Disease Information
General Information of the Disease (ID: DIS00201)
Name |
Leiomyosarcoma
|
---|---|
ICD |
ICD-11: 2B58
|
Resistance Map |
Type(s) of Resistant Mechanism of This Disease
ADTT: Aberration of the Drug's Therapeutic Target
UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
Doxorubicin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Key Molecule: Nanog homeobox (NANOG) | [1] | |||
Resistant Disease | Leiomyosarcoma [ICD-11: 2B58.0] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Doxorubicin | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Spheroid formation | Activation | hsa04140 | ||
Cell colony | Activation | hsa05200 | ||
Cell migration | Activation | hsa04670 | ||
In Vitro Model | SK-UT-1 cells | Uterus | Homo sapiens (Human) | CVCL_0533 |
In Vivo Model | BALB/c-nu female mice | Mus musculus | ||
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay; Flow cytometry assay; Transwell migration and invasion assay | |||
Mechanism Description | The expression levels of CSC-related markers in CD133+ subpopulation derived from SK-UT-1 cells, Western blotting was employed to detect the expression levels of CD44, ALDH1, BMI1, and Nanog. Expectedly, researchers found that CD133+subpopulation had higher expression levels of CD44, ALDH1, BMI1, and Nanog compared with those of CD133 subpopulation. Collectively, the above-mentioned results suggested that CD133+ subpopulation derived from SK-UT-1 cells possessed capabilities of resistance to apoptosis after treatment with DXR, as well as stemness feature of cancer stem-like cells. | |||
Key Molecule: Extracellular matrix receptor III (CD44) | [1] | |||
Resistant Disease | Leiomyosarcoma [ICD-11: 2B58.0] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Doxorubicin | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Spheroid formation | Activation | hsa04140 | ||
Cell colony | Activation | hsa05200 | ||
Cell migration | Activation | hsa04670 | ||
In Vitro Model | SK-UT-1 cells | Uterus | Homo sapiens (Human) | CVCL_0533 |
In Vivo Model | BALB/c-nu female mice | Mus musculus | ||
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay; Flow cytometry assay; Transwell migration and invasion assay | |||
Mechanism Description | The expression levels of CSC-related markers in CD133+ subpopulation derived from SK-UT-1 cells, Western blotting was employed to detect the expression levels of CD44, ALDH1, BMI1, and Nanog. Expectedly, researchers found that CD133+subpopulation had higher expression levels of CD44, ALDH1, BMI1, and Nanog compared with those of CD133 subpopulation. Collectively, the above-mentioned results suggested that CD133+ subpopulation derived from SK-UT-1 cells possessed capabilities of resistance to apoptosis after treatment with DXR, as well as stemness feature of cancer stem-like cells. | |||
Key Molecule: Polycomb complex protein BMI-1 (BMI1) | [1] | |||
Resistant Disease | Leiomyosarcoma [ICD-11: 2B58.0] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Doxorubicin | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Spheroid formation | Activation | hsa04140 | ||
Cell colony | Activation | hsa05200 | ||
Cell migration | Activation | hsa04670 | ||
In Vitro Model | SK-UT-1 cells | Uterus | Homo sapiens (Human) | CVCL_0533 |
In Vivo Model | BALB/c-nu female mice | Mus musculus | ||
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay; Flow cytometry assay; Transwell migration and invasion assay | |||
Mechanism Description | The expression levels of CSC-related markers in CD133+ subpopulation derived from SK-UT-1 cells, Western blotting was employed to detect the expression levels of CD44, ALDH1, BMI1, and Nanog. Expectedly, researchers found that CD133+subpopulation had higher expression levels of CD44, ALDH1, BMI1, and Nanog compared with those of CD133 subpopulation. Collectively, the above-mentioned results suggested that CD133+ subpopulation derived from SK-UT-1 cells possessed capabilities of resistance to apoptosis after treatment with DXR, as well as stemness feature of cancer stem-like cells. | |||
Key Molecule: Nanog homeobox (NANOG) | [1] | |||
Resistant Disease | Leiomyosarcoma [ICD-11: 2B58.0] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Doxorubicin | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Spheroid formation | Activation | hsa04140 | ||
Cell colony | Activation | hsa05200 | ||
Cell migration | Activation | hsa04670 | ||
In Vitro Model | SK-UT-1 cells | Uterus | Homo sapiens (Human) | CVCL_0533 |
In Vivo Model | BALB/c-nu female mice | Mus musculus | ||
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay; Flow cytometry assay; Transwell migration and invasion assay | |||
Mechanism Description | The expression levels of CSC-related markers in CD133+ subpopulation derived from SK-UT-1 cells, Western blotting was employed to detect the expression levels of CD44, ALDH1, BMI1, and Nanog. Expectedly, researchers found that CD133+subpopulation had higher expression levels of CD44, ALDH1, BMI1, and Nanog compared with those of CD133 subpopulation. Collectively, the above-mentioned results suggested that CD133+ subpopulation derived from SK-UT-1 cells possessed capabilities of resistance to apoptosis after treatment with DXR, as well as stemness feature of cancer stem-like cells. | |||
Key Molecule: Extracellular matrix receptor III (CD44) | [1] | |||
Resistant Disease | Leiomyosarcoma [ICD-11: 2B58.0] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Doxorubicin | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Spheroid formation | Activation | hsa04140 | ||
Cell colony | Activation | hsa05200 | ||
Cell migration | Activation | hsa04670 | ||
In Vitro Model | SK-UT-1 cells | Uterus | Homo sapiens (Human) | CVCL_0533 |
In Vivo Model | BALB/c-nu female mice | Mus musculus | ||
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay; Flow cytometry assay; Transwell migration and invasion assay | |||
Mechanism Description | The expression levels of CSC-related markers in CD133+ subpopulation derived from SK-UT-1 cells, Western blotting was employed to detect the expression levels of CD44, ALDH1, BMI1, and Nanog. Expectedly, researchers found that CD133+subpopulation had higher expression levels of CD44, ALDH1, BMI1, and Nanog compared with those of CD133 subpopulation. Collectively, the above-mentioned results suggested that CD133+ subpopulation derived from SK-UT-1 cells possessed capabilities of resistance to apoptosis after treatment with DXR, as well as stemness feature of cancer stem-like cells. | |||
Key Molecule: Polycomb complex protein BMI-1 (BMI1) | [1] | |||
Resistant Disease | Leiomyosarcoma [ICD-11: 2B58.0] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Doxorubicin | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
Spheroid formation | Activation | hsa04140 | ||
Cell colony | Activation | hsa05200 | ||
Cell migration | Activation | hsa04670 | ||
In Vitro Model | SK-UT-1 cells | Uterus | Homo sapiens (Human) | CVCL_0533 |
In Vivo Model | BALB/c-nu female mice | Mus musculus | ||
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay; Flow cytometry assay; Transwell migration and invasion assay | |||
Mechanism Description | The expression levels of CSC-related markers in CD133+ subpopulation derived from SK-UT-1 cells, Western blotting was employed to detect the expression levels of CD44, ALDH1, BMI1, and Nanog. Expectedly, researchers found that CD133+subpopulation had higher expression levels of CD44, ALDH1, BMI1, and Nanog compared with those of CD133 subpopulation. Collectively, the above-mentioned results suggested that CD133+ subpopulation derived from SK-UT-1 cells possessed capabilities of resistance to apoptosis after treatment with DXR, as well as stemness feature of cancer stem-like cells. |
Clinical Trial Drug(s)
1 drug(s) in total
Capivasertib
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
Aberration of the Drug's Therapeutic Target (ADTT) | ||||
Key Molecule: RAC-alpha serine/threonine-protein kinase (AKT1) | [2] | |||
Sensitive Disease | Leiomyosarcoma [ICD-11: 2B58.0] | |||
Molecule Alteration | Missense mutation | p.E17K (c.49G>A) |
||
Sensitive Drug | Capivasertib | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Breast | . | ||
Mechanism Description | The missense mutation p.E17K (c.49G>A) in gene AKT1 cause the sensitivity of Capivasertib by aberration of the drug's therapeutic target |
References
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