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Biomedical subjects

D Milliken

Publications and source records attributed to D Milliken.

7 recordsLinked to original sources
PubMed2005

Development, feasibility and compliance of a web-based system for very frequent QOL and symptom home self-assessment after hematopoietic stem cell transplantation.

We believe that many adverse events following hematopoietic stem cell transplantation (HSCT), particularly relapse and chronic graft-versus-host disease (CGVHD), are preceded by a subclinical period of development that is accessible by frequent psychometric assessment. Documenting these associations could improve future clinical care by extending the potential window for intervention. However, conventional methods of assessing quantity of lite (QOL) in patients in their homes, typically by mailed self-assessment questionnaires, are impractical for very frequent administration. We have developed and implemented a web-based system for measuring short-term (dynamic) changes in QOL by employing brief, online, daily QOL assessments and more extensive, monthly online assessments from patients' homes. Here we report the feasibility of collecting very frequent patient home self-assessments of QOL via the web for a 52 week participation period; we detail incidence of home web access, accrual, compliance, and satisfaction with the system in an HSCT patient sample. We also describe our integrated web-systems for administering patient recruitment, scheduling, monitoring, and analysis. Our results suggest that very frequent routine collection of QOL outcomes is entirely feasible using our web-based home assessment tool, with good patient compliance and high user satisfaction. We believe our methodology shows great promise for use with other cancer and health populations.

Adult↗
PubMed2001

Analysis of CC chemokine and chemokine receptor expression in solid ovarian tumours.

To understand the chemokine network in a tissue, both chemokine and chemokine receptor expression should be studied. Human epithelial ovarian tumours express a range of chemokines but little is known about the expression and localisation of chemokine receptors. With the aim of understanding chemokine action in this cancer, we investigated receptors for CC-chemokines and their ligands in 25 biopsies of human ovarian cancer. CC-chemokine receptor mRNA was generally absent from solid tumours, the exception being CCR1 which was detected in samples from 75% of patients. CCR1 mRNA localised to macrophages and lymphocytes and there was a correlation between numbers of CD8(+) and CCR1 expressing cells (P = 0.031). mRNA for 6 CC-chemokines was expressed in a majority of tumour samples. In a monocytic cell line in vitro, we found that CCR1 mRNA expression was increased 5-fold by hypoxia. We suggest that the CC-chemokine network in ovarian cancer is controlled at the level of CC-chemokine receptors and this may account for the phenotypes of infiltrating cells found in these tumours. The leukocyte infiltrate may contribute to tumour growth and spread by providing growth survival factors and matrix metalloproteases. Thus, CCR1 may be a novel therapeutic target in ovarian cancer.

Adenocarcinoma, Clear Cell↗
PubMed2001

Epithelial cancer cell migration: a role for chemokine receptors?

We investigated the possibility that chemokine gradients influence migration of human ovarian epithelial tumor cells. Of 14 chemokine receptors investigated, only CXCR4 was expressed on ovarian cancer cells. CXCR4 mRNA localized to a subpopulation of tumor cells in ovarian cancer biopsies. Ovarian cancer cell lines and cells freshly isolated from ascites expressed CXCR4 protein. The CXCR4 ligand, CXCL12, was found in ascites from 63 patients. CXCL12 elicited intracellular calcium flux and directed migration and changes in integrin expression in ovarian cancer cells. CXCR4 may influence cell migration in the peritoneum, a major route for ovarian cancer spread, and could be a therapeutic target.

Ascitic Fluid↗
PubMed1997

Increased frequency of P-glycoprotein gene amplification in colchicine-resistant Rat-1 clones transformed by v-src.

A rat fibroblast cell line (Rat-1) carrying a temperature-sensitive mutation of v-src was used to determine whether inducible cellular transformation altered the ability of cells to amplify the p-glycoprotein gene in response to colchicine selection. Transformed and nontransformed Rat-1 fibroblasts selected under 4 times the LD50 generated the same number of colchicine-resistant colonies. We next examined colchicine-resistant colonies derived from transformed cells and compared them to colchicine-resistant colonies derived from nontransformed cells. When Rat-1 cells were selected at 35 degrees C (transforming temperature), 7 out of 7 clones exhibited a 3- to 5-fold p-glycoprotein gene amplification. These results contrasted to those found at the nontransforming temperature (40 degrees C); none of the 8 colchicine-resistant clones examined had amplified the p-glycoprotein gene. Thus in Rat-1 cells carrying a temperature-sensitive v-src gene, p-glycoprotein gene amplification was observed at a high frequency only in transformed clones selected at the temperature permissive for v-src activity.

ATP Binding Cassette Transporter, Subfamily B, Mem↗