The primary function of the corpus luteum is secretion of the hormone progesterone, which is required for maintenance of normal pregnancy in mammals. The corpus luteum develops from residual follicular granulosal and thecal cells after ovulation. Luteinizing hormone (LH) from the anterior pituitary is important for normal development and function of the corpus luteum in most mammals, although growth hormone, prolactin, and estradiol also play a role in several species. The mature corpus luteum is composed of at least two steroidogenic cell types based on morphological and biochemical criteria and on the follicular source of origin. Small luteal cells appear to be of thecal cell origin and respond to LH with increased secretion of progesterone. LH directly stimulates the secretion of progesterone from small luteal cells via activation of the protein kinase A second messenger pathway. Large luteal cells are of granulosal cell origin and contain receptors for PGF(2alpha) and appear to mediate the luteolytic actions of this hormone. If pregnancy does not occur, the corpus luteum must regress to allow follicular growth and ovulation and the reproductive cycle begins again. Luteal regression is initiated by PGF(2alpha) of uterine origin in most subprimate species. The role played by PGF(2alpha) in primates remains controversial. In primates, if PGF(2alpha) plays a role in luteolysis, it appears to be of ovarian origin. The antisteroidogenic effects of PGF(2alpha) appear to be mediated by the protein kinase C second messenger pathway, whereas loss of luteal cells appears to follow an influx of calcium, activation of endonucleases, and an apoptotic form of cell death. If the female becomes pregnant, continued secretion of progesterone from the corpus luteum is required to provide an appropriate uterine environment for maintenance of pregnancy. The mechanisms whereby the pregnant uterus signals the corpus luteum that a conceptus is present varies from secretion of a chorionic gonadotropin (primates and equids), to secretion of an antiluteolytic factor (domestic ruminants), and to a neuroendocrine reflex arc that modifies the secretory patterns of hormones from the anterior pituitary (most rodents).

While the promise of the Human Genome Project provided significant insights into the structure of the human genome, the complexities of disease at the individual level have made it difficult to utilize –omic information in clinical decision making. Some of the existing constraints have been minimized by technological advancements that have reduced the cost of sequencing to a rate far in excess of Moore’s Law (a halving in cost per unit output every 18 months). The reduction in sequencing costs has made it economically feasible to create large data commons capturing the diversity of disease across populations. Until recently, these data have primarily been consumed in clinical research, but now increasingly being considered in clinical decision- making. Such advances are disrupting common diagnostic business models around which academic medical centers (AMCs) and molecular diagnostic companies have collaborated over the last decade. Proprietary biomarkers and patents on proprietary diagnostic content are no longer driving biomarker collaborations between industry and AMCs. Increasingly the scope of the data commons and biorepositories that AMCs can assemble through a nexus of academic and pharma collaborations is driving a virtuous cycle of precision medicine capabilities that make an AMC relevant and highly competitive. A rebalancing of proprietary strategies and open innovation strategies is warranted to enable institutional precision medicine asset portfolios. The scope of the AMC’s clinical trial and research collaboration portfolios with industry are increasingly dependent on the currency of data, and less on patents. Intrapeneurial support of internal service offerings, clinical trials and clinical laboratory services for example, will be important new points of emphasis at the academic-industry interface. Streamlining these new models of industry collaboration for AMCs are a new area for technology transfer offices to offer partnerships and to add value beyond the traditional intellectual property offering.

Innovation ecosystems tied to academic medical centers (AMCs) are inextricably linked to policy, practices, and infrastructure resulting from the Bayh-Dole Act in 1980. Bayh-Dole smoothed the way to patenting and licensing new drugs and, to some degree, medical devices and diagnostic reagents. Property rights under Bayh-Dole provided significant incentive for industry investments in clinical trials, clinical validation, and industrial scale-up of products that advanced health care. Bayh-Dole amplified private investment in biotechnology drug development and, from the authors' perspective, did not significantly interfere with the ability of AMCs to produce excellent peer-reviewed science. In today's policy environment, it is increasingly difficult to patent and license products based on the laws of nature-as the scope of patentability has been narrowed by case law and development of a suitable clinical and business case for the technology is increasingly a gating consideration for licensees. Consequently, fewer academic patents are commercially valuable. The role of technology transfer organizations in engaging industry partners has thus become increasingly complex. The partnering toolbox and organizational mandate for commercialization must evolve toward novel collaborative models that exploit opportunities for future patent creation (early drug discovery), data exchange (precision medicine using big data), cohort assembly (clinical trials), and decision rule validation (clinical trials). These inputs contribute to intellectual property rights, and their clinical exploitation manifests the commercialization of translational science. New collaboration models between AMCs and industry must be established to leverage the assets within AMCs that industry partners deem valuable.

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