34 research outputs found
Quantitative Evidence of Wear-Off Effect at the End of the Intravenous IgG (IVIG) Dosing Cycle in Primary Immunodeficiency
PROTECTIVE LEVELS OF VARICELLA-ZOSTER ANTIBODY DID NOT EFFECTIVELY PREVENT CHICKENPOX IN AN X-LINKED AGAMMAGLOBULINEMIA PATIENT
Long persistence of tumour necrosis factorâα antagonistâinduced autoantibodies under subsequent treatment with ustekinumab but no adverse effects: a case study of 14 patients with psoriasis
A Single-Cycle Glycoprotein D Deletion Viral Vaccine Candidate, ÎgD-2, Elicits Polyfunctional Antibodies That Protect against Ocular Herpes Simplex Virus
Improved IgG3 levels and reduced infection rate in a woman with CVID switched from intravenous to subcutaneous immunoglobulin therapy
Development of a Pharmacokinetic Model Describing Neonatal Fc ReceptorâMediated Recycling of HL2351, a Novel Hybrid FcâFused Interleukinâ1 Receptor Antagonist, to Optimize Dosage Regimen
Transcriptome Analyses Identify Deregulated <i>MYC</i> in Early Onset Colorectal Cancer
Despite a global decrease in colorectal cancer (CRC) incidence, the prevalence of early-onset colorectal cancer (EOCRC), or those occurring in individuals before the age of 50, has steadily increased over the past several decades. When compared to later onset colorectal cancer (LOCRC) in individuals over 50, our understanding of the genetic and molecular underpinnings of EOCRCs is limited. Here, we conducted transcriptomic analyses of patient-matched normal colonic segments and tumors to identify gene expression programs involved in carcinogenesis. Amongst differentially expressed genes, we found increased expression of the c-MYC proto-oncogene (MYC) and its downstream targets in tumor samples. We identified tumors with high and low differential MYC expression and found patients with high-MYC tumors were older and overweight or obese. We also detected elevated expression of the PVT1 long-non-coding RNA (lncRNA) in most tumors and found gains in copy number for both MYC and PVT1 gene loci in 35% of tumors evaluated. Our transcriptome analyses indicate that EOCRC can be sub-classified into groups based on differential MYC expression and suggest that deregulated MYC contributes to CRCs that develop in younger patients