ZMYM4 (Zinc Finger MYM-Type Containing 4)

In conclusion, ZMYM4 is specifically targeted by miR-34a-5p in HCC and promotes the malignant progression of HCC. This suggests that ZMYM4 may serve as a potential biomarker for both the treatment and prognosis of HCC.

Therefore, this study revealed that m6A-induced hsa_circ_0011536 elevated TFRC expression to induce ferroptosis by sponging hsa-miR-576-5p in NSCLC. These results might provide novel therapeutic targets for NSCLC treatment.

35 novel (21 unique) genes across 12 disorders were identified: ADNP, AOC3, CDC42EP2, CHTOP, CNN1, DES, FOXF1, FXR1, HLTF, KCNMB1, MTF2, MYH11, PLN, PNPLA2, REST, SGCA, SORBS1, SYNPO2, TAGLN, WAPL, and ZMYM4. These genes are proffered as potential biomarkers or therapeutic targets for the corresponding rare diseases discussed.

This study has uncovered the mutational landscape in three local childhood AML patients and contributes to a better understanding of the molecular mechanisms of relapsed AML.

Cancer treatment reduced most of the serum fusion transcript levels. Serum fusion gene machine learning models may serve as important tools in screening HCC and monitoring the impact of HCC treatment.

ODAM knockdown could reverse the repressive effect of circZMYM4 overexpression on cell proliferation, migration and invasion abilities. Overall, circZMYM4 regulates the miR-587/ODAM axis to suppress LUAD progression, which may become a potential biomarker and therapeutic target.

Our in-silico analysis demonstrates the importance of copy number alterations in the pathology of HCC. These findings open a door for future studies that evaluate our results by performing additional experiments.

In both GC and CC with MSI-H, ZMYM4 expression in ZMYM4-mutated cases was significantly lower than that in ZMYM4-nonmutated cases. Our study indicates that ZMYM4 is altered at multiple levels (frameshift mutation, mutational intratumoral heterogeneity, and loss of expression), suggesting their relations with MSI-H GC and CC.