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Dynamic full-field optical coherence tomography for extemporaneous high-resolution imaging of adrenal glands
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2025-02-19 DOI: 10.1016/j.yexmp.2025.104958
Irene A. Spiridon , Michel Vix , Didier Mutter , Barbara Seeliger

Background

There is an interindividual variance in postoperative adrenocortical capacity, and the minimal functional remnant size is unknown. New imaging technologies may allow for improved intraoperative assessment of adrenal tissue morphology, cell activity, and surgery-related changes. The aim of this experimental study was to provide a pilot assessment of adrenal gland architecture with dynamic full-field optical coherence tomography (D-FF-OCT) in comparison to standard hematoxylin-eosin (HE) examination.

Methods

D-FF-OCT was performed on freshly resected porcine adrenal glands to simultaneously assess both morphology and metabolic activity in real time, and for comparison with standard histopathology. Left and right adrenal glands were assessed from 8 pigs (1 M, 7 F, mean weight 43.9 ± 8.3 kg).

Results

The evaluation with D-FF-OCT proved fast in terms of acquisition time, averaging 32 min/specimen. The technique required a relatively short learning curve and provided morphological details similar to standard microscopy. In the comparative analysis of both methods, D-FF-OCT scans allowed easy identification of normal adrenal morphology and facilitated differentiation of the structural components of the cortical and medullary areas based on architectural and vascular patterns. Furthermore, it was possible to distinguish more accurately between cell subpopulations based on their metabolic activity.

Conclusion

While HE examination remains the gold standard for morphological evaluation, time weighs heavy on this ancillary technique. In our study, we prove that D-FF-OCT is effective in achieving a comparable level of morphological details, with added metabolic activity of the cells, a combination which can prove useful in the real-time assessment of various diseases requiring adrenal surgery.
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引用次数: 0
Diagnostic next-generation sequencing to detect MYD88 L265P in Lymphoplasmacytic lymphoma compared to ddPCR
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2025-02-15 DOI: 10.1016/j.yexmp.2025.104956
Lauren M. Wainman, Guohong Huang, Donald C. Green, Gregory J. Tsongalis, Laura J. Tafe, Wahab A. Khan, Prabhjot Kaur, Parth S. Shah , Jeremiah X. Karrs
Lymphoplasmacytic lymphoma (LPL) is a B-cell lymphoproliferative disorder typically involving the bone marrow with infiltration by small lymphocytes and plasma cells. Studies have identified MYD88 L265P mutation as a diagnostic marker to distinguish LPL from other small B-cell lymphomas. Detection rates for this mutation have varied depending on the analytic methodology, with previous data suggesting that routine next-generation sequencing (NGS) does not demonstrate the required sensitivity to reliably detect MYD88 L265P. NGS has become part of routine clinical testing because it allows detection of variants across multiple genes. To study the utility of NGS in the detection of MYD88 L265P, we performed droplet digital PCR (ddPCR) and routine NGS on a cohort of 34 cases of lymphoid neoplasms (22 LPL, 4 CLL, 1 MCL, 1 MGUS, 2 plasma cell myeloma, and 4 negative bone marrow cases). We utilized manual review and BAMtools to assess MYD88 L265P in NGS cases. Limit of detection for ddPCR was determined to be 0.4 % variant allele frequency (VAF) with 10 ng DNA input. MYD88 L265P VAF detection by NGS and ddPCR was comparable down to 0.5 % VAF (R2 = 0.968). Setting an appropriate threshold for detection based on ddPCR results resulted in zero NGS false positives. We found that low tumor content did not impact the detection of MYD88 L265P by NGS. This study demonstrates that NGS can be a sensitive and reliable method for detection of MYD88 L265P with adequate coverage and specific assessment parameters.
{"title":"Diagnostic next-generation sequencing to detect MYD88 L265P in Lymphoplasmacytic lymphoma compared to ddPCR","authors":"Lauren M. Wainman,&nbsp;Guohong Huang,&nbsp;Donald C. Green,&nbsp;Gregory J. Tsongalis,&nbsp;Laura J. Tafe,&nbsp;Wahab A. Khan,&nbsp;Prabhjot Kaur,&nbsp;Parth S. Shah ,&nbsp;Jeremiah X. Karrs","doi":"10.1016/j.yexmp.2025.104956","DOIUrl":"10.1016/j.yexmp.2025.104956","url":null,"abstract":"<div><div>Lymphoplasmacytic lymphoma (LPL) is a B-cell lymphoproliferative disorder typically involving the bone marrow with infiltration by small lymphocytes and plasma cells. Studies have identified MYD88 L265P mutation as a diagnostic marker to distinguish LPL from other small B-cell lymphomas. Detection rates for this mutation have varied depending on the analytic methodology, with previous data suggesting that routine next-generation sequencing (NGS) does not demonstrate the required sensitivity to reliably detect MYD88 L265P. NGS has become part of routine clinical testing because it allows detection of variants across multiple genes. To study the utility of NGS in the detection of MYD88 L265P, we performed droplet digital PCR (ddPCR) and routine NGS on a cohort of 34 cases of lymphoid neoplasms (22 LPL, 4 CLL, 1 MCL, 1 MGUS, 2 plasma cell myeloma, and 4 negative bone marrow cases). We utilized manual review and BAMtools to assess MYD88 L265P in NGS cases. Limit of detection for ddPCR was determined to be 0.4 % variant allele frequency (VAF) with 10 ng DNA input. MYD88 L265P VAF detection by NGS and ddPCR was comparable down to 0.5 % VAF (R<sup>2</sup> = 0.968). Setting an appropriate threshold for detection based on ddPCR results resulted in zero NGS false positives. We found that low tumor content did not impact the detection of MYD88 L265P by NGS. This study demonstrates that NGS can be a sensitive and reliable method for detection of MYD88 L265P with adequate coverage and specific assessment parameters.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"141 ","pages":"Article 104956"},"PeriodicalIF":2.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Matrix metalloproteinase-3 is a potent prognostic factor associated with cell proliferation and migration in prostate cancer
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2025-02-11 DOI: 10.1016/j.yexmp.2025.104954
Ai Sato , Kiyoshi Takagi , Mio Yamaguchi-Tanaka , Jotaro Okushima , Yuto Yamazaki , Akihiro Ito , Takashi Suzuki
Prostate cancer is a common malignancy in men around the world, and it is crucial to explore novel biomarkers to improve its treatment. Prostate cancer cells typically invade the surrounding stroma, and remodeling of the extracellular matrix (ECM) is a crucial step in the progress of prostate cancer. Matrix metalloproteinase-3 (MMP3) is an enzyme that degrades several ECM components and is implicated in human malignancies. However, the clinical and biological significance of MMP3 has not been well elucidated.
We therefore immunolocalized MMP3 in prostate cancer tissues (n = 117) and demonstrated that MMP3 immunoreactivity was correlated with aggressive phenotype of prostate cancer, including higher proliferation/invasion ability, and shorter disease-free survival. In addition, subsequent in vitro analysis revealed that overexpression of MMP3 significantly increased the proliferative and migratory abilities of PC-3 and DU-145 prostate cancer cell lines, depending on conditioned media from WMPY-1 prostate stromal cells.
It was concluded that MMP3 might contribute to prostate cancer progression by modifying the ECM surrounding prostate cancer cells and could serve as a potent prognostic factor in prostate cancer.
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引用次数: 0
Mediterranean diet improves liver health but does not protect against azoxymethane-induced colon tumorigenesis compared to Western diet in A/J mice
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2025-02-06 DOI: 10.1016/j.yexmp.2025.104953
Weimin Guo , Nicholas Crossland , Jimmy W. Crott

Introduction

Abundant evidence indicates that the Mediterranean (MED) diet pattern is beneficial for health, especially cardiovascular health. Epidemiological evidence indicates that the MED diet also affords protection against colorectal cancer (CRC). To date, preclinical models have only evaluated specific MED diet components and therefore, although supportive, fall short of confirming the chemoprotective capacity of this complex dietary pattern. We sought to address this gap.

Method

A/J mice were randomized to receive Western (WRN) or MED diets differing in their fat, protein, and carbohydrate sources. Azoxymethane (AOM) was used to initiate colon tumorigenesis and mice were maintained for 19 weeks after the final dose.

Result

Unexpectedly high mortality was observed amongst male mice following the second AOM dose. At the end of the study hepatic Cyp2E1, an enzyme that metabolize AOM, was lower in males than females. Livers from MED diet mice were significantly lighter, had lower histologic Non-Alcoholic Fatty Liver Disease (NAFLD) scores, and contained less triglycerides than WRN mice. Amongst females, serum alanine transaminase (ALT) was also lower in MED than WRN mice. Amongst male mice, those fed MED diet presented with significantly more colonic tumors than those on the WRN diet.

Conclusion

In this study male mice displayed elevated sensitivity to AOM-induced hepatotoxicity and mortality than females. In agreement with human and preclinical data, livers of MED-diet-fed mice were healthier than those fed WRN diets. We could not confirm the chemoprotective capacity of the MED diet. Additional studies are required to evaluate the purported anticancer effect of the MED diet.
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引用次数: 0
Modulation of IL-6 receptor/STAT3 downstream signaling in rheumatoid arthritis patients 类风湿关节炎患者IL-6受体/STAT3下游信号的调节
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2024-12-25 DOI: 10.1016/j.yexmp.2024.104951
Fabio Cacciapaglia , Simone Perniola , Stefano Stano , Vincenzo Venerito , Dorotea Natuzzi , Rita Bizzoca , Florenzo Iannone
Interleukin-6 (IL-6) is a relevant cytokine in rheumatoid arthritis (RA) pathogenesis, potentially activating Janus kinases (JAK)-1, −2, and tyrosine kinase 2 (TYK2), and thus, three signal transducer and activator of transcription (STAT)-1, −3 or − 5 pathways. This pilot study aims to explore differences in phosphorylated (p)STAT3 levels among patients with RA, those not classified as RA (nRA), and healthy donors (HD), providing some clues on the relative contribution of each JAK protein to the downstream of the IL-6-induced STAT3 pathway. Clinical data and blood samples from 80 subjects (41 RA, 14 nRA, and 25 HD) were collected. The activity of the JAK-STAT3 pathway was assessed by Western Blot and Real Time-PCR analysis for the quantification of STAT3 in peripheral blood mononuclear cells (PBMC). Furthermore, the impact of JAK-1, −2, and TYK2 inhibitors on pSTAT3 was assessed in vitro by FACS, with and without IL-6 stimulation in RA patients naïve to treatment with DMARD and steroids. The pSTAT3 (%) was significantly higher in PBMC from RA compared to nRA patients and HD. Furthermore, pSTAT3 (%) was significantly associated with inflammation and disease activity (ESR, CRP, and DAS28). The JAK-1 inhibitor was more effective in reducing pSTAT3 expression in CD14pos cells of RA patients, while the JAK-2 selective compound was more effective in CD4pos cells of RA patients. On the contrary, the TYK2 selective agent showed no significant effects. This study highlights the importance of the JAK/STAT3 pathway in RA. Some differences among various JAK proteins have been pointed out, with JAK1 and JAK2 standing as the most relevant mediators of the STAT3 pathway in this in-vitro model after IL-6R activation.
白细胞介素-6 (IL-6)是类风湿关节炎(RA)发病过程中的一种相关细胞因子,可能激活Janus激酶(JAK)-1、-2和酪氨酸激酶2 (TYK2),因此是三种信号转导和转录激活因子(STAT)-1、-3或- 5途径。本初步研究旨在探讨RA患者、非RA患者(nRA)和健康供者(HD)之间磷酸化(p)STAT3水平的差异,为每种JAK蛋白在il -6诱导的STAT3通路下游的相对贡献提供一些线索。收集了80例受试者(41例RA, 14例nRA, 25例HD)的临床资料和血液样本。Western Blot和Real - Time-PCR检测JAK-STAT3通路的活性,定量外周血单核细胞(PBMC)中STAT3的表达。此外,通过体外FACS评估JAK-1, -2和TYK2抑制剂对pSTAT3的影响,在RA患者中,有和没有IL-6刺激naïve对DMARD和类固醇治疗。与非RA患者和HD患者相比,RA患者PBMC中的pSTAT3(%)显著升高。此外,pSTAT3(%)与炎症和疾病活动性(ESR、CRP和DAS28)显著相关。JAK-1抑制剂在RA患者CD14pos细胞中降低pSTAT3表达更有效,而JAK-2选择性化合物在RA患者CD4pos细胞中更有效。与之相反,TYK2选择剂没有表现出明显的作用。本研究强调了JAK/STAT3通路在RA中的重要性。各种JAK蛋白之间存在一些差异,在IL-6R激活后的体外模型中,JAK1和JAK2是STAT3通路最相关的介质。
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引用次数: 0
Transcriptomic analysis of the HPT axis in a model of oligoasthenozoospermia induced by Adenine in rats 腺嘌呤诱导大鼠少弱精子症模型HPT轴转录组学分析。
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2024-12-18 DOI: 10.1016/j.yexmp.2024.104948
Nan Yang , Xiao-ge Wei , Kaiying Li , Fei Wang , Fei Song , Wenjing Sun , Yan Wang , Zhenning Zhao , Jing Mu , Huisheng Ma
Male infertility is most commonly caused by oligozoospermia, and its pathogenesis is still poorly understood at the molecular level. This study used RNA sequencing (RNA-Seq) technology to identify candidate genes and regulatory pathways that regulate semen quality in the hypothalamic, pituitary, and testicular tissues of healthy rats and Adenine-induced oligozoospermia model rats. Semen quality testing and histological analysis of testicular tissues were performed on both groups of rats. We identified 627, 692, and 437 differentially expressed genes in the hypothalamus, pituitary gland, and testes, respectively. Functional analysis indicates that “neuronal projections,” “positive regulation of hormone biosynthetic process,” and “neuroactive ligand-receptor interaction pathways” are closely related to the hypothalamic-pituitary-testicular (HPT) axis hormone regulation and sperm production. Seven genes (Pomc, Rxfp1, Tac1, Npy, Insl3, Hsd3b3, Lhcgr) have been identified as key candidate genes responsible for regulating sperm quality within the HPT axis, potentially affecting rat reproductive function by influencing testicular development and testosterone secretion. These data provide a theoretical basis for further understanding the molecular mechanisms of reproductive performance in a rat model of oligoasthenozoospermia.
男性不育症最常见的原因是少精子症,而人们对其发病机制的分子水平还知之甚少。本研究利用 RNA 测序(RNA-Seq)技术,在健康大鼠和腺嘌呤诱导的少精子症模型大鼠的下丘脑、垂体和睾丸组织中鉴定调控精液质量的候选基因和调控通路。我们对两组大鼠的精液质量进行了检测,并对睾丸组织进行了组织学分析。我们在下丘脑、垂体和睾丸中分别发现了 627、692 和 437 个差异表达基因。功能分析表明,"神经元投射"、"激素生物合成过程的正向调节 "和 "神经活性配体-受体相互作用途径 "与下丘脑-垂体-睾丸(HPT)轴激素调节和精子生成密切相关。七个基因(Pomc、Rxfp1、Tac1、Npy、Insl3、Hsd3b3、Lhcgr)被确定为负责调节 HPT 轴内精子质量的关键候选基因,可能通过影响睾丸发育和睾酮分泌来影响大鼠的生殖功能。这些数据为进一步了解少精症大鼠模型中生殖功能的分子机制提供了理论基础。
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引用次数: 0
In Silico analysis unveils rs2109069 of DPP9 as a potential catalyst for COVID-19 severity and risk of inflammatory symptoms In Silico分析揭示了DPP9的rs2109069是COVID-19严重程度和炎症症状风险的潜在催化剂
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.yexmp.2024.104946
Chi-Ying Lee , Zih-Yin Lai , Yung-Jen Chuang

Background

During the COVID-19 pandemic, the viral illness caused by SARS-CoV-2 spread through respiratory droplets, resulting in a global pandemic with a range of symptoms from mild to severe. Pathological inflammation posed a critical issue, yet the genetic mechanisms behind the excessive activation of inflammatory responses remained unclear. To uncover the genetic and regulatory basis of the pathogenesis, we first explored possible genetic mechanisms from phenome-wide association studies (PWAS) with different severity levels of COVID-19. PWAS is a genetic research approach that identifies pleiotropic risk variants that contribute to elucidating potential physiological mechanisms from different traits.

Methods

We used the PWAS approach to link the multiple clinical symptoms to the variants. We discovered a common variant, rs2109069, in dipeptidyl peptidase 9 (DPP9), which relates to the elevated odds ratio of developing severe illness from COVID-19. Interestingly, the proxy of rs2109069 has been identified as the susceptible locus of interstitial lung disease (ILD) and idiopathic pulmonary fibrosis (IPF). We thus examined the DPP9 expression patterns in selected organs, including the lungs, blood vessels, and skin.

Results

In silico analysis revealed conserved driver activation between COVID-19-induced inflammation and the association with ILD and IPF. Multi-omics analysis further verified the association of DPP9 with abnormal inflammatory responses in COVID-19. Lastly, gene homology analysis inferred a potential regulatory role of DPP9 in inhibiting inflammasome activation, which suggests that DPP9 deficiency may exacerbate inflammation observed in some COVID-19 patients.

Conclusions

Our in silico findings reveal that severe COVID-19 inflammatory responses and inflammatory lung diseases share the same genetic risk loci, helping to elucidate the underlying physiological mechanisms of severe COVID-19 inflammation. Additionally, the individual differences in immune sensitivity may contribute to the varying multi-organ inflammatory effects among patients. The rs2109069 of DPP9 could be a genetic marker to predict the risk of specific COVID-19 symptoms and severity.
在2019冠状病毒病大流行期间,由SARS-CoV-2引起的病毒性疾病通过呼吸道飞沫传播,导致全球大流行,症状从轻微到严重不等。病理性炎症是一个关键问题,但过度激活炎症反应背后的遗传机制尚不清楚。为了揭示发病机制的遗传和调控基础,我们首先通过不同严重程度的COVID-19全现象关联研究(PWAS)探索了可能的遗传机制。PWAS是一种识别多效性风险变异的遗传研究方法,有助于阐明不同性状的潜在生理机制。方法采用PWAS方法将多种临床症状与变异联系起来。我们在二肽基肽酶9 (DPP9)中发现了一种常见的变异rs2109069,它与COVID-19引发严重疾病的风险比升高有关。有趣的是,rs2109069的代理基因已被确定为间质性肺疾病(ILD)和特发性肺纤维化(IPF)的易感位点。因此,我们检查了DPP9在选定器官中的表达模式,包括肺、血管和皮肤。结果计算机分析显示,covid -19诱导的炎症与ILD和IPF之间存在保守的驱动因子激活。多组学分析进一步证实了DPP9与COVID-19异常炎症反应的相关性。最后,基因同源性分析推断DPP9在抑制炎症小体激活方面具有潜在的调节作用,这表明DPP9缺乏可能会加剧部分COVID-19患者的炎症。结论我们的研究结果表明,严重的COVID-19炎症反应与炎症性肺部疾病具有相同的遗传风险位点,有助于阐明严重的COVID-19炎症的潜在生理机制。此外,免疫敏感性的个体差异可能导致患者多器官炎症反应的不同。DPP9的rs2109069可能是预测特定COVID-19症状和严重程度风险的遗传标记。
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引用次数: 0
Corrigendum to “Irisin and neuroinflammation: Challenges and opportunities” [Experimental and Molecular Pathology 140 (2024) 104941] 鸢尾素与神经炎症:挑战与机遇》[《实验与分子病理学》140 (2024) 104941]。
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.yexmp.2024.104943
Erika Yolanda Hernández Sandoval, Zulma Dueñas
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引用次数: 0
Influence of diet and exercise on leukocyte telomere length, markers of oxidative stress and inflammation in rats 饮食和运动对大鼠白细胞端粒长度、氧化应激和炎症标志物的影响
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.yexmp.2024.104947
Mehmet Mustafa Tilekli , Ali Kerim Yılmaz , Yavuz Yasul , Nurhan Çon , Sevcan Mercan , Nilüfer Tek
Telomere length is an important biomarker of biological aging and is affected by nutrition and physical activity. This study investigated the effects of diets with different fat contents and increased physical activity on certain pro/anti-inflammatory and oxidative stress markers and aging. The study is performed in a randomized, experimental, and controlled design with 48 rats, 8 weeks old, divided into 6 different groups (Control (C), exercise (E), unsaturated fat diet (USF), saturated fat diet (SF), unsaturated fat diet + exercise (USF + E), and saturated fat diet + exercise (SF + E)). The rats performed aerobic swimming exercise for 50 days and were fed a diet with different fat content. TAS, TOS, and MDA levels were determined by colorimetric analysis while 8-OHdG, IL-10, and TNF-α were determined by ELISA. Additionally, leukocyte telomere length is determined by the PCR method. Weight changes were also recorded. Plasma TOS, OSI, and TNF-α were lowest in the USF group and highest in the SF and SF + E groups. MDA, 8-OHdG and TG levels were highest in the SF group. The lowest IL-10 level was detected in group C. TL level was the highest in the USF group. There was also a moderate, negative, and significant correlation between telomeres and TOS, OSI, and TNF-α. The groups with the highest body weight gain were C, SF, and SF + E. Diets low in saturated fat or high in unsaturated fat, and physical activity were associated with leukocyte telomere length and alteration of oxidative and pro/anti-inflammatory markers.
端粒长度是生物衰老的重要生物指标,受营养和体力活动的影响。本研究探讨了不同脂肪含量的饮食和增加体力活动对某些促/抗炎和氧化应激标志物以及衰老的影响。研究采用随机、实验和对照设计,将48只8周龄大鼠分为6个不同组(对照组(C)、运动组(E)、不饱和脂肪饮食(USF)、饱和脂肪饮食(SF)、不饱和脂肪饮食+运动组(USF + E)和饱和脂肪饮食+运动组(SF + E))。大鼠进行有氧游泳运动50天,并喂食不同脂肪含量的饮食。比色法测定TAS、TOS、MDA水平,ELISA法测定8-OHdG、IL-10、TNF-α水平。此外,白细胞端粒长度由PCR方法确定。体重变化也被记录下来。血浆TOS、OSI、TNF-α在USF组最低,SF和SF + E组最高。SF组MDA、8-OHdG和TG水平最高。c组IL-10水平最低,USF组IL-10水平最高。端粒与TOS、OSI和TNF-α之间也存在中度、负和显著相关。体重增加最多的组是C组、SF组和SF + e组。低饱和脂肪或高不饱和脂肪的饮食,体力活动与白细胞端粒长度以及氧化和促/抗炎标志物的改变有关。
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引用次数: 0
Corrigendum to “Anti-tumor effect of antibody-drug conjugate targeting cell adhesion molecule 1 on GIST cells representing small intestinal GIST” [Experimental and Molecular Pathology 139 (2024) 104922] 以细胞粘附分子 1 为靶点的抗体-药物共轭物对小肠 GIST 细胞的抗肿瘤作用》[实验与分子病理学 139 (2024) 104922] 勘误。
IF 2.8 4区 医学 Q2 PATHOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.yexmp.2024.104934
Makoto Yoshida , Jiayin Yuan , Takako Kihara , Neinei Kimura , Takashi Yamasaki , Mizuka Ohkouchi , Yuka Hashikura , Koji Isozaki , Man Hagiyama , Akihiko Ito , Seiichi Hirota
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引用次数: 0
期刊
Experimental and molecular pathology
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