General Information:

Id: 6,301
Diseases: Angioimmunoblastic T-Cell lymphoma
Cancer
Cutaneous T-cell lymphoma
Peripheral T-cell leukemia / lymphoma
Homo sapiens
peripheral T-cell lymphoma
article/cited
Reference: Quesada AE et al.(2014) Morphoproteomics identifies constitutive activation of the mTORC2/Akt and NF-kappaB pathways and expressions of IGF-1R, Sirt1, COX-2, and FASN in peripheral T-cell lymphomas: pathogenetic implications and therapeutic options Int J Clin Exp Pathol 7: 8732-8739 [PMID: 25674239]

Interaction Information:

Comment Bortezomib inhibits the NF-kappaB pathway activation.
Formal Description
Interaction-ID: 59022

drug/chemical compound

Bortezomib

decreases_activity of

process

NF-kappaB signaling

Drugbank entries Show/Hide entries for Bortezomib
Comment Metformin inhibits both NF-kappaB and mTORC2.
Formal Description
Interaction-ID: 60068

drug/chemical compound

Metformin

decreases_activity of

complex/PPI

NF-kappaB complex

Drugbank entries Show/Hide entries for Metformin
Comment Panobinostat inhibits Sirt1 pathway.
Formal Description
Interaction-ID: 60069

drug/chemical compound

Panobinostat

decreases_activity of

gene/protein

SIRT1

Comment 10 PTCL patients demonstrated nuclear and cytoplasmic staining (high expression) for p-Akt (Ser 473) and p-mTOR (Ser 2448) corresponding to mTORC 2, and all cases showed strong, diffuse nuclear translocation for p-NF-kappaBp65 (Ser 536). All ten cases also showed cytoplasmic staining for IGF-1R (Tyr1165/1166). In addition, high expression in the tumor cells (>50%) of nuclear Sirt1, and cytoplasmic COX-2 and FASN were detected in PTCL cells in 7, 9 and 8 out of 10 cases, respectively.
Formal Description
Interaction-ID: 60073

disease

Peripheral T-cell leukemia / lymphoma

increases_expression of

gene/protein

AKT1

Akt phosphorylated at Ser 473. Pattern of staining: Nuclear and Cytoplasmic.
Drugbank entries Show/Hide entries for AKT1
Comment Metformin inhibits both NF-kappaB and mTORC2.
Formal Description
Interaction-ID: 60078

drug/chemical compound

Metformin

decreases_activity of

complex/PPI

mTORC2 complex

Drugbank entries Show/Hide entries for Metformin
Comment 10 PTCL patients demonstrated nuclear and cytoplasmic staining (high expression) for p-Akt (Ser 473) and p-mTOR (Ser 2448) corresponding to mTORC 2, and all cases showed strong, diffuse nuclear translocation for p-NF-kappaBp65 (Ser 536). All ten cases also showed cytoplasmic staining for IGF-1R (Tyr1165/1166). In addition, high expression in the tumor cells (>50%) of nuclear Sirt1, and cytoplasmic COX-2 and FASN were detected in PTCL cells in 7, 9 and 8 out of 10 cases, respectively.
Formal Description
Interaction-ID: 60082

disease

Peripheral T-cell leukemia / lymphoma

increases_expression of

gene/protein

MTOR

MTOR phosphorylated at Ser 2448. Pattern of staining: Nuclear and Cytoplasmic.
Drugbank entries Show/Hide entries for MTOR
Comment 10 PTCL patients demonstrated nuclear and cytoplasmic staining (high expression) for p-Akt (Ser 473) and p-mTOR (Ser 2448) corresponding to mTORC 2, and all cases showed strong, diffuse nuclear translocation for p-NF-kappaBp65 (Ser 536). All ten cases also showed cytoplasmic staining for IGF-1R (Tyr1165/1166). In addition, high expression in the tumor cells (>50%) of nuclear Sirt1, and cytoplasmic COX-2 and FASN were detected in PTCL cells in 7, 9 and 8 out of 10 cases, respectively.
Formal Description
Interaction-ID: 60083

disease

Peripheral T-cell leukemia / lymphoma

increases_expression of

gene/protein

RELA

with NF-kappaB phosphorylated at Ser 536. Pattern of staining: Nuclear.
Drugbank entries Show/Hide entries for RELA
Comment 10 PTCL patients demonstrated nuclear and cytoplasmic staining (high expression) for p-Akt (Ser 473) and p-mTOR (Ser 2448) corresponding to mTORC 2, and all cases showed strong, diffuse nuclear translocation for p-NF-kappaBp65 (Ser 536). All ten cases also showed cytoplasmic staining for IGF-1R (Tyr1165/1166). In addition, high expression in the tumor cells (>50%) of nuclear Sirt1, and cytoplasmic COX-2 and FASN were detected in PTCL cells in 7, 9 and 8 out of 10 cases, respectively.
Formal Description
Interaction-ID: 60087

disease

Peripheral T-cell leukemia / lymphoma

increases_expression of

gene/protein

IGF1R

IGF-1R phosphorylated at Tyr1165/1166. Pattern of staining: Cyptoplasmic.
Drugbank entries Show/Hide entries for IGF1R
Comment 10 PTCL patients demonstrated nuclear and cytoplasmic staining (high expression) for p-Akt (Ser 473) and p-mTOR (Ser 2448) corresponding to mTORC 2, and all cases showed strong, diffuse nuclear translocation for p-NF-kappaBp65 (Ser 536). All ten cases also showed cytoplasmic staining for IGF-1R (Tyr1165/1166). In addition, high expression in the tumor cells (>50%) of nuclear Sirt1, and cytoplasmic COX-2 and FASN were detected in PTCL cells in 7, 9 and 8 out of 10 cases, respectively.
Formal Description
Interaction-ID: 60088

disease

Peripheral T-cell leukemia / lymphoma

increases_expression of

gene/protein

SIRT1

Pattern of staining: Nuclear.
Comment 10 PTCL patients demonstrated nuclear and cytoplasmic staining (high expression) for p-Akt (Ser 473) and p-mTOR (Ser 2448) corresponding to mTORC 2, and all cases showed strong, diffuse nuclear translocation for p-NF-kappaBp65 (Ser 536). All ten cases also showed cytoplasmic staining for IGF-1R (Tyr1165/1166). In addition, high expression in the tumor cells (>50%) of nuclear Sirt1, and cytoplasmic COX-2 and FASN were detected in PTCL cells in 7, 9 and 8 out of 10 cases, respectively.
Formal Description
Interaction-ID: 60089

disease

Peripheral T-cell leukemia / lymphoma

increases_expression of

gene/protein

PTGS2

Pattern of staining: Cyptoplasmic.
Drugbank entries Show/Hide entries for PTGS2
Comment 10 PTCL patients demonstrated nuclear and cytoplasmic staining (high expression) for p-Akt (Ser 473) and p-mTOR (Ser 2448) corresponding to mTORC 2, and all cases showed strong, diffuse nuclear translocation for p-NF-kappaBp65 (Ser 536). All ten cases also showed cytoplasmic staining for IGF-1R (Tyr1165/1166). In addition, high expression in the tumor cells (>50%) of nuclear Sirt1, and cytoplasmic COX-2 and FASN were detected in PTCL cells in 7, 9 and 8 out of 10 cases, respectively.
Formal Description
Interaction-ID: 60090

disease

Peripheral T-cell leukemia / lymphoma

increases_expression of

gene/protein

FASN

Pattern of staining: Cyptoplasmic.
Drugbank entries Show/Hide entries for FASN
Comment mTOR complex is comprised of two distinct complexes. The first, mTORC1 complex, is linked to the regulatory associated protein of mTOR, raptor. The other complex, mTORC2, is coupled to rictor. mTORC1 is in a primarily cytoplasmic distribution, whereas mTORC2 is abundant in both the cytoplasmic and nuclear compartment. (cited information)
Formal Description
Interaction-ID: 60110

gene/protein

MTOR

is_part_of

complex/PPI

mTORC1 complex

mTORC1 is in a primarily cytoplasmic distribution.
Drugbank entries Show/Hide entries for MTOR
Comment mTOR complex is comprised of two distinct complexes. The first, mTORC1 complex, is linked to the regulatory associated protein of mTOR, raptor. The other complex, mTORC2, is coupled to rictor. mTORC1 is in a primarily cytoplasmic distribution, whereas mTORC2 is abundant in both the cytoplasmic and nuclear compartment. (cited information)
Formal Description
Interaction-ID: 60111

gene/protein

MTOR

is_part_of

complex/PPI

mTORC2 complex

mTORC2 is abundant in both the cytoplasmic and nuclear compartment.
Drugbank entries Show/Hide entries for MTOR
Comment mTOR complex is comprised of two distinct complexes. The first, mTORC1 complex, is to the regulatory associated protein of mTOR, raptor. The other complex, mTORC2, is coupled to rictor. mTORC1 is in a primarily cytoplasmic distribution, whereas mTORC2 is abundant in both the cytoplasmic and nuclear compartment. (cited information)
Formal Description
Interaction-ID: 60112

complex/PPI

mTORC1 complex

is localized in

cellular component

cytoplasm

Comment mTOR complex is comprised of two distinct complexes. The first, mTORC1 complex, is linked to the regulatory associated protein of mTOR, raptor. The other complex, mTORC2, is coupled to rictor. mTORC1 is in a primarily cytoplasmic distribution, whereas mTORC2 is abundant in both the cytoplasmic and nuclear compartment. (cited information)
Formal Description
Interaction-ID: 60113

complex/PPI

mTORC2 complex

is localized in

cellular component

cytoplasm

Comment mTOR complex is comprised of two distinct complexes. The first, mTORC1 complex, is linked to the regulatory associated protein of mTOR, raptor. The other complex, mTORC2, is coupled to rictor. mTORC1 is in a primarily cytoplasmic distribution, whereas mTORC2 is abundant in both the cytoplasmic and nuclear compartment. (cited information)
Formal Description
Interaction-ID: 60114

complex/PPI

mTORC2 complex

is localized in

cellular component

nucleus

Comment Because mTOR phosphorylated at serine 2448 binds to both raptor and rictor, the finding of nuclear and cytoplasmic compartmentalization of p-mTOR (Ser 2448) in all cases and in this context, supports a role for mTORC2 in PTCL. This is reinforced, by the concurrent finding of nuclear and cytoplasmic p-Akt (Ser 473), a putative downstream product of mTORC2 signaling. From a pathogenetic standpoint, it is noteworthy that the mTOR signaling pathway has been implicated in T-cell lymphopoiesis.
Formal Description
Interaction-ID: 60115

complex/PPI

mTORC2 complex

affects_activity of

disease

Peripheral T-cell leukemia / lymphoma

Comment From a pathogenetic standpoint, it is noteworthy that the mTOR signaling pathway has been implicated in T-cell lymphopoiesis. (cited information)
Formal Description
Interaction-ID: 60116

process

TOR signaling

affects_activity of

process

T-cell lymphopoiesis

Comment The observations of COX-2 expression in 9 out of 10 of our cases, Sirt1 in 7 out of 10 cases and FASN in 8 out of the 10 cases support a central role of the mTORC2/Akt pathway in PTCL.
Formal Description
Interaction-ID: 60117

process

TORC2/AKT signaling

affects_activity of

disease

Peripheral T-cell leukemia / lymphoma

Comment COX-2 has been reported to be an upregulator of Akt and Akt signaling in turn, induces COX-2 expression. (cited information)
Formal Description
Interaction-ID: 60118

gene/protein

PTGS2

increases_expression of

gene/protein

AKT1

Drugbank entries Show/Hide entries for PTGS2 or AKT1
Comment Sirt1, reportedly deacetylates Akt and thereby, promotes phosphatidylinositol (3,4,5)-triphosphate binding to Akt and participates in its activation (cited information).
Formal Description
Interaction-ID: 60119

gene/protein

SIRT1

decreases_acetylation of

gene/protein

AKT1

Drugbank entries Show/Hide entries for AKT1
Comment IGF-1R is a tyrosine kinase receptor which, once it has bound to its ligand, stimulates the PI3K-AKT/mTOR (cited information).
Formal Description
Interaction-ID: 60120

gene/protein

IGF1R

increases_activity of

process

PI3K/AKT/TOR signaling

if bound to its ligand.
Drugbank entries Show/Hide entries for IGF1R
Comment Collaboratively, phospho-Akt has been reported to induce the expression of FASN and conversely, FASN has been reported to increase phospho-Akt (cited information).
Formal Description
Interaction-ID: 60121

gene/protein

AKT1

increases_expression of

gene/protein

FASN

if Akt is phosphorylated.
Drugbank entries Show/Hide entries for AKT1 or FASN
Comment Downstream signaling from constitutively activated Akt results in the activation of the NF-kappaB pathway and Akt upregulates a subset of NF-kappaB-dependent genes for T cell activation (cited information).
Formal Description
Interaction-ID: 60122

gene/protein

AKT1

increases_activity of

process

NF-kappaB signaling

if Akt is constitutively activated.
Drugbank entries Show/Hide entries for AKT1
Comment Vorinostat is able to dephosphorylate Akt on serine 473 by increasing the activity of protein phosphatase 1 (PP1), to downregulate SIRT1 mRNA, and to reduce Sirt1 deacetylase activity (cited information).
Formal Description
Interaction-ID: 60123

drug/chemical compound

Vorinostat

decreases_phosphorylation of

gene/protein

AKT1

on p-AKT-serine473 by increasing the activity of protein phosphatase 1 (PP1).
Drugbank entries Show/Hide entries for Vorinostat or AKT1
Comment Panobinostat acts by a similar mechanism as Vorinostat with protein phosphatase 1 involvement in the dephosphorylation of Akt. Parenthetically, panobinostat and other histone deacetylase inhibitors have been proven efficacious and are routinely used in the treatment of advanced cutaneous T-cell lymphoma (CTCL) (cited information).
Formal Description
Interaction-ID: 60124

drug/chemical compound

Panobinostat

decreases_phosphorylation of

gene/protein

AKT1

by increasing the activity of protein phosphatase 1 (PP1).
Drugbank entries Show/Hide entries for AKT1
Comment Celecoxib, a selective COX-2 inhibitor, in preclinical studies has been shown to decrease p-Akt protein expression in head and neck squamous cell carcinoma and to inhibit the NF-kappeB pathway leading to apoptosis in human glioblastoma cells (cited information).
Formal Description
Interaction-ID: 60125

drug/chemical compound

Celecoxib

decreases_activity of

gene/protein

PTGS2

Drugbank entries Show/Hide entries for Celecoxib or PTGS2
Comment Metformin, also in a preclinical study has been shown to decrease the stimulative effect of a high-energy diet on colon carcinoma growth in vivo associated with the attenuation of the phosphorylation of Akt and decreased expression of FASN (cited information).
Formal Description
Interaction-ID: 60126

drug/chemical compound

Metformin

decreases_phosphorylation of

gene/protein

AKT1

Drugbank entries Show/Hide entries for Metformin or AKT1
Comment COX-2 has been reported to be an upregulator of Akt and Akt signaling in turn, induces COX-2 expression (cited information).
Formal Description
Interaction-ID: 60131

increases_expression of

gene/protein

PTGS2

Drugbank entries Show/Hide entries for PTGS2
Comment Sirt1, reportedly deacetylates Akt and thereby, promotes phosphatidylinositol (3,4,5)-triphosphate binding to Akt and participates in its activation (cited information).
Formal Description
Interaction-ID: 60139

gene/protein

SIRT1

increases_activity of

gene/protein

AKT1

via promoting phosphatidylinositol (3,4,5)-triphosphate binding to Akt.
Drugbank entries Show/Hide entries for AKT1
Comment Collaboratively, phospho-Akt has been reported to induce the expression of FASN and conversely, FASN has been reported to increase phospho-Akt (cited information).
Formal Description
Interaction-ID: 60143

gene/protein

FASN

increases_expression of

gene/protein

AKT1

if Akt is phosphorylated.
Drugbank entries Show/Hide entries for FASN or AKT1
Comment Vorinostat is able to dephosphorylate Akt on serine 473 by increasing the activity of protein phosphatase 1 (PP1), to downregulate SIRT1 mRNA, and to reduce Sirt1 deacetylase activity (cited information).
Formal Description
Interaction-ID: 60154

drug/chemical compound

Vorinostat

increases_activity of

gene/protein

Protein phosphatase 1

thus, dephosphorylatingAkt on serine 473.
Drugbank entries Show/Hide entries for Vorinostat
Comment Vorinostat is able to dephosphorylate Akt on serine 473 by increasing the activity of protein phosphatase 1 (PP1), to downregulate SIRT1 mRNA, and to reduce Sirt1 deacetylase activity (cited information).
Formal Description
Interaction-ID: 60156

drug/chemical compound

Vorinostat

decreases_activity of

gene/protein

SIRT1

of SIRT1 mRNA and Sirt1 deacetylase activity.
Drugbank entries Show/Hide entries for Vorinostat
Comment Panobinostat acts by a similar mechanism as Vorinostat with protein phosphatase 1 involvement in the dephosphorylation of Akt. Parenthetically, panobinostat and other histone deacetylase inhibitors have been proven efficacious and are routinely used in the treatment of advanced cutaneous T-cell lymphoma (CTCL) (cited information).
Formal Description
Interaction-ID: 60159

drug/chemical compound

Panobinostat

decreases_activity of

disease

Cutaneous T-cell lymphoma

Comment Celecoxib, a selective COX-2 inhibitor, in preclinical studies has been shown to decrease p-Akt protein expression in head and neck squamous cell carcinoma and to inhibit the NF-kappeB pathway leading to apoptosis in human glioblastoma cells. (cited information)
Formal Description
Interaction-ID: 60161

drug/chemical compound

Celecoxib

decreases_expression of

gene/protein

AKT1

of pAKT in head and neck squamous cell carcinoma.
Drugbank entries Show/Hide entries for Celecoxib or AKT1
Comment Celecoxib, a selective COX-2 inhibitor, in preclinical studies has been shown to decrease p-Akt protein expression in head and neck squamous cell carcinoma and to inhibit the NF-kappeB pathway leading to apoptosis in human glioblastoma cells (cited information). Celecoxib inhibits NF-kappaB pathway activation independent of COX2.
Formal Description
Interaction-ID: 60162

drug/chemical compound

Celecoxib

decreases_activity of

process

NF-kappaB signaling

independent of COX2.
Drugbank entries Show/Hide entries for Celecoxib
Comment Celecoxib, a selective COX-2 inhibitor, in preclinical studies has been shown to decrease p-Akt protein expression in head and neck squamous cell carcinoma and to inhibit the NF-kappeB pathway leading to apoptosis in human glioblastoma cells (cited information).
Formal Description
Interaction-ID: 60164

drug/chemical compound

Celecoxib

increases_activity of

in human glioblastoma cells
Drugbank entries Show/Hide entries for Celecoxib
Comment Metformin, also in a preclinical study has been shown to decrease the stimulative effect of a high-energy diet on colon carcinoma growth in vivo associated with the attenuation of the phosphorylation of Akt and decreased expression of FASN (cited information).
Formal Description
Interaction-ID: 60173

drug/chemical compound

Metformin

decreases_expression of

gene/protein

FASN

Drugbank entries Show/Hide entries for Metformin or FASN
Comment Bortezomib inhibits the NF-kappeB pathway via inhibition of proteasome degradation. In addition, bortezomib, in preclinical studies has been shown to induce apoptosis and growth suppression in human medulloblastoma cells in association with a suppression of NF-kappaB signaling and reduction in phosphorylation of Akt. In prostate cancer cells it also caused dephosphorylation of phospho-Akt. Bortezomib should work collaboratively with celecoxib in inhibiting the nuclear translocation of p-NF-kappeBp65 (cited information).
Formal Description
Interaction-ID: 60174

drug/chemical compound

Bortezomib

decreases_activity of

Drugbank entries Show/Hide entries for Bortezomib
Comment Bortezomib inhibits the NF-kappeB pathway via inhibition of proteasome degradation. In addition, bortezomib, in preclinical studies has been shown to induce apoptosis and growth suppression in human medulloblastoma cells in association with a suppression of NF-kappaB signaling and reduction in phosphorylation of Akt. In prostate cancer cells it also caused dephosphorylation of phospho-Akt. Bortezomib should work collaboratively with celecoxib in inhibiting the nuclear translocation of p-NF-kappeBp65 (cited information).
Formal Description
Interaction-ID: 60175

drug/chemical compound

Bortezomib

increases_activity of

in human medulloblastoma cells
Drugbank entries Show/Hide entries for Bortezomib
Comment Bortezomib inhibits the NF-kappeB pathway via inhibition of proteasome degradation. In addition, bortezomib, in preclinical studies has been shown to induce apoptosis and growth suppression in human medulloblastoma cells in association with a suppression of NF-kappaB signaling and reduction in phosphorylation of Akt. In prostate cancer cells it also caused dephosphorylation of phospho-Akt. Bortezomib should work collaboratively with celecoxib in inhibiting the nuclear translocation of p-NF-kappeBp65 (cited information).
Formal Description
Interaction-ID: 60176

drug/chemical compound

Bortezomib

decreases_activity of

process

growth

in human medulloblastoma cells
Drugbank entries Show/Hide entries for Bortezomib
Comment Bortezomib inhibits the NF-kappeB pathway via inhibition of proteasome degradation. In addition, bortezomib, in preclinical studies has been shown to induce apoptosis and growth suppression in human medulloblastoma cells in association with a suppression of NF-kappaB signaling and reduction in phosphorylation of Akt. In prostate cancer cells it also caused dephosphorylation of phospho-Akt. Bortezomib should work collaboratively with celecoxib in inhibiting the nuclear translocation of p-NF-kappeBp65 (cited information).
Formal Description
Interaction-ID: 60177

affects_activity of

process

NF-kappaB signaling

Comment Bortezomib inhibits the NF-kappeB pathway via inhibition of proteasome degradation. In addition, bortezomib, in preclinical studies has been shown to induce apoptosis and growth suppression in human medulloblastoma cells in association with a suppression of NF-kappaB signaling and reduction in phosphorylation of Akt. In prostate cancer cells it also caused dephosphorylation of phospho-Akt. Bortezomib should work collaboratively with celecoxib in inhibiting the nuclear translocation of p-NF-kappeBp65 (cited information).
Formal Description
Interaction-ID: 60178

drug/chemical compound

Bortezomib

decreases_phosphorylation of

gene/protein

AKT1

also of AKT-phos in prostate cancer cells.
Drugbank entries Show/Hide entries for Bortezomib or AKT1
Comment Bortezomib inhibits the NF-kappeB pathway via inhibition of proteasome degradation. In addition, bortezomib, in preclinical studies has been shown to induce apoptosis and growth suppression in human medulloblastoma cells in association with a suppression of NF-kappaB signaling and reduction in phosphorylation of Akt. In prostate cancer cells it also caused dephosphorylation of phospho-Akt. Bortezomib should work collaboratively with celecoxib in inhibiting the nuclear translocation of p-NF-kappeBp65 (cited information).
Formal Description
Interaction-ID: 60179

drug/chemical compound

Bortezomib

increases_activity of

drug/chemical compound

Celecoxib

in inhibiting the nuclear translocation of p-NF-kappeBp65.
Drugbank entries Show/Hide entries for Bortezomib or Celecoxib
Comment Bortezomib inhibits the NF-kappeB pathway via inhibition of proteasome degradation. In addition, bortezomib, in preclinical studies has been shown to induce apoptosis and growth suppression in human medulloblastoma cells in association with a suppression of NF-kappaB signaling and reduction in phosphorylation of Akt. In prostate cancer cells it also caused dephosphorylation of phospho-Akt. Bortezomib should work collaboratively with celecoxib in inhibiting the nuclear translocation of p-NF-kappeBp65 (cited information).
Formal Description
Interaction-ID: 60180

drug/chemical compound

Celecoxib

increases_activity of

drug/chemical compound

Bortezomib

in inhibiting the nuclear translocation of p-NF-kappeBp65.
Drugbank entries Show/Hide entries for Celecoxib or Bortezomib
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60182

drug/chemical compound

CHOP

increases_activity of

drug/chemical compound

Bortezomib

Drugbank entries Show/Hide entries for
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60183

drug/chemical compound

Bortezomib

increases_activity of

drug/chemical compound

CHOP

Drugbank entries Show/Hide entries for Bortezomib
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60184

drug/chemical compound

Bortezomib

decreases_activity of

disease

Angioimmunoblastic T-Cell lymphoma

Drugbank entries Show/Hide entries for Bortezomib
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60185

drug/chemical compound

CHOP

decreases_activity of

disease

Angioimmunoblastic T-Cell lymphoma

Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60186

disease

Angioimmunoblastic T-Cell lymphoma

increases_expression of

gene/protein

BCL2

Drugbank entries Show/Hide entries for BCL2
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60187

disease

Angioimmunoblastic T-Cell lymphoma

increases_expression of

gene/protein

MTOR

Drugbank entries Show/Hide entries for MTOR
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60188

disease

Angioimmunoblastic T-Cell lymphoma

increases_expression of

gene/protein

AKT1

Drugbank entries Show/Hide entries for AKT1
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60189

disease

Angioimmunoblastic T-Cell lymphoma

increases_expression of

gene/protein

RELA

with NF-kappaBp65 (Ser536)
Drugbank entries Show/Hide entries for RELA
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60190

disease

Angioimmunoblastic T-Cell lymphoma

increases_expression of

gene/protein

PTGS2

Drugbank entries Show/Hide entries for PTGS2
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60191

disease

Angioimmunoblastic T-Cell lymphoma

increases_expression of

gene/protein

SIRT1

Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60192

disease

Angioimmunoblastic T-Cell lymphoma

increases_expression of

gene/protein

FASN

Drugbank entries Show/Hide entries for FASN
Comment A patient with AITL (Angioimmunoblastic T-Cell Lymphoma, a rare, aggressive (fast-growing) form of peripheral T-cell lymphoma (PTCL)) showed a remarkable durable response using a combination of conventional CHOP and bortezomib. All seven markers (p-mTOR (Ser 2448), p-Akt (Ser 473), p-NF-kappaBp65 (Ser 536), COX2, Bcl-2, FASN, and Sirt1) were highly expressed, indicating expressing constitutive activation of the mTORC2/NF-kappaB pathway in this patient who responded remarkably well to an NF-kappaB antagonist.
Formal Description
Interaction-ID: 60193

disease

Angioimmunoblastic T-Cell lymphoma

increases_activity of

process

TORC2/NF-kappaB signaling