Molecular Oncology最新文献

MET and NF2 alterations confer primary and early resistance to first-line alectinib treatment in ALK-positive non-small-cell lung cancer.

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 DOI: 10.1002/1878-0261.70029

Jie Hu, Ning Ding, Xiaobo Xu, Yedan Chen, Yong Zhang, Jingwen Liu, Jiebai Zhou, Hairong Bao, Donghui Zhang, Yijun Song, Yang Shao, Yuanlin Song

{"title":"MET and NF2 alterations confer primary and early resistance to first-line alectinib treatment in ALK-positive non-small-cell lung cancer.","authors":"Jie Hu, Ning Ding, Xiaobo Xu, Yedan Chen, Yong Zhang, Jingwen Liu, Jiebai Zhou, Hairong Bao, Donghui Zhang, Yijun Song, Yang Shao, Yuanlin Song","doi":"10.1002/1878-0261.70029","DOIUrl":"https://doi.org/10.1002/1878-0261.70029","url":null,"abstract":"Although first-line alectinib has prolonged survival in ALK-mutated non-small-cell lung cancers (NSCLCs), the response to treatment varies among patients, and the primary/early development of alectinib resistance mechanisms is still not fully understood. Here, we analyzed molecular profiles of 108 alectinib-treated patients (first-line and second-line after crizotinib) with confirmed relapse by targeted sequencing of cancer-related genes. After first-line treatment, off-target MET and NF2 alterations were more frequent than on-target alterations within the first 6 months, causing primary or early resistance. Conversely, on-target alterations became prevalent after 1 year of first-line alectinib treatment and predominantly after second-line. The incidence of acquired resistance also depended on EML4-ALK variants. In variant 1 (v1), off-target alterations were responsible for 50% of resistance cases after first-line alectinib therapy, whereas on-target mutations had no contribution in this subgroup. In variant 3 (v3), on-target alterations resulted in 46% of resistance cases, whereas only 18% were caused by off-target mutations. After second-line treatment, the most common mutations in v1 were L1196M (42%) and G1269A (25%), while G1202R was detected in 45% of v3 tumors. These findings emphasize the importance of stratifying resistance mechanisms to guide tailored treatment for ALK-positive NSCLCs.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":""},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Vertical inhibition of p110α/AKT and N-cadherin enhances treatment efficacy in PIK3CA-aberrated ovarian cancer cells. 垂直抑制 p110α/AKT 和 N-cadherin 可提高对 PIK3CA 异常卵巢癌细胞的治疗效果。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2024-11-14 DOI: 10.1002/1878-0261.13761

Shibo Zhang, Hei Ip Hong, Victor C Y Mak, Yuan Zhou, Yiling Lu, Guanglei Zhuang, Lydia W T Cheung

{"title":"Vertical inhibition of p110α/AKT and N-cadherin enhances treatment efficacy in PIK3CA-aberrated ovarian cancer cells.","authors":"Shibo Zhang, Hei Ip Hong, Victor C Y Mak, Yuan Zhou, Yiling Lu, Guanglei Zhuang, Lydia W T Cheung","doi":"10.1002/1878-0261.13761","DOIUrl":"10.1002/1878-0261.13761","url":null,"abstract":"Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha [PIK3CA, encoding PI3Kalpha (also known as p110α)] is one of the most commonly aberrated genes in human cancers. In serous ovarian cancer, PIK3CA amplification is highly frequent but PIK3CA point mutation is rare. However, whether PIK3CA amplification and PIK3CA driver mutations have the same functional impact in the disease is unclear. Here, we report that both PIK3CA amplification and E545K mutation are tumorigenic. While the protein kinase B (AKT) signaling axis was activated in both E545K knock-in cells and PIK3CA-overexpressing cells, the mitogen-activated protein kinase 3/1 (ERK1/2) pathway was induced selectively by E545K mutation but not PIK3CA amplification. Intriguingly, AKT signaling in these PIK3CA-aberrated cells increased transcriptional coactivator YAP1 (YAP) Ser127 phosphorylation and thereby cytoplasmic YAP levels, which in turn increased cell migration through Ras-related C3 botulinum toxin substrate 1 (RAC1) activation. In addition to the altered YAP signaling, AKT upregulated N-cadherin expression, which also contributed to cell migration. Pharmacological inhibition of N-cadherin reduced cell migratory potential. Importantly, co-targeting N-cadherin and p110α/AKT caused additive reduction in cell migration in vitro and metastases formation in vivo. Together, this study reveals the molecular pathways driven by the PIK3CA aberrations and the exploitable vulnerabilities in PIK3CA-aberrated serous ovarian cancer cells.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1132-1154"},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Stroma gene signature predicts responsiveness to chemotherapy in pancreatic ductal adenocarcinoma patient-derived xenograft models.

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2025-02-04 DOI: 10.1002/1878-0261.13816

Alessia Anastasia, Laura Formenti, Paola Ostano, Lucia Minoli, Andrea Resovi, Lavinia Morosi, Claudia Fioravanti, Edoardo Micotti, Cristina Matteo, Eugenio Scanziani, Giovanna Chiorino, Raffaella Giavazzi, Carmen Ghilardi, Dorina Belotti

{"title":"Stroma gene signature predicts responsiveness to chemotherapy in pancreatic ductal adenocarcinoma patient-derived xenograft models.","authors":"Alessia Anastasia, Laura Formenti, Paola Ostano, Lucia Minoli, Andrea Resovi, Lavinia Morosi, Claudia Fioravanti, Edoardo Micotti, Cristina Matteo, Eugenio Scanziani, Giovanna Chiorino, Raffaella Giavazzi, Carmen Ghilardi, Dorina Belotti","doi":"10.1002/1878-0261.13816","DOIUrl":"10.1002/1878-0261.13816","url":null,"abstract":"Despite many efforts to understand the molecular mechanisms of pancreatic ductal adenocarcinoma (PDAC) treatment resistance, there is still no reliable method for selecting patients who could benefit from standard pharmacological treatment. Here, four PDAC patient-derived xenografts (PDAC-PDXs) with different responses to gemcitabine plus nab-paclitaxel (nanoparticle albumin-bound paclitaxel) were studied to dissect the contribution of both tumor and host microenvironment to treatment response. PDAC-PDXs transplanted into the pancreas of immunodeficient mice retained the main genetic and histopathological characteristics of the original human tumors, including invasiveness and desmoplastic reaction. Response to chemotherapy was associated with a specific 294 stroma gene signature and was not due to the intrinsic responsiveness of tumor cells or differences in drug delivery. Human dataset analysis validated the expression of the 294 stroma gene signature in PDAC clinical samples, confirming PDAC-PDXs as a useful tool to study the biology of tumor-host interactions and to test drug efficacy. In summary, we identified a stroma gene signature that differentiates PDAC-PDXs that are responsive to gemcitabine plus Nab-paclitaxel treatment from those that are not, confirming the active role of the tumor microenvironment in the drug response.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1075-1091"},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143123384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Gut microbiota diversity is prognostic and associated with benefit from chemo-immunotherapy in metastatic triple-negative breast cancer. 肠道微生物群多样性预示着转移性三阴性乳腺癌的预后，并与化疗免疫疗法的获益相关。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2024-11-15 DOI: 10.1002/1878-0261.13760

Andreas Ullern, Kristian Holm, Andreas Hagen Røssevold, Nikolai Kragøe Andresen, Corinna Bang, Ole Christian Lingjærde, Bjørn Naume, Johannes R Hov, Jon Amund Kyte

{"title":"Gut microbiota diversity is prognostic and associated with benefit from chemo-immunotherapy in metastatic triple-negative breast cancer.","authors":"Andreas Ullern, Kristian Holm, Andreas Hagen Røssevold, Nikolai Kragøe Andresen, Corinna Bang, Ole Christian Lingjærde, Bjørn Naume, Johannes R Hov, Jon Amund Kyte","doi":"10.1002/1878-0261.13760","DOIUrl":"10.1002/1878-0261.13760","url":null,"abstract":"The gut microbiota influences multiple aspects of human health and disease. Several studies have indicated an association between the gut microbiota and response to immune checkpoint inhibitors in various cancers, but there is scarce data from breast cancer. The randomized ALICE trial demonstrated improved progression-free survival (PFS) from adding the programmed cell death 1 ligand 1 (PD-L1) inhibitor atezolizumab (atezo) to immunomodulating chemotherapy (chemo) in metastatic triple-negative breast cancer (mTNBC), even for PD-L1negative disease. Herein, we investigated the microbiota composition and dynamics in the ALICE patients and their association with clinical outcome, by analyzing fecal samples collected at baseline and after 8 weeks. We applied 16S (V3-V4) rRNA sequencing to characterize the diversity and taxonomic composition. Kaplan-Meier and Cox proportional hazard models were used for time-to-event analyses. We found that high alpha diversity by Faith's phylogenetic diversity (PD) at baseline was associated with prolonged PFS in the total study population and in the atezo-chemo arm, but not in the placebo-chemo arm. Moreover, Faith's PD appeared to be predictive of benefit from atezolizumab. Patients with high Faith's PD exhibited a PFS hazard ratio of 0.34 (P = 0.018) in favor of the atezo-chemo arm, compared to 0.83 (P = 0.62) in the low Faith's PD group. Faith's PD was significantly reduced during treatment. At baseline, Bifidobacterium was significantly overrepresented in patients without clinical benefit in the atezo-chemo arm, but not in the placebo-chemo arm. These findings suggest that alpha diversity by Faith's PD should be further investigated as a prognostic and predictive biomarker in patients with mTNBC receiving chemo-immunotherapy.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1229-1243"},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Plasma-activated media selectively induces apoptotic death via an orchestrated oxidative stress pathway in high-grade serous ovarian cancer cells. 血浆激活介质通过精心安排的氧化应激途径选择性诱导高级别浆液性卵巢癌细胞的凋亡死亡。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2024-12-03 DOI: 10.1002/1878-0261.13768

Lorena T Davies, Raja Ganesen, John Toubia, Sung-Ha Hong, Sushil Kumar Kc, Martin K Oehler, Carmela Ricciardelli, Endre J Szili, Nirmal Robinson, Melissa R Pitman

{"title":"Plasma-activated media selectively induces apoptotic death via an orchestrated oxidative stress pathway in high-grade serous ovarian cancer cells.","authors":"Lorena T Davies, Raja Ganesen, John Toubia, Sung-Ha Hong, Sushil Kumar Kc, Martin K Oehler, Carmela Ricciardelli, Endre J Szili, Nirmal Robinson, Melissa R Pitman","doi":"10.1002/1878-0261.13768","DOIUrl":"10.1002/1878-0261.13768","url":null,"abstract":"High-grade serous ovarian cancer (HGSOC) is the most common and aggressive type of ovarian cancer. Due to a lack of an early detection test and overt symptoms, many patients are diagnosed at a late stage where metastasis makes treatment very challenging. Furthermore, the current standard treatment for HGSOC patients, consisting of debulking surgery and platinum-taxane chemotherapy, reduces quality of life due to debilitating side-effects. Sadly, 80-90% of patients diagnosed with advanced stage ovarian cancer will die due to treatment resistance. As such, novel therapeutic strategies for HGSOC that are both more effective and less toxic are urgently required. Here we describe the assessment of cold atmospheric pressure (CAP) gas discharge technology as a novel treatment strategy in pre-clinical models of HGSOC. Plasma-activated media (PAM) was generated using cell growth media. HGSOC cell lines, patient ascites cells and primary tissue explants were tested for their response to PAM via analysis of cell viability, cell death and oxidative stress assays. Our data show that PAM treatment can be more effective than standard carboplatin chemotherapy at selectively targeting ovarian cancer cells in primary patient samples. Further, we also observed PAM to induce apoptosis in HGSOC cancer cell lines via induction of oxidative stress and mitochondrial-mediated apoptosis. These findings suggest that PAM is a viable therapeutic strategy to test in in vivo models of ovarian cancer, with a view to develop an intraperitoneal PAM-based therapy for HGSOC patients. Our studies validate the ability of PAM to selectively target tumour tissue and ascites cells. This work supports the development of PAM towards in vivo validation and translation into clinical practice.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1170-1187"},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Unraveling epigenetic heterogeneity across gastrointestinal adenocarcinomas through a standardized analytical framework. 通过标准化分析框架揭示胃肠道腺癌的表观遗传异质性。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2024-12-18 DOI: 10.1002/1878-0261.13772

Rita Pinto, Hege Marie Vedeld, Guro Elisabeth Lind, Marine Jeanmougin

{"title":"Unraveling epigenetic heterogeneity across gastrointestinal adenocarcinomas through a standardized analytical framework.","authors":"Rita Pinto, Hege Marie Vedeld, Guro Elisabeth Lind, Marine Jeanmougin","doi":"10.1002/1878-0261.13772","DOIUrl":"10.1002/1878-0261.13772","url":null,"abstract":"In this study, we propose an alternative approach for stratifying genome-scale DNA methylation profiles of gastrointestinal (GI) adenocarcinomas based on a robust analytical framework. A set of 978 GI adenocarcinomas and 120 adjacent normal tissues from public repositories was quality controlled and analyzed. Hierarchical consensus clustering of the tumors, based on differential epigenetic variability between malignant and normal samples, identified six distinct subtypes defined either by a pan-GI or a lower GI-specific phenotype. In addition to methylation levels, aberrant methylation frequencies and the degree of DNA methylation instability contributed to the characterization of each subtype. We found significant differences in the outcome of patients, with the poorest overall survival seen for those belonging to a pan-GI subtype with infrequent aberrant methylation. In conclusion, our standardized approach contributes to a refined characterization of the epigenetic heterogeneity in GI adenocarcinomas, offering insights into subtype-specific methylation with the potential to support prognostication.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1117-1131"},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Genomic landscape and preclinical models of angiosarcoma. 血管肉瘤的基因组图谱和临床前模型。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2024-10-05 DOI: 10.1002/1878-0261.13744

Annaleigh Benton, Bozhi Liu, Lauren E Gartenhaus, Jason A Hanna

引用次数: 0

Loss of SETD2 in wild-type VHL clear cell renal cell carcinoma sensitizes cells to STF-62247 and leads to DNA damage, cell cycle arrest, and cell death characteristic of pyroptosis. 野生型 VHL 透明细胞肾细胞癌中 SETD2 的缺失会使细胞对 STF-62247 敏感，并导致 DNA 损伤、细胞周期停滞和细胞死亡，这就是热核病的特征。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2024-11-26 DOI: 10.1002/1878-0261.13770

Mathieu Johnson, Sandra Turcotte

{"title":"Loss of SETD2 in wild-type VHL clear cell renal cell carcinoma sensitizes cells to STF-62247 and leads to DNA damage, cell cycle arrest, and cell death characteristic of pyroptosis.","authors":"Mathieu Johnson, Sandra Turcotte","doi":"10.1002/1878-0261.13770","DOIUrl":"10.1002/1878-0261.13770","url":null,"abstract":"Loss of chromosome 3p and loss of heterogeneity of the von Hippel-Lindau (VHL) gene are common characteristics of clear cell renal cell carcinoma (ccRCC). Despite frequent mutations on VHL, a fraction of tumors still grows with the expression of wild-type (WT) VHL and evolve into an aggressive subtype. Additionally, mutations on chromatin-modifying genes, such as the gene coding for the histone methyltransferase SET containing domain 2 (SETD2), are essential to ccRCC evolution. We previously identified STF-62247, a small molecule first discovered as a synthetically lethal molecule for VHL-deficient cells by blocking late stages of autophagy. This study investigated how other commonly mutated genes in ccRCC could impact the response to STF-62247. We showed that SETD2 inactivation in ccRCC cells expressing WT-VHL became vulnerable to STF-62247, as indicated by decreases in cell proliferation and survival. Furthermore, activation of the DNA damage response pathway leads to the loss of M-phase inducer phosphatase 1 (CDC25A) and cell cycle arrest in S phase. Cleavage of both caspase-3 and gasdermin E suggests that STF-62247 eliminates WT-VHL ccRCC cells through pyroptosis specifically when SETD2 is inactivated.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"1244-1264"},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142730727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Whole-genome sequencing of cell-free DNA reveals DNA of tumor origin in plasma from patients with colorectal adenomas. 无细胞DNA的全基因组测序揭示了结直肠腺瘤患者血浆中肿瘤起源的DNA。

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2025-01-20 DOI: 10.1002/1878-0261.13803

Amanda Frydendahl, Adam J Widman, Nadia Øgaard, Anushri Arora, Daniel Halmos, Jesper Nors, Johanne Ahrenfeldt, Tenna V Henriksen, Christina Demuth, Line Raaby, Mads H Rasmussen, Christina Therkildsen, Dan A Landau, Claus L Andersen

{"title":"Whole-genome sequencing of cell-free DNA reveals DNA of tumor origin in plasma from patients with colorectal adenomas.","authors":"Amanda Frydendahl, Adam J Widman, Nadia Øgaard, Anushri Arora, Daniel Halmos, Jesper Nors, Johanne Ahrenfeldt, Tenna V Henriksen, Christina Demuth, Line Raaby, Mads H Rasmussen, Christina Therkildsen, Dan A Landau, Claus L Andersen","doi":"10.1002/1878-0261.13803","DOIUrl":"10.1002/1878-0261.13803","url":null,"abstract":"The presence of circulating tumor DNA (ctDNA) in patients with colorectal adenomas remains uncertain. Studies using tumor-agnostic approaches report ctDNA in 10-15% of patients, though with uncertainty as to whether the signal originates from the adenoma. To obtain an accurate estimate of the proportion of patients with ctDNA, a sensitive tumor-informed strategy is preferred, as it ensures the detected signal originates from the adenoma. Here, tumor-informed whole-genome sequencing-based ctDNA analysis (MRD-EDGESNV) was applied to two independent cohorts. Cohort 1, comprising 93 patients with stage III colorectal cancer (CRC) and 40 healthy individuals, was used to establish the signal threshold at 95% specificity. This threshold was then applied to Cohort 2, consisting of 22 patients with symptomatic and 20 with asymptomatic adenomas. In stage III, MRD-EDGESNV had an area under the curve of 0.98. ctDNA was detected in 50% and 25% of patients with symptomatic and asymptomatic adenomas, respectively. The median adenoma plasma tumor fraction was 5.9 × 10-5. These finding not only demonstrate the feasibility of ctDNA detection in patients with colorectal adenomas, but also provides an estimate of the necessary sensitivity required to detect these lesions, paving the way for future ctDNA-based screening strategies.","PeriodicalId":18764,"journal":{"name":"Molecular Oncology","volume":" ","pages":"984-993"},"PeriodicalIF":6.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction to "hnRNPA2/B1 activates cyclooxygenase-2 and promotes tumor growth in human lung cancers".

IF 6.6 2区医学

Molecular Oncology Pub Date : 2025-04-01 Epub Date: 2025-03-10 DOI: 10.1002/1878-0261.70016

引用次数: 0