To the Editor, Since March 11, 2020, the World Health Organization defined coronavirus disease 2019 (COVID-19) as a pandemic, with a series of confirmed cases that currently exceeded 300,000 people worldwide and with approximately 14,500 deaths. 1 Accumulated evidence suggests that a subgroup of patients with severe COVID-19 could have a dysregulation of the immune response that allows the development of viral hyperinflammation. 2 Thus, all patients with severe COVID-19 should be screened for hyperinflammation using laboratory parameters to improve mortality. Neutrophil-to-lymphocyte ratio (NLR) and lymphocyte-to-C-reactive protein ratio (LCR) are established inflammation markers that reflect systemic inflammatory F I G U R E 1 Standardized mean difference (SMD) and 95% confidence interval (95% CI) of neutrophil-to-lymphocyte ratio and lymphocyte-to-C-reactive protein ratio in coronavirus disease 2019 (COVID-19) patients with or without severe disease 2018-000012-01NACF-07226) from the National Council of Science and Technology, CONACyT.

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FMS-like tyrosine kinase 3 (FLT3) is a proto-oncogene involved in crucial steps of haematopoiesis such as proliferation, differentiation and survival. In recent years, FLT3 has been an important marker in different haematological malignancies, highlighting in acute myeloid leukaemia, where FLT3 mutations have been associated with the clinical prognosis, treatment and survival of patients. The most common form of FLT3 mutation is an internal tandem duplication (ITD) that promotes ligand-independent auto-phosphorylation and constitutive activation of the receptor. FLT3-ITD has been strongly associated with a bad prognosis, leukocytosis, high blast counts, increased risk of relapse and shorter overall survival. In order to improve the clinical condition of FLT3-ITD-positive patients, several FLT3 inhibitors have been developed showing variable results. Currently, the main challenges to be overcome are the different forms of resistance to FLT3 inhibitors. Thus, the purpose of this review is to present, in a general way, the current role that FLT3-ITD mutation plays in patients with AML, with a particular emphasis on the molecular mechanisms associated with clinical prognosis, treatment, and survival of patients.

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Resistance to current cancer treatments is an important problem that arises through various mechanisms, but one that stands out involves an overexpression of several factors associated with DNA repair. To counteract this type of resistance, different drugs have been developed to affect one or more DNA repair pathways, therefore, to test different compounds of natural origin that have been shown to induce cell death in cancer cells is paramount. Since natural compounds target components of the DNA repair pathways, they have been shown to promote cancer cells to be resensitized to current treatments. For this and other reasons, natural compounds have aroused great curiosity and several research projects are being developed around the world to establish combined treatments between them and radio or chemotherapy. In this work, we summarize the effects of different natural compounds on the DNA repair mechanisms of cancer cells and emphasize their possible application to re-sensitize these cells.