A prognostic interpretation of preneoplastic lesions would have impact in bronchial carcinoma early diagnosis and through the study of Erb-B family receptors as they have an important role in lung carcinogenesis. The existence of drugs as tyrosine kinase inhibitors stressed the importance of studying gene alterations for selected chemoprevention schemes and characterization of carcinogenesis. Bronchial preneoplastic lesions were characterized by immunohistochemistry using the antibodies LP34 (high weigh molecular cytokeratin), CK7, chromogranin A, Ki67, p53, C-erbB-2 and EGFR. HER2 and EGFR gene copy number was also evaluated by fluorescent in situ hybridization in those lesions. The expected results defined the origin cell for basal cell hyperplasia and squamous metaplasia as adaptative lesions and dysplasia. By known experiences and published data, beyond the stem cell, the spectral evolution of bronchial preneoplastic lesions was demonstrated by characterizing basal cells (LP34) and their neoplastic potentiality. Dysplasias showed a higher expression of EGFR, Ki67 and p53 with a stepwise increase with the gravity of the respective grading. C-erbB-2 immunohistochemical overexpression was a rare event in preneoplastic lesions. Polysomy was the main mechanism for EGFR and HER2/ neu higher gene copy number and together with increased proliferation index (Ki67) will account to preview bronchial carcinogenesis.

Immune-mediated necrotizing myopathies (IMNM) are recognized as a subgroup of idiopathic inflammatory myopathies (IIM). IMNM are defined based on a combination of clinical presentation and laboratory studies, requiring a specific myopathological pattern on muscle biopsy for diagnosis. The authors describe a case of a patient with necrotizing myopathy, thought to be immune mediated, highlighting the challenge of its differential diagnosis. As clinical assessment and diagnostic tools sometimes fail to determine whether a necrotizing myopathy is immune mediated, leading to misdiagnosis and a compromise of the optimal therapeutic approach, distinguishing between IMNM and other myopathies is crucial.

Introduction. Superior vena cava (SVC) syndrome results from the obstruction of blood flow through the SVC, having distinct pathophysiological underlying mechanisms. Cancer is associated with an increased risk of thromboembolism that varies according to patient-, tumor-, and treatment-related factors. An individualized clinical approach is important to pursue the accurate diagnosis of the underlying pathology causing thromboembolism in cancer patients. Case Presentation. The authors present a case of a 58-year-old male with an infrequent presentation of an unknown colon carcinoma, who has never had any symptom until he was hospitalized with the diagnosis of superior vena cava syndrome and pulmonary thromboembolism. The patient had an advanced disease by the time of diagnosis and molecular alterations contributing to abnormal hemostasis. He presented venous and arterial thromboembolism and developed disseminated intravascular coagulopathy after surgery, anticoagulant and transfusion therapy, dying 40 days after the hospitalization. Conclusion. The authors discuss thromboembolic disease and tumor metastasis roles in a cancer patient with SVC syndrome. Thromboembolism in a malignancy context is a challenging clinical entity. A multifactorial perspective of the thrombotic disease is warranted to approach thromboembolism risk and stratify patients suitable to receive adequate anticoagulant prophylaxis and targeted therapies, aiming to improve clinical prognosis.

A prognostic interpretation of preneoplastic lesions would have impact in bronchial carcinoma early diagnosis and through the study of Erb-B family receptors as they have an important role in lung carcinogenesis. The existence of drugs as tirosine kinase inhibitors (TKis) stressed the importance of studying gene alterations for selected chemoprevention schemes and characterization of carcinogenesis.Bronchial preneoplastic lesions were characterized by immunohistochemistry using the antibodies LP34 (high weigh molecular cytokeratin), CK7, Chromogranin A, Ki67, p53, C-erbB-2 and EGFR. HER2 and EGFR gene copy number was also evaluated by fluorescent in situ hybridization (FISH) in those lesions.The expected results defined the origin cell for basal cell hyperplasia and squamous metaplasia as adaptative lesions and dysplasia. By known experiences and published data, beyond the stem cell, the spectral evolution of bronchial preneoplastic lesions was demonstrated by characterizing basal cells (LP34) and their neoplastic potentiality.Dysplasias showed a higher expression of EGFR, Ki67 and p53 with a stepwise increase with the gravity of the respective grading. C-erbB-2 immunohistochemical overexpression was a rare event in preneoplastic lesions. Polysomy was the main mechanism for EGFR and HER2/neu higher gene copy number and together with increased proliferation index (Ki67) will account to preview bronchial carcinogenesis.

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