Disease Information
General Information of the Disease (ID: DIS00108)
Name |
Pituitary cancer
|
---|---|
ICD |
ICD-11: 2F37
|
Resistance Map |
Type(s) of Resistant Mechanism of This Disease
ADTT: Aberration of the Drug's Therapeutic Target
EADR: Epigenetic Alteration of DNA, RNA or Protein
IDUE: Irregularity in Drug Uptake and Drug Efflux
RTDM: Regulation by the Disease Microenvironment
UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Drug
Approved Drug(s)
8 drug(s) in total
Bromocriptine
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Aberration of the Drug's Therapeutic Target (ADTT) | ||||
Key Molecule: Dopamine receptor D2 (DRD2) | [1] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Down-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
Mechanism Description | Generally, the effectiveness of BRC or CAB has been related to a decreased expression in DRs, as the expression of such receptors has been shown to correlate with responsiveness to therapy in lactotroph, somatotroph, corticotroph and in clinically nonfunctioning PitNET. | |||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Key Molecule: hsa-miR-17-5p | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell proliferation | Activation | hsa05200 | |
In Vitro Model | C4-2 cells | Prostate | Homo sapiens (Human) | CVCL_4782 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
CCK-8 assay | |||
Mechanism Description | Overexpression of mir-93 increased resistance to bromocriptine and cabergoline treatment. | |||
Key Molecule: hsa-mir-126 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-136 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Down-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-miR-142-3p | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-144 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-17 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-22 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-30a | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Down-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-382 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Down-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-451 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-miR-486-5p | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: Long non-protein coding RNA (lnc886) | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Key Molecule: hsa-mir-93 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | C4-2 cells | Prostate | Homo sapiens (Human) | CVCL_4782 |
KHM-5M cells | Pleural effusion | Homo sapiens (Human) | CVCL_2975 | |
Experiment for Drug Resistance |
Clinical diagnostic evaluation | |||
Mechanism Description | Hsa-mir-93, hsa-mir-17, hsa-mir-22*, hsa-mir-126*, hsa-mir-142-3p, hsa-mir-144*, hsa-mir-486-5p, hsa-mir-451, and hsa-mir-92a were up-regulated and hsa-mir-30a, hsa-mir-382, and hsa-mir-136 were down-regulated in bromocriptine-resistant prolactinomas in comparison with bromocriptine-sensitive prolactinomas. | |||
Regulation by the Disease Microenvironment (RTDM) | ||||
Key Molecule: Mothers against decapentaplegic homolog 3 (SMAD3) | [3] | |||
Resistant Disease | Prolactinomas [ICD-11: 2F37.2] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | TGF-beta 1/Smad3 pathway | Activation | hsa04350 | |
In Vitro Model | HS27 cells | Bone | Homo sapiens (Human) | CVCL_0E34 |
MMQ cells | Pituitary gland | Rattus norvegicus (Rat) | CVCL_2117 | |
Experiment for Molecule Alteration |
Western blotting assay | |||
Experiment for Drug Resistance |
CCK8 assay | |||
Mechanism Description | TGF-beta1 promotes the synthesis and secretion of collagen fibers in fibroblasts and that the TGF-beta1/Smad3 pathway is involved in the mechanism of prolactinoma resistance by increasing fibrosis through interactions with fibroblasts. | |||
Key Molecule: Mothers against decapentaplegic homolog 4 (SMAD4) | [3] | |||
Resistant Disease | Prolactinomas [ICD-11: 2F37.2] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | TGF-beta 1/Smad3 pathway | Activation | hsa04350 | |
In Vitro Model | HS27 cells | Bone | Homo sapiens (Human) | CVCL_0E34 |
MMQ cells | Pituitary gland | Rattus norvegicus (Rat) | CVCL_2117 | |
Experiment for Molecule Alteration |
Western blotting assay | |||
Experiment for Drug Resistance |
CCK8 assay | |||
Mechanism Description | TGF-beta1 promotes the synthesis and secretion of collagen fibers in fibroblasts and that the TGF-beta1/Smad3 pathway is involved in the mechanism of prolactinoma resistance by increasing fibrosis through interactions with fibroblasts. | |||
Key Molecule: TSPY like 2 (TSPYL2) | [3] | |||
Resistant Disease | Prolactinomas [ICD-11: 2F37.2] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | TGF-beta 1/Smad3 pathway | Activation | hsa04350 | |
In Vitro Model | HS27 cells | Bone | Homo sapiens (Human) | CVCL_0E34 |
MMQ cells | Pituitary gland | Rattus norvegicus (Rat) | CVCL_2117 | |
Experiment for Molecule Alteration |
Western blotting assay | |||
Experiment for Drug Resistance |
CCK8 assay | |||
Mechanism Description | TGF-beta1 promotes the synthesis and secretion of collagen fibers in fibroblasts and that the TGF-beta1/Smad3 pathway is involved in the mechanism of prolactinoma resistance by increasing fibrosis through interactions with fibroblasts. | |||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Key Molecule: Cyclin-dependent kinase inhibitor 1A (CDKN1A) | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Down-regulation |
||
Resistant Drug | Bromocriptine | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell invasion | Activation | hsa05200 | |
Cell migration | Activation | hsa04670 | ||
In Vitro Model | C4-2 cells | Prostate | Homo sapiens (Human) | CVCL_4782 |
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay | |||
Mechanism Description | Knockdown of mir-93 increased the sensitivity of MMQ cells to bromocriptine treatment, and these effects were abolished when p21 was knocked-down using siRNA. |
Cabergoline
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Aberration of the Drug's Therapeutic Target (ADTT) | ||||
Key Molecule: Dopamine receptor D2 (DRD2) | [1] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Down-regulation |
||
Resistant Drug | Cabergoline | |||
Experimental Note | Identified from the Human Clinical Data | |||
Mechanism Description | Generally, the effectiveness of BRC or CAB has been related to a decreased expression in DRs, as the expression of such receptors has been shown to correlate with responsiveness to therapy in lactotroph, somatotroph, corticotroph and in clinically nonfunctioning PitNET. | |||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Key Molecule: hsa-miR-17-5p | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Cabergoline | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell proliferation | Activation | hsa05200 | |
In Vitro Model | C4-2 cells | Prostate | Homo sapiens (Human) | CVCL_4782 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
CCK-8 assay | |||
Mechanism Description | Overexpression of mir-93 increased resistance to bromocriptine and cabergoline treatment. | |||
Key Molecule: hsa-mir-93 | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Cabergoline | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell proliferation | Activation | hsa05200 | |
In Vitro Model | C4-2 cells | Prostate | Homo sapiens (Human) | CVCL_4782 |
Experiment for Molecule Alteration |
Solexa sequencing assay; qRT-PCR | |||
Experiment for Drug Resistance |
CCK-8 assay | |||
Mechanism Description | Overexpression of mir-93 increased resistance to bromocriptine and cabergoline treatment. | |||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Key Molecule: Cyclin-dependent kinase inhibitor 1A (CDKN1A) | [2] | |||
Resistant Disease | Prolactin-secreting adenoma [ICD-11: 2F37.Y] | |||
Molecule Alteration | Expression | Down-regulation |
||
Resistant Drug | Cabergoline | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell proliferation | Activation | hsa05200 | |
In Vitro Model | C4-2 cells | Prostate | Homo sapiens (Human) | CVCL_4782 |
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
CCK-8 assay | |||
Mechanism Description | Knockdown of mir-93 increased the sensitivity of MMQ cells to bromocriptine treatment, and these effects were abolished when p21 was knocked-down using siRNA. |
Carboplatin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Key Molecule: Bcl-2-associated agonist of cell death (BAD) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Carboplatin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. | |||
Key Molecule: Baculoviral IAP repeat containing 2 (BIRC2) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Carboplatin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. | |||
Key Molecule: Baculoviral IAP repeat-containing protein 1 (BIRC1) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Carboplatin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. | |||
Key Molecule: E3 ubiquitin-protein ligase XIAP (XIAP) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Carboplatin | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. |
Colchicine
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Multidrug resistance protein 1 (ABCB1) | [5] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Colchicine | |||
Experimental Note | Revealed Based on the Cell Line Data | |||
In Vitro Model | GH4C1 cells | Pituitary gland | Rattus norvegicus (Rat) | CVCL_0276 |
Experiment for Molecule Alteration |
Immunocytochemical staining assay | |||
Experiment for Drug Resistance |
Lowry assay; Bradford assay | |||
Mechanism Description | Cells resistant to colchicine at 0.4 micrograms/ml, termed GH4C1/RC.4, exhibited the multidrug-resistance phenotype, as the LD50 values for colchicine, puromycin, actinomycin D, and doxorubicin were between 8 and 30 times greater than the corresponding values for the parental GH4C1 cells.Immunocytochemical staining with a monoclonal antibody, C219, to the 170-kilodalton P-glycoprotein showed directly that GH4C1/RC.4 cells overexpress P-glycoprotein. |
Doxorubicin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Multidrug resistance protein 1 (ABCB1) | [5] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Doxorubicin | |||
Experimental Note | Revealed Based on the Cell Line Data | |||
In Vitro Model | GH4C1 cells | Pituitary gland | Rattus norvegicus (Rat) | CVCL_0276 |
Experiment for Molecule Alteration |
Immunocytochemical staining assay | |||
Experiment for Drug Resistance |
Lowry assay; Bradford assay | |||
Mechanism Description | Cells resistant to colchicine at 0.4 micrograms/ml, termed GH4C1/RC.4, exhibited the multidrug-resistance phenotype, as the LD50 values for colchicine, puromycin, actinomycin D, and doxorubicin were between 8 and 30 times greater than the corresponding values for the parental GH4C1 cells.Immunocytochemical staining with a monoclonal antibody, C219, to the 170-kilodalton P-glycoprotein showed directly that GH4C1/RC.4 cells overexpress P-glycoprotein. |
Etoposide
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Key Molecule: Bcl-2-associated agonist of cell death (BAD) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Etoposide | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. | |||
Key Molecule: Baculoviral IAP repeat containing 2 (BIRC2) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Etoposide | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. | |||
Key Molecule: Baculoviral IAP repeat-containing protein 1 (BIRC1) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Etoposide | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. | |||
Key Molecule: E3 ubiquitin-protein ligase XIAP (XIAP) | [4] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Etoposide | |||
Experimental Note | Identified from the Human Clinical Data | |||
In Vitro Model | Pituitary tumour stem-like cells | Pituitary | Homo sapiens (Human) | N.A. |
In Vivo Model | NOD/SCID mice xenograft model | Mus musculus | ||
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 proliferation assay | |||
Mechanism Description | Stem cells are generally known to preferentially express antiapoptotic genes, such as BCL-2, cIAP1, NAIP, and XIAP.The expression levels of these antiapoptotic genes in PASC1 were one- to sixfolds higher than those in its daughter cells. |
Octreotide
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Key Molecule: Forkhead box protein O3 (FOXO3) | [6] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Octreotide | |||
Experimental Note | Identified from the Human Clinical Data | |||
Cell Pathway Regulation | Cell apoptosis | Inhibition | hsa04210 | |
In Vitro Model | HCT8 cells | Colon | Homo sapiens (Human) | CVCL_2478 |
LN-18 cells | Brain | Homo sapiens (Human) | CVCL_0392 | |
ATCC 293T cells | Fetal kidney | Homo sapiens (Human) | CVCL_0063 | |
SH-1-V3 cells | Esophagus | Homo sapiens (Human) | N.A. | |
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
WST-1 assay | |||
Mechanism Description | miR-34a upregulation leads not only to increased cell proliferation and GH secretion in vitro, but also induces resistance to the antiproliferative and hormonal effects of the first-generation somatostatin analog, octreotide. |
Temozolomide
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Key Molecule: DNA mismatch repair protein Msh6 (MSH6) | [7] | |||
Resistant Disease | Pituitary cancer [ICD-11: 2F37.0] | |||
Molecule Alteration | Structural variation | Copy number loss |
||
Resistant Drug | Temozolomide | |||
Experimental Note | Identified from the Human Clinical Data | |||
Experiment for Molecule Alteration |
Low throughput experiment assay | |||
Mechanism Description | Loss of MSH6 occurred during the progression from an atypical prolactinoma to a pituitary carcinoma, which may have caused resistance to TMZ treatment. |
Investigative Drug(s)
2 drug(s) in total
Actinomycin D
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Multidrug resistance protein 1 (ABCB1) | [5] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Actinomycin D | |||
Experimental Note | Revealed Based on the Cell Line Data | |||
In Vitro Model | GH4C1 cells | Pituitary gland | Rattus norvegicus (Rat) | CVCL_0276 |
Experiment for Molecule Alteration |
Immunocytochemical staining assay | |||
Experiment for Drug Resistance |
Lowry assay; Bradford assay | |||
Mechanism Description | Cells resistant to colchicine at 0.4 micrograms/ml, termed GH4C1/RC.4, exhibited the multidrug-resistance phenotype, as the LD50 values for colchicine, puromycin, actinomycin D, and doxorubicin were between 8 and 30 times greater than the corresponding values for the parental GH4C1 cells.Immunocytochemical staining with a monoclonal antibody, C219, to the 170-kilodalton P-glycoprotein showed directly that GH4C1/RC.4 cells overexpress P-glycoprotein. |
Puromycin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Irregularity in Drug Uptake and Drug Efflux (IDUE) | ||||
Key Molecule: Multidrug resistance protein 1 (ABCB1) | [5] | |||
Resistant Disease | Pituitary adenoma [ICD-11: 2F37.1] | |||
Molecule Alteration | Expression | Up-regulation |
||
Resistant Drug | Puromycin | |||
Experimental Note | Revealed Based on the Cell Line Data | |||
In Vitro Model | GH4C1 cells | Pituitary gland | Rattus norvegicus (Rat) | CVCL_0276 |
Experiment for Molecule Alteration |
Immunocytochemical staining assay | |||
Experiment for Drug Resistance |
Lowry assay; Bradford assay | |||
Mechanism Description | Cells resistant to colchicine at 0.4 micrograms/ml, termed GH4C1/RC.4, exhibited the multidrug-resistance phenotype, as the LD50 values for colchicine, puromycin, actinomycin D, and doxorubicin were between 8 and 30 times greater than the corresponding values for the parental GH4C1 cells.Immunocytochemical staining with a monoclonal antibody, C219, to the 170-kilodalton P-glycoprotein showed directly that GH4C1/RC.4 cells overexpress P-glycoprotein. |
References
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