| General information | Literature | Expression | Regulation | Mutation | Interaction |
Basic Information | |
|---|---|
Gene ID | 57167 |
Name | SALL4 |
Synonymous | DRRS|HSAL4|ZNF797|dJ1112F19.1;sal-like 4 (Drosophila);SALL4;sal-like 4 (Drosophila) |
Definition | sal-like protein 4|zinc finger protein 797|zinc finger protein SALL4 |
Position | 20q13.2 |
Gene type | protein-coding |
Cancer type | Abstract |
| rhabdoid Tumor;Neurological | Malignant rhabdoid tumor is a highly aggressive pediatric neoplasm molecularly characterized by inactivating mutations of the SMARCB1 gene, a potent tumor suppressor and member of the SWI/SNF chromatin remodeling complex. It has been suggested that oncogenesis in SMARCB1-deficient cancers, such as malignant rhabdoid tumors, is driven not by the loss of SWI/SNF function but by an aberrant functioning of the BRG1-containing SWI/SNF complex. Since Brg1 is required for self-renewal and pluripotency of mouse embryonic stem cells, we hypothesized that the human malignant rhabdoid tumors may express pluripotency genes such as SALL4, LIN28 , OCT3 and OCT4 (OCT3/4) , NANOG , and TCL1 . To test this hypothesis, we studied the immunohistochemical expression of SALL4, LIN28, OCT3/4, NANOG, and TCL1 in 11 malignant rhabdoid tumors of the central nervous system (atypical teratoid/rhabdoid tumors) and 5 malignant rhabdoid tumors of the kidney. Of the 16 malignant rhabdoid tumors, 14 (88%) tumors showed robust SALL4 and/or LIN28 expression. No tumor showed any significant OCT3/4, NANOG, or TCL1 expression. Our results suggest that malignant rhabdoid tumors may arise from and/or share features with embryonic stem cells or germ cells. |