Biochemistry and Biophysics Reports最新文献

{"title":"Deciphering tryptophan metabolism in colorectal cancer through multi-omics analysis.","authors":"Chengcheng Zhang, Zhijing Rao, Xiangyang Zhan, Jingru Qin, Lu Yang, Qianqian Yin, Junqing Ji, Xiaoxue Zhao, Yiyi Liu, Zhanhui Lu, Guoying Wang, Xingshuai Huang, Wenbo Shi, Wan Su, Zhongqi Wang","doi":"10.1016/j.bbrep.2025.102157","DOIUrl":"10.1016/j.bbrep.2025.102157","url":null,"abstract":"<p><p>Metabolic reprogramming is essential for colorectal cancer (CRC) progression, and recent studies have pointed to tryptophan metabolism as a crucial modulator of the tumor immune microenvironment. In this study, we performed untargeted metabolomics analyses and identified significant differences between CRC tissues and matched adjacent tissues, highlighting alterations in tryptophan metabolism. Targeted metabolomics, combined with public single-cell RNA sequencing datasets, further validated enhanced tryptophan metabolism activity in CRC, correlating closely with tumor purity and poor patient prognosis. Using multiple machine learning algorithms, we developed and validated a prognostic risk model based on key tryptophan metabolism-related genes across several independent cohorts. Single-cell transcriptomic analyses also revealed a distinct tumor cell subcluster (C1), characterized by elevated tryptophan metabolism and associated with tumor progression. Additionally, increased tryptophan metabolism correlated positively with M2 macrophage infiltration, and our in vitro co-culture assays confirmed that CRC cell-derived tryptophan metabolites could directly induce M2 macrophage polarization. Together, these results indicate that tryptophanmetabolism is pivotal in CRC development and immune escape, presenting potential novel targets for therapeutic intervention.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102157"},"PeriodicalIF":2.2,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12361607/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between VEGF gene polymorphisms and breast cancer risk.","authors":"Hala Osman, Mozan Hassan, Mohamed Alfaki, Ghada Haj-Ali","doi":"10.1016/j.bbrep.2025.102202","DOIUrl":"10.1016/j.bbrep.2025.102202","url":null,"abstract":"<p><strong>Introduction: </strong>Breast cancer (BC) poses a significant global health challenge. In Sudan, the absence of a national cancer registry has resulted in an underestimation of BC incidence. BC is notably the most common cancer among Sudanese women, especially affecting those under 50, with many cases diagnosed at advanced stages. Angiogenesis, driven by vascular endothelial growth factor (VEGF), plays a critical role in the progression and recurrence of BC. This study examines the relationship between the VEGF (rs699947) gene polymorphism and BC among Sudanese women in Khartoum State in 2022. <b>Methodology</b>: A case-control study was conducted with 30 BC patients, and tissue samples were collected for molecular analysis. DNA was extracted and genotyped for the VEGF (rs699947) polymorphism using allele-specific PCR.</p><p><strong>Results: </strong>No statistically significant association was found between the VEGF-2578 C > A polymorphism and BC risk in our study population. Although the A allele was more prevalent in tumor tissues compared to normal tissues, with no significant correlation with tumor stage or grade. The study revealed that BC in Sudanese women often presents at younger ages and is predominantly invasive ductal carcinoma, with stage II being the most common.</p><p><strong>Conclusion: </strong>These findings emphasize the necessity for continued research to explore additional genetic factors and improve our understanding of BC and associated risks. Advancing early detection and prevention methods is vital, particularly for underrepresented populations. However, the small sample size in this study may limit the statistical power to detect significant associations, and thus, findings should be interpreted with caution.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102202"},"PeriodicalIF":2.2,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12361601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxicity of ubiquitous tire rubber antiozonant <i>N</i>-(1,3-dimethylbutyl)-<i>N</i>'-phenyl-<i>p</i>-phenylenediamine (6PPD) and its transformation product 6PPD-quinone (6PPD-Q) in primary human hepatocytes and liver spheroids.","authors":"Daniel J Yeisley, Lijun Ren, Katy S Papineau, Laura K Schnackenberg, Gonçalo Gamboa da Costa, Tucker A Patterson, Suzanne C Fitzpatrick, Qiang Shi","doi":"10.1016/j.bbrep.2025.102199","DOIUrl":"10.1016/j.bbrep.2025.102199","url":null,"abstract":"<p><p>The tire rubber antioxidant <i>N</i>-(1,3-dimethylbutyl)-<i>N'</i>-phenyl-<i>p</i>-phenylenediamine (6PPD) and its oxidation product 6PPD-quinone (6PPD-Q) were recently found in human bodies. Though 6PPD/6PPD-Q showed species-dependent toxicity in animals, human relevant data are scarce. Here, primary human hepatocytes (PHHs), the gold standard in vitro model for hepatotoxicity, were used for acute and subacute toxicity assessments, with test concentrations normalized to average human serum concentrations (C_ave). Acute exposure in sandwich cultured PHHs decreased glutathione starting at 100-fold C_ave of 6PPD (10 ng/mL) or 500-fold C_ave of 6PPD-Q (100 ng/mL), and inhibited albumin starting at 10,000-fold C_ave of 6PPD, or 2500-fold C_ave of 6PPD-Q. Urea was suppressed by 6PPD-Q, but not 6PPD, starting at 2500-fold C_ave. Lactate dehydrogenase (LDH) leakage, a measurement of cell death, was unaffected. Subacute exposure of primary human liver spheroids to 6PPD-Q showed no cell death, while 6PPD increased caspase 3/7 activity and LDH leakage and decreased adenosine triphosphate at 50,000-fold C_ave. Of 10 cytokines involved in hepatotoxicity, interleukin-8 was increased by 6PPD and 6PPD-Q starting from 200- and 50-fold C_ave, respectively. At 50 to 300-fold C_ave, the in vivo-relevant concentrations in humans, GSH, caspase 3/7 activity, and interleukin-8 were the only endpoints that were significantly affected by 6PPD and/or 6PPD-Q, and no cell death was observed. These data indicate that 6PPD/6PPD-Q may cause liver dysfunctions and trigger immunotoxicity in heavily exposed individuals but are unlikely to induce significant cell death at regular environmental exposure levels.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102199"},"PeriodicalIF":2.2,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12358658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of a hypoxia- and immune-related prognostic signature for pancreatic cancer.","authors":"Ganghua Yang, Jiawei Yu, Xuqi Li, Fandi Meng, Yong Wan, Zhengyang Lu, Zheng Wang, Qinhong Xu","doi":"10.1016/j.bbrep.2025.102205","DOIUrl":"10.1016/j.bbrep.2025.102205","url":null,"abstract":"<p><p>Pancreatic cancer is a lethal disease with a poor prognosis. Immunity and hypoxia are critical characteristics of the tumor microenvironment and are closely associated with cancer prognosis. The present study aimed to identify a novel hypoxia- and immune-related gene signature for the prediction of prognosis in patients with pancreatic cancer. The status of hypoxia or immunity was determined via the NMF method by using data from the TCGA database. A total of 27 hypoxia- or immune-related DEGs were identified. A 6-gene hypoxia- and immune-related prognostic signature (<i>GALR2</i>, <i>AGT</i>, <i>MAPT</i>, <i>PRKCG</i>, <i>CAMK2B</i> and <i>PKP1</i>) was further identified via LASSO regression. Survival analysis revealed that the overall survival of patients with pancreatic cancer was inversely associated with the prognostic signature. A ROC curve indicated the excellent performance of the prognostic signature, with an AUC of 0.713. A similar prognostic value of the prognostic signature was further confirmed in 2 independent GEO cohorts. In addition, a nomogram was constructed with the prognostic signature and clinical factors, including sex, age and histological grade, and the performance of the nomogram was assessed via calibration plots and decision curve analysis. Thus, our study identified a hypoxia- and immune-related prognostic signature and established a nomogram, which may be helpful for survival prediction in patients with pancreatic cancer.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102205"},"PeriodicalIF":2.2,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12361614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D alveolar organoid drug screening model for targeting TGF-β1 in pulmonary fibrosis.","authors":"Hyeong-Jun Han, Hyunyoung Kim","doi":"10.1016/j.bbrep.2025.102191","DOIUrl":"10.1016/j.bbrep.2025.102191","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a prototype of chronic, progressive, and fibrotic lung disease. Excessive deposition of extracellular matrix (ECM) results in fibrotic remodeling, alveolar destruction, and irreversible lung dysfunction. In addition to myofibroblast activation and ECM deposition, repetitive lung epithelial cell damage and reprogramming areconsidered to be closely involved in IPF pathogenesis. Transforming growth factor (TGF)-β1 plays an important role in IPF and cancer; it is a major pro-fibrotic cytokine, and is a potential target for treating fibrotic diseases.TGF-β1 binds to TGF-βRII, phosphorylating TGF-βRI, and enhances ECM expression via the suppressor of mothers against decapentaplegic (SMAD) phosphorylation signaling pathway. Current medical interventions for IPF are predominantly anti-fibrotic medications such as pirfenidone and nintedanib, which are effective in delaying lung function deterioration, reducing acute symptom exacerbations, and increasing overall life expectancy. However, these pharmaceutical agents cannot repair fibrotic pulmonary tissues or impede disease progression. To bridge this gap, we constructed a model of TGF-β1-induced fibrosis and screened for potential drugs. From 320 anti-fibrotic drugs, 9 hits were found in the TGF-β1-induced fibrosis model, and after validation, the final 7 hits were identified as TGF-β1 inhibitors. All the 7 hits were confirmed as TGF-βRI inhibitors, which showed that the model could quickly and easily discover new compounds that can act as TGF-β1 inhibitors. This study is significantbecausewe useda 3D model to swiftly and precisely identify TGF-β1 inhibitors, potentially accelerating the clinical translation of TGF-β1-targeted therapies for fibrotic diseases.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102191"},"PeriodicalIF":2.2,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12358629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"PAK4 inhibition significantly potentiates gemcitabine activity in PDAC cells via inhibition of Wnt/β-catenin, p-ERK/MAPK and p-AKT/PI3K pathways\" [Biochemistry and Biophysics Reports, (35), September 2023, 1-8 / 101544].","authors":"Charudatt Samant, Ramesh Kale, Anand Bokare, Mahip Verma, K Sreedhara Ranganath Pai, Mandar Bhonde","doi":"10.1016/j.bbrep.2025.102201","DOIUrl":"10.1016/j.bbrep.2025.102201","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1016/j.bbrep.2023.101544.].</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102201"},"PeriodicalIF":2.2,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145038948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An integrated environmental toxicity risk assessment framework combining deep learning and molecular simulation: A case study on pyrethrins and breast cancer.","authors":"Jinghui Sung, Zikang Jiang, Wen-Pei Sung, Weijie Li, Yixin Zhuang, Yuanpeng Huang","doi":"10.1016/j.bbrep.2025.102141","DOIUrl":"10.1016/j.bbrep.2025.102141","url":null,"abstract":"<p><p>This study develops and validates a multi-scale integrative computational toxicology framework to systematically investigate the potential association between the natural pesticides pyrethrin I and II and breast cancer risk. The proposed approach integrates deep learning-based drug-target interaction prediction (via DeepPurpose), molecular docking and dynamics (MD) simulations, and protein-protein interaction (PPI) network modeling, forming a traceable risk inference chain from molecular-level interactions to clinically relevant outcomes. Experimental results revealed that pyrethrin I exhibits stable and high-affinity binding to key breast cancer-related proteins, including RPS6KB1, TNKS2, and MAOB, with a minimum binding free energy (ΔG) reaching -27.37 kcal/mol. These interactions potentially modulate tumor progression through key oncogenic pathways such as PI3K/AKT, Wnt/β-catenin, and metabolic reprogramming. RPS6KB1 is implicated in estrogen receptor-positive (ER+) breast cancer proliferation, while TNKS2 is closely associated with stemness maintenance and the aggressiveness of triple-negative breast cancer (TNBC). MAOB demonstrates the highest structural stability among complexes, making it a promising candidate for toxicological modeling. The study further introduces a cross-scale risk indicator modeling strategy, constructing a mechanistically interpretable chain from compound structure to protein modules, carcinogenic pathways, and clinical risks. This integrative methodology supports environmental exposure monitoring and toxicological policy development. The open-source, containerized analytical toolchain developed herein is highly extensible and adaptable for future toxicological evaluations of other natural compounds and emerging environmental pollutants.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102141"},"PeriodicalIF":2.2,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12355571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"mRNA expression, tumor heterogeneity, and response to therapy in patients with advanced renal cell carcinoma treated with immune-based combinations (ARON-1α).","authors":"Cristina Aguzzi, Simona De Summa, Javier Molina-Cerrillo, Teresa Alonso-Gordoa, Massimo Nabissi, Mimma Rizzo, Annalisa Zeppellini, Kaisa Sunela, Giulia Sorgentoni, Cinzia Ortega, Francesco Massari, Fernando Sabino Marques Monteiro, Nicola Battelli, Camillo Porta, Giorgio Santoni, Matteo Santoni","doi":"10.1016/j.bbrep.2025.102162","DOIUrl":"10.1016/j.bbrep.2025.102162","url":null,"abstract":"<p><strong>Background: </strong>Renal Cell Carcinoma (RCC) represents a spectrum of tumors, characterized by heterogeneous growth patterns, histology and response to immune-based combinations.</p><p><strong>Objectives: </strong>The aim of the present retrospective analysis was to investigate the mRNA expression of 32 genes associated with RCC carcinogenesis and their potential involvement in patients treated with first-line immune-based combination therapies. Additionally, we examined the role of tumor heterogeneity by comparing mRNA expression levels between primary renal tumors and metastatic sites in a group of patients included in the ARON-1 study.</p><p><strong>Patients and methods: </strong>The study included patients with advanced RCC treated with first-line immune-based therapies. Total RNA was extracted from fixed paraffin-embedded tissue slices using the RNeasy FFPE Mini Kit. Quantitative RT-PCR was performed using the IQ5 Multicolor real-time PCR detection system. Coefficient of variations were calculated for each gene and compared between primary and metastatic samples.</p><p><strong>Results: </strong>17 patients were included in this analysis; 9 of them had both primary and metastatic samples available. Three of the 4 patients showing the highest mRNA expression levels of the 32 analyzed genes reported complete remissions, while 2 of the 3 patients with the lowest expression levels were primary refractory to first-line therapy. As for tumor heterogeneity, <i>VEGFA</i> was the only gene significantly deregulated in the paired comparison.</p><p><strong>Conclusions: </strong>We showed differences in mRNA expression between primary and metastatic sites, and proposed a possible link to the response to first-line immune combination therapies. Additional research is required to clarify their potential as prognostic or predictive biomarkers.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102162"},"PeriodicalIF":2.2,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12354808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduction of Heterogeneous nuclear ribonucleoprotein A1 levels in retinal pigment epithelial cells induces inflammation and inhibits autophagy flux: pathology of age-related macular degeneration.","authors":"Tomofumi Yatsu, Ayaka Nagata, Takuya Chiba, Yoshiki Miyata","doi":"10.1016/j.bbrep.2025.102195","DOIUrl":"10.1016/j.bbrep.2025.102195","url":null,"abstract":"<p><p>Heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1) regulates RNA metabolism and inhibits various aging processes. It has also been reported as an inhibitor of inflammation; however, its role in the retina, particularly in retinal pigment epithelial (RPE) cells-a major source of inflammatory cytokines in the retina-remains unclear. Retinal inflammation is a key factor in the development of dry age-related macular degeneration (AMD), an age-related disease that can lead to blindness and currently lacks an established treatment. Therapeutic strategies are focused on preventing the suppression of autophagy, a precursor to inflammation. However, the factors regulating autophagy in RPE cells are not yet fully understood. In this study, we investigated the role of HNRNPA1 in RPE cells to evaluate its potential as a therapeutic target for dry AMD. <i>HNRNPA1</i> knockdown experiments were conducted, followed by RNA sequencing (RNA-seq) and Gene Ontology term analyses to elucidate the impact of HNRNPA1 reduction. The results revealed that reduced HNRNPA1 levels induced the increased expression of CXCL8 and IL1B, decreased autolysosome formation, and increased autophagosome formation, showing that HNRNPA1 reduction induces inflammation and suppressed autophagy, demonstrating its essential role in maintaining autophagy and mitigating inflammation under normal conditions. Furthermore, in an NaIO3-induced dryAMD model, RPE degeneration was accompanied by a reduction in HNRNPA1. These findings raise the possibility that decreased HNRNPA1 levels play a role in the onset and progression of dry AMD, and support the rationale for further exploring HNRNPA1 as a potential therapeutic target for this currently untreatable condition.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102195"},"PeriodicalIF":2.2,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12354792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predicting raw material impact on cell culture parameters in commercial biotherapeutic manufacturing.","authors":"Phyllis C Pugh, Bijay R Khanal, Jenna L Lemons, Mario A Murillo, Jacika N Patel, Preeya K Boppana, Veera Padmanabhan","doi":"10.1016/j.bbrep.2025.102192","DOIUrl":"10.1016/j.bbrep.2025.102192","url":null,"abstract":"<p><p>Complex, chemically-undefined media components are often used as nutrients in the production of biological products via mammalian cell culture. Variability in the compositions of these complex raw materials can significantly impact product yields. This paper investigates the influence of raw material quality on the cell culture process by developing data-based models to estimate final productivity in an industrial antibody production operation at AstraZeneca. Fourier Transform Infrared (FTIR) spectroscopy measurements of selected raw material components were obtained. These measurements were processed, derivatized, and used to create Partial Least Squares (PLS) regression chemometric models. The resulting models were then employed to predict the influence of such raw variability on the yields of biotherapeutic molecules.</p>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"43 ","pages":"102192"},"PeriodicalIF":2.2,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12354791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}