Thyroid Cancer Incidence Trends

xlomafota13 shared this article with you from Inoreader Thyroid Cancer Incidence Trends Among Filipinos in the United States Via The Laryngoscope Objective To analyze thyroid cancer incidence trends among Filipinos relative to non-Filipino Asians and non-Hispanic Whites in the US. Study Design Population-based analysis of cancer incidence data. Methods Population-based analysis of cancer incidence data from Surveillance, Epidemiology, and End Results 9 detailed Asian/Pacific Islander subgroup incidence and population datasets. Adult patients aged 20 and older with thyroid cancer diagnosed in 2004 to 2014 were included. Annual percent change (APC) of the incidence rates were calculated using joinpoint regression analysis. Results The incidence rates were 19.57 (95% CI 19.03–20.12) per 100,000 for Filipinos, 10.45 (95% CI 10.22–10.68) per 100,000 for non-Filipino Asians, and 13.94 (95% CI 13.85–14.02) per 100,000 for non-Hispanic Whites. The highest increase was seen among non-Hispanic Whites (average APC 5.04, 95% CI 4.61–5.46). Incidence rates of tumors ≤ 2 cm remained stable among Filipinos but increased in non-Filipino Asians (average APC 5.38, 95% CI 2.51–8.34) and non-Hispanic Whites (average APC 5.81 95% CI 4.52–7.11). Conclusion Filipinos have high incidence of thyroid cancer compared with other racial/ethnic groups. However, non-Hispanic Whites have the highest increase in incidence rates, resulting in a significant narrowing of the gap in incidence rates between Filipinos and non-Hispanic Whites. This is most likely due to enhanced detection of small tumors in non-Hispanic Whites. Laryngoscope, 2021 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Concomitant Variants in NF1, LZTR1, and GNAZ Genes Probably Contribute to the Aggressiveness of Plexiform Neurofibroma and Warrant Treatment with MEK Inhibitor

xlomafota13 shared this article with you from Inoreader Concomitant Variants in NF1, LZTR1, and GNAZ Genes Probably Contribute to the Aggressiveness of Plexiform Neurofibroma and Warrant Treatment with MEK Inhibitor Via Experimental Dermatology Abstract Neurofibromatosis 1 (NF1) is caused by germline mutations in the NF1 gene and manifests as proliferation of various tissues, including plexiform neurofibromas. The plexiform neurofibroma phenotype varies from indolent to locally aggressive, suggesting contributions of other modifiers in addition to somatic loss of NF1. Here, we investigated a life-threatening plexiform neurofibroma in a 9-month-old female infant with NF1. Germline mutations in two Rasopathy-associated genes were identified using whole exome sequencing - a de-novo pathogenic variant in the NF1 gene, and a known pathogenic variant in the LZTR1 gene. Somatic analysis of the plexiform neurofibroma revealed NF1 loss of heterozygosity and a variant in GNAZ, a gene encoding a G Protein Coupled Receptor. Cells expressing mutant GNAZ exhibited increased ERK 1,2 activation compared to those expressing wild type GNAZ. Taken together, we suggest the variants in NF1, LZRT1, and GNAZ act synergistically in our patient, leading to MAPK pathway activation and contributing to the severity of the patient's plexiform neurofibromatosis. After treatment with the MEK inhibitor, trametinib, a prominent clinical improvement was observed in this patient. This case study contributes to the knowledge of germline and somatic non-NF1 variants affecting the NF1 clinical phenotype and supports use of personalized, targeted therapy. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.