BRCA2 Cancer Research Results
BRCA2, BReast CAncer gene 2: Click to Expand ⟱
| Source: CGL-Driver Genes |
| Type: TSG |
BRCA1 and BRCA2 are tumor suppressor genes, which, when they function normally, keep tumors from forming.
BRCA2 mutations are associated with an increased risk for:
Breast cancer
Ovarian cancer
Melanoma
Pancreatic cancer
Prostate cancer
|
Scientific Papers found: Click to Expand⟱
BRCA1↑,
BRCA2↑,
ATM↓,
OS↑, In 2008, a cohort study of breast cancer survivors identified that patients who consistently exercised for greater than 2.5 hours per week following diagnosis had a greater than 60% reduction in the risk of all deaths compared with patients who were
IGF-1↓, Table 1, IGF1 Decreased levels, IGFBP3 Increased levels
IGFBP3↑,
BRCA1↑, BRCA1 Increased expression
BRCA2↑, BRCA2 Increased expression
RAS↓, RAS family oncogenes Suppressed activity
P53↑, P53 Enhanced activity
HSPs↑, Heat shock proteins Enhanced activity
Leptin↓, Leptin Reduced activity
Irisin↓, Irisin Enhanced activity
Resistin↓, Resistin Reduced activity
NK cell↑, NK cells Enhanced activity
CRP↓, C-reactive protein, interleukin-6, TNFα Reduced activity
IL6↓,
TNF-α↓,
PGE1↓, Prostaglandins Reduced activity
COX2/PTGS2↓, Cox-2 Reduced activity
*GSH↑, Glutathione, Catalase and Superoxide dismutase Increased activity
*Catalase↑,
*SOD↑,
*monoA↑, Monoamines Higher levels
*EndoR↑, Endorphins Increased release
*testos↑, testosterone increases immediately after vigorous exercise in some but not all studies. lasting for 20–60 minutes post-exercise
ROS↑, Physical activity, especially if strenuous, produces reactive oxidative species (ROS)
QoL↑, Adverse cancer-related symptoms, which have been shown to be alleviated by exercise, include fatigue, muscle weakness, thromboembolism, weight gain, loss of bone density, quality of life (QOL), psychological distress, incontinence and sexual dysfunct
BMD↑, the rate of decline in BMD was significantly less in the resistance exercise group, with a greater benefit seen in the aerobic exercise group
BowelM↑, Exercise reduces bowel transit time and ameliorates constipation and its associated abdominal cramps
JNK↑, indole-3-carbinol has been shown to activate the stress-induced MAP kinases p38 and c-jun N-terminal kinase (JNK) in prostate cancer cells (66), and to inhibit constitutively active STAT3,
STAT3↓,
TumCCA↑, Indole-3-carbinol and DIM exhibit the ability to cause G1 arrest in breast and prostate cancer cells
P21↑, upregulation of the CDK inhibitors p21WAF1 and p27kip1, and the concurrent downregulation of cyclin D1, cyclin E, and CDKs 2, 4, and 6,
p27/CDKN1B↑,
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
AhR↑, indole-3-carbinol has been reported to increase AhR expression in MCF-7 cells
ER-α36↓, Indole-3-carbinol is a negative regulator of ERα signaling in human tumor cells
ChemoSen↑, Consequently, indole-3-carbinol could cooperate with tamoxifen to inhibit breast cancer proliferation
ER Stress↑, indole-3-carbinol and DIM induced endoplasmic reticulum stress responses in cancer cells via unfolded protein response pathways,
UPR↑,
BRCA1↑, indole-3-carbinol/DIM-induced endoplasmic reticulum stress and upregulation of the expression of the tumor suppressor genes BRCA1 and BRCA2 in prostate and breast cancer cells
BRCA2↑,
TumCMig↓, Indole-3-carbinol has been reported to inhibit the migration and invasion of breast cancer cells
TumCI↓,
VEGF↓, decreased vascular endothelial growth factor (VEGF), increased interleukin-8 (IL-8) secretion, and decreased activities of MMP-2 and MMP-9
IL8↓,
MMP2↓,
MMP9↓,
RadioS↑, Chemo- and radiosensitizing effects of indole-3-carbinol/DIM
Akt↓, Inhibition of Akt/NF-κB signaling
NF-kB↓,
DR4↑, Induction of death receptor (DR)4 and DR5 expression
DR5↑,
Showing Research Papers: 1 to 3 of 3
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
ROS↑, 1,
Cell Death(tgid=5) ⓘ
AhR↑, 1, Akt↓, 1, DR4↑, 1, DR5↑, 1, JNK↑, 1, p27/CDKN1B↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
BowelM↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, HSPs↑, 1, UPR↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
ATM↓, 1, BRCA1↑, 3, BRCA2↑, 3, P53↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK2↓, 1, CDK4↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
IGF-1↓, 1, IGFBP3↑, 1, RAS↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
ER-α36↓, 1, MMP2↓, 1, MMP9↓, 1, TumCI↓, 1, TumCMig↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, CRP↓, 1, IL6↓, 1, IL8↓, 1, NF-kB↓, 1, NK cell↑, 1, PGE1↓, 1, Resistin↓, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1, Irisin↓, 1, Leptin↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, RadioS↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BMD↑, 1, BRCA1↑, 3, CRP↓, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
OS↑, 1, QoL↑, 1,
Total Targets: 51
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↑, 1, GSH↑, 1, SOD↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
EndoR↑, 1, monoA↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
testos↑, 1,
Total Targets: 6
Scientific Paper Hit Count for: BRCA2, BReast CAncer gene 2
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#:33 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
Home Page