<![CDATA[Background: Hydatidiform mole, a type of gestational trophoblastic disease, arises from abnormal placental tissue and has the potential for malignant transformation. The condition’s incidence varies globally, with notable prevalence in Indonesia. Advanced maternal age, dietary factors, and a history of previous moles contribute to recurrence risks. Understanding the molecular and cellular mechanisms is critical for effective management.Methods: This narrative review synthesizes findings from primary studies and reviews exploring the molecular and cellular characteristics of hydatidiform mole. Data were sourced from Google Scholar, PubMed, and ScienceDirect using keywords like “hydatidiform mole,” “molecular mechanisms,” and “cell signaling pathways.”Results: The pathogenesis involves chromosomal abnormalities, particularly in complete moles characterized by a diploid genome lacking maternal DNA. P57KIP2 expression serves as a diagnostic marker, distinguishing complete from partial moles. Molecular genotyping, including short tandem repeat (STR) analysis, aids in accurate diagnosis and risk stratification for malignancy. Genetic factors, including mutations in NLRP7 and KHDC3L, are associated with recurrence in familial cases.Conclusion: The cellular and molecular insights into hydatidiform moles enhance understanding of their pathophysiology and inform diagnostic strategies. Recognizing genetic predispositions enables better patient management, emphasizing the need for continued research into the condition’s underlying mechanisms to improve clinical outcomes and therapeutic approaches.]]>
