PubMed Health⌕ Search

Biomedical subjects

Debra Friedman

Publications and source records attributed to Debra Friedman.

7 recordsLinked to original sources
PubMed2007

Assessment of health-related quality of life of adolescent cancer patients using the Minneapolis-Manchester Quality of Life Adolescent Questionnaire.

BACKGROUND: Improved survival after childhood cancer has shifted the focus to health-related quality of life (HRQL)-an understudied problem, especially among adolescents. PROCEDURE: We assessed HRQL among adolescents utilizing a validated self-report tool, the Minneapolis-Manchester Quality of Life (MMQL) Adolescent Form, consisting of 46 items comprising seven domains: physical, cognitive, psychological and social functioning, body image, intimate relations, and outlook on life, and computed an overall QoL score. The MMQL Adolescent Form was administered to 226 adolescent survivors of childhood cancer a median of 7.8 years from diagnosis (off therapy-median age: 16.2 years), 136 adolescent cancer patients undergoing therapy (on therapy-median age: 16.4 years), and 134 healthy adolescents (controls-median age: 15.5 years). Primary diagnoses included leukemia (46%), lymphoma (26%), brain tumors (5%), and other solid tumors (23%). RESULTS: Compared to healthy controls, on-therapy patients were at increased risk for reporting poor overall QoL [Odds Ratio (OR) = 3.3, P = 0.002)] and poor physical functioning (OR = 11.8, P < 0.001). Off-therapy survivors did not differ significantly from healthy controls for overall QoL (OR = 1.6, P = 0.5) or any HRQL domains. Female patients, both on- and off-therapy, were more likely to report poorer overall QoL, physical, psychological and cognitive functioning as well as poorer body image when compared with male patients. CONCLUSIONS: While adolescent cancer patients undergoing active therapy report poor physical functioning, there is no evidence of long-term QoL sequelae.

Adolescent↗
PubMed2005

Health-related quality of life in young survivors of childhood cancer using the Minneapolis-Manchester Quality of Life-Youth Form.

OBJECTIVE: To assess the health-related quality of life (HRQL) of 8- to 12-year-old children undergoing therapy for cancer or childhood-cancer survivors by using the Minneapolis-Manchester Quality of Life-Youth Form (MMQL-YF), a comprehensive, multidimensional self-report instrument with demonstrable reliability and validity. DESIGN, SETTING, AND PATIENTS: The MMQL-YF consists of 32 items comprising 4 scales: physical functioning, psychologic functioning, physical symptoms, and outlook on life. Scoring on the MMQL ranges from 1 to 5; 5 indicates maximal HRQL. An overall quality-of-life (QOL) score is also computed. By using a cross-sectional study design, the MMQL-YF was administered to 90 off-therapy cancer survivors, 72 children with cancer undergoing active therapy, and 481 healthy children without a history of cancer or other chronic disease. RESULTS: Compared with healthy controls, children actively undergoing cancer treatment report low overall QOL, physical functioning, and outlook-on-life scores. However, off-therapy survivors report a superior overall QOL, compared with age-matched healthy controls. CONCLUSIONS: Young survivors of childhood cancer report a favorable HRQL relative to healthy controls. These results are reassuring, suggesting that this group of survivors may have been too young to encounter some of the negative psychosocial impacts of cancer and its treatment.

Case-Control Studies↗
PubMed2004

Breast cancer after childhood cancer: a report from the Childhood Cancer Survivor Study.

BACKGROUND: Survivors of childhood cancer are at risk for secondary breast cancer. Other than previous chest radiation therapy, risk factors for secondary breast cancer have not been established. OBJECTIVE: To identify risk factors for breast cancer among female survivors of childhood cancer. DESIGN: Retrospective cohort study. SETTING: The Childhood Cancer Survivor Study (CCSS), a multicenter study of persons who survived more than 5 years after childhood cancer diagnosed from 1970 to 1986. PARTICIPANTS: Among 6068 women in the CCSS, 95 women had 111 confirmed cases of breast cancer. MEASUREMENTS: Standardized incidence ratios for breast cancer were calculated by using age-specific incidence rates in the general population. Breast cancer incidence was evaluated with respect to primary cancer diagnosis and therapy, age at and time since primary diagnosis, menstrual and reproductive history, and family history of cancer. RESULTS: Breast cancer risk was increased in survivors who were treated with chest radiation therapy (standardized incidence ratio, 24.7 [95% CI, 19.3 to 31.0]) and survivors of bone and soft-tissue sarcoma who were not treated with chest radiation therapy (standardized incidence ratios, 6.7 and 7.6, respectively). Family history of breast cancer (relative rate, 2.7 [CI, 1.3 to 5.0]) and history of thyroid disease (relative rate, 1.7 [CI, 1.1 to 2.6]) were independently associated with increased risk, and exposure to pelvic radiation was protective (relative rate, 0.6 [CI, 0.4 to 0.9]). Age at primary cancer diagnosis and menstrual and reproductive histories did not statistically significantly modify risk. LIMITATIONS: This cohort has not yet attained an age at which breast cancer risk is greatest. CONCLUSION: Survivors of childhood sarcomas and those who received chest radiation therapy are at risk for secondary breast cancer. When assessing a survivor's risk, clinicians should consider primary diagnosis, previous radiation therapy, family cancer history, and history of thyroid disease.

Adult↗
PubMed2004

XRCC1 and glutathione-S-transferase gene polymorphisms and susceptibility to radiotherapy-related malignancies in survivors of Hodgkin disease.

BACKGROUND: One of the most serious late effects of treatment for childhood cancer is the occurrence of subsequent malignancy. Survivors of Hodgkin disease (HD), in particular, have been shown to be at high risk of subsequent malignancy, the occurrence of which has been associated strongly with exposure to radiotherapy. METHODS: In the current study, the authors investigated the association between polymorphisms in 3 genes--glutathione-S-transferase M1 (GSTM1), glutathione-S-transferase T1 (GSTT1), and XRCC1, with roles in protection from a variety of DNA-damaging agents-and the risk of subsequent malignancy in 650 survivors of HD enrolled in the Childhood Cancer Survivor Study who had received radiotherapy. RESULTS: Individuals lacking GSTM1 but not GSTT1 were at increased risk of any subsequent malignancy (odds ratio [OR], 1.5; 95% confidence interval [CI], 1.0-2.3), and for subsequent cancer within the radiation field (OR, 1.4; 95% CI, 0.9-2.1). A nonsignificant increased risk of thyroid carcinoma was observed in individuals lacking either GSTM1 (OR, 2.9; 95% CI, 0.8-10.9) or GSTT1 (OR, 3.7; 95% CI, 0.6-23.5). Individuals having the genotype of the arginine/glutamine polymorphism at codon 399 in the XRCC1 gene (R399) showed a nonsignificant increased risk of breast carcinoma compared with those without (OR, 1.4; 95% CI, 0.7-2.7), and a nonsignificant decreased risk against a subsequent thyroid carcinoma (OR, 0.6; 95% CI, 0.2-1.6). No differences in genotype frequencies were observed between survivors with basal cell carcinoma when compared with survivors without a subsequent cancer. CONCLUSIONS: These data illustrated the potential value of incorporating the collection of genomic DNA in longitudinal cohort studies of populations with well defined, potentially carcinogenic exposures. Evaluation of additional genetic polymorphisms in this cohort may help define genes that influence individual sensitivity to radiotherapy.

Adolescent↗
PubMed2003

TP53, BRCA1, and BRCA2 tumor suppressor genes are not commonly mutated in survivors of Hodgkin's disease with second primary neoplasms.

PURPOSE: Despite recognition that second malignant neoplasms (SMNs) contribute significantly to mortality after the successful treatment of Hodgkin's disease (HD), little is known about the molecular events leading to secondary tumors. Factors contributing to second cancer risk include the carcinogenic effects of ionizing radiation and chemotherapy, in combination with possible host susceptibility. To clarify whether host genetic factors contribute to secondary tumorigenesis, we performed mutational analyses of the TP53, BRCA1, and BRCA2 tumor suppressor genes in a cohort of 44 HD patients developing one or more SMN. PATIENTS AND METHODS: Family cancer histories and constitutional DNA samples were obtained from 44 HD patients with SMNs identified. Using DNA-based sequencing, we evaluated the TP53 gene in all 44 patients. Nineteen female patients developing one or more secondary breast cancer were also analyzed for mutations in the BRCA1 and BRCA2 breast cancer-susceptibility genes. RESULTS: Nineteen patients (43%) had more than one SMN, and 12 patients (27%) had a positive family history of cancer. One of 44 patients tested for TP53 harbored a novel homozygous germline abnormality. One of 19 patients tested for BRCA2 carried a previously described heterozygous inactivating mutation. We identified no germline BRCA1 mutations. CONCLUSION: Despite features suggestive of genetic predisposition, the TP53, BRCA1, and BRCA2 genes were not frequently mutated in this cohort of HD patients developing SMNs. Larger studies of these genes or investigations of other genes involved in cellular DNA damage response pathways may identify host genetic factors that contribute to secondary tumorigenesis.

Adult↗