Pathology, research and practice最新文献

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The clinicopathological characteristics of co-mutations in exon 2 and 3 of the KRAS gene in patients with colorectal cancer

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-24 DOI: 10.1016/j.prp.2025.155990

Huizhen Peng, Hongtian Yao, Xiaojun Jiang, Huijuan Zhu, Jun Li, Hui Tang

KRAS, one of the most frequently mutated oncogenes in colorectal cancer (CRC), with mutations in approximately 40 % of all CRC cases. KRAS mutations exhibit considerable diversity. Studies have shown that patients with mutations at codon 13 (G13) of the KRAS gene have a higher risk of mortality, while mutations at codon 12 (G12) of the KRAS gene are also associated with prognosis, though their impact on mortality risk is lower than that of codon 13 mutations. Therefore, identifying the specific KRAS mutation type is crucial for assessing patient prognosis and developing personalized treatment plans. KRAS mutations typically occur in a single exon, whereas co-mutations in exon 2 (G12/G13) and exon 3 (Q61) in a single tissue haven’t been reported yet. In this study, we reported a co-mutation in two exons (exon 2 and exon 3) of the KRAS gene in a 72-year-old male with CRC, adenocarcinoma located at 8 cm from the anus. NGS and ARMS-PCR revealed that two exons of KRAS were co-mutated in this patient-- Q61H in exon 3, with a mutation frequency of 21.09 % and G13D in exon 2, with a variance frequency of 6.06 %. A copy number increase (copy number: 5.65) in MET gene was also found in this patient simultaneously. The clinicopathological characteristics were analyzed, and the possible mechanisms were further discussed. However, due to the CRC patients with co-mutations in two exons of the KRAS are exceedingly rare, a cohort study with more patients’ clinical data is urged.

{"title":"The clinicopathological characteristics of co-mutations in exon 2 and 3 of the KRAS gene in patients with colorectal cancer","authors":"Huizhen Peng, Hongtian Yao, Xiaojun Jiang, Huijuan Zhu, Jun Li, Hui Tang","doi":"10.1016/j.prp.2025.155990","DOIUrl":"10.1016/j.prp.2025.155990","url":null,"abstract":"<div><div><em>KRAS,</em> one of the most frequently mutated oncogenes in colorectal cancer (CRC), with mutations in approximately 40 % of all CRC cases. <em>KRAS</em> mutations exhibit considerable diversity. Studies have shown that patients with mutations at codon 13 (G13) of the <em>KRAS</em> gene have a higher risk of mortality, while mutations at codon 12 (G12) of the <em>KRAS</em> gene are also associated with prognosis, though their impact on mortality risk is lower than that of codon 13 mutations. Therefore, identifying the specific <em>KRAS</em> mutation type is crucial for assessing patient prognosis and developing personalized treatment plans. <em>KRAS</em> mutations typically occur in a single exon, whereas co-mutations in exon 2 (G12/G13) and exon 3 (Q61) in a single tissue haven’t been reported yet. In this study, we reported a co-mutation in two exons (exon 2 and exon 3) of the <em>KRAS</em> gene in a 72-year-old male with CRC, adenocarcinoma located at 8 cm from the anus. NGS and ARMS-PCR revealed that two exons of <em>KRAS</em> were co-mutated in this patient-- Q61H in exon 3, with a mutation frequency of 21.09 % and G13D in exon 2, with a variance frequency of 6.06 %. A copy number increase (copy number: 5.65) in <em>MET</em> gene was also found in this patient simultaneously. The clinicopathological characteristics were analyzed, and the possible mechanisms were further discussed. However, due to the CRC patients with co-mutations in two exons of the <em>KRAS</em> are exceedingly rare, a cohort study with more patients’ clinical data is urged.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155990"},"PeriodicalIF":2.9,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143873477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Defining molecular signatures of the solid/pseudopapillary and pseudoglandular patterns in so-called “solid-tubulocystic intrahepatic cholangiocarcinoma vs. NIPBL::NACC1 fusion hepatic carcinoma”

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-23 DOI: 10.1016/j.prp.2025.155962

Prachi Bajpai , Fatme Ghandour , Ekta Jain , Raima Memon , Chirag R. Patel , Santhosh Kumar Karthikeyan , Sankarasubramanian Jagadesan , Babu Guda , Farrukh Afaq , Amr Elkholy , Sooryanarayana Varambally , Upender Manne , Sameer Al Diffalha

Solid-tubulocystic variant of intrahepatic cholangiocarcinoma (ST-iCCA) is newly described entity characterized by two distinct histologic growth patterns: (1) solid sheets of tumor cells with focal necrosis giving pseudopapillary appearance and (2) tubular or pseudoglandular structures containing pink, colloid-like material. Tumor cells are inhibin-positive and harbor NIPBL::NACC1 fusion gene. To date, only 28 cases of ST-iCCA have been documented. While prior molecular studies provided insights into ST-iCCA, genetic profiles of individual histologic components have not been explored. This study presents first transcriptomic analysis comparing the solid/pseudopapillary and pseudoglandular components of ST-iCCA. Two cases of histologically confirmed ST-iCCA were identified for RNA sequencing which was performed on solid/pseudopapillary component, pseudoglandular component, and normal tissue. Analysis revealed distinct gene expression profiles for each pattern. Solid/pseudopapillary component uniquely overexpressed DMRTA1, NEXMIF, PRDM6, SORCS3, and NALF, while pseudoglandular component exhibited unique overexpression of HRG, ITIH3, TAT, APOA2, CP, ALDOB, CPS1, F2, KHG1, SERPINC1, HPX, C9, ADGRF1, MUC21, SAA2, SPRR2A, SAA1, FGL1, CFHR1, and LBP. These findings establish unique gene signatures for these variants of ST-iCCA, providing potential biomarkers for differential diagnosis, prognosis and targeted therapy. The distinct genetic profiles may also uncover novel therapeutic targets to address the aggressive nature of ST-iCCA.

{"title":"Defining molecular signatures of the solid/pseudopapillary and pseudoglandular patterns in so-called “solid-tubulocystic intrahepatic cholangiocarcinoma vs. NIPBL::NACC1 fusion hepatic carcinoma”","authors":"Prachi Bajpai , Fatme Ghandour , Ekta Jain , Raima Memon , Chirag R. Patel , Santhosh Kumar Karthikeyan , Sankarasubramanian Jagadesan , Babu Guda , Farrukh Afaq , Amr Elkholy , Sooryanarayana Varambally , Upender Manne , Sameer Al Diffalha","doi":"10.1016/j.prp.2025.155962","DOIUrl":"10.1016/j.prp.2025.155962","url":null,"abstract":"<div><div>Solid-tubulocystic variant of intrahepatic cholangiocarcinoma (ST-iCCA) is newly described entity characterized by two distinct histologic growth patterns: (1) solid sheets of tumor cells with focal necrosis giving pseudopapillary appearance and (2) tubular or pseudoglandular structures containing pink, colloid-like material. Tumor cells are inhibin-positive and harbor <em>NIPBL::NACC1</em> fusion gene. To date, only 28 cases of ST-iCCA have been documented. While prior molecular studies provided insights into ST-iCCA, genetic profiles of individual histologic components have not been explored. This study presents first transcriptomic analysis comparing the solid/pseudopapillary and pseudoglandular components of ST-iCCA. Two cases of histologically confirmed ST-iCCA were identified for RNA sequencing which was performed on solid/pseudopapillary component, pseudoglandular component, and normal tissue. Analysis revealed distinct gene expression profiles for each pattern. Solid/pseudopapillary component uniquely overexpressed <em>DMRTA1, NEXMIF, PRDM6, SORCS3,</em> and <em>NALF,</em> while pseudoglandular component exhibited unique overexpression of HRG<em>, ITIH3, TAT, APOA2, CP, ALDOB, CPS1, F2, KHG1, SERPINC1, HPX, C9, ADGRF1, MUC21, SAA2, SPRR2A, SAA1, FGL1, CFHR1,</em> and <em>LBP.</em> These findings establish unique gene signatures for these variants of ST-iCCA, providing potential biomarkers for differential diagnosis, prognosis and targeted therapy. The distinct genetic profiles may also uncover novel therapeutic targets to address the aggressive nature of ST-iCCA.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155962"},"PeriodicalIF":2.9,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143867798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The critical role of GLP-1 signaling pathways in the pathology of Parkinson's disease and diabetes

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-22 DOI: 10.1016/j.prp.2025.155985

Jinhao Chen , Xiang Dong , Yichen Lin , Cunming Lv

This review assesses the roles of GLP-1 and its receptor agonists (GLP-1RAs) in the treatment of diabetes and Parkinson’s disease, integrating current theories and research. GLP-1, a vital endogenous hormone, regulates insulin secretion, delays gastric emptying, and promotes satiety, showing significant potential for diabetes management. However, its brief lifespan and restricted blood-brain barrier penetration limit its clinical application. To overcome these constraints, researchers have developed GLP-1 receptor agonists that prolong its action and exhibit high efficacy in diabetes treatment. Recent studies further reveal GLP-1’s neuroprotective effects, notably its potential in managing neurodegenerative disorders such as Parkinson’s disease. GLP-1RAs mitigate neuroinflammation, reduce oxidative stress, and enhance neuroprotection, suggesting substantial potential for treating neurodegenerative diseases. Additionally, to enhance GLP-1RAs’ efficacy in the nervous system, researchers have introduced novel drug delivery approaches, including nanoparticle carriers and molecular modifications, to improve stability and targeting accuracy. In conclusion, this review comprehensively analyzes the mechanisms, clinical applications, and challenges of GLP-1 and its receptor agonists in managing diabetes and Parkinson’s disease, while identifying future research and clinical opportunities.

{"title":"The critical role of GLP-1 signaling pathways in the pathology of Parkinson's disease and diabetes","authors":"Jinhao Chen , Xiang Dong , Yichen Lin , Cunming Lv","doi":"10.1016/j.prp.2025.155985","DOIUrl":"10.1016/j.prp.2025.155985","url":null,"abstract":"<div><div>This review assesses the roles of GLP-1 and its receptor agonists (GLP-1RAs) in the treatment of diabetes and Parkinson’s disease, integrating current theories and research. GLP-1, a vital endogenous hormone, regulates insulin secretion, delays gastric emptying, and promotes satiety, showing significant potential for diabetes management. However, its brief lifespan and restricted blood-brain barrier penetration limit its clinical application. To overcome these constraints, researchers have developed GLP-1 receptor agonists that prolong its action and exhibit high efficacy in diabetes treatment. Recent studies further reveal GLP-1’s neuroprotective effects, notably its potential in managing neurodegenerative disorders such as Parkinson’s disease. GLP-1RAs mitigate neuroinflammation, reduce oxidative stress, and enhance neuroprotection, suggesting substantial potential for treating neurodegenerative diseases. Additionally, to enhance GLP-1RAs’ efficacy in the nervous system, researchers have introduced novel drug delivery approaches, including nanoparticle carriers and molecular modifications, to improve stability and targeting accuracy. In conclusion, this review comprehensively analyzes the mechanisms, clinical applications, and challenges of GLP-1 and its receptor agonists in managing diabetes and Parkinson’s disease, while identifying future research and clinical opportunities.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155985"},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143867794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of extracellular vesicles in the pathophysiology, diagnosis, and prognosis of gynecological cancers

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-22 DOI: 10.1016/j.prp.2025.155987

Treena Rica D. Teh , Von Novi O. de Leon , Ourlad Alzeus G. Tantengco

Gynecological cancers account for one-sixth of disability-adjusted life years of women with malignancies. The burden of these diseases is more remarkable in low- and middle-income countries with limited access to human papillomavirus vaccines. Thus, early diagnosis and prompt treatment are vital in disease management. In connection, extracellular vesicles (EVs) are gaining traction in tumor biology. Biomolecular cargoes within EVs can be nucleic acids, proteins, or lipids that can reflect the biological state of the cell from which they are derived such as cancer cells, and consequently the influence of cancer cells to recipients including cancer and non-cancer cells. Combining this with the stability and detectability of EVs in biological samples, EVs present potential utility in the diagnosis and prognostic monitoring of gynecological malignancies. Therefore, this review discusses the role of extracellular vesicles in the pathophysiology of cervical, uterine, and ovarian cancers, and how these roles are exploited in the diagnosis and prognosis of patients with these malignancies through the presentation of evidence from in vitro, in vivo, and clinical studies.

{"title":"Role of extracellular vesicles in the pathophysiology, diagnosis, and prognosis of gynecological cancers","authors":"Treena Rica D. Teh , Von Novi O. de Leon , Ourlad Alzeus G. Tantengco","doi":"10.1016/j.prp.2025.155987","DOIUrl":"10.1016/j.prp.2025.155987","url":null,"abstract":"<div><div>Gynecological cancers account for one-sixth of disability-adjusted life years of women with malignancies. The burden of these diseases is more remarkable in low- and middle-income countries with limited access to human papillomavirus vaccines. Thus, early diagnosis and prompt treatment are vital in disease management. In connection, extracellular vesicles (EVs) are gaining traction in tumor biology. Biomolecular cargoes within EVs can be nucleic acids, proteins, or lipids that can reflect the biological state of the cell from which they are derived such as cancer cells, and consequently the influence of cancer cells to recipients including cancer and non-cancer cells. Combining this with the stability and detectability of EVs in biological samples, EVs present potential utility in the diagnosis and prognostic monitoring of gynecological malignancies. Therefore, this review discusses the role of extracellular vesicles in the pathophysiology of cervical, uterine, and ovarian cancers, and how these roles are exploited in the diagnosis and prognosis of patients with these malignancies through the presentation of evidence from in vitro, in vivo, and clinical studies.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155987"},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143873476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression of functionally glycosylated PSGL-1 in ALK-positive anaplastic large cell lymphoma

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-21 DOI: 10.1016/j.prp.2025.155988

Natsumi Yonemoto , Mana Fukushima , Hitomi Hoshino , Yusuke Fukiage , Akifumi Muramoto , Yasuharu Kaizaki , Yasuni Nakanuma , Yukinori Inadome , Takuya Komeno , Haruo Ohtani , Motohiro Kobayashi

Anaplastic lymphoma kinase (ALK)-positive (ALK+) anaplastic large cell lymphoma (ALCL) is defined as a CD30-positive mature T-cell lymphoma characterized by proliferation of large anaplastic cells and aberrant ALK protein expression. These cells often infiltrate lymphatic sinuses, proliferate and exhibit intercellular cohesiveness and accumulate around blood vessels. However, molecular mechanisms underlying such vascular-related histogenesis remain to be elucidated. Since PSGL-1 is more highly expressed in ALK+ ALCL than in other T-cell lymphomas and sLe^x glycan expression has been reported in ALK+ ALCL, the interaction between PSGL-1, which is functionally glycosylated with sLe^x, and P-selectin, which is expressed on endothelial cells, may contribute to such vascular-related histogenesis. To analyze glycans on PSGL-1 expressed in ALK+ ALCL in the context of P-selectin binding function, we first performed immunohistochemical analysis of 12 cases of ALK+ ALCL to identify those that express both PSGL-1 and sLe^x glycans and found that a substantial portion of both molecules co-localizes in those cases. We then conducted western blot analysis, together with glycosyltransferase gene expression analysis, of ALK+ ALCL cells and observed that PSGL-1 is decorated with sLe^x glycans, especially those displayed on core 2 O-glycans. Finally, we carried out a P-selectin•IgM chimera binding assay to show that ALK+ ALCL cells bind to P-selectin. These results indicate that the PSGL-1 glycoform expressed on ALK+ ALCL cells is functional and that interaction of functionally glycosylated PSGL-1 with P-selectin may be partially responsible for the vascular-related histogenesis characteristics of ALK+ ALCL.

{"title":"Expression of functionally glycosylated PSGL-1 in ALK-positive anaplastic large cell lymphoma","authors":"Natsumi Yonemoto , Mana Fukushima , Hitomi Hoshino , Yusuke Fukiage , Akifumi Muramoto , Yasuharu Kaizaki , Yasuni Nakanuma , Yukinori Inadome , Takuya Komeno , Haruo Ohtani , Motohiro Kobayashi","doi":"10.1016/j.prp.2025.155988","DOIUrl":"10.1016/j.prp.2025.155988","url":null,"abstract":"<div><div>Anaplastic lymphoma kinase (ALK)-positive (ALK+) anaplastic large cell lymphoma (ALCL) is defined as a CD30-positive mature T-cell lymphoma characterized by proliferation of large anaplastic cells and aberrant ALK protein expression. These cells often infiltrate lymphatic sinuses, proliferate and exhibit intercellular cohesiveness and accumulate around blood vessels. However, molecular mechanisms underlying such vascular-related histogenesis remain to be elucidated. Since PSGL-1 is more highly expressed in ALK+ ALCL than in other T-cell lymphomas and sLe<sup>x</sup> glycan expression has been reported in ALK+ ALCL, the interaction between PSGL-1, which is functionally glycosylated with sLe<sup>x</sup>, and P-selectin, which is expressed on endothelial cells, may contribute to such vascular-related histogenesis. To analyze glycans on PSGL-1 expressed in ALK+ ALCL in the context of P-selectin binding function, we first performed immunohistochemical analysis of 12 cases of ALK+ ALCL to identify those that express both PSGL-1 and sLe<sup>x</sup> glycans and found that a substantial portion of both molecules co-localizes in those cases. We then conducted western blot analysis, together with glycosyltransferase gene expression analysis, of ALK+ ALCL cells and observed that PSGL-1 is decorated with sLe<sup>x</sup> glycans, especially those displayed on core 2 <em>O</em>-glycans. Finally, we carried out a P-selectin•IgM chimera binding assay to show that ALK+ ALCL cells bind to P-selectin. These results indicate that the PSGL-1 glycoform expressed on ALK+ ALCL cells is functional and that interaction of functionally glycosylated PSGL-1 with P-selectin may be partially responsible for the vascular-related histogenesis characteristics of ALK+ ALCL.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155988"},"PeriodicalIF":2.9,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumor-educated platelet, a potential liquid biopsy biosource in pancreatic cancer: A review

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-21 DOI: 10.1016/j.prp.2025.155986

Majid Zaki-Dizaji , Zahra Taheri , Mohammad Heiat , Kiavash Hushmandi

Pancreatic cancer (PC) is a frequent and aggressive digestive system cancer with a very poor prognosis. The best chance for recovery lies in early surgical removal of the tumor. Unfortunately, because PC often develops without noticeable symptoms, diagnosis is frequently delayed. Limited treatment options, the metastasis potential of pancreatic cancer cells, and its generally poor prognosis mean that patients are often diagnosed late, significantly reducing the effectiveness of treatment. Consequently, there's a critical need for new biomarkers and technologies to improve early detection through screening. Recently, the liquid biopsy has developed as a powerful means for detecting and monitoring cancer at the molecular level. Its advantages include the ease and non-invasive nature of sample collection and its ability to reflect the dynamic changes within a tumor. Platelets, the second most numerous type of blood cell, offer a particularly promising source for liquid biopsy. It is known that cancer affects various aspects of platelets, including their number, size, activation state, and the proteins and RNA they contain. However, the full implications of these changes for cancer detection have not yet been fully integrated into routine clinical practice. Platelets have a unique ability to captivate nucleic acids and proteins from their surroundings, and they alter their transcriptome in response to external signals. This leads to the development of tumor-educated platelets (TEPs). Liquid biopsies that utilize TEP biomarkers hold considerable potential for screening, early detection, prognosis, guiding personalized treatment strategies, ongoing monitoring of the disease, and predicting recurrence. Encouraging results from preclinical studies have highlighted the potential of platelets as a novel liquid biopsy source for a wide range of cancers. This review will explore the potential of using platelets as a liquid biopsy method, specifically for pancreatic cancer.

{"title":"Tumor-educated platelet, a potential liquid biopsy biosource in pancreatic cancer: A review","authors":"Majid Zaki-Dizaji , Zahra Taheri , Mohammad Heiat , Kiavash Hushmandi","doi":"10.1016/j.prp.2025.155986","DOIUrl":"10.1016/j.prp.2025.155986","url":null,"abstract":"<div><div>Pancreatic cancer (PC) is a frequent and aggressive digestive system cancer with a very poor prognosis. The best chance for recovery lies in early surgical removal of the tumor. Unfortunately, because PC often develops without noticeable symptoms, diagnosis is frequently delayed. Limited treatment options, the metastasis potential of pancreatic cancer cells, and its generally poor prognosis mean that patients are often diagnosed late, significantly reducing the effectiveness of treatment. Consequently, there's a critical need for new biomarkers and technologies to improve early detection through screening. Recently, the liquid biopsy has developed as a powerful means for detecting and monitoring cancer at the molecular level. Its advantages include the ease and non-invasive nature of sample collection and its ability to reflect the dynamic changes within a tumor. Platelets, the second most numerous type of blood cell, offer a particularly promising source for liquid biopsy. It is known that cancer affects various aspects of platelets, including their number, size, activation state, and the proteins and RNA they contain. However, the full implications of these changes for cancer detection have not yet been fully integrated into routine clinical practice. Platelets have a unique ability to captivate nucleic acids and proteins from their surroundings, and they alter their transcriptome in response to external signals. This leads to the development of tumor-educated platelets (TEPs). Liquid biopsies that utilize TEP biomarkers hold considerable potential for screening, early detection, prognosis, guiding personalized treatment strategies, ongoing monitoring of the disease, and predicting recurrence. Encouraging results from preclinical studies have highlighted the potential of platelets as a novel liquid biopsy source for a wide range of cancers. This review will explore the potential of using platelets as a liquid biopsy method, specifically for pancreatic cancer.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155986"},"PeriodicalIF":2.9,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143867797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Vaccination and personalized cancer vaccines focusing on common cancers in women: A narrative review

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-18 DOI: 10.1016/j.prp.2025.155983

Seyed Sadeq Mousavi Ghahfarrokhi , Pegah Karimi , Fateme-Sadat Mahdigholi , Mohadeseh Haji Abdolvahab

Immunotherapy has recently cast great attention on cancer vaccines in order to aim to decrease tumor growth, elicit persistent anti-tumor memory, and avert adverse reactions. Moreover, cancer vaccines employ tumor antigens to stimulate anti-tumor immunity using different platforms, for example, whole cells, nucleic acids, peptides, etc. Recent findings have classified cancer vaccines into cell-based, virus-based, peptide-based, and nucleic acid-based types. Personalized cancer vaccines, also known as neoantigens, have exhibited acceptable safety and efficacy in eliciting immune responses against melanoma and glioblastoma. Neoantigen-based vaccines, concentrating on tumor antigens present only in cancer cells, bring intriguing opportunities for different types of cancer, including melanoma, lung, bladder, breast, renal, head and neck, and colorectal cancers. Furthermore, breast cancer research underscores ongoing trials of vaccines targeting α-lactalbumin to prevent the recurrence of triple-negative breast cancer. Lung cancer studies have discovered interesting outcomes with liposomal vaccines and the potential of CIMAvax-EGF in the prevention of lung cancer. Studies on ovarian cancer highlight personalized cancer vaccines using dendritic cells and various tumor-associated antigens to elicit T-cell responses against cancer cells. Overall, such advancements suggest great promise for future clinical translation of cancer novel immunotherapy-based approaches to effectively counter various types of cancer.

{"title":"Vaccination and personalized cancer vaccines focusing on common cancers in women: A narrative review","authors":"Seyed Sadeq Mousavi Ghahfarrokhi , Pegah Karimi , Fateme-Sadat Mahdigholi , Mohadeseh Haji Abdolvahab","doi":"10.1016/j.prp.2025.155983","DOIUrl":"10.1016/j.prp.2025.155983","url":null,"abstract":"<div><div>Immunotherapy has recently cast great attention on cancer vaccines in order to aim to decrease tumor growth, elicit persistent anti-tumor memory, and avert adverse reactions. Moreover, cancer vaccines employ tumor antigens to stimulate anti-tumor immunity using different platforms, for example, whole cells, nucleic acids, peptides, etc. Recent findings have classified cancer vaccines into cell-based, virus-based, peptide-based, and nucleic acid-based types. Personalized cancer vaccines, also known as neoantigens, have exhibited acceptable safety and efficacy in eliciting immune responses against melanoma and glioblastoma. Neoantigen-based vaccines, concentrating on tumor antigens present only in cancer cells, bring intriguing opportunities for different types of cancer, including melanoma, lung, bladder, breast, renal, head and neck, and colorectal cancers. Furthermore, breast cancer research underscores ongoing trials of vaccines targeting α-lactalbumin to prevent the recurrence of triple-negative breast cancer. Lung cancer studies have discovered interesting outcomes with liposomal vaccines and the potential of CIMAvax-EGF in the prevention of lung cancer. Studies on ovarian cancer highlight personalized cancer vaccines using dendritic cells and various tumor-associated antigens to elicit T-cell responses against cancer cells. Overall, such advancements suggest great promise for future clinical translation of cancer novel immunotherapy-based approaches to effectively counter various types of cancer.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155983"},"PeriodicalIF":2.9,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143855735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mutational landscape of ovarian carcinomas: An Australian study of 116 patients

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-17 DOI: 10.1016/j.prp.2025.155958

Julie Robin , Noel Djitro , Liyan Song , Patricia Pyrchla , Bin Yuan , Pamela Htain , Anna Fong Na Goh , Janice Lee , Robert Quach , Broden Krause , Amit Kumar , Priscillia Siswara , Wendy Hutchison , Suzanne Svobodova , Beena Kumar , Kate Webber , Pranav Dorwal

Understanding genetic biomarkers in ovarian cancer allows for access to targeted clinical management. This retrospective mutational analysis of 116 Australian patients with ovarian cancer complements the development of current knowledge on ovarian cancer biomarkers. In the 116 samples, nearly 500 variants were identified including 19 variants of strong clinical significance, 212 variants of potential clinical significance and 268 variants of uncertain clinical significance (VUS) as per the Association for Molecular Pathology (AMP) guidelines. The most frequently altered gene was TP53 which was altered in 75 % of tumours. Other commonly altered genes included PIK3CA, PTEN, ARID1A, KRAS and BRCA1. Moreover, the biggest differences in between mutational profile was observed in between tumour subtypes, more specifically in between HGSOC and endometrioid tumour. Minimal differences in mutational landscape were identified between primary and metastatic lesions, with only PTEN being significantly more prevalent in primary lesions. PTEN and ARID1A pathogenic variants were more frequently reported in younger patient group. These genetic markers could be used to support clinical care, providing information for diagnosis, prognosis and therapeutic option for the patient.

{"title":"Mutational landscape of ovarian carcinomas: An Australian study of 116 patients","authors":"Julie Robin , Noel Djitro , Liyan Song , Patricia Pyrchla , Bin Yuan , Pamela Htain , Anna Fong Na Goh , Janice Lee , Robert Quach , Broden Krause , Amit Kumar , Priscillia Siswara , Wendy Hutchison , Suzanne Svobodova , Beena Kumar , Kate Webber , Pranav Dorwal","doi":"10.1016/j.prp.2025.155958","DOIUrl":"10.1016/j.prp.2025.155958","url":null,"abstract":"<div><div>Understanding genetic biomarkers in ovarian cancer allows for access to targeted clinical management. This retrospective mutational analysis of 116 Australian patients with ovarian cancer complements the development of current knowledge on ovarian cancer biomarkers. In the 116 samples, nearly 500 variants were identified including 19 variants of strong clinical significance, 212 variants of potential clinical significance and 268 variants of uncertain clinical significance (VUS) as per the Association for Molecular Pathology (AMP) guidelines. The most frequently altered gene was <em>TP53</em> which was altered in 75 % of tumours. Other commonly altered genes included <em>PIK3CA, PTEN, ARID1A, KRAS and BRCA1.</em> Moreover, the biggest differences in between mutational profile was observed in between tumour subtypes, more specifically in between HGSOC and endometrioid tumour. Minimal differences in mutational landscape were identified between primary and metastatic lesions, with only <em>PTEN</em> being significantly more prevalent in primary lesions. <em>PTEN</em> and <em>ARID1A</em> pathogenic variants were more frequently reported in younger patient group. These genetic markers could be used to support clinical care, providing information for diagnosis, prognosis and therapeutic option for the patient.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155958"},"PeriodicalIF":2.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The untold story of CD82: Exploring its non-canonical roles in cancer

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-17 DOI: 10.1016/j.prp.2025.155979

Shutao Zheng , Yao Zhang , Ren Cai , Bangwu Cai , Shujuan Luo , Shuo He , Tianyuan Peng , Wei Wang , Hong Cui , Huifang Li , Xiaomei Lu

CD82, traditionally recognized as a metastasis suppressor within the tetraspanin family, has emerged as a key player in diverse cancer-related processes beyond its canonical functions. This review highlights recent research on the non-canonical roles of CD82 in cancer progression, with a particular focus on its regulation of immune cell interactions, its impact on tumor microenvironment modulation, and its potential as both a therapeutic target and a biomarker. By examining the novel functions of CD82 in immune modulation and its influence on key signaling pathways, we propose that CD82 offers promising avenues for therapeutic interventions in cancer. This paper provides a comprehensive synthesis of the current understanding of CD82’s expanded roles, underscoring its potential in improving cancer diagnosis and therapy.

引用次数: 0

Moderate exercise relieves heart failure-induced skeletal muscle atrophy through the inhibition of MAPK/SOCS3 signaling

IF 2.9 4区医学 Q2 PATHOLOGY

Pathology, research and practice

Pub Date : 2025-04-17 DOI: 10.1016/j.prp.2025.155982

Ying Zhao , Ying Zhang , Rui Song , Ying He , Liqing Yao

Heart failure (HF) is a structural or functional abnormality of the heart, often accompanied by skeletal muscle atrophy and other complications. Exercise plays an important role in preventing muscle atrophy. However, the underlying molecular mechanisms related to skeletal muscle atrophy in HF still remain poorly understood. In this study, we constructed an HF rat model by abdominal aortic coarctation (AAC) and a C2C12 muscle atrophy cell model induced by angiotensin II (Ang II). The relevant protein expressions were analyzed using western blotting. The damage of myocardial tissue, gastrocnemius tissue and cells were assessed through echocardiography, ELISA, HE staining, and immunofluorescence staining. Findings from this study indicated that moderate exercise has beneficial effects on pathological damage in the myocardial and gastrocnemius tissues of rats, resulting in a reduction of NT-proBNP levels in the blood. Furthermore, it was observed that the expression levels of MAFbx and MuRF1 were downregulated, while MHC and MyoD expressions were elevated, and the expression of endoplasmic reticulum stress (ERS)-related proteins GRP78, p-eIF2α, p-IRE1α, p-PERK, CHOP, ATF6 was inhibited, and finally alleviated HF-induced skeletal muscle atrophy. The mechanism involves moderate exercise working to alleviate ERS by inhibiting the MAPK/SOCS3 signaling pathway, thus alleviating skeletal muscle atrophy induced by HF. Our study elucidates the positive role of moderate exercise in HF-induced skeletal muscle atrophy, reveals its potential molecular mechanism, and provides a new scientific basis for the comprehensive treatment of skeletal muscle atrophy in HF.

{"title":"Moderate exercise relieves heart failure-induced skeletal muscle atrophy through the inhibition of MAPK/SOCS3 signaling","authors":"Ying Zhao , Ying Zhang , Rui Song , Ying He , Liqing Yao","doi":"10.1016/j.prp.2025.155982","DOIUrl":"10.1016/j.prp.2025.155982","url":null,"abstract":"<div><div>Heart failure (HF) is a structural or functional abnormality of the heart, often accompanied by skeletal muscle atrophy and other complications. Exercise plays an important role in preventing muscle atrophy. However, the underlying molecular mechanisms related to skeletal muscle atrophy in HF still remain poorly understood. In this study, we constructed an HF rat model by abdominal aortic coarctation (AAC) and a C2C12 muscle atrophy cell model induced by angiotensin II (Ang II). The relevant protein expressions were analyzed using western blotting. The damage of myocardial tissue, gastrocnemius tissue and cells were assessed through echocardiography, ELISA, HE staining, and immunofluorescence staining. Findings from this study indicated that moderate exercise has beneficial effects on pathological damage in the myocardial and gastrocnemius tissues of rats, resulting in a reduction of NT-proBNP levels in the blood. Furthermore, it was observed that the expression levels of MAFbx and MuRF1 were downregulated, while MHC and MyoD expressions were elevated, and the expression of endoplasmic reticulum stress (ERS)-related proteins GRP78, p-eIF2α, p-IRE1α, p-PERK, CHOP, ATF6 was inhibited, and finally alleviated HF-induced skeletal muscle atrophy. The mechanism involves moderate exercise working to alleviate ERS by inhibiting the MAPK/SOCS3 signaling pathway, thus alleviating skeletal muscle atrophy induced by HF. Our study elucidates the positive role of moderate exercise in HF-induced skeletal muscle atrophy, reveals its potential molecular mechanism, and provides a new scientific basis for the comprehensive treatment of skeletal muscle atrophy in HF.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"270 ","pages":"Article 155982"},"PeriodicalIF":2.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143867799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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