RESUMEN
BACKGROUND AND PURPOSE: Leukoerythroblastic reaction (LER) is characterized by the presence of immature erythroid cells and myeloid precursors (metamyelocytes, myelocytes, promyelocytes, myeloblasts, and blasts) as well as, exclusively in myelofibrotic disorders, teardrop cells in the peripheral blood (J Pathol Bacteriol, 42, 1936, 541; Semaine Med, 22, 1902, 373). Research on how to interpret LER and its meaning in clinical practice is scarce, and there is no consensus on the diagnostic criteria. We summarize the current evidence with the aim of clarifying the knowledge on this subject. METHODS: We conducted a comprehensive search of the PubMed-MEDLINE, EMBASE and ELSEVIER databases, the Cochrane Library, Google Scholar, and medical journals to identify relevant papers. RESULTS: Our search identified 425 papers, of which, 35 (11 trials and 24 case reports) ultimately met the inclusion criteria. These showed two principal groups of diseases associated with leukoerythroblastosis (LEB), corresponding to solid and hematological malignancies. The other etiologies, in order of frequency, were hemolytic diseases, infection, and others, while hemorrhage was only reported in the trials group. CONCLUSION: The literature on LER is scarce and heterogeneous. The etiological factors of LER are diverse, and its presence in malignant disease is an indicator of disease progression and an adverse prognosis suggesting poor survival. In those cases where LER had neither hematological nor solid neoplasms, its manifestation, prognosis and its impact on our daily clinical practice are unknown.
Asunto(s)
Susceptibilidad a Enfermedades , Células Eritroides/patología , Leucocitos/patología , Trastornos Mieloproliferativos/diagnóstico , Trastornos Mieloproliferativos/etiología , Animales , Manejo de la Enfermedad , Humanos , Anamnesis , Trastornos Mieloproliferativos/terapiaRESUMEN
The fragile histidine triad (FHIT) gene encloses an active common chromosomal fragile site, FRA3B. This gene is known to be associated with genomic instability, apoptosis and DNA damage. FHIT disturbances have been related to carcinogenesis in different types of human tumor. Despite this, there are some controversies about the exact role of the FHIT gene in relation to tumor biology. Several pieces of evidence support the hypothesis that FHIT acts as a tumor suppressor gene. A loss or decrease in the Fhit protein expression appears to be related to tumor progression, poor prognostic factors and lower survival rates. The most frequent causes of FHIT expression changes are gene mutations, epigenetic alteration and loss of heterozygosity. This literature review aims to clarify the involvement of the FHIT gene in carcinogenesis, tumor progression and clinical outcome in prevalent solid malignancies, such as breast, lung, cervical, esophageal, gastric and colorectal cancers.