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Purpose of Review: The purpose of this review is to contextualize findings from the first 25 years of PTSD genetics research, focusing on the most robust findings and interpreting results in light of principles that have emerged from modern genetics studies., Recent Findings: Genome-wide association studies (GWAS) encompassing tens of thousands of participants enabled the first molecular genetic heritability and genetic correlation estimates for PTSD in 2017. In 2018, highly promising loci for PTSD were reported, including variants in and near the CAMKV, KANSL1, and TCF4 genes. Twin studies from 25 years ago established that PTSD is genetically influenced and foreshadowed the molecular genetic findings of today. Discoveries that were impossible with smaller studies have been achieved via collaborative/team-science efforts. Most promisingly, individual genomic loci offer entirely novel clues about PTSD etiology, providing the raw material for transformative discoveries, and the future of PTSD research is bright.

All-trans-retinoic acid (RA) has been demonstrated to inhibit the growth of numerous breast carcinoma cell lines. In this study we demonstrated that RA inhibits estradiol stimulation of proliferation of the estrogen-dependent breast carcinoma cell lines MCF-7 and ZR-75. RA inhibition of MCF-7 breast carcinoma cell proliferation is associated with the marked stimulation of the synthesis and secretion of a 75,000 molecular weight protein. Minor stimulation of the synthesis and secretion of other proteins was also noted, including 160,000, 95,000, 89,000, 82,000, 52,000 and 46,000 molecular weight proteins. Increased synthesis and secretion of the Mr 75,000 protein was noted with as little as 10 nM RA. Stimulation of the synthesis and secretion of this protein occurred within 24 h of adding the retinoid and at the time of RA inhibition of cellular proliferation. RA stimulated the production and secretion of this protein both in the absence and presence of estradiol. Stimulation of the secretion and synthesis was not noted in the presence of difluoromethyl-ornithine or tamoxifen, both of which significantly inhibited cellular proliferation. The estrogen-dependent breast carcinoma cell line ZR-75 when exposed to RA also expressed increased synthesis of the Mr 75,000 and 46,000 proteins but increased synthesis was not noted in the RA-resistant cell line MDA-MB-231. Stimulation of the synthesis and secretion of the Mr 75,000 and/or 46,000 proteins may be intimately involved in RA inhibition of cellular proliferation.