pathology of severe acute respiratory syndrome in Toronto.
The severe acute respiratory syndrome (SARS) pandemic in Toronto resulted in a large number of autopsies on its victims. We describe the pulmonary pathology of patients who died in the 2003 Toronto outbreak. Autopsy material from the lungs of 20 patients who died between March and July 2003 were characterized by histology, molecular biology, and immunohistochemistry for cytokeratins, thyroid transcription factor-1, CD68, Epstein-Barr virus, cytomegalovirus, and human herpes simplex viruses. ⋯ Two cases were complicated by invasive fungal disease consistent with Aspergillosis, and another by coinfection with cytomegalovirus. Our findings indicate that the lungs of patients who die of SARS are almost always positive for the SARS-associated coronavirus by RT-PCR, and may show features of both diffuse alveolar damage and acute fibrinous and organizing pneumonia patterns of acute injury. Cases of SARS may be complicated by coexistent infections and therapy-related lung injury.
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Comparative Study
Aberrant expression of cell cycle regulators in Hodgkin and Reed-Sternberg cells of classical Hodgkin's lymphoma.
The characteristic Hodgkin and Reed-Sternberg cells of classical Hodgkin's lymphoma, although highly positive for proliferation markers, do not accumulate to excessive cell numbers. These cells are characterized by abortive mitotic cycles, leading to multinucleation or cell death in mitosis. We have previously described high expression of G1-phase cyclins in classical Hodgkin's lymphoma, which could explain the high percentage of cells staining for proliferation markers. ⋯ In addition, 98% of Hodgkin's and Reed-Sternberg cells in 99% (250/253) of the cases stained strongly positive for cyclin A. These findings further corroborate the hypothesis that Hodgkin and Reed-Sternberg cells exhibit a disturbed cell cycle with an abnormally short or even absent G1-phase. In contrast to other tumors, expression of PCNA or cyclin A had no prognostic value for patient survival.
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Comment Letter Comparative Study
A distinct expression pattern and point mutation of c-KIT in papillary renal cell carcinomas.
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Nonspecific interstitial pneumonia, a recently described form of idiopathic interstitial pneumonia, is characterized by uniform involvement of the alveolar septae with interstitial inflammation and variable amounts of fibrosis. Histological observations differentiate nonspecific interstitial pneumonia from usual interstitial pneumonia and clinically, patients with a nonspecific interstitial pneumonia pattern show better prognosis than those with usual interstitial pneumonia. We have genetically analyzed a family with a history of usual interstitial pneumonia. ⋯ DNA sequence analyses of the surfactant protein C gene in children with nonspecific interstitial pneumonia and adults with usual interstitial pneumonia exhibit a common heterozygous mutation located in exon 5. The mutation causes a Leu188 to Gln188 change in the carboxy-terminal region of prosurfactant protein C, possibly affecting peptide processing. These observations suggest that individuals with this particular mutation in surfactant protein C gene might be at increased risk of interstitial lung disease of variety of types.