| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
© Oxford University Press 2008.
IN THIS ISSUE
Adjuvant Chemotherapy After Gastric Cancer SurgeryThe value of adjuvant chemotherapy in patients who have undergone complete surgical resection for gastric cancer is not clear. Di Costanzo et al. (p. 388) randomly assigned 258 patients who had been surgically treated for gastric cancer to intravenous treatment with four cycles of chemotherapy that consisted of cisplatin, epirubicin, leucovorin, and flurouracil (PELF) or to follow-up alone. Chemotherapy did not increase disease-free or overall survival. The authors stress the need for additional trials to test newer drug combinations and to analyze the association of clinical variables and molecular factors with survival.
In an editorial, Wu and Ji (p. 376) summarize the results from Asian and Western clinical trials of adjuvant therapy for gastric cancer and suggest that one goal of future research should be the identification of subgroups of patients who are most likely to benefit.
Specialized Care and Survival of Dutch Ovarian Cancer Patients
In some countries, referral guidelines recommend that patients with ovarian cancer be treated in specialized (regional) centers. However, in The Netherlands, treatment of ovarian cancer is not regionalized. Vernooij et al. (p. 399) used data from the Netherlands Cancer Registry to investigate the magnitude of the association between hospital type and survival of all Dutch patients diagnosed with ovarian cancer from 1996 through 2003 to assess whether care under the current system was optimal. Hospital type was statistically significantly associated with survival among patients with early-stage ovarian cancer but not among patients with advanced ovarian cancer. Patients with early-stage cancer who were treated in specialized or semi-specialized hospitals survived longer than patients treated in general hospitals. The authors conclude that, during the study period, the system in The Netherlands was not sufficient to deliver optimal care to all Dutch patients with ovarian cancer and suggest that regionalized care thus seems necessary.
In an editorial, Schrag (p. 378) points out that the value of cancer registries could be increased by adding data on patient comorbidities and performance status and by linking cancer registry data with databases that contain physician characteristics. Because it is impossible to evaluate every clinical intervention and healthcare strategy with a randomized trial, observational population-based data in registries remain important. She concludes that working across international borders to develop consensus on data collection, metrics, and timing rules should make registry data even more valuable.
Risk Factor Profiles for HPV-16–Positive and –Negative HNSCCs
High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). Gillison et al. (p. 407) conducted a hospital-based case–control study of HNSCC to compare the risk factor profiles for HPV-16–positive and HPV-16–negative HNSCCs. HPV-16–positive HNSCC was independently associated with several measures of sexual behavior and use of marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Conversely, HPV-16–negative HNSCC was associated with tobacco smoking, alcohol drinking, and poor oral hygiene but not with sexual behavior or marijuana use. The authors conclude that HNSCCs are a heterogeneous group of malignancies with at least two etiologically distinct pathways for HNSCC pathogenesis, one mediated by tobacco and alcohol and the other by HPV infection.
COX-2 in Atypical Hyperplasia and Breast Cancer Risk
Cyclooxygenase-2 (COX-2) is overexpressed in invasive and in situ breast cancers, and atypical hyperplasia in breast tissue, although benign, is associated with a high risk of breast cancer. Visscher et al. (p. 421) investigated the relationship between COX-2 expression in atypia specimens and the risk of subsequent breast cancer. They found that the risk of developing breast cancer, relative to that in a control population, increased in association with increasing COX-2 expression in atypia specimens, albeit with borderline statistical significance. Overexpression of COX-2 in atypias was statistically significantly associated with the type of atypia (lobular over ductal), increasing numbers of atypical foci in the biopsy specimen, and older age at biopsy examination. The authors conclude that COX-2 appears to be a biomarker that further stratifies breast cancer risk among women with atypical hyperplasia, and they suggest that it may be a relevant target for chemoprevention.
Cancer in Atomic Bomb Survivors Exposed In Utero or in Childhood
Exposure to radiation in utero and during childhood is associated with increased cancer risks in childhood and adulthood, respectively, but the association between exposure in utero and cancer risk in adulthood is unclear. To examine this association, Preston et al. (p. 428) analyzed excess risks of solid cancers at ages 12–55 among nearly 18,000 atomic bomb survivors of Nagasaki and Hiroshima who were in utero or 5 years old or younger at the time of the bombings. In each group, excess relative risks of solid cancers increased with radiation dose (excess relative risk for those exposed in utero was 1.0 per sievert [Sv] and for those exposed in childhood was 1.7 per Sv); in the combined cohort, excess relative risks declined with attained age. Excess absolute risks increased with attained age among those who were exposed after birth (estimated excess absolute risk at age 50 was 56 per 10,000 person-years per Sv) but not among those who were exposed in utero. The authors conclude that more follow-up is required to determine whether lifetime risks after radiation exposure are lower for those exposed in utero than for those exposed during early childhood.
Genetic Variations in AKAP9 and Breast Cancer Risk
Genetic polymorphisms in the A-kinase anchoring proteins (AKAPs), which are involved in signal transduction, have been suggested to be associated with carcinogenesis. Frank et al. (p. 437) genotyped six single-nucleotide polymorphisms (SNPs) in the AKAP genes that were predicted to disrupt the function of the encoded proteins. Using a case–control design in a German population of 1,110 familial breast cancer patients and 1,131 control subjects, they found that two SNPs in AKAP9, M463I and N2792S, were associated with increased risk for familial breast cancer. Both SNPs were in close linkage disequilibrium. When the analysis of the AKAP9 M463I SNP was extended to 9,523 breast cancer patients and 13,770 control subjects in seven independent studies in Europe and Australia, this SNP was found to be associated with increased risks of both familial breast cancer and breast cancer overall.
Related Articles in JNCI
![]()
CiteULike
Connotea
Del.icio.us What's this?
J Natl Cancer Inst 2008 100: 407-420.
J Natl Cancer Inst 2008 100: 399-406.
J Natl Cancer Inst 2008 100: 421-427.
J Natl Cancer Inst 2008 100: 437-442.
J Natl Cancer Inst 2008 100: 428-436.
J Natl Cancer Inst 2008 100: 388-398.
J Natl Cancer Inst 2008 100: 376-377.
J Natl Cancer Inst 2008 100: 378-379.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||