Unraveling the Influence of Social, Economic, and Demographic Factors in Texas on Breast Cancer Survival.

Background: According to the Centers for Disease Control (CDC), breast cancer is the second most common cancer among women in the United States. Affected people are financially challenged due to the high out-of-pocket cost of breast cancer treatment, as it is the most expensive treatment. Using a 16-year cohort study of breast cancer survival data in Texas, we investigate the factors that might explain why some breast cancer patients live longer than others. Methods: Performing a survival analysis consisting of the log-rank test, a survival time regression, and Cox proportional hazards regression, we explore the breast cancer survivors' specific attributes to identify the main determinants of survival time. Results: Analyses show that the factors: stage, grade, primary site of the cancer, number of cancers each patient has, histology of the cancer, age, race, and income are among the main variables that enlighten why some breast cancer survivors live much longer than others. For instance, compared to White non-Hispanics, Black non-Hispanics have a shorter length of survival with a hazard ratio of (1.282). The best prognostic for White non-Hispanics, Hispanics (all races), and Black non-Hispanics is a woman aged between 40 to 49 years old, diagnosed with localized stage and grade one with Axillary tail of breast as a primary site with only one cancer and with a household income of 75,000.00 and over. Conclusion: Policymakers should promote early diagnosis and screening and better assist the older and the poor to improve the survival time for breast cancer patients.

HHV-8-Associated Multicentric Castleman Disease, a Diagnostic Challenge in a Patient With Acquired Immunodeficiency Syndrome and Fever.

Patients with acquired immunodeficiency syndrome (AIDS) are at an increased susceptibility to pathogens and associated malignancies which can present with a unique constellation of symptoms. In this article, we describe a case of Castleman disease in a patient with AIDS, nonadherent with antiretroviral therapy (ART), who presented with fevers, constant abdominal pain, nausea, and vomiting. After an extensive work up, a lymph node biopsy confirmed a diagnosis of human herpesvirus-8 (HHV-8)-associated multicentric Castleman disease. Patients presenting with AIDS and fever have broad differential diagnoses; therefore, reaching a diagnosis as rare as Castleman disease can be challenging. HHV-8 has a propensity to CD20 positive B cells, which allows rituximab to be an effect treatment.

AAV2/8-hSMAD3 gene delivery attenuates aortic atherogenesis, enhances Th2 response without fibrosis, in LDLR-KO mice on high cholesterol diet.

BACKGROUND: Inflammation is a key etiologic component in atherogenesis and transforming growth factor beta 1 (TGFß1) is a well known anti-inflammatory cytokine which potentially might be used to limit it. Yet TGFß1 is pleiomorphic, causing fibrosis, cell taxis, and under certain circumstances, can even worsen inflammation. SMAD3 is an important member of TGFß1's signal transduction pathway, but is a fully intracellular protein. OBJECTIVES: With the hope of attenuating TGFß1's adverse systemic effects (eg. fibrosis) and accentuating its anti-inflammatory activity, we proposed the use of human (h)SMAD3 as an intracellular substitute for TGFß1. STUDY DESIGN: To test this hypothesis adeno-associated virus type 2/8 (AAV)/hSMAD3 or AAV/Neo (control) was tail vein injected into the low density lipoprotein receptor knockout (LDLR-KO) mice, then placed on a high-cholesterol diet (HCD). RESULTS: The hSMAD3 delivery was associated with significantly lower atherogenesis as measured by larger aortic cross sectional area, thinner aortic wall thickness, and lower aortic systolic blood velocity compared with Neo gene-treated controls. HSMAD3 delivery also resulted in fewer aortic macrophages by immunohistochemistry for CD68 and ITGAM, and quantitative reverse transcriptase polymerase chain reaction analysis of EMR and ITGAM. Overall, aortic cytokine expression showed an enhancement of Th2 response (higher IL-4 and IL-10); while Th1 response (IL-12) was lower with hSMAD3 delivery. While TGFß1 is often associated with increased fibrosis, AAV/hSMAD3 delivery exhibited no increase of collagen 1A2 or significantly lower 2A1 expression in the aorta compared with Neo-delivery. Connective tissue growth factor (CTGF), a mediator of TGFß1/SMAD3-induced fibrosis, was unchanged in hSMAD3-delivered aortas. In the liver, all three of these genes were down-regulated by hSMAD3 gene delivery. CONCLUSION: These data strongly suggest that AAV/hSMAD3 delivery gave anti-atherosclerosis therapeutic effect without the expected undesirable effect of TGFß1-associated fibrosis.

Hair depigmentation during chemotherapy with dasatinib, a dual Bcr-Abl/Src family tyrosine kinase inhibitor.

Hair depigmentation has been shown to occur with disruption of the interaction between the ligand stem cell factor (SCF) with its class III receptor tyrosine kinase c-kit, also called the stem cell factor receptor. This article reports the case of a patient who experienced depigmentation of her eyelashes, eyebrows, and temporal scalp hair six-to-eight weeks after initiating treatment with dasatinib (BMS-354825 or Sprycel), a novel dual Bcr-Abl/Src family tyrosine kinase inhibitor for chronic myeloid leukemia (CML). This case illustrates a previously unreported side-effect of dasatinib that is most likely due to the drug's inhibition of the c-kit, Src family, and platelet-derived growth factor receptor beta (PDGFRbeta) tyrosine kinases. Further study of hair depigmentation as a side effect of multi-kinase inhibitors can provide useful information on hair and melanocyte physiology.

Plasma cell granuloma: a case report of multiple lesions in the lung and review of the literature.

BACKGROUND: Although plasma cell granuloma is a rare tumor in the lung, it must be considered in the differential diagnosis of lung cancer. It typically presents as a solitary lesion. Involvement with multiple lesions can be a presenting picture of plasma cell granuloma; however, the incidence is much lower than that of a solitary lesion. PROCEDURES AND FINDINGS: A 35-year-old man was evaluated for intermittent chest pain over a 6-year period. CT showed the presence of one mass and three nodules in the left lung. The initial diagnosis was metastatic lung cancer. CT guided biopsy suggested the diagnosis of plasma cell granuloma. All the lesions were resected with a thoracotomy procedure. Pathology evaluation confirmed the diagnosis. For the 3 years he received follow-up care, he remained asymptomatic. CONCLUSIONS: Multiple lung nodules or masses can be a presenting manifestation of plasma cell granuloma. It should be differentiated from metastatic neoplasm. Surgery resection is the treatment of choice.

Sperm protein 17 expression defines 2 subsets of primary esthesioneuroblastoma.

Esthesioneuroblastomas (ENBs) are rare malignant tumors of the nasal vault, the origin, diagnosis, and management of which are still subjects of discussion. That there is no related prognostic factor or generally recognized therapeutic regimen highlights the need for further analyses of its underlying biologic features and investigations of new marker proteins that allow more reliable clinical testing. We here show that sperm protein 17 (Sp17) is expressed in the ciliated cells of the normal olfactory epithelium and in a proportion of primary ENB lesions. We found an association between Sp17 expression and metastases at relapse (P = .035), chromogranin expression (P = .014), and a female sex prevalence. A statistically nonsignificant relation was found between Sp17 and S-100, synaptophysin, and neurofilament expression. No correlation was also found between Sp17 expression and the proliferative capacity of the lesion that was evaluated by Ki-67 immunohistochemistry. The results of this study show the usefulness of Sp17 as a means of discriminating 2 subsets of primary ENB lesions and seem to suggest the existence of 2 distinct cell pathways in their origin and development.