Although biological evidence suggests that tea consumption may protect against non-Hodgkin lymphoma (NHL), epidemiological evidence has been unclear. The aim of this study was to examine the association between tea-drinking habits and the risk of NHL in a large nationwide prospective cohort of postmenopausal US women. 68 854 women who were enrolled from 1993 through 1998 in the Women’s Health Initiative Observational Study and responded to year 3 annual follow-up questionnaire comprised the analytic cohort. Newly diagnosed NHL cases after the year 3 visit were confirmed by medical and pathology reports. Multivariable-adjusted Cox proportional hazards models were performed to assess the associations of tea-drinking habits (specifically, the amounts of caffeinated/herbal/decaffeinated tea intake) with the overall risk of NHL and three major subtypes (diffuse large B-cell lymphoma (n 195, 0·3 %), follicular lymphoma (n 128, 0·2 %) and chronic lymphocytic leukaemia/small lymphocytic lymphoma (n 51, 0·1 %)). Among 62 622 participants, a total of 663 (1·1 %) women developed NHL during a median follow-up of 16·51 (sd 6·20) years. Overall, different amounts of type-specific tea intake were not associated with the risk of NHL regardless of its histologic subtypes after adjustment for confounders. Our findings suggest that tea intake at the current consumption level does not influence the risk of NHL, regardless of its histologic types.

Today, cancer is one of the leading causes of death worldwide. Lately, cytokine and chemokine imbalances have gained attention amongst different involved pathways in cancer development and attracted much consideration in cancer research. CXCL16, as a member of the CXC subgroup of chemokines, has been attributed to be responsible for immune cell infiltration into the tumour microenvironment. The aberrant expression of CXCL16 has been observed in various cancers. This chemokine has been shown to play a conflicting role in tumour development through inducing pro-inflammatory conditions. The infiltration of various immune and non-immune cells such as lymphocytes, cancer-associated fibroblasts and myeloid-derived suppressor cells by CXCL16 into the tumour microenvironment has complicated the tumour fate. Given this diverse role of CXCL16 in cancer, a better understanding of its function might build-up our knowledge about tumour biology. Hence, this study aimed to review the impact of CXCL16 in cancer and explored its therapeutic application. Consideration of these findings might provide opportunities to achieve novel approaches in cancer treatment and its prognosis.

Limited studies have investigated the effects of serum carotenoids on the risk of non-Hodgkin lymphoma (NHL), and the findings have been inconclusive. This study aims to assess the association between serum total or specific carotenoid levels and NHL risk. This 1:1 matched, hospital-based case–control study enrolled 512 newly diagnosed (within 1 month) NHL patients and 512 healthy controls who were matched by age (±5 years) and sex in Urumqi, China. Serum carotenoid levels were measured by HPLC. Conditional logistic regression showed that higher serum total carotenoid levels and their subtypes (e.g. α-carotene, β-carotene, β-cryptoxanthin and lycopene) were dose-dependently associated with decreased NHL risk. The multivariable-adjusted OR and their 95 % CI for NHL risk for quartile 4 (v. quartile 1) were 0·31 (95 % CI 0·22, 0·48; Pfor trend < 0·001) for total carotenoids, 0·52 (95 % CI 0·33, 0·79; Pfor trend: 0·003) for α-carotene, 0·63 (95 % CI 0·42, 0·94; Pfor trend: 0·031) for β-carotene, 0·73 (95 % CI 0·49, 1·05; Pfor trend: 0·034) for β-cryptoxanthin and 0·51 (95 % CI 0·34, 0·75; Pfor trend: 0·001) for lycopene. A null association was observed between serum lutein + zeaxanthin and NHL risk (OR 0·89, 95 % CI 0·57, 1·38; Pfor trend: 0·556). Significant interactions were observed after stratifying according to smoking status, and inverse associations were more evident among current smokers than past or never smokers for total carotenoids, α-carotene and lycopene (Pfor heterogeneity: 0·047, 0·042 and 0·046). This study indicates that higher serum carotenoid levels might be inversely associated with NHL risk, especially among current smokers.

The present study explored the association between dietary vitamin D and non-Hodgkin's lymphoma (NHL) risk. The multiethnic cohort (MEC) includes more than 215 000 Caucasians, African Americans, Native Hawaiians, Japanese Americans and Latinos, aged 45–75. After 10 years of follow-up, 939 incident NHL cases were identified. Risk was estimated using proportional hazards' models adjusted for possible confounders. Vitamin D intake was not associated with NHL risk in the entire cohort (Ptrend = 0·72 for men and Ptrend = 0·83 for women), but significantly lowered disease risk in African American women (hazard ratio (HR) = 0·50, 95 % CI: 0·28, 0·90, Ptrend = 0·03) and was borderline protective in African American men (HR = 0·68; 95 % CI: 0·39, 1·19; Ptrend = 0·31) when the highest to the lowest tertile was compared. In NHL subtype analyses, a 19, 36 and 32 % lowered risk, although not significant, was observed for diffuse large B-cell lymphoma, follicular lymphoma and small lymphocytic lymphoma/chronic lymphocytic leukemia in women, respectively. High dietary intake of vitamin D did not show a protective effect against NHL within the MEC except among African Americans, possibly because vitamin D production due to sun exposure is limited in this population.

Despite recent advances, treatment of patients with aggressive Non-Hodgkin'slymphoma (NHL2) has yet to be optimally designed. Notwithstanding the contribution ofmolecular treatments, intensification of chemotherapeutic regimens may still be beneficial.Hoping to aid in the design of intensified chemotherapy, we put forward a mathematicaland computational model that analyses the effect of Doxorubicin on NHL over a widerange of patho-physiological conditions. The model represents tumour growth both indiffusion-limited settings, that is, in small avascular tumours and tumour cords, and inperfusion-limited settings, e.g. in well-vascularized tumours. Model simulations indicatedthe presence of a critical regimen intensity below which treatment will fall short of tumourelimination. Taking this critical intensity into account, we compared two regimenintensification strategies: Dose escalation and regimen densification, i.e. reducing theinter-dosing interval. In the diffusion-limited setting, dose escalation was somewhat moreefficient than regimen densification. In the perfusion-limited setting, both intensificationstrategies yielded similar results. The present study coupled with a realistic myelotoxicitymodel may add insight on the optimisation of NHL intensified chemotherapy design.