Longer Times of Receipt of Adjuvant Endocrine Therapy Correspond to Improved Functional Capacity and Lower Adiposity in Women Receiving Adjuvant Therapy

Purpose

To study the use of functional capacity (FC) level and duration of aromatase inhibitor (AI) therapy with adiposity parameters in women with breast cancer.

Salvage treatment of disseminated strongyloidiasis in an immunocompromised patient: therapy success with subcutaneous ivermectin

Disseminated strongyloidiasis is a disease with high mortality rate, especially in immunocompromised individuals. Paralytic ileus and intestinal malabsorption are frequent symptoms caused by this severe disease. As there are no licensed parenteral anthelmintic drugs for human use, off-label formulations are often used in the treatment of this disease. In this case report, the use of subcutaneous ivermectin is described as a successful therapy for this life-threatening infection.     

In utero origin of t(8;21) AML1-ETO translocations in childhood acute myeloid leukemia

Recent reports have established the prenatal origin of leukemia translocations and resultant fusion genes in some patients, including MLL-AF4 translocations in infants and TEL-AML1 translocations in children. We now report evidence for the prenatal origin of a translocation in childhood acute myeloid leukemia (AML). The t(8;21) AML1-ETO translocations were sequenced at the genomic level in 10 diagnostic leukemia samples from children with available neonatal Guthrie blood spots. Clonotypic genomic AML1-ETO sequences were detected in the Guthrie spots for 5 individuals, providing unambiguous evidence of prenatal origin in these cases. Two of these patients were older than 10 years of age at diagnosis, indicative of a protracted postnatal latency. Three of the patients were assessed for the persistence of genomic fusion sequences in complete clinical remission samples and were found to be positive. These data indicate that t(8;21) in childhood AML can arise in utero, possibly as an initiating event in childhood AML, and may establish a long-lived or stable parental clone that requires additional secondary genetic alterations to cause leukemia.