1. Overexpression of CMTM7 inhibits cell growth and migration in liver cancer
   Zi‐Ming Huang et al, 2019, The Kaohsiung Journal of Medical Sciences CrossRef
2. Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
   Wen Guo et al, 2019, Aging CrossRef
3. Bioinformatics-Based Discovery of CKLF-Like MARVEL Transmembrane Member 5 as a Novel Biomarker for Breast Cancer
   Juan Zhou et al, 2020, Frontiers in Cell and Developmental Biology CrossRef
4. Oncogenic and tumor suppressor genes expression in myeloproliferative neoplasms: The hidden side of a complex pathology
   Elham Abedi et al, 2022, Journal of Clinical Laboratory Analysis CrossRef
5. CMTM Family and Gastrointestinal Tract Cancers: A Comprehensive Review
   Jie Li et al, 2022, Cancer Management and Research CrossRef
6. Expressions of ZNF436, β-catenin, EGFR, and CMTM5 in breast cancer and their clinical significances
   Zhi Chen et al, 2021, European Journal of Histochemistry CrossRef
7. Low expression of PDK1 inhibits renal cell carcinoma cell proliferation, migration, invasion and epithelial mesenchymal transition through inhibition of the PI3K-PDK1-Akt pathway
   Wei-Min Zhou et al, 2019, Cellular Signalling CrossRef
8. Research insights into the chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family (CMTM): their roles in various tumors
   Sai-Li Duan et al, 2024, PeerJ CrossRef
9. CMTM5 inhibits the development of prostate cancer via the EGFR/PI3K/AKT signaling pathway
   Linjin Li et al, 2021, Molecular Medicine Reports CrossRef
10. Identification of prognostic biomarkers in the CMTM family genes of human ovarian cancer through bioinformatics analysis and experimental verification
    Mengjun Zhang et al, 2022, Frontiers in Genetics CrossRef
11. Chemokine-Like Factor-Like MARVEL Transmembrane Domain-Containing Family in Hepatocellular Carcinoma: Latest Advances
    Mengxia Li et al, 2020, Frontiers in Oncology CrossRef