Cancer Genetics最新文献

{"title":"YME1L facilitates the development of non-small cell lung cancer by promoting activation of mitochondria-Gαi1-Akt pathway","authors":"MinDan Wu ,&nbsp;WenXia Qian ,&nbsp;MeiJie Xu,&nbsp;JieRu Zhang,&nbsp;Feng Gao,&nbsp;LiXiu Chen,&nbsp;SongHua Huang","doi":"10.1016/j.cancergen.2025.10.101","DOIUrl":"10.1016/j.cancergen.2025.10.101","url":null,"abstract":"<div><div>As a key regulatory enzyme in mitochondria, YME1L is crucial for regulation of mitochondrial dynamic balance and metabolic plasticity in tumors. Yet its role in non-small cell lung cancer (NACLC) and underlying mechanism are still unclear. In this study, we found YME1L was highly expressed at both protein and RNA levels in NSCLC tissues, which was consistent with the result of database analysis. The bioinformatics analysis also showed that YME1L expression negatively correlated with survival rate. The significance of YME1L was investigated through gain- and loss-of-function studies in vivo and vitro. As expected, the protease activity was consistent with the expression of YME1L. Knockdown of YME1L significantly inhibited mitochondrial activity, proliferation and migration of NACLC cell lines, and suppressed the growth of xenografted tumors in nude mice. While over-expression of YME1L promoted the development of tumors. Further study revealed that YME1L increased the proportion of S-phase and reduced the number of G0/G1 ratio in NSCLC cells, suggesting the strong proliferation activity. Mechanically, knockdown of YME1L decreased the expression of Gαi1 and the phosphorylation of Akt, and on the contrary, YME1L over-expression increased the Gαi1 expression and Akt activation, which in turn stimulated cell proliferation, migration and survival, and promoted the progression of NSCLC. In this study, we revealed that YME1L played a novel oncogenic role in promoting NSCLC tumorigenesis and progression via the mitochondria-Gαi1-AKT axis, providing a new target for the treatment of lung cancer.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 212-220"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145410670","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}

{"title":"Clonal cytogenetic abnormality in IgG4-related disease","authors":"Prasad Koduru ,&nbsp;Sara Monaghan ,&nbsp;Rolando Garcia ,&nbsp;Weina Chen","doi":"10.1016/j.cancergen.2025.10.102","DOIUrl":"10.1016/j.cancergen.2025.10.102","url":null,"abstract":"<div><div>Inflammatory conditions in which immunoglobulin G4 secreting plasma cells infiltrate the affected tissue and form a systemic immune-mediated fibroinflammatory lesion is recognized as IgG4+ related disease. Patients with this disease are at an increased risk for developing neoplasm. Lymphadenopathy is common in patients with IgG4+ related disease; and may clinically resemble lymphoma. Here we describe a patient presented with an IgG4+ related lymphadenopathy (disease) and harbored a clonal cytogenetic abnormality; to our knowledge this is the first report.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 237-241"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145446313","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}

{"title":"Villin1 predicts survival and adjuvant TACE response in hepatocellular carcinoma","authors":"Dongjun Luo ,&nbsp;Chen Wang ,&nbsp;Beicheng Sun ,&nbsp;Zhu Xu","doi":"10.1016/j.cancergen.2025.11.003","DOIUrl":"10.1016/j.cancergen.2025.11.003","url":null,"abstract":"<div><div>Adjuvant transcatheter arterial chemoembolization (TACE) has traditionally been performed as an effective treatment for hepatocellular carcinoma (HCC). The present study aims to explore key genes associated with TACE treatment for HCC. We used weighted gene co-expression network analysis (WGCNA) to identify the core gene related to the efficacy of TACE for HCC. The raw data of GSE104580 were downloaded from the Gene Expression Omnibus (GEO), and the differentially expressed genes (DEGs) were analyzed. WGCNA was used to identify the key modules related to the efficacy of TACE for HCC, and the protein-protein interaction (PPI) network was used to screen the core genes. Villin1 (VIL1) was identified as a core gene for predicting TACE response. VIL1 was highly expressed in HCC compared to normal tissues, and high expression of VIL1 was strongly correlated with the poor prognosis of HCC patients. Finally, we used one cohort from our center to validate that high expression of VIL1 was closely related to low TACE efficacy in HCC patients. Our study identified the Villin1 gene that may play an important role in the efficacy of TACE for HCC and may become a potential predictive biomarker for evaluating the efficacy of TACE in HCC patients.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 280-284"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145519826","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}

{"title":"Expression and clinical significance of the imprinted gene PHLDA2 in colorectal cancer","authors":"Haohui Li ,&nbsp;Chenting Jin ,&nbsp;Fangfang Zhou ,&nbsp;Man Bao ,&nbsp;Canliang Tan ,&nbsp;Zhenchao Luo ,&nbsp;Ninglei Li ,&nbsp;Yiyi Jin ,&nbsp;Luzhe Han ,&nbsp;Gang Xiao ,&nbsp;Jian Yan","doi":"10.1016/j.cancergen.2025.10.104","DOIUrl":"10.1016/j.cancergen.2025.10.104","url":null,"abstract":"<div><h3>Background</h3><div>Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide and a leading cause of cancer-related mortality. Tumor progression and metastasis, particularly to the lymph nodes, are critical factors contributing to poor patient outcomes. Identifying molecular markers that predict disease progression and patient survival is essential for improving CRC prognosis and therapeutic strategies.</div></div><div><h3>Objective</h3><div>This study aims to investigate the clinical significance of PHLDA2 expression in CRC and its potential as a prognostic marker.</div></div><div><h3>Methods</h3><div>PHLDA2 expression levels in CRC tissues were analyzed using Oncomine database and validated through immunohistochemistry. Mean optical density (MOD) scores were used to quantify PHLDA2 protein expression, and mRNA levels were analyzed in tissue samples. Kaplan-Meier survival analysis was performed to determine the effect of PHLDA2 expression on overall survival (OS). The impact of PHLDA2 on CRC cell behavior was examined by knocking out PHLDA2 in HCT 116 and DLD-1 cell lines, followed by assessments of cell proliferation, migration, invasion, and colony formation in vitro. Additionally, the effects of PHLDA2 knockout were evaluated in xenograft models.</div></div><div><h3>Results</h3><div>PHLDA2 expression was significantly upregulated in CRC tissues compared to adjacent normal tissues. Elevated PHLDA2 levels were associated with lymph node metastasis, with a high expression in 69.23% of rectal cancer patients with metastasis compared to 33.33% in those without metastasis (p = 0.0363). Patients with higher PHLDA2 expression (2+/3+) had significantly worse OS than those with low or no expression (p &lt; 0.05). Functional assays revealed that PHLDA2 knockout significantly reduced proliferation, migration, invasion, and colony formation in HCT 116 and DLD-1 cells. In vivo, PHLDA2 knockout markedly decreased tumor growth in xenograft models.</div></div><div><h3>Conclusions</h3><div>Increased PHLDA2 expression is associated with more advanced CRC, particularly in cases with lymph node metastasis, and is linked to poorer survival outcomes. These findings suggest that PHLDA2 may be a valuable prognostic marker in CRC.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 227-236"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145439194","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}

{"title":"Influence of lynch syndrome on the incidence of side effects to antineoplastic treatment of patients with colorectal cancer","authors":"Ana Valeria Silva Alencar,&nbsp;Giulianna Aparecida Vieira Barreto,&nbsp;Maria Cláudia dos Santos Luciano,&nbsp;Clarissa Picanço Albuquerque,&nbsp;Rosane Oliveira de Sant’Ana,&nbsp;Paulo Goberlânio de Barros Silva,&nbsp;Flávio da Silveira Bittencourt,&nbsp;Valeska Portela Lima,&nbsp;Maria Júlia Barbosa Bezerra","doi":"10.1016/j.cancergen.2025.10.001","DOIUrl":"10.1016/j.cancergen.2025.10.001","url":null,"abstract":"<div><div>To analyze the influence of Lynch Syndrome on the incidence of adverse reactions to antineoplastic treatment in patients with colorectal cancer. Observational and retrospective study based on analyzing electronic medical records of patients treated at Hospital Haroldo Juaçaba/Ceará Cancer Institute (HHJ/ICC). Patients with NCCN clinical criteria for Lynch Syndrome and a diagnosis of colorectal cancer were included, comparing the profile of adverse reactions to chemotherapy between those with and without pathogenic mutations associated with the syndrome. The sample consisted of 161 patients with suspected Lynch Syndrome, all undergoing chemotherapy. A higher frequency of adverse reactions was observed among patients without a pathogenic mutation for Lynch Syndrome. Approximately two-thirds of the sample reported adverse reactions, with nausea being the most common adverse event, followed by neurotoxicity and diarrhea. Patients with colorectal cancer without a pathogenic mutation for Lynch syndrome had a higher incidence of adverse reactions to chemotherapy. This finding may be related to biological and physiological factors, including greater cellular variability, the need for more intensive therapeutic regimens, and the influence of individual genetic variability. These results highlight the importance of personalized approaches in managing the side effects of cancer treatment.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 169-179"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145287500","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}

{"title":"Segregation of the rare TP53 germline missense variant c.314G>T, p.Gly105Val in Algerian family with Li-Fraumeni Syndrome: First report","authors":"Farid Cherbal ,&nbsp;Djamel-Eddine Seddik ,&nbsp;Mouchira Saidi ,&nbsp;Fatiha Gachi","doi":"10.1016/j.cancergen.2025.11.001","DOIUrl":"10.1016/j.cancergen.2025.11.001","url":null,"abstract":"<div><h3>Background</h3><div>Li-Fraumeni syndrome (LFS) is an autosomal dominant disease caused by heterozygous germline pathogenic variant in <em>TP53</em> gene and frequently predisposes to a broad spectrum of cancers including early-onset cancers. To date, clinical and genetic features of LFS are largely unknown in Algerian population. In this study, we performed germline variants screening in <em>TP53</em> gene in an Algerian LFS family and we have reclassified the <em>TP53</em> germline missense variant c.314G&gt;<em>T</em>/ (p.Gly105Val).</div></div><div><h3>Patients and Methods</h3><div>We selected an LFS family with strong history of cancer along three generations that meets updated Chompret clinical criteria. Four family members were affected with various tumors. The proband in this family, a 4-year-old girl has been diagnosed with rhabdomyosarcoma at age 3 years old and she developed a secondary cancer in the right lung after radiotherapy. Her mother developed an early-onset breast cancer at age 30 years old, her maternal grandmother and her maternal aunt have also been diagnosed with breast cancer at age 33 and 27 years, respectively. We screened <em>TP53</em> exons 3–11 using PCR-Sanger sequencing in 4 members of this LFS family: the proband, her mother and her father (trio) and her kid brother aged of 2 years old, respectively.</div></div><div><h3>Results</h3><div>The analysis identified the rare germline missense variant <em>TP53</em> c.314G&gt;<em>T</em>/ (p.Gly105Val) in heterozygous status in three members of the LFS family: the proband, her mother and her kid brother, respectively. The father has been tested negative for the variant. As the <em>TP53</em> missense germline variant c.314G&gt;<em>T</em> co-segregates within cancer in our LFS family along two generations, we can classify it for the first time as Class 4 variant with the status “Likely Pathogenic” according to ACMG nomenclature.</div></div><div><h3>Conclusions</h3><div>Our study highlights the importance of the identification, the interpretation and the reclassification of <em>TP53</em> missense variants detected in carriers in order to improve prognosis, treatment strategies, and LFS patients monitoring and identifying high risk family members.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 268-273"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145514372","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}

{"title":"Decoding the genetic complexity in a pediatric case of B-ALL through long-read genomic sequencing and RNA sequencing","authors":"Mei Ling Chong ,&nbsp;Sok Meng Evelyn Ng ,&nbsp;Hongyan Chai ,&nbsp;Autumn Diadamo ,&nbsp;Aron Flagg ,&nbsp;Nicole Marie Owen ,&nbsp;Peining Li ,&nbsp;Jiadi Wen","doi":"10.1016/j.cancergen.2025.11.002","DOIUrl":"10.1016/j.cancergen.2025.11.002","url":null,"abstract":"<div><div>B-cell acute lymphoblastic leukemia (B-ALL) is a heterogeneous hematologic malignancy caused by diverse genetic alterations. While cytogenetic methods such as karyotyping and FISH are routinely used in diagnostics, cryptic and novel oncogenic gene fusions often go undetected. We report a 15-year-old male diagnosed with high-risk B-ALL, presenting with anemia, leukocytosis, and significant lymphoblast burden. Initial karyotyping identified an abnormal clone with a t(7;20)(q34;q13.3) and FISH detected a partial deletion of the <em>ABL1</em> gene. Chromosome microarray analysis revealed a deletion at 9p21.3 encompassing <em>CDKN2A</em>/<em>CDKN2B</em> and several contiguous copy number aberrations at 9q34.12q34.2. Further long-read genomic sequencing uncovered cryptic <em>NUP214::ABL1</em> and <em>ABL1::TSC1</em> fusions, as well as a novel <em>VAPB::TRBV30</em> rearrangement from the t(7;20). RNA sequencing confirmed the transcripts for both <em>ABL1</em> fusions and a noncoding rearrangement involving the TCRB locus. Notably, the presence of <em>NUP214::ABL1</em> identified a clinically actionable target, supporting the use of tyrosine kinase inhibitors (TKIs) such as imatinib. This case underscores the critical role of integrated sequencing approaches in identifying cryptic genetic alterations in B-ALL for precise classification of oncogenic drivers and for targeted therapeutic strategies to improve patient outcomes.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 274-279"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145514415","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}

{"title":"Unfavorable disease progression in patients with chronic myeloid leukemia and concurrent t(6;9) translocation (DEK::NUP214 fusion) or inversion 16 (CBFB::MYH11 fusion)","authors":"Ying Zhang ,&nbsp;Jack Reid ,&nbsp;Deepa Jeyakumar ,&nbsp;Kapitolina Semenova ,&nbsp;Naqvi Kiran ,&nbsp;Lisa Lee ,&nbsp;Angela Fleishman ,&nbsp;Sherif Rezk ,&nbsp;Xiaohui Zhao ,&nbsp;Fabiola Quintero-Rivera","doi":"10.1016/j.cancergen.2025.08.004","DOIUrl":"10.1016/j.cancergen.2025.08.004","url":null,"abstract":"<div><div>The occurrence of additional specific chromosomal abnormalities in Philadelphia chromosome-positive (pH+) cells is associated with disease progression in chronic myeloid leukemia (CML), and is considered a marker that defines the accelerated/blast phase of CML. Both DEK::NUP214 fusion and CBFB rearrangement are extremely rare in CML, and their prognostic significance is unknown. Here we present two CML cases, with one case having concurrent translocation 6;9 [t(6;9)] leading to DEK::NUP214 fusion, and the other one presenting with concurrent inversion 16 -inv(16)- leading to CBFB::MYH11 fusion. The t(6;9) is usually associated with poor prognosis in acute myeloid leukemia (AML) patients. In this case, the patient failed to achieve remission and expired. This suggests that the t(6;9) is also associated with poor prognosis in CML. However, more data is needed to verify this association. Detection of inv(16) by karyotyping is technically challenging. In addition, FISH for CBFB is not usually run in the context of CML, thus raising the possibility that similar cases may have been underdiagnosed. With the routine use of next-generation sequencing (NGS) for gene fusion detection, more patients like this one should be diagnosed and treated accordingly. These cases illustrate the importance of a comprehensive molecular/cytogenetic diagnostic work-up.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 20-26"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908235","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}

{"title":"Unraveling complex karyotype clonal architecture: co-existing double TP53 mutations alongside DNMT3A, TET2, and NF1 mutations – a case study","authors":"Suhaib Mohammad Ali Abunaser ,&nbsp;Anurita Pais ,&nbsp;Manu Venkatesan ,&nbsp;Uzma Zaidi ,&nbsp;Cigdem Pala Ozturk","doi":"10.1016/j.cancergen.2025.08.007","DOIUrl":"10.1016/j.cancergen.2025.08.007","url":null,"abstract":"<div><div>Complex chromosomal changes in Acute Myeloid Leukemia (AML) are highly heterogeneous, with disease progression shaped by both the number and nature of abnormalities. Rarely do, multiple unrelated clones with independent chromosomal changes coexist at diagnosis.</div><div>Present study showcases a comprehensive characterization of two cytogenetically distinct complex clones in AML, driven by non-cyclic and chromoplexy mechanisms, highlighting their co-existence with key molecular alterations (<em>TP53, NF1, DNMT3A, TET2</em>) along with their potential contribution to clonal evolution.</div><div>In the present study a refined assessment of clonal chromosomal complexity is provided, with each clone exhibiting distinct alterations involving chromosomes 5, 14, and 17 along with variant structural formation of chromosomes ie. isochromosome 5p, partial monosomy 7 and derivative 17, defining the heterogeneity of clonal architecture.</div><div>Additionally, we propose a probable association between mutational burden and chromosomal complexity, as evidenced by the coexistence of distinct clones with varying mutation loads and cytogenetic profiles, reflecting parallel clonal evolution.</div><div>Our integrated approach combining karyotyping and fluorescence <em>in situ</em> hybridization (FISH) was essential in unraveling the clonal architecture, providing valuable insights into the personalized chromosomal alterations and pathogenetic mechanisms that would be helpful for refining prognosis and guiding AML management.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 63-68"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145018563","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}

{"title":"The multidimensional role of laminin γ2 (LAMC2) on cancer progression","authors":"Xiaojuan Zhang ,&nbsp;Juan Xie ,&nbsp;Tao Fu ,&nbsp;Zhen Gao ,&nbsp;Hengrui Liu ,&nbsp;Zhenshan Yang","doi":"10.1016/j.cancergen.2025.09.007","DOIUrl":"10.1016/j.cancergen.2025.09.007","url":null,"abstract":"<div><div>Laminin, a critical component of the basement membrane, plays an indispensable role in numerous biological processes. Among its subunits, laminin γ2 (LAMC2) emerges as a key player in the progression of cancer. This review delves into the current understanding of LAMC2′s role, highlighting its significant contribution to cancer development through promoting cell proliferation, invasion, and vasculogenic mimicry, as well as inhibiting apoptosis. Notably, LAMC2 expression is markedly increased in cancerous tissues compared to normal counterparts, with higher levels of LAMC2 correlating with poorer survival rates. This correlation underscores LAMC2′s potential as a diagnostic and prognostic marker across various cancers. Furthermore, the increasing importance of LAMC2 as a viable target for cancer therapy is explored. This review aims to provide a thorough overview of LAMC2′s involvement in cancer progression, prognostic implications, potential therapeutic target, and involved signaling pathway, and to outline future research directions in this promising field.</div></div>","PeriodicalId":49225,"journal":{"name":"Cancer Genetics","volume":"298 ","pages":"Pages 122-127"},"PeriodicalIF":2.1,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109630","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}