In Their Own Words: A Qualitative Descriptive Study of Patient and Caregiver Perspectives on Follow-Up Care after Palliative Radiotherapy.

PURPOSE: To explore patients' and caregivers' views on follow-up care after palliative radiotherapy. METHODOLOGY: A qualitative study design was used. Patients receiving palliative radiotherapy or their caregivers were eligible to participate following informed consent. Participants attended a single interview. The interviews were guided by a set of open-ended questions designed to explore the participants' understanding of the purpose and preference for follow-up care after palliative radiotherapy. Interviews were recorded and transcribed verbatim. Themes were identified in the transcripts and described with consideration of the individual participant's demographics and cancer experiences. RESULTS: Nine participants (five patients and four caregivers) of eleven approached consented, and were interviewed. The median age of the participants was 60 years (range, 47-80 years). All participants had an Eastern Cooperative Oncology Group performance status of ≤1. Median time from the patient's initial cancer diagnosis to the study interview was 4.5 years (range, 3-35 years). Follow-up appointments were expected to provide an evaluation of treatment outcomes, complications, and current situations. Scheduled appointments were appreciated by some as they provided a dedicated opportunity to ask questions of their health care team. The receiving radiation oncology team's contact information was felt to be helpful because the patients could ask treatment-related questions. Many participants were comfortable with and expected the medical oncologist or referral physician to provide follow-up care for patients who received palliative radiotherapy. CONCLUSIONS: Palliative patients have diverse physical and emotional care needs. Within this study sample, participants valued follow-up because it provided an evaluation of their clinical status. They also viewed their established primary oncologist as the most appropriate person to provide follow-up care, supplemented by an efficient way of contacting their radiation oncology team as needed.

Epigenetic and phenotypic consequences of a truncation disrupting the imprinted domain on distal mouse chromosome 7.

The distal end of mouse chromosome 7 (Chr 7) contains a large cluster of imprinted genes. In this region two cis-acting imprinting centers, IC1 (H19 DMR) and IC2 (KvDMR1), define proximal and distal subdomains, respectively. To assess the functional independence of IC1 in the context of Chr 7, we developed a recombinase-mediated chromosome truncation strategy in embryonic stem cells and generated a terminal deletion allele, DelTel7, with a breakpoint in between the two subdomains. We obtained germ line transmission of the truncated Chr 7 and viable paternal heterozygotes, confirming the absence of developmentally required paternally expressed genes distal of Ins2. Conversely, maternal transmission of DelTel7 causes a midgestational lethality, consistent with loss of maternally expressed genes in the IC2 subdomain. Expression and DNA methylation analyses on DelTel7 heterozygotes demonstrate the independent imprinting of IC1 in absence of the entire IC2 subdomain. The evolutionarily conserved linkage between the subdomains is therefore not required for IC1 imprinting on Chr 7. Importantly, the developmental phenotype of maternal heterozygotes is rescued fully by a paternally inherited deletion of IC2. Thus, all the imprinted genes located in the region and required for normal development are silenced by an IC2-dependent mechanism on the paternal allele.

Syntaxin 5 is required for cytokinesis and spermatid differentiation in Drosophila.

Syntaxin 5 is a Golgi-localized SNARE protein that has been shown to be required for ER-Golgi traffic in yeast and Golgi reassembly following cell division in mammalian cells. Here, we describe the characterization of the Drosophila ortholog of syntaxin 5, dSyx5, and show that, like its mammalian and yeast counterparts, the protein is localized to the Drosophila Golgi and binds to alpha-SNAP. Null mutations in dSyx5 are larval lethal and demonstrate impaired transport of a GFP-tagged membrane protein. A hypomorphic allele of dSyx5 caused by insertion of an EP element results in impenetrant lethality, and escaping adult flies are male sterile. The male sterility results both from failure of germ cells to complete cytokinesis and from defects in spermatid elongation and maturation. Ectopic expression of dSyx5 from the EP element can rescue the cytokinesis defect, but high levels of expression are required to restore maturation and fertility. Together, these results show that dSyx5 is required for the proper function of the Golgi apparatus and that an efficiently functioning Golgi apparatus is required for the steps leading to the completion of cytokinesis and formation of mature sperm.