In this work, we used global differential gene expression profiling to better understand the transcriptional activity of diffuse intrinsic pontine gliomas in the brainstem. We discovered that 10 of the top 1% of transcripts that were most differentially expressed between tumors of patients who survived greater or less than six months were non-coding RNA transcripts, both microRNA and snoRNAs, by comparing the transcriptomes of tumors from patients who survived greater or less than six months. These non-coding RNA transcripts may be employed as a diagnostic tool. More specifically, SNORA22 levels were significantly higher in tumors of patients who survived for more than 6 months, and SNORA22 levels in each patient's tumor also displayed a linear correlation with the amount of time each patient survived, though this correlation was not statistically significant to 95 percent confidence. SNORA22 is a member of the H/ACA box of snoRNAs, which direct the conversion of uridine to pseudouridine in substrate RNAs, primarily ribosomal RNAs (rRNAs) (7). Exosomal RNA SNORA22 has been shown to be overexpressed in pancreatic ductal adenocarcinoma (PDAC) (8). In a study of prostate cancer xenografts, SNORA22 was discovered to be expressed differently in metastatic and non-metastatic xenografts (9). Breast cancer (10), ovarian cancer (11), gastric cancer (12), and hepatocellular carcinoma (12) have all been linked to miR939 (13). Prostate cancer (14, 15), colorectal cancer (16), hepatocellular carcinoma (17), and non-small cell lung carcinoma (18) have all been linked to miR154 (18). Nonsmall cell lung cancer (19), gastric carcinoma (20), ovarian cancer (21), colorectal cancer (22-23), bladder cancer (24), breast cancer (25), and esophageal carcinoma (26) have all been linked to miR429 expression (26). Breast cancer (27-29), gastric cancer (30, 31), bladder cancer (32), lung adenocarcinoma (33), liver cancer (34), prostate cancer (35), and hepatocellular carcinoma (36), have all been linked to miR485 in some way (36, 37). One intriguing miR485 regulatory circuit included NF-YB regulation by miR-485-3p, which ultimately resulted in variations in DNA topoisomerase II expression, resulting in variations in responsiveness to topoisomerase inhibitor (38). Both rhabdomyosarcoma Rh30 cell and the leukemia CEM/VM-1-5 cell line were used in these experiments (38). In terms of miR595, the transcription factor Sox7 was regulated by mir595, which aided the growth of human glioblastoma cell lines (39). Ovarian cancer (40), neuroblastoma (41) and hepatocellular carcinoma (42) have all been linked to miR595 expression (42). We discovered that individuals with diffuse intrinsic pontine glioma differently express a number of non-coding RNA transcripts, including microRNAs and snoRNAs, by analyzing the transcriptomes of tumors from patients who lived longer or less than six months. Except for one ncRNA transcript, SNORA22, all 10 differentially expressed ncRNA transcripts were significantly lower in the tumours of patients who survived more than 6 months. The length of time each patient lived (overall survival) was linearly associated with the expression of SNORA22 and SNORA22 alone, and this association approached but did not reach statistical significance (95 percent confidence). All of the microRNAs that were shown to be differently expressed in DIPG depending on patient outcomes have previously been linked to cancer etiology in a variety of malignancies. This is the first study to show that the expression of these microRNAs differs depending on the patient's outcome in DIPG. These findings warrant further investigation into the contribution of each of these microRNA and snoRNA in the etiology of DIPG, as well as whether any of them can be used to stratify patients at the time of diagnosis into groups who will have more severe disease courses and may benefit from more intensive radiation therapy. Understanding the disease's transcriptional landscape is the initial step in identifying treatment targets and developing new treatment methods for DIPG patients.