Lymphoma patients treated with autologous transplantation (ASCT) live an increasingly long life with the recent advancement in therapeutic modalities. This has resulted in an increase in the incidence of therapy-related myeloid neoplasms (t-MN), which is one of the leading causes of non-relapse mortality. Several observational studies have linked the development of t-MN after ASCT with the intensity and frequency of chemotherapy, particularly alkylating agents, use of total body irradiation (TBI), and peripheral blood progenitor cells. In addition, role of genetic factors is increasingly being identified. It is postulated that the use of chemotherapy prior to ASCT results in DNA damage of progenitor cells, mitochondrial dysfunction, and altered gene expression related to DNA repair, metabolism as well as hematopoietic regulation. Cytogenetic studies have shown the presence of abnormalities in the peripheral blood progenitor cells prior to ASCT. It is, therefore, likely that the reinfusion of peripheral blood progenitor cells, proliferative stress on infused progenitor cells during hematopoietic regeneration and associated telomere shortening ultimately result in clonal hematopoiesis and blastic transformation. Cytopenias, myelodysplasia, or cytogenetic abnormalities are common and can be transient after ASCT; therefore, only when present together, they do confirm the diagnosis of t-MN. Attempts to reduce the occurrence of t-MN should be directed toward minimizing the exposure to the identified risk factors. Although the median survival is few months to less than a year, studies have shown the promising role of allogeneic transplantation in select young t-MN patients without high-risk cytogenetics. In this review we will explain the recent findings in the field of t-MN in lymphoma patients that have implications for identifying the molecular and genetic mechanisms of leukemogenesis and discuss potential strategies to reduce the risk of t-MN in this patient population.

Anticoagulation is thought to be associated with the risk of intracranial hemorrhage (ICH) in patients with brain metastases; however, the data on this topic are limited. This study was conducted to determine the incidence of ICH associated with anticoagulant use in adult patients with brain metastases. Consecutive patients with brain metastases occurring from 2006 to 2014 were identified from a single-institution database. Long-term anticoagulant therapy was defined as outpatient anticoagulation therapy of > 1 month. Chi-square tests and Fisher's exact test were used to compare rates of ICH by groups. This cohort included 125 patients with brain metastases. Of these, 64 had primary of non-small cell lung cancer (51.2%). Of these patients, 12/125 (9.6%) patients developed ICH. Neither the primary tumor site nor the number of brain metastases was associated with the development of ICH. ICH incidence was not associated with the use of anticoagulant therapy, with 8/67 (11.94%) patients on outpatient anticoagulation and 4/58 (6.9%) not on anticoagulation experiencing ICH (p = 0.33). The type of treatment did not significantly influence ICH, although those having combined WBRT and SRS were numerically more likely to experience ICH (4/15; 26.67%) of this cohort. In patients on enoxaparin, there was no difference in the incidence of ICH for daily versus twice-daily dosing (p = 1.0). Long-term anticoagulant use is not associated with an increased incidence of ICH in patients with intracranial metastases.

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