Feasibility and Preliminary Efficacy of Tailored Yoga in Survivors of Head and Neck Cancer: A Pilot Study.

PURPOSE: Treatment for head and neck cancer (HNC) results in long-term toxicities and increased physical and psychosocial survivor burden. There are a limited number of treatments for these late effects. Yoga postures, breath work, relaxation, and meditation, may improve these late effects. The purpose of this study was to examine the feasibility of a tailored yoga program in HNC survivors and obtain preliminary efficacy data. METHODS: This was a randomized wait-list control study of yoga-naive HNC survivors who were >3 months post-cancer treatment. Baseline data were collected. Participants were randomized to either an 8-week hatha yoga intervention group or a wait-list group. Feasibility and efficacy data were collected. At 4 and 8 weeks, patients underwent a repeat assessment of health. Wait-list control group participants were offered the yoga program after data collection. Descriptive statistics evaluated feasibility. Mixed effects general linear models were used to generate estimates of the efficacy outcomes. RESULTS: Seventy-three individuals were screened and 40 were eligible. All eligible individuals consented and enrolled. Five of the intervention group discontinued early and none in the wait-list control group. Feasibility was affirmed as participants were recruited and retained in the study, there were no adverse events, fidelity to protocol was demonstrated, and satisfaction rates were high. Efficacy measures indicated potential benefit for shoulder range of motion ( d = 0.57-0.86, P < .05), pain ( d = 0.67-0.90, P ≤ .005), and anxiety ( d = 0.59, P = .015). CONCLUSION: A tailored hatha yoga program is feasible and potentially efficacious for HNC survivors. Preliminary data supports further investigation of yoga in this population is needed.

Retroviral insertions in the VISION database identify molecular pathways in mouse lymphoid leukemia and lymphoma.

AKXD recombinant inbred (RI) strains develop a variety of leukemias and lymphomas due to somatically acquired insertions of retroviral DNA into the genome of hematopoetic cells that can mutate cellular proto-oncogenes and tumor suppressor genes. We generated a new set of tumors from nine AKXD RI strains selected for their propensity to develop B-cell tumors, the most common type of human hematopoietic cancers. We employed a PCR technique called viral insertion site amplification (VISA) to rapidly isolate genomic sequence at the site of provirus insertion. Here we describe 550 VISA sequence tags (VSTs) that identify 74 common insertion sites (CISs), of which 21 have not been identified previously. Several suspected proto-oncogenes and tumor suppressor genes lie near CISs, providing supportive evidence for their roles in cancer. Furthermore, numerous previously uncharacterized genes lie near CISs, providing a pool of candidate disease genes for future research. Pathway analysis of candidate genes identified several signaling pathways as common and powerful routes to blood cancer, including Notch, E-protein, NFkappaB, and Ras signaling. Misregulation of several Notch signaling genes was confirmed by quantitative RT-PCR. Our data suggest that analyses of insertional mutagenesis on a single genetic background are biased toward the identification of cooperating mutations. This tumor collection represents the most comprehensive study of the genetics of B-cell leukemia and lymphoma development in mice. We have deposited the VST sequences, CISs in a genome viewer, histopathology, and molecular tumor typing data in a public web database called VISION (Viral Insertion Sites Identifying Oncogenes), which is located at http://www.mouse-genome.bcm.tmc.edu/vision .

Tnfrsf13c (Baffr) is mis-expressed in tumors with murine leukemia virus insertions at Lvis22.

In susceptible strains of mice, leukemia is caused by the somatic integration of murine leukemia retroviruses into the host genome. Integration sites that are common to several tumors are likely to affect genes that are important in oncogenesis. Here we present the analysis of a common site of retroviral integration on mouse chromosome 15, which includes the genomic structure of three genes near the integration site. One of the genes misexpressed at the insertion site has recently been characterized as a B-cell receptor, Tnfrsf13c (formerly Baffr), indicating that this approach is useful in defining genes that function in lymphocyte development and tumor progression. Current genome databases provide powerful resources for the rapid identification of genes at common proviral insertion sites. The characterization of these genes in tumor samples will allow a function to be assigned to many novel loci identified by the genome sequencing projects.