Weight gain during adjuvant chemotherapy has been reported by several authors. Because increased body weight at diagnosis is associated with an increased risk of disease recurrence, we have assessed the prevalence of weight gain in a series of patients receiving adjuvant treatment, as well as the association of weight gain with type of treatment and risk of recurrence. We first assembled an inception cohort of 237 patients who had all undergone pretreatment evaluation and treatment at one institution, and had already been followed for at least 12 months. Body weight at the start and completion of treatment was recorded, as was type of treatment and status at last followup. Ninety-six percent of patients gained weight during treatment and none lost weight (mean increase 4.3 kg). Weight gain was strongly associated with treatment, and was least in patients receiving single agent chemotherapy, greatest in patients treated with ovarian ablation and prednisone, and intermediate in those receiving combination chemotherapy. There was no association between weight gain and disease recurrence.

Purpose/Objectives We previously reported that combination of mean lung dose (MLD), and inflammatory cytokines (IL-8 and TGF-β1) may provide a more accurate model for radiation-induced lung toxicity (RILT) prediction in 58 patients with non-small cell lung cancer (NSCLC). This study is to validate the previous findings with new patients and explore new models with more cytokines. Materials/Methods 142 patients with stage I–III NSCLC treated with definitive radiation therapy (RT) from prospective studies were included. Sixty-five new patients were used to validate previous findings, and all 142 patients to explore new models. Thirty inflammatory cytokines were measured in plasma samples before RT, 2 weeks and 4 weeks during RT (pre, 2w, 4w). Grade ≥2 RILT defined as grade 2 and higher radiation pneumonitis or symptomatic pulmonary fibrosis was the primary endpoint. Logistic regression was performed to evaluate the risk factors of RILT. The area under the curve (AUC) for the Receiver Operating Characteristic (ROC) curves was used for model assessment. Results Sixteen of 65 patients (24.6%) developed RILT2. Lower pre IL-8 and higher TGF-β1 2w/pre ratio were associated with higher risk of RILT2. The AUC increased to 0.73 by combining MLD, pre IL-8 and TGF-β1 2w/pre ratio compared with 0.61 by MLD alone to predict RILT. In all 142 patients, 29 patients (20.4%) developed grade ≥2 RILT. Among the 30 cytokines measured, only IL-8 and TGF-β1 were significantly associated with the risk of RILT2. MLD, pre IL-8 level and TGF-β1 2w/pre ratio were included in the final predictive model. The AUC increased to 0.76 by combining MLD, pre IL-8 and TGF-β1 2w/pre ratio compared with 0.62 by MLD alone. Conclusions We validated that a combination of mean lung dose, pre IL-8 level and TGF-β1 2w/pre ratio provided a more accurate model to predict the risk of RILT2 compared to MLD alone.

Background Prostaglandin E2 (PGE2) induces aromatase expression in adipose tissue leading to increased estrogen production that may promote the development and progression of breast cancer. However, few studies have simultaneously investigated systemic levels of PGE2 and estrogen in relation to postmenopausal breast cancer risk. Methods Here we determined urinary estrogen metabolites (EMs) using mass spectrometry in a case-cohort study (295 incident breast cancer cases and 294 subcohort members), and using linear regression estimated the effect of urinary levels of a major PGE2 metabolite (PGE-M) on EMs. Hazard ratios (HRs) for the risk of developing breast cancer in relation to PGE-M and EMs were compared between Cox regression models with and without mutual adjustment. Results PGE-M was a significant predictor of estrone (E1), but not estradiol (E2) levels in multivariable analysis. Elevated E2 levels were associated with an increased risk of developing breast cancer (HRQ5vs.Q1 =1.54, 95% CI: 1.01–2.35), and this association remained unchanged after adjustment for PGE-M (HRQ5vs.Q1 =1.52, 95% CI: 0.99–2.33). Similarly, elevated levels of PGE-M were associated with increased risk of developing breast cancer (HRQ4vs.Q1 =2.01, 95% CI: 1.01–4.29), and this association was only nominally changed after consideration of E1 or E2 levels. Conclusions Urinary levels of PGE-M and estrogens were independently associated with future risk of developing breast cancer among these postmenopausal women. Impact Increased breast cancer risk associated with PGE-M might not be fully explained by the estrogens-breast cancer association alone but also by additional effects related to inflammation.

The pretreatment neutrophil/lymphocyte ratio (NLR), derived from differential white blood cell counts, has been previously associated with poor prognosis in breast cancer. Little data exist, however, concerning this association in Black patients, who are known to have lower neutrophil counts than other racial groups. We conducted a retrospective cohort study of 236 Black and 225 non-Hispanic White breast cancer patients treated at a single institution. Neutrophil and lymphocyte counts were obtained from electronic medical records. Univariate and multivariate Cox regression models were used to determine hazard ratios (HRs) and 95% confidence intervals (95% CIs) of all-cause mortality and breast cancer-specific mortality in relation to pretreatment NLR. Overall, there were no associations between an elevated pretreatment NLR (NLR ≥3.7) and all-cause or breast cancer-specific mortality. Among patients without metastasis at the time of diagnosis, an elevated pretreatment NLR was independently associated with all-cause mortality, with a multivariable HR of 2.31 (95% CI: 1.10–4.86). Black patients had significantly lower NLR values than White patients, but there was no evidence suggesting racial heterogeneity of the prognostic utility of NLR. Pretreatment NLR was an independent predictor of all-cause mortality but not breast cancer-specific mortality in non-metastatic breast cancer patients.