Table 2.
Genomic alteration of ATP-dependent chromatin-remodeling factors in cancer.
| Tumors | Genomic Alteration | Molecular Functions | Refs. |
|---|---|---|---|
| Ovarian carcinomas | ARID1A mutations |
ARID1A mutations induce early transformation of endometriosis into cancer. | [32] |
| Ovarian clear cell carcinoma | ARID1A mutations | Aberrant ARID1A contributes to the pathogenesis of OCCC. | [33] |
| Clear cell carcinoma | PBRM1/BAF180 truncating mutations | Truncating mutations of PBRM1 contribute to aberrant chromatin biology. | [34] |
| Lung cancer | Concomitant loss of BRG1/BRM | Loss of BRG1/BRM is correlated with poor prognosis. | [35] |
| Rhabdoid tumors | SMARCB1 biallelic mutations | Inactivation of SMARCB1 upregulates cell cycle progression. | [40] |
| Lung primary tumor | SMARCA4 inactivating mutations | Inactivation of SMARCA4 contributes to the development of lung primary tumor. | [41] |
| Breast tumor | Low BRD7 expression | Low BRD7 expression promotes tumorigenicity. | [37] |
| Non-small-cell lung cancer | SMARCA4 loss | SMARCA4 loss exhibits a synthetic lethality with CDK4/6 inhibition. | [38] |
| Malignant rhabdoid tumor | SMARCA4 inactivation | SMARCA4-deficient causes long-lasting response to pembrolizumab treatment. | [39] |
| Lung adenocarcinoma | SMARCA4/BRG1 Inactivation | Inactivation of SMARCA4 promotes transformation and early metastasis. | [42] |
| Leukemia | SMARCD2/ BAF60b loss-of-function mutations |
Loss-of-function mutations of SMARCD2 promote acute myeloid leukemia. | [43] |
| Glioblastoma | SMARCB1/BAF47 | A SMARCB1 mutation predisposes to earlier development of glioblastoma. | [44] |
| Thyroid Tumor | SWI/SNF complex mutations | SWI/SNF complex mutations promote thyroid tumor progression and resistance to redifferentiation therapies. | [45] |
| Lung cancer | Inactivation of SMARCA2 | SMARCA2 promoter hypermethylation plays an oncogenetic role. | [46] |
| Clear cell meningioma | SMARCE1/BAF57 mutations | SMARCE1 mutations cause spinal and cranial clear cell meningioma. Germline SMARCE1 mutations were found in familial pediatric clear cell meningioma. |
[47,48] |
| Squamous Cell Carcinoma | ACTL6A/BAF53A co-amplified with p63 | ACTL6A is co-amplified with p63 and acts as an oncogenic driver in squamous cell carcinoma. | [49] |
| Synovial sarcomas | SS18: SSX fusion | SS18: SSX fusion acts as an oncogenic driver in synovial sarcomas. | [50] |
| Endometroid and ovarian clear cell cancers | ARID1A/BAF250A loss-of-function mutations | ARID1A mutations impacts numerous signals important in oncogenesis. | [51] |
| Colorectal cancer | ARID1B/ BAF250B inactivation mutation | ARID1B inactivation mutation may play a role in microsatellite unstable colorectal cancer. | [52] |
| Lung cancer | ARID2/BAF200 mutations | ARID2 deficiency increases tumor progression and chemotherapy resistance in lung cancer. | [53] |
| Lung cancer | PBRM1/BAF180 mutation | PBRM1 mutation may be a negative predictive biomarker for immunotherapy in NSCLC. | [54] |
| Ewing sarcoma/primitive neuroectodermal tumor | EWSR1-SMARCA5/SNF2H fusion | EWSR1-hSNF2H may act as an oncogenic chromatin-remodeling factor. | [55] |
| Lung adenocarcinoma | SMARCA1/ SNF2L mutations | SMARCA1 mutations were associated with metastasis. | [56] |
| Soft-tissue sarcoma | SMARCA1 | SMARCA1 loss affects the differentiation process | [19] |
| Gastric cancer | SMARCA1 aberrant methylation | SMARCA1 loss promotes cancer cell growth | [57] |
| Breast cancer, gastric cancer, acute myeloid leukemia, pancreatic ductal adenocarcinoma | SMARCA5 overexpressed | Overexpression of SMARCA5 promotes cancer progression. | [58,59,60,61] |
| Bladder cancer, breast cancer, | circ-SMARCA5 silent | circ-SMARCA5 acts as a potential prognostic marker. | [62,63] |
| Prostate cancer | CHD1 deletion | CHD1 shows a key role in prostate cancer biology, | [64,65,66] |
| Metastatic prostate cancer | CHD1 loss | CHD1 loss is a cause of antiandrogen resistance. | [67] |
| Prostate cancer | CHD1 deletions | CHD1 deletions were correlated with disease phenotype and progression. | [66] |
| Breast implant-associated anaplastic large-cell lymphoma, mantle-cell lymphoma | CHD2 mutation | CHD2 mutation is an oncogenic event. | [68,69] |
| Acute myeloid leukemia | CHD4 mutation | CHD4 mutations enrich in primary chemoresistance patients. | [70] |
| Spinal schwannoma | CHD4 mutation | CHD4 is a frequently mutated cancer-related gene in spinal schwannoma. | [71] |
| Human cancer | CHD5 deletion | CHD5 deletion controls proliferation, apoptosis, and senescence. | [72] |
| Neuroblastoma | CHD5 and ARID1A deletion | CHD5 and ARID1A deletion links to poor prognosis of neuroblastoma. | [73] |
| Bladder cancer | CHD6 aberration | CHD6 aberration might be a hallmark of bladder cancer. | [74] |
| Colorectal carcinomas | CHD7 and CHD8 mutation | Mutations in CHD7 and CHD8 occurred frequently in CpG island methylator phenotype 1 colorectal carcinomas. | [75] |
| Lung cancer | CHD7 rearrangement | Recurrently rearrangement of CHD7 occurs in tobacco-smoking small-cell lung cancer patients. | [76] |
| Human cancers | CHD7 gained/amplified and mutated | CHD7 is associated with poor prognosis in human cancer. | [77] |
| Pancreatic cancer | INO80C deletion | INO80C deletion is associated with worse prognosis of patients. | [78] |
| Burkitt-like lymphoma | NFRKB aberration | NFRKB aberration is a positional candidate. |
[79,80] |
| Colorectal cancer | INO80 variants | INO80 is candidate gene with a higher risk for colorectal cancer. | [81] |
| Hepatosplenic T-cell lymphoma | INO80 and ARID1B mutation | INO80 and ARID1B mutations linked to Hepatosplenic T-cell lymphoma pathogenesis. | [82] |
| Colon cancer | INO80 haploinsufficiency | INO80 haploinsufficiency suppresses colon cancer tumorigenesis. | [83] |
| Non-small-cell lung cancer | INO80 highly expressed | INO80 promotes oncogenic transcription and NSCLC tumorigenesis | [84] |
| Melanoma | INO80 elevated | Elevated INO80 induces melanoma progression. | [85] |