Citations

BackgroundFewer than 5 % of cancer patients participate in clinical research. Although this paltry rate has led to extensive research on this topic, previous studies have not sought verbatim comments in a real‐time, comprehensive manner to understand why patients decline.MethodsThis study used a low‐risk, non‐interventional parent study that focused on cancer‐associated weight loss to understand patients' reasons for declining research participation. A research assistant wrote down the name and verbatim reason of all patients who declined to participate. These comments with accompanying patient demographic data are the subject of this report.ResultsOf the 334 patients, 51 (15 %) declined parent study enrollment; three comment‐related themes emerged: (1) a repelling sense of too much institutional research, (2) overwhelming personal health issues, and (3) a low likelihood of returning to the institution. In univariate and multivariate analyses, only age (older) and gender (female) were associated with non‐enrollment. Interestingly, 41 patients with fatigue scores of 7 or worse and 26 with pain scores of 7 or worse were enrolled.ConclusionsAlthough many factors were associated with declining to participate in research, symptom severity was not. Upfront education might help cancer patients better prioritize their participation in research, particularly as some patients felt overwhelmed by too much research in the institution; and for now, investigators should continue to keep asking patients for their participation.

Abstract Background: Little is known about the causes of adult leukemia. A few small studies have reported a reduced risk associated with regular use of nonsteroidal anti-inflammatory drugs (NSAID). Methods: In a population-based case–control study, we evaluated analgesic use among 670 newly diagnosed myeloid leukemia cases [including 420 acute myeloid leukemias (AML) and 186 chronic myeloid leukemias (CML)] and 701 controls aged 20 to 79 years. Prior use of aspirin, ibuprofen, acetaminophen, other NSAIDs, and COX-2 inhibitors was assessed and included frequency, duration, and quantity. ORs and 95% CIs were calculated using unconditional logistic regression adjusting for potential confounders. Results: Regular/extra strength aspirin use was inversely associated with myeloid leukemia in women (OR = 0.59, 95% CI = 0.37–0.93) but not in men (OR = 0.85, 95% CI = 0.58–1.24). In contrast, acetaminophen use was associated with an increased risk of myeloid leukemia in women only (OR = 1.60, 95% CI = 1.04–2.47). These relationships were stronger with increasing dose and duration. When stratified by leukemia type, aspirin use was inversely associated with AML and CML in women. No significant overall associations were found with ibuprofen or COX-2 inhibitors for either sex; however, a decreased risk was observed with other anti-inflammatory analgesic use for women with AML or CML (OR = 0.47, 95% CI = 0.22–0.99; OR = 0.31, 95% CI = 0.10–0.92, respectively). Conclusions: Our results provide additional support for the chemopreventive benefits of NSAIDs, at least in women. Because leukemia ranks fifth in person-years of life lost due to malignancy, further investigation is warranted. Impact: NSAIDs may reduce, whereas acetaminophen may increase, myeloid leukemia risk in women. Cancer Epidemiol Biomarkers Prev; 20(8); 1741–50. ©2011 AACR.

Abstract Rash from epidermal growth factor receptor inhibitors is common and negatively impacts the quality of life of cancer patients. Published guidelines recommend holding cancer therapy if the rash is severe. Does this recommendation hinge solely on improving patients' quality of life, or does it also hinge on the prevention of a potentially fatal, cutaneous adverse event? In other words, do patients die from rashes from epidermal growth factor receptor inhibitors? To our knowledge, the latter question has never before been asked and answered in an evidence-based fashion. Therefore, we conducted a systematic review of the published, prospectively conducted clinical trial literature on epidermal growth factor receptor inhibitors. The primary aim was to determine whether rash-related death has ever been reported in such trials. Among 117 such trials, which included 8,998 cancer patients, the rate of rash development was >50%, as expected. However, there were no reported deaths from a rash. Although we cannot conclude that a rash-related death from this class of agents can never occur, this systematic review provides evidence-based guidance on how best to counsel cancer patients who develop a rash from an epidermal growth factor receptor inhibitor. It suggests that quality of life issues should remain at the forefront as cancer patients and health care providers make decisions about holding cancer therapy.

The mechanisms underlying CD4+ T cell depletion in human immunodeficiency virus (HIV) infection are not well understood. Comparative studies of lymphoid tissues, where the vast majority of T cells reside, and peripheral blood can potentially illuminate the pathogenesis of HIV-associated disease. Here, we studied the effect of HIV infection on the activation and depletion of defined subsets of CD4+ and CD8+ T cells in the blood, gastrointestinal (GI) tract, and lymph node (LN). We also measured HIV-specific T cell frequencies in LNs and blood, and LN collagen deposition to define architectural changes associated with chronic inflammation. The major findings to emerge are the following: the GI tract has the most substantial CD4+ T cell depletion at all stages of HIV disease; this depletion occurs preferentially within CCR5+ CD4+ T cells; HIV-associated immune activation results in abnormal accumulation of effector-type T cells within LNs; HIV-specific T cells in LNs do not account for all effector T cells; and T cell activation in LNs is associated with abnormal collagen deposition. Taken together, these findings define the nature and extent of CD4+ T cell depletion in lymphoid tissue and point to mechanisms of profound depletion of specific T cell subsets related to elimination of CCR5+ CD4+ T cell targets and disruption of T cell homeostasis that accompanies chronic immune activation.