CD11b Cancer Research Results
CD11b, CD11b: Click to Expand ⟱
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CD11b’s (also known as integrin αM or ITGAM).
Markers CD14 and CD11b is one of the important characteristics of differentiation.
High levels of CD11b are often noted in the tumor microenvironment.
A high density of CD11b⁺ cells in the tumor microenvironment has been associated with adverse prognosis. For example, an abundance of MDSCs (which are CD11b⁺) is linked to immunosuppression, tumor progression, and resistance to therapies. High levels of CD11b⁺ cell infiltration have been correlated with:
-Faster tumor progression.
-Increased metastasis.
-Reduced response to immunotherapies.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
AML, |
HL-60 |
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in-vitro, |
AML, |
KG-1 |
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in-vitro, |
lymphoma, |
U937 |
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TumCD↓, The SUV39H1 inhibitor (chaetocin) and the G9a inhibitor (UNC0638) caused cell death in AML cells at high concentrations.
SUV39H↓,
CD11b↑, only chaetocin-induced CD11b expression and differentiation of AML cells at non-cytotoxic concentration.
Diff↑,
H3K9↓, Long-term incubation of chaetocin led to downregulation of SUV39H1 and reduction of H3K9 tri-methylation in HL-60 and KG-1a cells.
eff↑, Combination of chaetocin with suberoylanilide hydroxamic acid (SAHA, a histone deacetylase inhibitor) or JQ (a BET (bromodomain extra terminal) bromodomain inhibitor) showed synergistic cytotoxicity.
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NA, |
APL, |
APL NB4 |
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vitro+vivo, |
NA, |
NA |
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TumCCA↑, ATO and ATRA at therapeutic and sub-therapeutic doses, there was an increase in sub-G0/G1 cells, annexin V/PI-positive-apoptotic cells and DNA fragmentation.
DNAdam↑,
TumCP↓, this reduction in proliferation and increase in apoptosis was accompanied by enhanced myeloid differentiation as indicated by an increased expression of CD11b.
Apoptosis↑,
Diff↑,
CD11b↑,
eff↑, Fucoidan synergizes ATO-mediated apoptosis in APL cells
Dose↝, Decreased proliferation was observed at both low (0.25, 0.5 μM) and clinical doses of ATO (1 μM).
CD14↑,
CD11b↑,
ROS↑, Shikonin result in the predominance of cell death because the oxidative stress is more severe and overcome the antioxidative capacity of Nrf2/ARE pathway, resulting in cell death.
GSH↓,
GSH/GSSG↓,
GPx↑, mRNA expression levels of GPX and CAT were markedly upregulated by Shikonin in a dose-dependent manner
Catalase↓, Shikonin causes apoptosis in human glioma cells by interrupting intracellular redox homeostasis, which included CAT downregulation
Diff↑, Shikonin-induced HL-60 cell differentiation
Showing Research Papers: 1 to 3 of 3
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
H3K9↓, 1, SUV39H↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↓, 1, GPx↑, 1, GSH↓, 1, GSH/GSSG↓, 1, ROS↑, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 1, TumCD↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
Diff↑, 3,
Migration(tgid=13) ⓘ
CD11b↑, 3, TumCP↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD14↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
Dose↝, 1, eff↑, 2,
Total Targets: 17
Pathway results for Effect on Normal Cells:
Total Targets: 0
Scientific Paper Hit Count for: CD11b, CD11b
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1067 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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