Presentation is loading. Please wait.

Presentation is loading. Please wait.

NSG mice transplanted with human primary ALK-positive ALCL tumor grafts were administered either doxorubicin, 10 mg/kg i.v. or CEP-28122 orally, 100 mg/kg,

Published byRatna Chandra Modified over 4 years ago

Similar presentations

Presentation on theme: "NSG mice transplanted with human primary ALK-positive ALCL tumor grafts were administered either doxorubicin, 10 mg/kg i.v. or CEP-28122 orally, 100 mg/kg,"— Presentation transcript:

1 NSG mice transplanted with human primary ALK-positive ALCL tumor grafts were administered either doxorubicin, 10 mg/kg i.v. or CEP orally, 100 mg/kg, twice daily, or doxorubicin following by CEP NSG mice transplanted with human primary ALK-positive ALCL tumor grafts were administered either doxorubicin, 10 mg/kg i.v. or CEP orally, 100 mg/kg, twice daily, or doxorubicin following by CEP Tumor diameters were measured and recorded every day, presented as mean ± SEM (A) or individual value (B). b.i.d., twice daily dose. Mangeng Cheng et al. Mol Cancer Ther 2012;11: ©2012 by American Association for Cancer Research

Download ppt "NSG mice transplanted with human primary ALK-positive ALCL tumor grafts were administered either doxorubicin, 10 mg/kg i.v. or CEP-28122 orally, 100 mg/kg,"

Similar presentations

A, Effect of folate-FITC (500 nmol/kg, 5 days/week) and/or sunitinib (20 mg/kg daily) therapy on the growth of M109 tumors in Balb/c mice. A, Effect of.

A, Effect of folate-FITC (500 nmol/kg, 5 days/week) and/or sunitinib (20 mg/kg daily) therapy on the growth of M109 tumors in Balb/c mice. A, Effect of.
SCC244 significantly inhibited c-Met–driven tumor growth in cancer CDX models. SCC244 significantly inhibited c-Met–driven tumor growth in cancer CDX models.

SCC244 significantly inhibited c-Met–driven tumor growth in cancer CDX models. SCC244 significantly inhibited c-Met–driven tumor growth in cancer CDX models.
Selinexor combines with immune checkpoint blockade to slow B16F10 melanoma tumor growth. Selinexor combines with immune checkpoint blockade to slow B16F10.

Selinexor combines with immune checkpoint blockade to slow B16F10 melanoma tumor growth. Selinexor combines with immune checkpoint blockade to slow B16F10.
Dose-escalation patient response.

Dose-escalation patient response.
Treatment with BLU9931 leads to tumor regression in the FGF19-overexpressing PDX-derived xenograft LIXC012. Treatment with BLU9931 leads to tumor regression.

Treatment with BLU9931 leads to tumor regression in the FGF19-overexpressing PDX-derived xenograft LIXC012. Treatment with BLU9931 leads to tumor regression.
Antitumor activity of BAY in patient-derived tumor models.

Antitumor activity of BAY in patient-derived tumor models.
Combined A2A receptor and PD-1 blockade is not effective in IFNγ−/− mice. Combined A2A receptor and PD-1 blockade is not effective in IFNγ−/− mice. AT-3ovadim.

Combined A2A receptor and PD-1 blockade is not effective in IFNγ−/− mice. Combined A2A receptor and PD-1 blockade is not effective in IFNγ−/− mice. AT-3ovadim.
Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16.

Inhibition of FGFR signaling and tumor growth in SNU-16 xenograft model by administration of E7090. Inhibition of FGFR signaling and tumor growth in SNU-16.
Treatment with BLU9931 leads to tumor regression in the FGF19-amplified Hep 3B liver cancer model. Treatment with BLU9931 leads to tumor regression in.

Treatment with BLU9931 leads to tumor regression in the FGF19-amplified Hep 3B liver cancer model. Treatment with BLU9931 leads to tumor regression in.
CD8+ T cells were immunomodulated and required for the efficacy of anti–4-1BB/anti–PD-1 combination treatment. CD8+ T cells were immunomodulated and required.

CD8+ T cells were immunomodulated and required for the efficacy of anti–4-1BB/anti–PD-1 combination treatment. CD8+ T cells were immunomodulated and required.
Effect of 11-day oral administration of vehicle (n = 4) or 6-day oral administration of enalapril 10 mg/kg per day (n = 19), followed by 5-day oral administration.

Effect of 11-day oral administration of vehicle (n = 4) or 6-day oral administration of enalapril 10 mg/kg per day (n = 19), followed by 5-day oral administration.
Activity of MAC-321 (i. v. and p. o

Activity of MAC-321 (i. v. and p. o
Effect of MI-773 dosing on long-term efficacy.

Effect of MI-773 dosing on long-term efficacy.
A: The change of plasma glucose in opioid μ-receptor knockout diabetic mice and wild-type controls receiving an oral intake of metformin (100 mg/kg). A:

A: The change of plasma glucose in opioid μ-receptor knockout diabetic mice and wild-type controls receiving an oral intake of metformin (100 mg/kg). A:
IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells. IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells.

IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells. IL-6 signaling affects response to erlotinib in head and neck (HNSCC) cells.
A: Chemical structure of pterosin A

A: Chemical structure of pterosin A
CO-1686 does not inhibit WT EGFR signaling in vivo and is active in EGFR-mutant transgenic mouse lung cancer models. CO-1686 does not inhibit WT EGFR signaling.

CO-1686 does not inhibit WT EGFR signaling in vivo and is active in EGFR-mutant transgenic mouse lung cancer models. CO-1686 does not inhibit WT EGFR signaling.
Mice immunized twice with RRBC showed superior protection to tumor challenge with αGal-positive MC38 colon carcinoma cells compared with mock-immunized.

Mice immunized twice with RRBC showed superior protection to tumor challenge with αGal-positive MC38 colon carcinoma cells compared with mock-immunized.
Antitumor immunity caused by DS-8201a.

Antitumor immunity caused by DS-8201a.
Skin tumor size following ligand activation of PPARβ/δ and inhibition of COX2. Skin tumor size following ligand activation of PPARβ/δ and inhibition of.

Skin tumor size following ligand activation of PPARβ/δ and inhibition of COX2. Skin tumor size following ligand activation of PPARβ/δ and inhibition of.

Similar presentations

Ads by Google