Mammalian Genome最新文献

{"title":"Mammalian genome research resources available from the National BioResource Project in Japan","authors":"Saori Mizuno-Iijima, Shoko Kawamoto, Masahide Asano, Tomoji Mashimo, Shigeharu Wakana, Katsuki Nakamura, Ken-ichi Nishijima, Hitoshi Okamoto, Kuniaki Saito, Sawako Yoshina, Yoshihiro Miwa, Yukio Nakamura, Moriya Ohkuma, Atsushi Yoshiki","doi":"10.1007/s00335-024-10063-2","DOIUrl":"https://doi.org/10.1007/s00335-024-10063-2","url":null,"abstract":"<p>Mammalian genome research has conventionally involved mice and rats as model organisms for humans. Given the recent advances in life science research, to understand complex and higher-order biological phenomena and to elucidate pathologies and develop therapies to promote human health and overcome diseases, it is necessary to utilize not only mice and rats but also other bioresources such as standardized genetic materials and appropriate cell lines in order to gain deeper molecular and cellular insights. The Japanese bioresource infrastructure program called the National BioResource Project (NBRP) systematically collects, preserves, controls the quality, and provides bioresources for use in life science research worldwide. In this review, based on information from a database of papers related to NBRP bioresources, we present the bioresources that have proved useful for mammalian genome research, including mice, rats, other animal resources; DNA-related materials; and human/animal cells and microbes.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"90 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142200549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying new molecular signatures and potential therapeutics for idiopathic pulmonary fibrosis: a network medicine approach","authors":"Mecbure Nur Akca, Ceyda Kasavi","doi":"10.1007/s00335-024-10069-w","DOIUrl":"https://doi.org/10.1007/s00335-024-10069-w","url":null,"abstract":"<p>Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease characterized by excessive collagen deposition and fibrosis of the lung parenchyma, leading to respiratory failure. The molecular mechanisms underlying IPF pathogenesis remain incompletely understood, hindering the development of effective therapeutic strategies. We have used a network medicine approach to comprehensively analyze molecular interactions and identify novel molecular signatures and potential therapeutics associated with IPF progression. Our integrative analysis revealed dysregulated molecular networks that are central to IPF pathophysiology. We have highlighted key molecular players and signaling pathways that are implicated in aberrant fibrotic processes. This systems-level understanding enables the identification of new biomarkers and therapeutic targets for IPF, providing potential avenues for precision medicine. Drug repurposing analysis revealed several drug candidates with anti-fibrotic, anti-inflammatory, and anti-cancer activities that could potentially slow fibrotic progression and improve patient outcomes. This study offers new insights into the molecular underpinnings of IPF and highlights network medicine approaches in uncovering complex disease mechanisms. The molecular signatures and therapeutic targets identified hold promise for developing precision therapies tailored to individual patients, ultimately advancing the management of this debilitating lung disease.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"59 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142200547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Commentary: The International Mouse Phenotyping Consortium: high-throughput in vivo functional annotation of the mammalian genome","authors":"K. C. Kent Lloyd","doi":"10.1007/s00335-024-10068-x","DOIUrl":"https://doi.org/10.1007/s00335-024-10068-x","url":null,"abstract":"<p>The International Mouse Phenotyping Consortium (IMPC) is a worldwide effort producing and phenotyping knockout mouse lines to expose the pathophysiological roles of all genes in human diseases and make mice and data available and accessible to the global research community. It has created new knowledge on the function of thousands of genes for which little to anything was known. This new knowledge has informed the genetic basis of rare diseases, posited gene product influences on common diseases, influenced research on targeted therapies, revealed functional pleiotropy, essentiality, and sexual dimorphism, and many more insights into the role of genes in health and disease. Its scientific contributions have been many and widespread, however there remain thousands of “dark” genes yet to be illuminated. Nearing the end of its current funding cycle, IMPC is at a crossroads. The vision forward is clear, the path to proceed less so.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"3 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142200548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The interplay of hydrogen sulfide and microRNAs in cardiovascular diseases: insights and future perspectives.","authors":"Yunjia Song, Shuo Cao, Xutao Sun, Guozhen Chen","doi":"10.1007/s00335-024-10043-6","DOIUrl":"10.1007/s00335-024-10043-6","url":null,"abstract":"<p><p>Hydrogen sulfide (H₂S) is recognized as the third gasotransmitter, after nitric oxide (NO) and carbon monoxide (CO). It is known for its cardioprotective properties, including the relaxation of blood vessels, promotion of angiogenesis, regulation of myocardial cell apoptosis, inhibition of vascular smooth muscle cell proliferation, and reduction of inflammation. Additionally, abnormal H₂S generation has been linked to the development of cardiovascular diseases (CVD), such as pulmonary hypertension, hypertension, atherosclerosis, vascular calcification, and myocardial injury. MicroRNAs (miRNAs) are non-coding, conserved, and versatile molecules that primarily influence gene expression by repressing translation and have emerged as biomarkers for CVD diagnosis. Studies have demonstrated that H₂S can ameliorate cardiac dysfunction by regulating specific miRNAs, and certain miRNAs can also regulate H₂S synthesis. The crosstalk between miRNAs and H₂S offers a novel perspective for investigating the pathophysiology, prevention, and treatment of CVD. The present analysis outlines the interactions between H₂S and miRNAs and their influence on CVD, providing insights into their future potential and advancement.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":" ","pages":"309-323"},"PeriodicalIF":2.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141248187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic patterns of selection in morphometric traits across diverse Indian cattle breeds.","authors":"Divya Rajawat, Sonali Sonejita Nayak, Karan Jain, Anurodh Sharma, Subhashree Parida, Sarada Prasanna Sahoo, Bharat Bhushan, D B Patil, Triveni Dutt, Manjit Panigrahi","doi":"10.1007/s00335-024-10047-2","DOIUrl":"10.1007/s00335-024-10047-2","url":null,"abstract":"<p><p>This study seeks a comprehensive exploration of genome-wide selective processes impacting morphometric traits across diverse cattle breeds, utilizing an array of statistical methods. Morphometric traits, encompassing both qualitative and quantitative variables, play a pivotal role in characterizing and selecting livestock breeds based on their external appearance, size, and physical attributes. While qualitative traits, such as color, horn structure, and coat type, contribute to adaptive features and breed identification, quantitative traits like body weight and conformation measurements bear a closer correlation with production characteristics. This study employs advanced genotyping technologies, including the Illumina BovineSNP50 Bead Chip and next-generation sequencing methods like Reduced Representation sequencing, to identify genomic signatures associated with these traits. We applied four intra-population methods to find evidence of selection, such as Tajima's D, CLR, iHS, and ROH. We found a total of 40 genes under the selection signature, that were associated with morphometric traits in five cattle breeds (Kankrej, Tharparkar, Nelore, Sahiwal, and Gir). Crucial genes such as ADIPDQ, DPP6, INSIG1, SLC35D2 in Kankrej, LPL, ATP6V1B2, CDC14B in Tharparkar, HPSE2, PLAG1 in Nelore, PCSK1, PRKD1 in Sahiwal, and GNAQ, HPCAL1 in Gir were identified in our study. This approach provides valuable insights into the genetic basis of variations in body weight and conformation traits, facilitating informed selection processes and offering a deeper understanding of the evolutionary and domestication processes in diverse cattle breeds.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":" ","pages":"377-389"},"PeriodicalIF":2.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal genetic diversity and phylogenetic analysis of Indian riverine and swamp buffaloes: insights from complete mitochondrial genomes.","authors":"Sonika Ahlawat, Upasna Sharma, Pooja Chhabra, Reena Arora, Rekha Sharma, Karan Veer Singh, R K Vijh","doi":"10.1007/s00335-024-10048-1","DOIUrl":"10.1007/s00335-024-10048-1","url":null,"abstract":"<p><p>This study explored the genetic diversity and evolutionary history of riverine and swamp buffaloes in India, utilizing complete mitochondrial genome sequences. Through comprehensive sampling across varied agro-climatic zones, including 91 riverine buffaloes from 12 breeds and 6 non-descript populations, along with 16 swamp buffaloes of the Luit breed, this study employed next-generation sequencing techniques to map the mitogenomic landscape of these subspecies. Sequence alignments were performed with the buffalo mitochondrial reference genome to identify mitochondrial DNA (mtDNA) variations and distinct maternal haplogroups among Indian buffaloes. The results uncovered the existence of 212 variable sites in riverine buffaloes, yielding 67 haplotypes with high haplotype diversity (0.991), and in swamp buffaloes, 194 variable sites resulting in 12 haplotypes, displaying haplotype diversity of 0.950. Phylogenetic analyses elucidated the genetic relationships between Indian buffaloes and the recognized global haplogroups, categorizing Indian swamp buffaloes predominantly into the SA haplogroup. Intriguingly, the haplogroup SB2b was observed for the first time in swamp buffaloes. Conversely, riverine buffaloes conformed to established sub-haplogroups RB1, RB2, and RB3, underscoring the notion of Northwestern India as a pivotal domestication site for riverine buffaloes. The study supports the hypothesis of independent domestication events for riverine and swamp buffaloes, highlighting the critical role of genetic analysis in unraveling the complex evolutionary pathways of domestic animals. This investigation contributes to the global understanding of buffalo mitogenome diversity, offering insights into this important livestock species' domestication and dispersal patterns.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":" ","pages":"390-398"},"PeriodicalIF":2.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141419784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tachol1 QTL on mouse chromosome 1 is responsible for hypercholesterolemia and diet-induced obesity.","authors":"Jung Han Kim, Marvin A Simpkins, Nicholas T Williams, Emma Cimino, Jadyn Simon, Tanner R Richmond, Jared Youther, Hannah Slutz, James Denvir","doi":"10.1007/s00335-024-10045-4","DOIUrl":"10.1007/s00335-024-10045-4","url":null,"abstract":"<p><p>Hypercholesterolemia raises the risk for cardiovascular complications and overall health. Hypercholesterolemia is common, affecting 10% of the general population of the US, and heritable. Most individuals with hypercholesterolemia have a polygenic predisposition to the condition. Previously we identified a quantitative trait locus, Tachol1, linked to hypercholesterolemia on mouse chromosome 1 (Chr1) in a cross between C57BL/6J (B6) and TALLYHO/JngJ (TH) mice, a polygenic model for human obesity, type 2 diabetes and hyperlipidemia. Subsequently, using congenic mice that carry a TH-derived genomic segment of Chr1 on a B6 background, we demonstrated that the distal segment of Chr1, where Tachol1 maps, is necessary to cause hypercholesterolemia, as well as diet-induced obesity. In this study, we generated overlapping subcongenic lines to the distal segment of congenic region and characterized subcongenic mice carrying the smallest TH region of Tachol1, ~ 16.2 Mb in size (B6.TH-Chr1-16.2 Mb). Both male and female B6.TH-Chr1-16.2 Mb mice showed a significantly increased plasma total cholesterol levels compared to B6 on both chow and high fat (HF) diet. B6.TH-Chr1-16.2 Mb mice also had greater fat mass than B6 on HF diet, without increasing food intake. The gene and protein expression levels of absent in melanoma 2 (Aim2) gene were significantly upregulated in B6.TH-Chr1-16.2 Mb mice compared to B6. In summary, we confirmed the effect of Tachol1 on hypercholesterolemia and diet-induced obesity using subcongenic analysis.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":" ","pages":"324-333"},"PeriodicalIF":2.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11339885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141248185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fine mapping and candidate gene analysis of Dravet syndrome modifier loci on mouse chromosomes 7 and 8.","authors":"Nicole A Hawkins, Nathan Speakes, Jennifer A Kearney","doi":"10.1007/s00335-024-10046-3","DOIUrl":"10.1007/s00335-024-10046-3","url":null,"abstract":"<p><p>Dravet syndrome is a developmental and epileptic encephalopathy (DEE) characterized by intractable seizures, comorbidities related to developmental, cognitive, and motor delays, and a high mortality burden due to sudden unexpected death in epilepsy (SUDEP). Most Dravet syndrome cases are attributed to SCN1A haploinsufficiency, with genetic modifiers and environmental factors influencing disease severity. Mouse models with heterozygous deletion of Scn1a recapitulate key features of Dravet syndrome, including seizures and premature mortality; however, severity varies depending on genetic background. Here, we refined two Dravet survival modifier (Dsm) loci, Dsm2 on chromosome 7 and Dsm3 on chromosome 8, using interval-specific congenic (ISC) mapping. Dsm2 was complex and encompassed at least two separate loci, while Dsm3 was refined to a single locus. Candidate modifier genes within these refined loci were prioritized based on brain expression, strain-dependent differences, and biological relevance to seizures or epilepsy. High priority candidate genes for Dsm2 include Nav2, Ptpn5, Ldha, Dbx1, Prmt3 and Slc6a5, while Dsm3 has a single high priority candidate, Psd3. This study underscores the complex genetic architecture underlying Dravet syndrome and provides insights into potential modifier genes that could influence disease severity and serve as novel therapeutic targets.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":" ","pages":"334-345"},"PeriodicalIF":2.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11329421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predicting the potential deterioration of Barrett's esophagus based on gut microbiota: a Mendelian randomization analysis.","authors":"Conghan Li, Panyin Shu, Taiyu Shi, Yuerong Chen, Ping Mei, Yizhong Zhang, Yan Wang, Xinyan Du, Jianning Wang, Yixin Zhang, Bin Liu, Zhijin Sheng, Shixin Chan, Zhangyong Dan","doi":"10.1007/s00335-024-10042-7","DOIUrl":"10.1007/s00335-024-10042-7","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Esophageal adenocarcinoma (EAC) is one of the most malignant tumors in the digestive system. To make thing worse, the scarcity of treatment options is disheartening. However, if detected early, there is a possibility of reversing the condition. Unfortunately, there is still a lack of relevant early screening methods. Considering that Barrett's esophagus (BE), a precursor lesion of EAC, has been confirmed as the only known precursor of EAC. Analyzing which BE cases will progress to EAC and understanding the processes and mechanisms involved is of great significance for early screening of such patients. Considering the significant alterations in the gut microbiota of patients with BE and its potential role in the progression to EAC, this study aims to analyze the relationship between BE, EAC, and GM to identify potential diagnostic biomarkers and therapeutic targets. This study utilized comprehensive statistical data on gut microbiota from a large-scale genome-wide association meta-analysis conducted by the MiBioGen consortium (n = 18,340). Subsequently, we selected a set of single nucleotide polymorphisms (SNPs) that fell below the genome-wide significance threshold (1 × 10-5) as instrumental variables. To investigate the causal relationship between gut microbiota and BE and EAC, we employed various MR analysis methods, including Inverse Variance Weighting (IVW), MR-Egger regression, weighted median (WM), and weighted mean. Additionally, we assessed the level of pleiotropy, heterogeneity, and stability of genetic variations through MR-Egger intercept test, MR-PRESSO, Cochran's Q test, and \"leave-one-out\" sensitivity analysis. Furthermore, we conducted reverse MR analysis to identify the causal relationships between gut microbiota and BE and EAC. The results from the Inverse Variance-Weighted (IVW) analysis indicate that Alistipes (P = 4.86 × 10&lt;sup&gt;-2&lt;/sup&gt;), Lactobacillus (P = 2.11 × 10&lt;sup&gt;-2&lt;/sup&gt;), Prevotella 7 (P = 4.28 × 10&lt;sup&gt;-2&lt;/sup&gt;), and RuminococcaceaeUCG004 (P = 4.34 × 10&lt;sup&gt;-2&lt;/sup&gt;) are risk factors for Barrett's esophagus (BE), while Flavonifractor (P = 8.81 × 10&lt;sup&gt;-3&lt;/sup&gt;) and RuminococcaceaeUCG004 (P = 4.99 × 10&lt;sup&gt;-2&lt;/sup&gt;) are risk factors for esophageal adenocarcinoma (EAC). On the other hand, certain gut microbiota genera appear to have a protective effect against both BE and EAC. These include Eubacterium (nodatum group) (P = 4.51 × 10&lt;sup&gt;-2&lt;/sup&gt;), Holdemania (P = 1.22 × 10&lt;sup&gt;-2&lt;/sup&gt;), and Lactococcus (P = 3.39 × 10&lt;sup&gt;-2&lt;/sup&gt;) in the BE cohort, as well as Eubacterium (hallii group) (P = 4.07 × 10&lt;sup&gt;-2&lt;/sup&gt;) and Actinomyces (P = 3.62 × 10&lt;sup&gt;-3&lt;/sup&gt;) in the EAC cohort. According to the results of reverse MR analysis, no significant causal effects of BE and EAC on gut microbiota were observed. Furthermore, no significant heterogeneity or pleiotropy was detected in the instrumental variables. We have established a causal relationship between the gut microbiota and BE and EAC. This study holds profound si","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":" ","pages":"399-413"},"PeriodicalIF":2.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141419785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the causal relationship between immune cells and prostatitis: evidence from bidirectional mendelian randomization analysis.","authors":"Genyi Qu, Weimin Jiang, Zhaohui Long, Xing Zhou, Yijie Wang, Guang Yang, Cheng Tang, Yong Xu","doi":"10.1007/s00335-024-10044-5","DOIUrl":"10.1007/s00335-024-10044-5","url":null,"abstract":"<p><p>Prostatitis represents a common disease of the male genitourinary system, significantly impacting the physical and mental health of male patients. While numerous studies have suggested a potential link between immune cell activity and prostatitis, the exact causal role of immune cells in prostatitis remains uncertain. This study aims to explore the causal relationship between immune cell characteristics and prostatitis using a bidirectional Mendelian randomization approach. This study utilizes data from the public GWAS database and employs bidirectional Mendelian randomization analysis to investigate the causal relationship between immune cells and prostatitis. The causal relationship between 731 immune cell features and prostatitis was primarily investigated through inverse variance weighting (IVW), complemented by MR-Egger regression, a simple model, the weighted median method, and a weighted model. Ultimately, the results underwent sensitivity analysis to assess the heterogeneity, horizontal pleiotropy, and stability of Single Nucleotide Polymorphisms (SNPs) in immune cells and prostatitis. MR analysis revealed 17 immune cells exhibiting significant causal effects on prostatitis. In contrast, findings from reverse MR indicated a significant causal relationship between prostatitis and 13 immune cells. Our study utilizes bidirectional Mendelian Randomization to establish causal relationships between specific immune cell phenotypes and prostatitis, highlighting the reciprocal influence between immune system behavior and the disease. Our findings suggest targeted therapeutic approaches and the importance of including diverse populations for broader validation and personalized treatment strategies.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":" ","pages":"474-483"},"PeriodicalIF":2.7,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141179799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}