Publication for HOXA6 and HOXA9
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| hsa | HOXA6 | homeobox A6 | 3203 | [link] | ||
| hsa | HOXA9 | homeobox A9 | 3205 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 28130639 | 0.98 | HOXA6, HOXA9, PENK, UPK3A and IGF2BP1) could successfully identify recurrent tumors and could be used as epigenetic biomarkers to effectively predict a pattern of global DNA methylation in meningioma. |
| 0.97 | HOXA6, HOXA9, OTX2, MAL2, and PAX3. | |
| 0.95 | HOXA6, and HOXA9 were reported in aggressive meningiomas by several studies but our analysis did not identify these genes as important predictors of outcome. | |
| 0.90 | HOXA6, and HOXA9, there were significant differences with increased levels of methylation in the MM-UNFAV group compared to MM-FAV group (findings limited to the validation dataset) (Online resource 9) confirming the findings in the literature. | |
| 19549311 | 0.98 | HOXA9, HOXA7, HOXA5 and HOXA3 were found to be generally upregulated in samples carrying MLL translocation, both in ALL and AML, while HOXA11 and HOXA6 showed common overexpression in AML/MLL+ cases. |
| 26517675 | 0.98 | HOXA6 (P = 3.34 x 10-7), HOXA9 (P = 4.72 x 10-8), HOXA10 (P = 5.83 x 10-8), HOXB2 (P = 5.95 x 10-8), HOXB3 (P = 5.61 x 10-5), HOXB4 (P = 1.37 x 10-6), HOXB5 (P = 3.90 x 10-6), HOXB6 (P = 2.65 x 10-3), HOXB7 (P = 2.21 x 10-3), HOXB8 (P = 1.78 x 10-2), MEIS1 (P = 6.18 x 10-7), and PBX3 (P = 5.02 x 10-4). |
| 31964111 | 0.98 | HOXA6, HOXA9, and HOXA11, induces silencing and downregulation of target tumor suppressors. |
| 26444494 | 0.97 | HOXA6, HOXA7, HOXA9 and HOXA10 compared with NPM1 wild-type samples in the The Cancer Genome Atlas (TCGA) cohort (Supplementary Fig. 4). |
| 0.88 | HOXA6, HOXA7, HOXA9 and HOXA10 (Supplementary Data 4). | |
| 0.74 | HOXA6, HOXA7, HOXA9 and HOXA10 in the LSC epigenetic signature (Fig. 1b-d and Supplementary Data 2). | |
| 23349797 | 0.97 | HOXA6 and HOXA9) tend to coincide with the binding sites of polycomb repressive complexes (PRC) in early developmental stages. |
| 0.94 | HOXA6 and HOXA9 has also been implicated in recurrent meningiomas according to another study. | |
| 26101774 | 0.97 | HOXA6, HOXA9, PENK, UPK3A, and IGF2BP1) was proposed. |
| 31426381 | 0.96 | HOXA6 expression in pro-B ALL (fold change = 2.01); (iii) HOXA7 expression in AML (fold change = 2.03); (iv) HOXA9 expression in AML (fold change = 2.99) and pro-B ALL (fold change = 7.21); and (v) HOXA10 expression in AML (fold change = 2.17) and pro-B ALL (fold change = 4.80). |
| 0.96 | HOXA6, HOXA7, HOXA9, and HOXA10 were significantly correlated with poor overall survival (OS, P < 0.05) in all of the AML patients (Figure 3). | |
| 0.87 | HOXA6, HOXA7, HOXA9, and HOXA10 was upregulated in patients with leukemia (Table 1). | |
| 20339440 | 0.96 | HOXA6, HOXA7, HOXA9, HOXB3, HOXB5, HOXB6, and HOXB7 as well as the non-clustered (type II) homeobox genes, MEIS1 and PBX3. |
| 29163771 | 0.96 | HOXA6 or HOXA9 alone has little effect on AML cells, but their double knock-down induces cell death and also increases their sensitivity to cytarabine. |
| 29221119 | 0.96 | HOXA6, HOXA7, HOXA9, HOXB9 and MEIS1 were observed in NPM1 mutated cells, as well as AML with MLL abnormalities. |
| 29770198 | 0.96 | HOXA6, HOXA9, PENK, UPK3A, and IGF2bP1) was reported to provide 80 to 90% sensitivity and specificity in predicting recurrence of meningiomas, independent of tumor grade . |
| 22498108 | 0.95 | HOXA6 and HOXA9) were silenced in all samples of this study. |
| 25539595 | 0.94 | HOXA6, HOXA9, HOXA10 and HOXB4 (Figure 4). |
| 0.90 | HOXA6, HOXA7, HOXA9, HOXA10, HOXB5 and HOXB6 distinguished leukemic cells of the M5a and M5b FAB subtypes from the matched normal counterparts, represented by the sorted M3 and M4 population, respectively (Additional file 8: Figure S7A and 7B). | |
| 27183470 | 0.94 | HOXA6, HOXA7 and HOXA9 expression in EB or FL cells treated with RA and AM580 (mean +/- SEM from n=4 independent experiments, see Supplementary Table 7 for statistics source data). |
| 25266220 | 0.92 | HOXA6, HOXA9, PBX3 and MEIS1), whose common expression signature was shown to influence overall survival in CN-AML. |
| 26485654 | 0.91 | HOXA6, HOXA7, HOXA9, HOXA10 and HOXA11 from HOXA-cluster. |
| 21339820 | 0.79 | HOXA6, HOXA7, HOXA9 and HOXA10 (Table 6). |
| 31970090 | 0.76 | HOXA6, HOXA9, PENK, UPK3A, and IGF2bP1). |
| 20068170 | 0.65 | HOXA9 expression in our tumor sets, also demonstrated a substantially lower correlation coefficient in the samples from Sun et al. Since HOXA6 and HOXA13 do not correlate with HOXA9 expression in all 3 tested tumor sets, a mechanism of chromosomal amplification encompassing the entire HOXA locus may not adequately explain the presence of such transcriptionally-active domains. |
| 29928480 | 0.65 | HOXA6, HOXA9 and HOXA10. |
| 31333881 | 0.54 | HOXA6, HOXA7, HOXA9, and HOXB9 genes and the MEIS1 and PBX3 genes. |
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