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Genetic alteration and loss of expression of tumor suppressor gene PTEN has been found in carcinomas of the breast, prostate, and endometrium, as well as in gliomas. PTEN expression in neural crest/neuroendocrine (NC/NE) tissues and in neoplasms has not been reported. This study examines PTEN expression in embryonal, fetal, and adult tissues by immunohistochemistry. The authors found high PTEN expression in embryonal, fetal, and adult NC/NE tissues. The authors also study the PTEN expression in NC/NE neoplasms (N ‫ס‬ 37), including 5 melanocytic nevi, 2 melanomas, 9 carcinoids, 2 moderately differentiated neuroendocrine carcinomas, 13 poorly differentiated neuroendocrine carcinomas, 2 paragangliomas, 2 pheochromocytomas, 2 medullary thyroid carcinomas, and 1 neuroblastoma. All carcinoid tumors and melanocytic nevi showed moderate or strong immunostaining for PTEN. In contrast, the majority of poorly differentiated neuroendocrine carcinomas (7 of 13) were negative for PTEN (54%); the remainder showed diminished reactivity. The two melanomas studied were also negative for PTEN immunostaining. The paragangliomas, pheochromocytomas, medullary thyroid carcinomas, and neuroblastoma all showed a strong PTEN stain. The authors postulate that PTEN is a differentiation marker for NC/NE tissue and tumors and that loss of PTEN expression may represent an important step in the progression of NE tumors. K e y W o r d s : P T E N -t u m o r s u p p r e s s o r g e n e -Immunohistochemistry-Neuroendocrine-Carcinoid-Neuroendocrine carcinoma.AppliedImmunohistochemistry&MolecularMorphology 10 (2): 139-146, 2002.

Sir, we report a rare autopsy case of microscopic polyangiitis (MPA) with myocardial infarction (MI) and pulmonary hemorrhage. A 41-year-old black woman presented with recent onset of severe headache, arthralgia, myalgia, and chest pain. Physical examination revealed macular facial rash. No oral ulcers, photosensitivity, alopecia, weight loss, fever, or Raynaud's phenomenon were present. Past medical history was unremarkable. The white blood count, hemoglobin, hematocrit, platelets, sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, creatinine, glucose, and liver enzyme studies were normal. The erythrocyte sedimentation rate (ESR) was 27 mm/h. The antinuclear antibody (ANA) titer was 1:2560 with a speckled pattern. Rheumatoid factor was negative. Creatine phosphokinase (CK) was 99 mU/ml. Her electrocardiogram (EKG) showed normal sinus rhythm. The patient was given 400 mg ibuprofen twice a day. One month later, her symptoms were not relieved and prednisone 15 mg/day was initiated by her primary care physician. There was no improvement. Prednisone was discontinued at the patient's request. Three months later the patient was hospitalized due to dyspnea and chest pain of 5-day duration. Physical examination revealed bilateral basilar crepitations in the lungs. Cardiovascular and neurological examinations were insignificant. EKG and chest roentgenogram (CXR) were normal. There were no skin lesions or joint tenderness. Further immunological studies showed: ANA titer 1:1280; negative anti-double strand DNA, anti-ribonucleoprotein, anti-Smith, antineutrophil cytoplasmic antiantibody (ANCA), anti-SSA, anti-SSB, and anti-glomerular basement membrane (GBM) antibodies. Rapid plasma reagin was non-reactive. C3 and C4 were 103 mg/dl and 14.4 mg/dl, respectively. Prothrombin (PT) was 13.3 s and partial thromboplastin time (PTT) was 53.5 s. ESR was 27 mm/h. Urinalysis showed protein 100 mg/dl, red blood cells, and white blood cells 5-10/HPF. Erythromycin and trimethoprim-sulfamethoxazole were prescribed. On the third day of admission, her respiratory status deteriorated. CXR and computerized tomography angiogram showed bilateral alveolar infiltrates. Arterial blood gases showed pH 7.42, pCO 2 39 mmHg, pO 2 59 mmHg and O 2 saturation 88%. Blood cultures were negative. Bronchial washings were negative for pneumocystis carinii, fungi, and acid fast organisms. Human immunodeficiency virus serology was negative. On the fifth hospital day she complained of severe chest pain. EKG showed inferior lateral ST segment elevation. Serum CK was 607 mU/ml and CK-MB fraction was 26.7%. Ischemic heart disease was considered. She was started on heparin, nitroglycerine and lopressor. On the ninth day she still had persistent ST segment elevation on EKG. CK was 500 mU/ml and troponin I was 40 ng/ml. She expired on the tenth day after admission.At autopsy, the heart (419 g) exhibited mild, bilateral ventricular dilatation. The left ventricular papillary muscles were focally hemorrhagic. Otherwise, the heart was unremarkable grossly. T...

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