Publication for CD33 and CLEC12A
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| hsa | CD33 | CD33 molecule | 945 | [link] | ||
| hsa | CLEC12A | C-type lectin domain family 12 member A | 160364 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 31695916 | 0.97 | CD33, CD123 and CLL-1 (SGN-CD33A, IMGN779, IMGN632, CLT030) are under active development. |
| 0.90 | CD33 and CD123, CLL-1 is completely absent on normal HSCs, making it an ideal therapeutic target for AML. | |
| 29316944 | 0.96 | CLL-1+, CD33+, and CD34+ cells in primary AML samples (n = 37-40, from a diverse range of AML subtypes; see Additional file 1: Table S1); NS not significant. |
| 0.93 | CD33 and CD34 are classic markers for AML, we measured the expression of these two markers in combination with CLL-1 on primary AML samples. | |
| 0.89 | CLL-1, while most of the granulocyte and monocyte precursor cells (CD34+CD33+) expressed CLL-1 at high levels, in contrast CD34+CD33- cells showed virtually no expression of CLL-1. | |
| 29946192 | 0.95 | CD33 (98.1%), CD123 (98.1%), CLL1 (71.4%), TIM3 (80.0%) and CD244 (97.1%). |
| 0.94 | CD33/TIM3 or CLL1/TIM3 may enhance therapeutic efficacy without aggravating toxicity in immunotherapy of AML. | |
| 0.94 | CD33, CD123, CLL1, TIM3 and CD7. | |
| 0.91 | CD33, CLL1, TIM3 and CD244 to be significantly less expressed on LSC, both at initial diagnosis and at relapse. | |
| 0.90 | CD33/TIM3 and CLL1/TIM3 revealed non-overlapping expression patterns in normal tissues: Excluding organs with known immune infiltration, dual expression of CD33/TIM3 was only found in bladder. | |
| 0.88 | CD33/TIM3 and CLL1/TIM3 to be highly positive in AML compared with normal hematopoiesis and non-hematopoietic tissues. | |
| 0.83 | CD33 (96.4%), CD123 (97.0%), CLL1 (80.1%), TIM3 (87.3%) and CD244 (96.7%). | |
| 0.66 | CD33, CD123, CLL1, TIM3 or CD244 may have antileukemic efficacy in most AML patients. | |
| 0.64 | CD33, CD123, CLL1, TIM3 and CD244 in most cases at initial diagnosis and relapse, irrespective of the genetic background. | |
| 0.55 | CD33, CD123, CLL1, CD47, CD96, CD157, CD244, TIM3 and CD7, have been reported to be expressed on leukemic stem cells (LSC). | |
| 25056598 | 0.95 | CLL-1 targeting BiFab, alphaCLL1-alphaCD3, and a comparison of its in vitro and in vivo activity to a similarly constructed CD33 targeting BiFab, alphaCD33-alphaCD3. |
| 0.93 | CD33 and CLL1 expression levels (U937: CD33 and CLL1 high; KASUMI-3: CD33 and CLL1 medium; and KG-1A: CD33 and CLL1 low; see Fig. S3) were used to compare the cytotoxicities of BiFabs after a 24h incubation period. | |
| 0.90 | CD33 and CLL1 expression in patients reveals simultaneous expression in most patients, but cases of single antigen expression (CD33+/CLL1- or CD33-/CLL1+) have also been reported in the literature and were observed in our AML patient samples. | |
| 0.86 | CD33- and CLL1- human B-lymphoblast cell line, RS4;11 (Fig. S2). | |
| 29716633 | 0.95 | CD33, CD123, CD38, CD44v6, FRbeta, PR1/HLA-A2, CLL-1, and LeY. CD33 and CD123 are highly expressed on primary AML cells and are the most commonly used antigens for AML treatment by CAR-T therapy. |
| 31623224 | 0.95 | CLEC12A), which is highly expressed also on CD33- AML cells and could better contribute to myeloid leukemia targeting by NK cells. |
| 32185132 | 0.95 | CD33, C-type lectin-like molecule 1 (CLL-1), and Lewis-Y. Additional targets under preclinical investigation include CD135 (FLT-3 receptor), Folate receptor beta, CD44v6, WT1, B7-H3, CD70, and CD7. |
| 31014360 | 0.93 | CLL1/CD33/CD38/CD56/CD123 from China is enrolling patients with refractory or relapsed AML; it plans to enroll 10 patients between 2 and 75 years old and aims to evaluate the feasibility, safety, and efficacy of the fourth generation CAR-T cells, estimated completion date is December 31, 2020. |
| 0.87 | CLL-1 or CD33-positive on both AML cell lines and primary AML cells. | |
| 0.76 | CLL-1 are mainly on anti-CLL-1 antibodies, the first successful utilization in human has inspired more interests in targeting CLL-1 for AML, it can be expected an increasing number of researches on CLL-1 CAR-T will emerge, especially the combination with other markers such as CD123 or CD33 or with novel agents such as FLT3 or BCL-2 inhibitor. | |
| 0.59 | CLL-1-CD33 CAR-T cells was firstly used after T cell-depleting conditioning therapy with fludarabine 30 mg/m2 and cyclophosphamide 500 mg/m2 for 3 consecutive days. | |
| 27872732 | 0.93 | CD33, CD44) and a marker cocktail (CLL-1/TIM-3/CD7/CD11b/CD22/CD56) in one fluorescence channel. |
| 30953030 | 0.92 | CD33 and CLL-1 (CD371) compared to CD34+/CD38- MCL cells (Figure 2, Table 2). |
| 31547472 | 0.90 | CD33, CLL1, TIM3, CD244, CD47, CD96, CD157 and CD7 were ubiquitously expressed on AML bulk cells at diagnosis and relapse, irrespective of genetic features. |
| 31470642 | 0.87 | CD33, CD44, CD123, CD135 (FLT3), CD371 (CLL-1), and Lewis Y (LeY). |
| 0.79 | CD33, CD123, and CLEC12A/CLL-1 (CD371). | |
| 30524966 | 0.84 | CD33, CD45, CD123, FLT3, Lewis-Y, and CLL-1 [reviewed in ]. |
| 29799854 | 0.82 | C-type lectin-like molecule-1 (CLL-1, also known as CLEC12A), CD13/CD33, CD44 and CD47 in a differentiation-stage specific manner. |
| 31221785 | 0.81 | CLL-1, which was targeted in the above-mentioned combinatorial approach in combination with CD33 by Liu et al. also has potential utility as a standalone antigen, with pre-clinical data suggesting that differential expression between malignant and healthy blasts may be sufficient to preserve hematopoeisis. |
| 0.52 | CD33-CLL1 CART (CLL1=C-type lectin molecule-1) were reported at the American Society of Hematology (ASH) annual meeting in 2018, though no data have been presented to date for the rest of this cohort (clinicaltrials.gov identifier: 03795779). | |
| 29017060 | 0.78 | CLL1, CD33, CD44, CD96, CD47, CD32 and CD25, TIM3, CD99, adding another 80 proteins (Figure 1 - orange boxes and Figure S1B). |
| 0.66 | CD33+ADGRE2, CLEC12A+CCR1, CD33+CD70 and LILRB2+CLEC12A, in greater depth, examining their expression in primary AML specimens. |
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