Risk Factors for Lung Cancer Mortality in a Referral Center.

BACKGROUND: Lung cancer is one of the most common causes of death that is rising in many countries including Iran. This study aimed to determine the impact of factors on survival of lung cancer patients at a referral center of lung diseases in Tehran, Iran. MATERIALS AND METHODS: A retrospective study was conducted on adult lung cancer cases admitted to a referral center for lung diseases from 2011 to 2015. Multivariate analysis was performed to determine the risk factors for all-cause mortality. RESULTS: Of a total 933 patients with lung cancer, 53.4% died, 49.3% of them at the hospital. Overall median follow-up time was 7 months. The most common histological type of cancer was adenocarcinoma with a 13 month median survival time. Age ≥55 and smoking remained significant for all-cause mortality on Cox analysis, whereas gender was not. CONCLUSIONS: The survival of lung cancer patients is poor and the patients with history of smoking and age ≥55 are at increased risk of death. Having a large hospital-based registry provides a good measurement of prognostic statistics for lung cancer. Further investigations are necessary to establish reasons for mortality.

Epstein-Barr virus burden in adolescents with systemic lupus erythematosus.

OBJECTIVE: We sought to determine whether patients with systemic lupus erythematosus (SLE) and a presumed primary or reactivated Epstein-Barr virus (EBV) serologic response had evidence of an active EBV infection. BACKGROUND: Patients with SLE often have what appears to be a primary or reactivated EBV serologic response. If these patients then present with fever, fatigue, adenopathy or leukopenia, it is not clear whether these symptoms are caused by worsening SLE or EBV infection. Establishing the correct diagnosis is crucial for management. METHODS: We examined the EBV burden in 13 adolescents with SLE and a presumed primary or reactivated EBV serologic response. All were taking prednisone; 2 each were also on azathioprine or intravenous pulse cyclophosphamide. EBV serologies were performed for all, and EBV burdens were assessed via immortalization assays and EBV DNA amplification of blood and saliva at least once. RESULTS: Seven patients had serologic patterns indicative of a primary EBV infection, while six had serologies indicative of a reactivated (secondary) EBV infection. Two of the latter were the only ones in whom a small amount of biologically active EBV was detected. CONCLUSION: In our series active EBV infection was not seen in most patients, despite serologic data that could be interpreted as a primary or reactivated infection. Thus the serologic profiles were more likely a consequence of immune dysregulation secondary to SLE or its therapy rather than rampant infection with EBV.

Subcutaneous metastasis from transitional cell carcinoma of the bladder diagnosed by fine needle aspiration biopsy. A case report.

BACKGROUND: Metastasis of transitional cell carcinoma (TCC) of the bladder to the skin and subcutaneous tissue is an uncommon finding. CASE: A 58-year-old man with a known case of high grade TCC of the bladder, presented with a right paraspinal mass. Clinically an abscess was suspected. Fine needle aspiration (FNA) showed many clusters and isolated malignant cells in an inflammatory background. The smears were diagnosed as positive for malignancy. CONCLUSION: It is essential to differentiate tumors metastatic to the skin and subcutaneous tissue from inflammatory lesions. FNA helped with the diagnosis in this case and prevented unnecessary biopsy.

CD8+ T cell-mediated suppression of human immunodeficiency virus replication in older children with acquired immunodeficiency syndrome.

BACKGROUND: Suppression of HIV replication by CD8+ T cells and/or their products correlated with the survival of infants. We sought to elucidate the role of CD8+ T cell-mediated suppression in seven older children with AIDS. METHODS: After separation of each child's CD4+ and CD8+ T cells, three different HIV culture assays were performed: (1) patient CD4+ T cells and phytohemagglutinin (PHA)-stimulated donor peripheral blood mononuclear cells (PBMC); (2) patient CD8+ T cells added to the CD4+ T cells and the PHA-stimulated donor PBMC (to test for CD8-mediated T cell suppression of HIV); (3) patient CD8+ cells added across a semipermeable membrane to the CD4+ T cells and the PHA-stimulated donor PBMC [to determine whether the CD8 cells secreted a soluble factor(s) that suppressed HIV]. RESULTS: Cultures from four of seven children showed greater HIV replication with CD4 cells alone than with CD4 and CD8 cells together, demonstrating CD8 suppression; evidence of soluble suppression was also seen. Cultures from two of the seven children showed HIV replication and no evidence of CD8 cell suppression. Cultures from one of the seven children had no appreciable replication of HIV even after removal of CD8 cells. CONCLUSIONS: CD8-mediated suppression is present in at least some children with AIDS. Additional mechanisms may be operating to slow the progression of the disease.

Epstein-Barr virus-infected marmoset cells transfected with c-myc do not form lymphomas in mice with severe combined immunodeficiency.

Epstein-Barr virus (EBV) has been associated with several malignant processes in man, most notably Burkitt lymphoma in previously healthy individuals and lesions resembling large cell non-Hodgkin lymphomas in organ transplant recipients. Mice with the severe combined immunodeficiency phenotype (SCID mice) are exquisitely susceptible to the development of EBV-associated lymphoproliferative lesions following the intraperitoneal (ip) inoculation of EBV-infected human lymphocytes. Recently, we reported that EBV-infected marmoset lymphocytes do not form lymphomas in SCID mice following ip injection, while human lymphocytes infected with the same EBV strains do. On the assumption that the EBV-infected marmoset cells were lacking a factor necessary for tumor formation, we transfected a plasmid containing c-myc into EBV-infected marmoset cells (B95-8, FF41, and W91 cells). Despite expression of the c-myc protein as determined by immunoblot and flow cytometry when probed with a monoclonal antibody, no increase over baseline lesion development was seen in SCID mice inoculated with 5 x 10(6) c-myc-expressing marmoset lymphoblastoid cells. Thus, cells that express c-myc and harbor EBV are not sufficient to form lymphomas in certain immunocompromised hosts.

Potential in vitro activity of Kutapressin against Epstein-Barr virus.

BACKGROUND: Kutapressin (KU), a porcine liver extract with bradykinin-potentiating effects but no vitamin B 12 activity, has been used in the treatment of Herpes zoster. We examined a phenol-free preparation of this drug for in vitro activity against Epstein-Barr Virus (EBV). MATERIALS AND METHODS: Immortalization-inhibition assays were used to assess EBV infectivity. Mitogen stimulation and cell viability assays were used to assess kutapression toxicity. Lytic replication assays and flow cytometry were used to assess the mechanism of drug activity. RESULTS: Seventy-five hundred mcg/ml of KU blocked the infection of 2 x 10(5) human umbilical cord mononuclear cells when added together with two strains of EBV (B95-8 and FF41). Doses as low as 250 mcg/ml were occasionally effective as well. Unlike acyclovir, KU does not inhibit viral DNA polymerase nor does it appear to compete with EBV as it binds to its receptor on the B-cell surface. CONCLUSIONS: The mechanism whereby KU may inhibit EBV immortalization remains to be determined. KU, a drug which is safe in humans, deserves further study as an agent with potential to block EBV-induced immortalization of B-lymphocytes.

Epstein-Barr virus-infected marmoset cells do not form lymphomas in mice with severe combined immunodeficiency.

EBV has been associated with several malignancies in humans. EBV can also infect marmoset B lymphocytes, which, as opposed to human B cells, are permissive for lytic Epstein-Barr viral replication. Mice with a severe combined immunodeficiency phenotype (SCID mice) are extremely susceptible to EBV-induced lymphomagenesis when inoculated with EBV-infected lymphocytes. We inoculated SCID mice with human and marmoset lymphoblastoid cells infected with the same EBV isolates. The marmoset cells never gave rise to lymphomas, even after the administration of acyclovir or an anti-natural killer cell antibody and observation periods of up to 16 wk. In contrast, the human lymphoblastoid cells nearly always gave rise to lymphomas within 8 wk. Furthermore, human lymphoblastoid cells genetically engineered to permit lytic EBV replication also readily formed tumors in the SCID mouse. Thus, in this system, it is the cellular milieu that is crucial in determining whether a given lymphoblastoid cell will give rise to a tumor, not the EBV isolate harbored by the cell or whether the virus is permitted to undergo lytic replication.

The role of natural-killer-cells in the pathogenesis of epstein-barr virus-associated burkitt-lymphoma in a scid mouse model.

Epstein-Barr virus (EBV) is associated with both benign and malignant lymphoproliferative processes. Recently, mice with severe combined immunodeficiency (SCID) have been described that develop EBV-induced lymphomas when inoculated with peripheral blood lymphocytes from EBV-seropositive individuals. To investigate the pathogenesis of EBV-associated Burkitt lymphomas, we intraperitoneally inoculated SCID mice with cells from EBV-infected Burkitt lymphoma (BL) cell lines. In general, cells from BL lines developed into BL-like tumors. Certain BL cell lines, however, were not particularly tumorigenic in these animals. Antibody capable of depleting mice of natural killer cells (anti-asialo GM1) favored the development of these Burkitt lymphomas. The pathogenetic implications of this animal model for human disease is discussed.