PFS Cancer Research Results

PFS, progression-free survival: Click to Expand ⟱
Source:
Type:

PFS (progression-free survival) is the time from a defined starting point—usually randomization or treatment initiation—until documented disease progression or death, whichever occurs first
Scientific Papers found: Click to Expand⟱
7311- Gos,    Systematic Review of Gossypol/AT-101 in Cancer Clinical Trials
- Review, CLL, NA
Dose↝, orally applied gossypol/AT-101 at low doses (30 mg daily or lower) was determined as well tolerable either as monotherapy or in combination with chemo-radiation.
toxicity↓,
PFS↓, Within these trials, a potential benefit was observed in high-risk patients or in some patients with prolongation in progression-free survival or in overall survival.
OS↑,
eff↑, most recent clinical trial combined low dose AT-101 with docetaxel, fluorouracil, and radiation, achieving complete responses in 11 of 13 patients with gastroesophageal carcinoma (median duration of 12 months) and a median progression-free survival o
BioAv↑, The gossypol (−)-enantiomer—also called AT-101—is degraded more slowly and is therefore the more biologically active form
Bcl-2↓, AT-101, a natural Bcl-2 homology domain 3 (BH3) mimetic, is a small molecule inhibitor that downregulates anti-apoptotic Bcl-2 and Bcl-2-related proteins in human cancer cells
ROS↑, In addition, gossypol-induced intrinsic apoptosis might occur also as reactive oxygen species (ROS)-independent
MOMP↑, In gossypol-treated cancer cells, alterations on the mitochondrial outer membrane permeabilization (MOMP) cause the release of large amounts of apoptotic markers, such as cytochrome c and apoptosis-inducing factor (AIF),
Dose↑, Thereby, the maximum tolerated gossypol dose was determined to be 0.8 mg/kg per day (50–60 mg/day),
Casp3↑, Gossypol-induced apoptosis appears to proceed via the caspase-dependent pathway by activation of caspase-3 and caspase-9
Casp9↑,
MMP↑, as well as mitochondrial membrane depolarization
VEGF↓, suppression of vascular endothelial growth factor (VEGF) stimulating intracellular pro-angiogenic kinases phosphorylation could be inhibited by AT-101
APE1/APEX1↓, addition of gossypol leads to inhibition of APE1 and enhances the activity of cisplatin in non-small cell lung cancer
ChemoSen↑,
RadioS↑, Moreover, AT-101 was demonstrated to radiosensitize prostate cancer in vitro and in vivo without augmenting toxicity
toxicity↑, hematologic toxicities are common treatment related toxicities
AST↑, he majority of related AEs were GI and nervous system disorders, increased AST/ALT, of grade 1/2 toxicities
ALAT↑,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

APE1/APEX1↓, 1,   PFS↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↑, 1,  

Cell Death(tgid=5) ⓘ

Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   MOMP↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   Dose↑, 1,   Dose↝, 1,   eff↑, 1,   RadioS↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↑, 1,   AST↑, 1,  

Functional Outcomes(tgid=23) ⓘ

OS↑, 1,   toxicity↓, 1,   toxicity↑, 1,  
Total Targets: 21

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PFS, progression-free survival
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#:1559  State#:%  Dir#:1
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