Risk Factors of Ovarian Cancer in PKU Muhammadiyah Teaching Hospital Yogyakarta

Introduction: Ovarian cancer is non-communicable diseases that has a high mortality rate. In PKU Muhammadiyah Teaching Hospital Yogyakarta in 2014-2017, ovarian cancer is 5th out of all types cancers diagnosed. Most of them are asymptomatic in early stage and come to hospital at late stage. Recognize and identify the risk factors of ovarian cancer are very important to prevent the patient from morbidity and mortality. The purpose of this study was to know the relationship between low parity, infertility, age, and family history with ovarian cancer in PKU Muhammadiyah Teaching  Hospital Yogyakarta.Methods: This study was an observational analytical study with cross sectional design. The sample was medical record of women with ovarian cancer and non ovarian cancer in PKU Muhammadiyah Teaching Hospital Yogyakarta period of April 2014-September 2017 with inclusion and exclusion criteria. Data analysis used chi-square test.Result: The bivariat analysis showed that there is no relationship between low parity with ovarian cancer (p=0,790 OR=0,87; 95% CI 0,305-2,466), there is no relation between infertility with ovarian cancer (p=0,104 OR=2,48; 95% CI 0,815-7,545), and there is no relation between family history with ovarian cancer (p=0,304 OR=3,18; 95% CI 0,315-32,039). But there is a relationship between age with ovarian cancer (p=0,01 OR=0,11; 95% CI 0,022-0,510).Conclusion: There are no relations between low parity, infertility, and family history with ovarian cancer. But there is a relationship between age with ovarian cancer

In vivo tumor cell adhesion in the pulmonary microvasculature is exclusively mediated by tumor cell - endothelial cell interaction

<p>Abstract</p> <p>Background</p> <p>Metastasis formation is the leading cause of death among colon cancer patients. We established a new in-situ model of in vivo microscopy of the lung to analyse initiating events of metastatic tumor cell adhesion within this typical metastatic target of colon cancer.</p> <p>Methods</p> <p>Anaesthetized CD rats were mechanically ventilated and 10⁶human HT-29LMM and T84 colon cancer cells were injected intracardially as single cell suspensions. Quantitative in vivo microscopy of the lung was performed in 10 minute intervals for a total of 40 minutes beginning with the time of injection.</p> <p>Results</p> <p>After vehicle treatment of HT-29LMM controls 15.2 ± 5.3; 14.2 ± 7.5; 11.4 ± 5.5; and 15.4 ± 6.5 cells/20 microscopic fields were found adherent within the pulmonary microvasculature in each 10 minute interval. Similar numbers were found after injection of the lung metastasis derived T84 cell line and after treatment of HT-29LMM with unspecific mouse control-IgG. Subsequently, HT-29LMM cells were treated with function blocking antibodies against β1-, β4-, and αv-integrins wich also did not impair tumor cell adhesion in the lung. In contrast, after hydrolization of sialylated glycoproteins on the cells' surface by neuraminidase, we observed impairment of tumor cell adhesion by more than 50% (p < 0.05). The same degree of impairment was achieved by inhibition of P- and L-selectins via animal treatment with fucoidan (p < 0.05) and also by inhibition of the Thomson-Friedenreich (TF)-antigen (p < 0.05).</p> <p>Conclusions</p> <p>These results demonstrate that the initial colon cancer cell adhesion in the capillaries of the lung is predominantly mediated by tumor cell - endothelial cell interactions, possibly supported by platelets. In contrast to reports of earlier studies that metastatic tumor cell adhesion occurs through integrin mediated binding of extracellular matrix proteins in liver, in the lung, the continuously lined endothelium appears to be specifically targeted by circulating tumor cells.</p

SERPINB5 and AKAP12 -- Expression and promoter methylation of metastasis suppressor genes in pancreatic ductal adenocarcinoma

<p>Abstract</p> <p>Background</p> <p>Early metastasis and infiltration are survival limiting characteristics of pancreatic ductal adenocarcinoma (PDAC). Thus, PDAC is likely to harbor alterations in metastasis suppressor genes that may provide novel diagnostic and therapeutic opportunities. This study investigates a panel of metastasis suppressor genes in correlation to PDAC phenotype and examines promoter methylation for regulatory influence on metastasis suppressor gene expression and for its potential as a diagnostic tool.</p> <p>Methods</p> <p>Metastatic and invasive potential of 16 PDAC cell lines were quantified in an orthotopic mouse model and mRNA expression of 11 metastasis suppressor genes determined by quantitative RT-PCR. Analysis for promoter methylation was performed using methylation specific PCR and bisulfite sequencing PCR. Protein expression was determined by Western blot.</p> <p>Results</p> <p>In general, higher metastasis suppressor gene mRNA expression was not consistent with less aggressive phenotypes of PDAC. Instead, mRNA overexpression of several metastasis suppressor genes was found in PDAC cell lines vs. normal pancreatic RNA. Of the investigated metastasis suppressor genes, only higher <it>AKAP12 </it>mRNA expression was correlated with decreased metastasis (P < 0.05) and invasion scores (P < 0.01) while higher <it>SERPINB5 </it>mRNA expression was correlated with increased metastasis scores (P < 0.05). Both genes' promoters showed methylation, but only increased <it>SERPINB5 </it>methylation was associated with loss of mRNA and protein expression (P < 0.05). <it>SERPINB5 </it>methylation was also directly correlated to decreased metastasis scores (P < 0.05).</p> <p>Conclusions</p> <p><it>AKAP12 </it>mRNA expression was correlated to attenuated invasive and metastatic potential and may be associated with less aggressive phenotypes of PDAC while no such evidence was obtained for the remaining metastasis suppressor genes. Increased <it>SERPINB5 </it>mRNA expression was correlated to increased metastasis and mRNA expression was regulated by methylation. Thus, <it>SERPINB5 </it>methylation was directly correlated to metastasis scores and may provide a diagnostic tool for PDAC.</p

Strategien bei der Anlage in auslaendischen festverzinslichen Wertpapieren

Goettingen, Univ., Diss., 1994Available from Bibliothek des Instituts fuer Weltwirtschaft, ZBW, Duesternbrook Weg 120, D-24105 Kiel A 205945 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

Economic Perspective of Cancer Care and Its Consequences for Vulnerable Groups

Within healthcare systems in all countries, vulnerable groups of patients can be identified and are characterized by the reduced utilization of available healthcare. Many different reasons can be attributed to this observation, summarized as implementation barriers involving acceptance, accessibility, affordability, acceptability and quality of care. For many patients, cancer care is specifically associated with the occurrence of vulnerability due to the complex disease, very different target groups and delivery situations (from prevention to palliative care) as well as cost-intensive care. Sociodemographic factors, such as educational level, rural/remote location and income, are known determinants for these vulnerable groups. However, different forms of financial burdens likely influence this vulnerability in cancer care delivery in a distinct manner. In a narrative review, these socioeconomic challenges are summarized regarding their occurrence and consequences to current cancer care. Overall, besides direct costs such as for treatment, many facets of indirect costs including survivorship costs for the cancer patients and their social environment need to be considered regarding the impact on vulnerability, treatment compliance and abundance. In addition, individual cancer-related financial burden might also affect the society due to the loss of productivity and workforce availability. Healthcare providers are requested to address this vulnerability during the treatment of cancer patients