24 research outputs found

    Effect of ploidy, recruitment, environmental factors, and tamoxifen treatment on the expression of sigma-2 receptors in proliferating and quiescent tumour cells

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    Recently, we demonstrated that sigma-2 receptors may have the potential to be a biomarker of tumour cell proliferation (Mach et al (1997) Cancer Res57: 156–161). If sigma-2 receptors were a biomarker of tumour cell proliferation, they would be amenable to detection by non-invasive imaging procedures, thus eliminating many of the problems associated with the flow cytometric measures of tumour cell proliferation presently used in the clinic. To be a good biomarker of tumour cell proliferation, the expression of sigma-2 receptors must be essentially independent of many of the biological, physiological, and/or environmental properties that are found in solid tumours. In the investigation reported here, the mouse mammary adenocarcinoma lines, 66 (diploid) and 67 (aneuploid), 9L rat brain tumour cells, and MCF-7 human breast tumour cells were used to study the extent and kinetics of expression of sigma-2 receptors in proliferative (P) and quiescent (Q) tumour cells as a function of species, cell type, ploidy, pH, nutrient depletion, metabolic state, recruitment from the Q-cell compartment to the P-cell compartment, and treatment with tamoxifen. In these experiments, the expression of sigma-2 receptors solely reflected the proliferative status of the tumour cells. None of the biological, physiological, or environmental properties that were investigated had a measurable effect on the expression of sigma-2 receptors in these model systems. Consequently, these data suggest that the proliferative status of tumours and normal tissues can be non-invasively assessed using radiolabelled ligands that selectively bind sigma-2 receptors. © 1999 Cancer Research Campaig

    Willingness to pay for cancer genetic testing in a tertiary healthcare centre

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    Increasing use of predictive genetic testing to address hereditary cancer risk has been commonly assessed by cost sharing practices. Little is known about how demographics, knowledge, attitude and practices may influence these individuals’ willingness to pay for cancer genetic testing. The objective of this research was to determine factors associated with willingness to pay for cancer genetic testing. A self-administered questionnaire was distributed to 175 respondents in the oncology and day care unit in one of tertiary healthcare centre. The respondents comprised cancer patients, their family members and the community. A total of 117 (66.9%) participants were willing to pay for cancer genetic testing. Ninety three (79.5%) of respondents were willing to pay from their own pocket with a mean of MYR1201.77 (SD976.72) and 95 (54.3%) respondents were willing to pay, shared with insurance. There were significant associations between willingness to pay with status of respondent as patients or family members or community, gender, race, educational level, income, knowledge and attitude. This is the first study to evaluate factors associated with willingness to pay not only among cancer patients but also their family members and the community. These findings reveal that majority of respondents believe there is valuable personal benefit based on genetic risk information and they are willing to pay for it

    Willingness to pay for cancer genetic testing in a tertiary healthcare centre

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    INTRODUCTION: Increasing use of predictive genetic testing to address hereditary cancer risk has been commonly assessed by cost sharing practices. Little is known about how demographics, knowledge, attitude and practices may influence these individuals’ willingness to pay for cancer genetic testing. The objective of this research was to determine factors associated with willingness to pay for cancer genetic testing. MATERIALS AND METHODS: A self-administered questionnaire was distributed to 175 respondents in the oncology and day care unit in one of tertiary healthcare centre. The respondents comprised cancer patients, their family members and the community. RESULTS: A total of 117 (66.9%) participants were willing to pay for cancer genetic testing. Ninety three (79.5%) of respondents were willing to pay from their own pocket with a mean of MYR1201.77 (SD976.72) and 95 (54.3%) respondents were willing to pay, shared with insurance. There were significant associations between willingness to pay with status of respondent as patients or family members or community, gender, race, educational level, income, knowledge and attitude. CONCLUSION: This is the first study to evaluate factors associated with willingness to pay not only among cancer patients but also their family members and the community. These findings reveal that majority of respondents believe there is valuable personal benefit based on genetic risk information and they are willing to pay for it

    Clinical and biochemical features of aromatic L-amino acid decarboxylase deficiency

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    none25siObjective: To describe the current treatment; clinical, biochemical, and molecular findings; and clinical follow-up of patients with aromatic l-amino acid decarboxylase (AADC) deficiency. Method: Clinical and biochemical data of 78 patients with AADC deficiency were tabulated in a database of pediatric neurotransmitter disorders (JAKE). A total of 46 patients have been previously reported; 32 patients are described for the first time. Results: In 96% of AADC-deficient patients, symptoms (hypotonia 95%, oculogyric crises 86%, and developmental retardation 63%) became clinically evident during infancy or childhood. Laboratory diagnosis is based on typical CSF markers (low homovanillic acid, 5-hydroxyindoleacidic acid, and 3-methoxy-4-hydroxyphenolglycole, and elevated 3-O-methyl-l-dopa, l-dopa, and 5-hydroxytryptophan), absent plasma AADC activity, or elevated urinary vanillactic acid. A total of 24 mutations in the DDC gene were detected in 49 patients (8 reported for the first time: p.L38P, p.Y79C, p.A110Q, p.G123R, p.I42fs, c.876G>A, p.R412W, p.I433fs) with IVS6+ 4A>T being the most common one (allele frequency 45%). Conclusion: Based on clinical symptoms, CSF neurotransmitters profile is highly indicative for the diagnosis of aromatic l-amino acid decarboxylase deficiency. Treatment options are limited, in many cases not beneficial, and prognosis is uncertain. Only 15 patients with a relatively mild form clearly improved on a combined therapy with pyridoxine (B6)/pyridoxal phosphate, dopamine agonists, and monoamine oxidase B inhibitors.Erratum in Neurology. 2010 Aug 10;75(6):576. Dosage error in article textmixedBrun L; Ngu LH; Keng WT; Ch'ng GS; Choy YS; Hwu WL; Lee WT; Willemsen MA; Verbeek MM; Wassenberg T; Régal L; Orcesi S; Tonduti D; Accorsi P; Testard H; Abdenur JE; Tay S; Allen GF; Heales S; Kern I; Kato M; Burlina A; Manegold C; Hoffmann GF; Blau N.Brun, L; Ngu, Lh; Keng, Wt; Ch'Ng, Gs; Choy, Ys; Hwu, Wl; Lee, Wt; Willemsen, Ma; Verbeek, Mm; Wassenberg, T; Régal, L; Orcesi, S; Tonduti, D; Accorsi, P; Testard, H; Abdenur, Je; Tay, S; Allen, Gf; Heales, S; Kern, I; Kato, M; Burlina, A; Manegold, C; Hoffmann, Gf; Blau, N

    The Cockayne Syndrome Natural History (CoSyNH) study: clinical findings in 102 individuals and recommendations for care

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    Manuscrito. -- 2 h.; papel; folio. -- Fondo Universidad de Salamanca; sección Claustros; serie Borradores de claustros. -- Buena conservación. -- Fechas: 06/07/1780
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