Diffuse large b-cell lymphoma with hemophagocytic syndrome in an HIV+ patient treated with CCR5- bone marrow transplant

Abstract

Collective evidence points to a prominent role of stress in cancer growth and metastasis. Despite these results an etio-pathogenetic role has not been widely accepted. Reasons of controversies are the coexistence in stressed patients of high risk habits, the sample size, the heterogeneity and the retrospective origins of these studies. Experimental data and clinical observations argue about the possibility of an interaction between psychosocial events and tumours. However the number of involved variables and the long period of observation prevent with current technologies the definition of causal versus chaotic sequences of this hypothetical relationship. Psychotherapy may help to face up to stressful events, but its role e remains uncertain. Stress works through sympathetic nervous system and hypothalamic– pituitary–adrenal axis activation, along with related hormones, that have functionally and biologically significant impacts on the tumor microenvironment. This paper collects evidences through the hypothesis of correlation between stress, psychological factors and cancer focusing both on psychology and on molecular biology. Knowledge on stress induced neuroendocrine dynamics in the tumor microenvironment might allow the development of integrated pharmacological and bio-behavioral strategies to create more successful cancer therapies.