RESUMO
Acute Lymphocytic Leukemia (ALL) is a malignancy that originates from immature lymphoid cells and is clinically established with flow cytometry through disease-specific markers. Variation between ethnic groups is an epidemiological aspect of ALL. Higher incidence rates have been observed in Latin American patients and ALL in Latinos carries a dismal prognosis. The cell of origin in ALL is derived from immature cells of either the B or T lineage. Most reported data among Latinos either exclusively looks at B cell precursor ALL or do not distinguish between subtypes. We used the National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) database to delineate the differences in incidence rates of B-ALL and T-ALL across ethnic groups in the United States. Data from SEER-18 was used to compare incidence rates of T-ALL and B-ALL. Due to the utilization of cytogenetics and subsequent changes in ICD coding over the years examined the most recent data reported from 2002 to 2017. We compared rates in Non-Hispanic Whites (NHWs), Latinos, Blacks and Asian-Pacific Islanders (API). Age-adjusted incidence rates per 100,000 person-years were calculated. The incidence rate of B-ALL in the Latino population was consistently higher than other race/ethnicities throughout the years, ranging from 1.0 per 100,000 in 2002 to 2.5 per 100,000 in 2017. Blacks had the lowest age adjusted incidence rate (AAIR) of B-ALL overall, with rates approximately one third of those found in Latinos and the highest AAIR of T-ALL with an AAIR of 0.5 per 100,000.
Assuntos
Imunofenotipagem/métodos , Grupos Minoritários/estatística & dados numéricos , Leucemia-Linfoma Linfoblástico de Células Precursoras/epidemiologia , Programa de SEER/estatística & dados numéricos , Adolescente , Adulto , Criança , Pré-Escolar , Feminino , Seguimentos , Humanos , Incidência , Lactente , Masculino , Pessoa de Meia-Idade , Leucemia-Linfoma Linfoblástico de Células Precursoras/imunologia , Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia , Prognóstico , Estados Unidos/epidemiologia , Adulto JovemRESUMO
BACKGROUND: Prostate cancer is one of leading causes of cancer death among men worldwide. Androgen deprivation therapy is a central part of the prostate cancer treatment algorithm, however, resistance to androgen deprivation commonly leads to disease progression. Mutations in the phosphoinositide-3-kinase pathway (PI3K) have been implicated in cancer progression and the development of castration-resistance. Thus, inhibitors of this pathway and its downstream signaling partners have been studied as potential therapeutic agents to treat metastatic castration resistant prostate cancer (mCRPC). In this article, we review recent clinical results for novel targeted therapies against the PI3K-AKT-mTOR pathway. MATERIALS AND METHODS: Trials included in this systemic review were identified through conference abstracts, citations in review articles, PubMed, and ClinicalTrials.gov. Trial eligibility was independent of clinical setting or sample size. RESULTS: A total of 13 prospective clinical trials between 2012 and 2020 were reviewed: Two trials for pan-PI3K inhibitors, 2 trials for selective PI3K inhibitors, 4 trials for AKT inhibitors, 5 trials for mTOR inhibitors, and 1 for a combined PI3K and mTOR inhibitor. All studies were phase I or II studies with primary outcomes of either safety and tolerability or efficacy. CONCLUSION: Overall, pan-PI3K inhibitors and selective-PI3K inhibitors have not demonstrated clinical efficacy and may have significant adverse effects. AKT inhibitors may have significant adverse effects, but showed some evidence of improved survival. mTORC1 inhibitors show modest efficacy and significant adverse effects.