Core Insights - The research published in "Nature" reveals a significant advancement in understanding mammalian jaw joint evolution, proposing a four-stage sequence that outlines the transformation of this critical anatomical structure [1][2][3] Group 1: Research Findings - The study identifies two fossil specimens that were overlooked for decades, which have now provided new insights into the evolution of the jaw joint in mammals [1] - The first fossil, from Sichuan, exhibits a unique secondary jaw joint structure, challenging previous notions about the morphology of secondary joints in quadrupeds [1][2] - The second fossil, from Yunnan, has led to the identification of a new genus and species, providing empirical support for the hypothesis regarding the origin of the mammalian jaw joint [2] Group 2: Evolutionary Mechanisms - The research proposes that the evolution of the jaw joint involved multiple independent origins, with previously identified features being re-evaluated in their significance for mammalian classification [2][3] - The study introduces the concept of environmentally induced developmental variation as a potential driver of jaw joint diversity, moving beyond the previously popular hypothesis of size reduction [2][3] Group 3: Implications for Future Research - This research not only enhances the understanding of mammalian jaw joint evolution but also establishes a framework for studying the evolutionary pathways of primitive and secondary jaw joints [3] - The findings underscore the interplay of biomechanical, ecological, and behavioral factors in shaping the evolutionary trajectory of jaw joints, offering valuable insights for vertebrate morphology and functional evolution studies [3]

Core Viewpoint - The article discusses a recent study that highlights the role of fetal-like transcription programs in promoting phenotypic plasticity in colorectal cancer, which is crucial for cancer progression, metastasis, and treatment resistance [2][3]. Group 1: Research Development - A patient-derived organoid model (CiPDO) was developed to capture the fetal-like plasticity state in colorectal cancer [4]. - The CiPDO system was cultivated under specific conditions using EGF, CHIR99021, LDN-214117, and FGF2, allowing for long-term expansion of colorectal cancer cells while retaining fetal-like characteristics [7]. Group 2: Key Findings - The research identified an oncofetal state (OnFS) enriched in advanced tumors, associated with key plasticity features including epithelial-mesenchymal transition, increased metastasis, and enhanced treatment resistance [8]. - Mechanistically, the FGF2-AP-1 signaling pathway was shown to maintain the OnFS program and related phenotypic plasticity in colorectal cancer [9]. Group 3: Implications - The patient-derived organoid model provides a powerful platform for studying the fetal-like characteristics of cancer cells and their roles in tumor progression and treatment resistance in colorectal cancer [11].