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Biomedical subjects

Susanne B Haga

Publications and source records attributed to Susanne B Haga.

10 recordsLinked to original sources
PubMed2006

Prescribing BiDil: is it black and white?

The approval of BiDil as an adjunct treatment in self-identified blacks with heart failure raises questions regarding the underlying etiology of drug response in this target population and the ability to accurately identify patients who are most likely to benefit. Preliminary data have indicated that differences in nitric oxide synthesis between groups may account for differences in response to BiDil and genetic studies have begun to elucidate the mechanism of these differences. Until more accurate selection criteria are developed to identify patients who are most likely to benefit, both clinicians and the general public will need to consider the unique issues raised by BiDil.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Teaching resources for genetics.

Genetics education is essential for preparing the public to engage in an informed debate about the future of genetics research and how its applications affect human health and the environment. This article provides an overview of genetics education resources that are available online, and is relevant to students in secondary education, health professionals, geneticists and the public. It also describes an integrated approach to teaching genetics, emphasizes the need for continuing teacher education, and encourages the involvement of geneticists and health professionals in providing a teaching resource.

Computer-Assisted Instruction↗
PubMed2006

Defining the spectrum of genome policy.

Many achievements in the genome sciences have been facilitated by policies that have prioritized genome research, secured funding and raised public and health-professional awareness. Such policies should address ethical, legal and social concerns, and are as important to the scientific and commercial development of the field as the science itself. On occasion, policy issues take precedence over science, particularly when impasses are encountered or when public health or money is at stake. Here we discuss the spectrum of current issues and debates in genome policy, and how to actively engage all affected stakeholders to promote effective policy making.

Advisory Committees↗
PubMed2006

Adding pharmacogenetics information to drug labels: lessons learned.

The US Food and Drug Administration approved a revised package insert for two cancer drugs to include information about the increased risk of severe adverse events owing to enzyme deficiencies caused by genetic variants. The label revisions stopped short of recommending or requiring pharmacogenetic testing prior to or following an adverse event. Despite (or because of) the lack of specific recommendations, we believe the actions taken by US Food and Drug Administration will have implications for pharmacogenetics research, clinical integration, and other policy considerations. We review the reasons behind the cautious label changes and discuss some of the lessons that can be learned from these experiences.

Antineoplastic Agents↗
PubMed2006

Translating genomic biomarkers into clinically useful diagnostics.

The landmark sequencing of the human genome has ushered in a new field of large-scale research. Advances in understanding the molecular basis of disease have opened up new opportunities to develop genomics-based tools to diagnose, predict disease onset or recurrence, tailor treatment options, and assess treatment response. Although still in the early stages of research and development, genomic biomarker research has the capability of providing a comprehensive insight into pathophysiological processes as well as more precise predictors of outcome not previously attainable with traditional biomarkers. Before genomic biomarkers are incorporated into clinical practice, several issues will need to be addressed in order to generate the necessary levels of evidence to demonstrate analytical and clinical validity and utility. In addition, efforts will be needed to educate health professionals and the public about genomics-based tools, revise regulatory oversight mechanisms, and ensure privacy safeguards of the information generated from these new tests.

Biomarkers↗
PubMed2003

Genetics. FDA races in wrong direction.

Despite recent genetic evidence and the promise of individualized medicine, there is a continuing interest in using self-identified categories of race and ethnicity as variables in scientific and medical research. The U.S. Food and Drug Administration recently proposed a standardized approach for the collection of race and ethnicity data in clinical trials. We believe that this move fails to acknowledge new scientific data and recommend that relevant data from individuals be collected and used rather than broad group statistics. We also encourage that increased funding be committed to this important issue.

Clinical Trials as Topic↗
PubMed2002

BP1, a homeodomain-containing isoform of DLX4, represses the beta-globin gene.

In earlier studies we identified a putative repressor of the human beta-globin gene, termed beta protein 1 (BP1), which binds to two silencer DNA sequences upstream of the adult human beta-globin gene and to a negative control region upstream of the adult delta-globin gene. Further studies demonstrated an inverse correlation between the binding affinity of the BP1 protein for the distal beta-globin silencer sequence and the severity of sickle cell anemia, suggesting a possible role for BP1 in determining the production of hemoglobin S. We have now cloned a cDNA expressing the BP1 protein. Sequencing revealed that BP1 is a member of the homeobox gene family and belongs to the subfamily called Distal-less (DLX), genes important in early development. Further analysis showed that BP1 is an isoform of DLX4. BP1 protein has repressor function towards the beta-globin promoter, acting through the two beta-globin DNA silencers, demonstrated in transient transfection assays. Strong BP1 expression is restricted to placenta and kidney tissue, with no expression in 48 other human tissues. BP1 exhibits regulated expression in the human erythroid cell line MB-02, where its expression decreases upon induction of the beta-globin gene. BP1 is thus the first member of the DLX family with known DNA binding sites and a function in globin gene regulation.

Adult↗