Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
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Frozen section analysis is an essential tool for assessing margins intra-operatively to assure complete resection. Many institutions evaluate surgical defect edge tissue provided by the surgeon after the main lesion has been removed. With the increasing use of transoral laser microsurgery, this method is becoming even more prevalent. ⋯ However, when considering only the frozen section cases where tumor was ultimately identified (either at the time of frozen section or on permanent sections) the sampling error rate for two-level sectioning was 15.3 versus 7.4% for three-level sectioning. This difference was statistically significant (P=0.006). Cutting a single additional 'deeper' level at the time of frozen section identifies more tumor-bearing specimens and may reduce the number of sampling errors.
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Loss of E-cadherin expression has been linked to the invasive phenotypes of a variety of neoplasms, including lobular breast cancer. The expression of E-cadherin in variants of urothelial carcinoma relative to usual-type urothelial carcinoma, maximum depth of invasion and angiolymphatic invasion has not been well characterized. A total of eight cases of micropapillary urothelial carcinoma, four cases of plasmacytoid urothelial carcinoma, two cases of urothelial carcinoma with signet ring cell differentiation and two cases of urothelial carcinoma with mixed plasmacytoid and signet ring cell differentiation, all obtained from cystectomy/cystoprostatectomy cases, were identified. ⋯ All nine additional cases of usual-type high-grade urothelial carcinoma were diffusely positive for E-cadherin. E-cadherin is diffusely positive in usual-type urothelial carcinoma and micropapillary urothelial carcinoma, irrespective of pathological stage and angiolymphatic invasion. Loss of E-cadherin expression may be a marker of plasmacytoid and signet ring cell differentiation in urothelial carcinoma.
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Graft-versus-host disease is the major complication after allogeneic hematopoietic stem cell transplantation and is attributable to donor T-cell recognition of recipient alloantigens. In patients undergoing autologous hematopoietic stem cell transplantation in which there is no genetic disparity to induce an alloresponse, a syndrome similar to allogeneic graft-versus-host disease has been described. Designated as autologous graft-versus-host disease, it typically involves the skin and has reportedly caused little morbidity in this patient population. ⋯ Outcomes ranged from a prompt, complete resolution of symptoms to death. Patients treated with autologous hematopoietic stem cell transplantation, particularly those with multiple myeloma, may develop a potentially life-threatening syndrome pathologically identical to allogeneic graft-versus-host disease. This diagnosis must be considered when interpreting biopsies from patients with gastrointestinal symptoms following autologous hematopoietic stem cell transplantation.
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In March and early April 2009, cases of a new swine-origin influenza A (H1N1) virus were diagnosed in Mexico and the United States. Influenza virus presents as a respiratory infection with high morbidity and mortality. We describe the postmortem findings of eight confirmed cases of influenza A/H1N1 in a medical examiner setting. ⋯ A wide range of histopathological findings including tracheitis, necrotizing bronchiolitis, alveolitis, intra-alveolar hemorrhage, and hyaline membranes, both in a focal and in a diffuse distribution, were identified. Influenza A/H1N1 viral infection presents with a wide range of histological findings in a diffuse or focal distribution; most consistently with tracheitis, necrotizing bronchiolitis, and alveolitis with extensive alveolar hemorrhage. These histopathological findings at autopsy along with a clinical history of flu-like symptoms should raise suspicion for influenza A/H1N1 infection, and postmortem analysis by the reverse transcription-polymerase chain reaction (RT-PCR) is recommended for an accurate diagnosis.
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Multifocal micronodular pneumocyte hyperplasia is a rare pulmonary manifestation of tuberous sclerosis complex (TSC) that is a tumor suppressor gene disorder characterized by many hamartomas. A purported mechanism of hamartomatous proliferation in TSC is constitutive activation of the mammalian target of rapamycin (mTOR) signaling pathway dysregulated by a functional loss of TSC genes. Although multifocal micronodular pneumocyte hyperplasia develops locally as self-limited, benign lesions, it is morphologically similar to the preinvasive lesion of pneumocytes that characterize atypical adenomatous hyperplasia or bronchioloalveolar carcinoma. ⋯ Loss of heterozygosity of TSC was found in the preinvasive lesions of pneumocytes, equal to or less than multifocal micronodular pneumocyte hyperplasia. In contrast, phospho-Akt was expressed in the preinvasive lesions of pneumocytes more frequently than multifocal micronodular pneumocyte hyperplasia, but the other mTOR-related proteins were less frequently expressed in the former than in the latter. These outcomes suggest that functional loss of TSCs and consequent hyperphosphorylation of mTOR-related proteins in multifocal micronodular pneumocyte hyperplasia may cause its benign neoplastic proliferation of pneumocytes.