Publisher Correction: The long tail of oncogenic drivers in prostate cancer

Armenia, Joshua; Wankowicz, Stephanie A.; Liu, David; Gao, Jianjiong; Kundra, Ritika; Reznik, Ed; Chatila, Walid K.; Chakravarty, Debyani; Han, Guangming; Coleman, Ilsa; Montgomery, Bruce; Pritchard, Colin C.; Morrissey, Colm; Barbieri, Christopher E.; Beltran, Himisha; Sboner, Andrea; Miranda, Susana; Bielski, Craig M.; Penson, A.; Tolonen, Charlotte; Huang, Franklin W.; Robinson, Dan R.; Lonigro, Robert J.; Garraway, Levi A.; Demichelis, Francesca; Taplin, Mary‐Ellen; Abida, Wassim; Taylor, Barry S.; Scher, Howard I.; Nelson, Peter S.; Bono, Johann S. de; Rubin, Mark A.; Sawyers, Charles L.; Chinnaiyan, Arul M.; Pcf,; Schultz, Nikolaus; Allen, Eliezer M. Van

doi:10.1038/s41588-019-0451-6

Cited by 9 publications

(5 citation statements)

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“…Additionally, mutations have been detected in 20% of patients with MDS/myeloproliferative neoplasms and 15% of patients with chronic lymphocytic leukemia (CLL) [ 146 , 148 – 150 ]. Furthermore, mutations in SF3B1 have been reported at low frequencies in patients with acute myeloid leukemia, breast cancer, prolactinomas, uveal melanoma, leptomeningeal melanoma, blue nevus-like cutaneous melanoma, pancreatic ductal adenocarcinoma, and prostate cancer [ 151 – 159 ].…”

Section: Splicing Factors That Affect Cancer Progressionmentioning

confidence: 99%

The role of alternative pre-mRNA splicing in cancer progression

Choi,

Cho,

Kim

et al. 2023

Cancer Cell Int

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Alternative pre-mRNA splicing is a critical mechanism that generates multiple mRNA from a single gene, thereby increasing the diversity of the proteome. Recent research has highlighted the significance of specific splicing isoforms in cellular processes, particularly in regulating cell numbers. In this review, we examine the current understanding of the role of alternative splicing in controlling cancer cell growth and discuss specific splicing factors and isoforms and their molecular mechanisms in cancer progression. These isoforms have been found to intricately control signaling pathways crucial for cell cycle progression, proliferation, and apoptosis. Furthermore, studies have elucidated the characteristics and functional importance of splicing factors that influence cell numbers. Abnormal expression of oncogenic splicing isoforms and splicing factors, as well as disruptions in splicing caused by genetic mutations, have been implicated in the development and progression of tumors. Collectively, these findings provide valuable insights into the complex interplay between alternative splicing and cell proliferation, thereby suggesting the potential of alternative splicing as a therapeutic target for cancer.

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Section: Splicing Factors That Affect Cancer Progressionmentioning

confidence: 99%

The role of alternative pre-mRNA splicing in cancer progression

Choi,

Cho,

Kim

et al. 2023

Cancer Cell Int

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“…TCGA Dataset, CRC: [58], GC: TCGA Dataset, CSCC: TCGA Dataset, EAC: [59], HNC: TCGA Dataset, RMS: [60], PAC: [61], DLBCL: TCGA Dataset, HCC: TCGA Dataset, AC: Ampullary carcinoma [62], UCS: TCGA Dataset, BUC: TCGA Dataset, RCC: TCGA Dataset, PA: [63], CC: [64], GC: [65], PDTC & ATC: [66,67], OSC: TCGA Dataset, BC: [68], CCRCC: TCGA Dataset, CLL: [69], DG: [70]. [50], DM [51], CM: TCGA Dataset, BCC: [52], LA: [53], EC: TCGA Dataset, VV-SCC: [54], NSCLC: [55], UTUC [56], CTCL: [57], AS: TCGA Dataset, CRC: [58], GC: TCGA Dataset, CSCC: TCGA Dataset, EAC: [59], HNC: TCGA Dataset, RMS: [60], PAC: [61], DLBCL: TCGA Dataset, HCC: TCGA Dataset, AC: Ampullary carcinoma [62], UCS: TCGA Dataset, BUC: TCGA Dataset, RCC: TCGA Dataset, PA: [63], CC: [64], GC: [65], PDTC & ATC: [66,67], OSC: TCGA Dataset, BC: [68], CCRCC: TCGA Dataset, CLL: [69], DG: [70].…”

Section: Somatic Mutations Of Trkc In Cancermentioning

confidence: 99%

Roles of TrkC Signaling in the Regulation of Tumorigenicity and Metastasis of Cancer

Jin

2020

Cancers

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Tropomyosin receptor kinase (Trk) C contributes to the clinicopathology of a variety of human cancers, and new chimeric oncoproteins containing the tyrosine kinase domain of TrkC occur after fusion to the partner genes. Overexpression of TrkC and TrkC fusion proteins was observed in patients with a variety of cancers, including mesenchymal, hematopoietic, and those of epithelial cell lineage. Both microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) were involved in the regulation of TrkC expression through transcriptional and posttranscriptional alteration. Aberrant activation of TrkC and TrkC fusion proteins markedly induces the epithelial-mesenchymal transition (EMT) program, growth rate, tumorigenic capacity via constitutive activation of Ras-MAP kinase (MAPK), PI3K-AKT, and the JAK2-STAT3 pathway. The clinical trial of TrkC or TrkC fusion-positive cancers with newly developed Trk inhibitors demonstrated that Trk inhibitors were highly effective in inducing tumor regression in patients who do not harbor mutations in the kinase domain. Recently, there has been a progressive accumulation of mutations in TrkC or the TrkC fusion protein detected in the clinic and its related cancer cell lines caused by high-throughput DNA sequencing. Despite given the high overall response rate against Trk or Trk fusion proteins-positive solid tumors, acquired drug resistance was observed in patients with various cancers caused by mutations in the Trk kinase domain. To overcome acquired resistance caused by kinase domain mutation, next-generation Trk inhibitors have been developed, and these inhibitors are currently under investigation in clinical trials.

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“…Given the genomic complexity and phenotypic heterogeneity that characterize prostate tumors, a single somatic or germline variant is unlikely prognostic. Various genomic changes are enriched in mCRPC compared to the primary diseases, such as loss of function mutations in the tumor-suppressor genes TP53, RB1, and PTEN, deficiency of DNA damage repair pathway, a gain of function mutations in oncogenes, and copy-number alterations [6][7][8][9] . However, despite significant advances in molecular genetics and genome analysis, our ability to distinguish lethal mCRPC from non-lethal indolent prostate cancer is still limited.…”

Section: The Landscape Of Neuroendocrine Prostate Cancermentioning

confidence: 99%