Cellular Radiosensitivity: How much better do we understand it?

Purpose: Ionizing radiation exposure gives rise to a variety of lesions in DNA that result in genetic instability and potentially tumorigenesis or cell death. Radiation extends its effects on DNA by direct interaction or by radiolysis of H2O that generates free radicals or aqueous electrons capable of interacting with and causing indirect damage to DNA. While the various lesions arising in DNA after radiation exposure can contribute to the mutagenising effects of this agent, the potentially most damaging lesion is the DNA double strand break (DSB) that contributes to genome instability and/or cell death. Thus in many cases failure to recognise and/or repair this lesion determines the radiosensitivity status of the cell. DNA repair mechanisms including homologous recombination (HR) and non-homologous end-joining (NHEJ) have evolved to protect cells against DNA DSB. Mutations in proteins that constitute these repair pathways are characterised by radiosensitivity and genome instability. Defects in a number of these proteins also give rise to genetic disorders that feature not only genetic instability but also immunodeficiency, cancer predisposition, neurodegeneration and other pathologies. Conclusions: In the past fifty years our understanding of the cellular response to radiation damage has advanced enormously with insight being gained from a wide range of approaches extending from more basic early studies to the sophisticated approaches used today. In this review we discuss our current understanding of the impact of radiation on the cell and the organism gained from the array of past and present studies and attempt to provide an explanation for what it is that determines the response to radiation

The course of anxiety and depression for patients with Hodgkin’s lymphoma or diffuse large B cell lymphoma: a longitudinal study of the PROFILES registry

Purpose The purpose of this study is to prospectively assess anxiety and depression among patients with Hodgkin lymphoma (HL) and diffuse large B cell lymphoma (DLBCL). Also, to compare its prevalence with a normative population, identify subgroups with more anxiety and depression, and assess its impact on health-related quality of life (HRQoL). Methods The population-based Eindhoven Cancer Registry was used to select patients diagnosed with HL or DLBCL from 1999 to 2010, 489 responded (T1). The HADS was completed four times (T1–T4), with a 1-year interval. Linear mixed-models were used to assess the course of anxiety and depression and identify high-risk subgroups. Results Both anxiety and depression were reported more often by patients compared to the normative population (p < 0.05). Over the four time points, approximately 10 % of patients reported to be always and 15 % reported to be sometimes anxious or depressed. Anxiety and depression did not improve in time. Patients with comorbidity and patients who were lower educated reported higher anxiety and depression scores (p < 0.05). Younger DLBCL patients reported higher anxiety scores, whereas older DLBCL patients reported higher depression scores over time (p < 0.05). Global health status/HRQoL was clinically relevant lower in patients with anxiety and depression and this appeared to be constant over time. Conclusion More HL and DLBCL patients experience anxiety and depression compared to their counterparts in the general population and it did not improve in time.Implication for Cancer SurvivorsClinicians should be aware that former lymphoma patients with anxiety and depression have a deteriorated global health status/HRQoL and refer patients to suitable aftercare when necessary

Acute lymphoblastic leukemia in a 2-year-old girl whose mother was previously diagnosed with antiphospholipid syndrome: a case report

BACKGROUND: The role of maternal exposures and conditions in the origin of childhood cancer has been a subject of growing interest, but current evidence is inconclusive. CASE PRESENTATION: We present a case detected in a multicenter case–control study evaluating the association between parental risk factors and childhood acute lymphoblastic leukemia (ALL). The patient is a Colombian girl who was diagnosed with ALL-L1 when she was 2 years old. Her mother had been diagnosed with antiphospholipid syndrome before pregnancy and had also been treated with subcutaneous injections of heparin. Other potentially relevant maternal and patient exposures are also reported in this paper. CONCLUSION: We hypothesize that the maternal autoimmune disease could be a contributor in the causality network of the daughter’s leukemia. However, the role of other exposures cannot be excluded