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Jason E Long

Publications and source records attributed to Jason E Long.

5 recordsLinked to original sources

Enozertinib Is a Selective, Brain-Penetrant EGFR Inhibitor for Treating Non-Small Cell Lung Cancers with EGFR Exon 20 and Atypical Mutations.

UNLABELLED: EGFR mutations are common oncogenic drivers in non-small cell lung cancer (NSCLC), and approximately half of patients develop brain metastases over the course of their disease. Patients with nonclassic EGFR mutations, such as insertions in exon 20, are a high unmet need with a worse prognosis compared with patients with classic EGFR mutations. Here, we describe the discovery and development of enozertinib (formerly ORIC-114), a highly brain-penetrant, orally bioavailable, irreversible inhibitor that targets EGFR exon 20 mutations with unparalleled kinome selectivity. Preclinical studies revealed strong potency and tumor regressions driven by enozertinib across a broad range of atypical EGFR-mutant models. In a phase I clinical trial of enozertinib in patients with advanced NSCLC bearing atypical mutations in EGFR, a patient harboring an EGFR exon 20 insertion experienced sustained complete response of all systemic and brain metastases. Together, these findings identify enozertinib as a promising investigational inhibitor to address the unmet need for brain-penetrant therapies in NSCLC with EGFR exon 20 insertions or other atypical mutations. SIGNIFICANCE: Preclinical and initial phase I clinical data demonstrate the potency, kinome selectivity, efficacy, and brain penetration of enozertinib in NSCLC with EGFR exon 20 insertions and atypical mutations, warranting further clinical development.

Carcinoma, Non-Small-Cell Lung↗

Cellular patterns of transcription factor expression in developing cortical interneurons.

Most gamma-aminobutyric acidergic interneurons in the neocortex and hippocampus are derived from subpallial progenitors in the medial ganglionic eminence and migrate tangentially to the pallium, where they differentiate into a diverse set of neuronal subtypes. Toward elucidating the mechanisms underlying the generation of interneuron diversity, we have studied in mice the expression patterns in differentiating and mature neocortical interneurons of 8 transcription factors, including 6 homeobox (Dlx1, Dlx2, Dlx5, Arx, Lhx6, Cux2), 1 basic helix-loop-helix, (NPAS1), and 1 bZIP (MafB). Their patterns of expression change during interneuron differentiation and show distinct distributions within interneuron subpopulations in adult neocortex. This study is a first step to define the combinatorial codes of transcription factors that participate in regulating the specification and function of cortical interneuron subtypes.

Aging↗

Short- and long-range attraction of cortical GABAergic interneurons by neuregulin-1.

Most cortical interneurons arise from the subcortical telencephalon, but the molecules that control their migration remain largely unidentified. Here, we show that different isoforms of Neuregulin-1 are expressed in the developing cortex and in the route that migrating interneurons follow toward the cortex, whereas a population of the migrating interneurons express ErbB4, a receptor for Neuregulin-1. The different isoforms of Neuregulin-1 act as short- and long-range attractants for migrating interneurons, and perturbing ErbB4 function in vitro decreases the number of interneurons that tangentially migrate to the cortex. In vivo, loss of Neuregulin-1/ErbB4 signaling causes an alteration in the tangential migration of cortical interneurons and a reduction in the number of GABAergic interneurons in the postnatal cortex. These observations provide evidence that Neuregulin-1 and its ErbB4 receptor directly control neuronal migration in the nervous system.

Animals↗

Identification and characterization of a novel transcript down-regulated in Dlx1/Dlx2 and up-regulated in Pax6 mutant telencephalon.

By using a custom-made array containing cDNAs preferentially expressed in the mouse embryonic telencephalon (Porteus et al. [1992] Brain Res Mol Brain Res 12:7-22; and Alessandro Bulfone, unpublished data), we studied the gene expression profile of the Dlx1/Dlx2(-/-) subpallium and Pax6(-/-) pallium. We identified a transcript corresponding to Unigene Cluster Mm.94021 and rat Evf-1, which is down-regulated in the Dlx1/Dlx2(-/-) subpallium and up-regulated in the Pax6(-/-) pallium. Here, we report the expression pattern of this transcript, designated mouse Evf1 (mEvf1), in the prenatal forebrain of wild-type, Dlx1/Dlx2(-/-) and Pax6(-/-) mice using RNA in situ hybridization and reverse transcriptase-polymerase chain reaction. In the wild-type forebrain mEvf1 expression is restricted to the ventral thalamus, hypothalamus, and subpallial telencephalon (caudal, lateral, and medial ganglionic eminences and septal primordia), whereas it is down-regulated in the Dlx1/Dlx2(-/-) subpallium (mainly in caudal, lateral, and medial ganglionic eminences), and up-regulated in the Pax6(-/-) lateral and ventral pallium at embryonic day 12.5 and in the dorsal, lateral, and ventral pallium at embryonic day 14.5.

Animals↗

DLX5 regulates development of peripheral and central components of the olfactory system.

Induction, neurogenesis, and synaptogenesis of the olfactory bulb are thought to require interactions with the olfactory epithelium. The Dlx family of homeobox genes is expressed in both the olfactory bulb and olfactory epithelium. In particular, Dlx5 is expressed in the olfactory placode, olfactory epithelium, and local circuit neurons of the olfactory bulb. Here we analyzed mice lacking DLX5 function. The Dlx5-/- mutation reduces the size of the olfactory epithelium. Although some olfactory neurons are formed, they fail to generate olfactory axons that innervate the olfactory bulb. Despite the lack of innervation, the olfactory bulb forms, and neurogenesis of projection and local circuit neurons proceeds. However, the mutation has a cell-autonomous effect on the ability of neural progenitors to produce olfactory bulb local circuit neurons, with granule cells more severely affected than periglomerular cells. In addition, the mutation has a noncell-autonomous effect on the morphogenesis of mitral cells.

Animals↗