CD31/PECAM-1 Cancer Research Results

CD31/PECAM-1, platelet endothelial cell adhesion molecule-1 (PECAM-1): Click to Expand ⟱

Source:

Type: marker

CD31, also known as platelet endothelial cell adhesion molecule-1 (PECAM-1), is a transmembrane receptor that plays a crucial role in various cellular processes, including cell adhesion, migration, and signaling.
High CD31 expression has been linked to poor prognosis and increased metastasis. (except Leukemia and brain cancers).
CD31 is a marker that is commonly used to identify microvessels in tissue sections.

Scientific Papers found: Click to Expand⟱

557-

ART/DHA,

Artemisinin and Its Derivatives in Cancer Care

Review,

Var,

100-250mg/d

400 mg 3x/day dosed it every other week

*BioAv↓, with High fat and high calorie meals
*BioAv↑, DHA dihydroartemisinin have improved bioavailability
Apoptosis↑,
EGFR↓,
CD31/PECAM-1↓,
Ki-67↓,
P53↓,
TfR1/CD71↑,
P-gp/ABCB1↓, many artemisinin derivatives act as P-gp inhibitors
PD-1↝, Caution when used with mmunotherapy (PD1/PDL1 inhibitors)

2773-

Bos,

Targeted inhibition of tumor proliferation, survival, and metastasis by pentacyclic triterpenoids: Potential role in prevention and therapy of cancer

Review,

Var,

Inflam↓, BA has been shown to be effective against chronic inflammation-driven diseases such as adjuvant or bovine serum albumin-induced arthritis, osteoarthritis, Crohnâs disease, ulcerative colitis, and ileitis, and galactosamine/endotoxin-induced hepa
TumCCA↑, BA induced apoptosis was mediated by cell cycle arrest in the G1 phase and by activating caspases 3, 8 and 9 in HT-29 cells
Casp3↑,
Casp8↑,
Casp9↑,
STAT3↑, BA inhibited the growth of multiple myeloma cells by suppression of STAT3 pathway and by activation of protein tyrosine phosphatase SHP1
SHP1↓,
NF-kB↓, BA down regulated the expression of NF-kB, cyclin D1, COX2, Ki-67, CD-31 and IAPs in the tumor tissue.
cycD1/CCND1↓,
COX2/PTGS2↓,
Ki-67↓,
CD31/PECAM-1↓,
IAP1↓,
MMPs↓, AKBA induced cell cycle arrest was mediated by down-regulating the expression of cyclinD1, suppresses MMP activity, and also induced apoptosis by suppressing Bcl-2, and Bcl-xL expression
Bcl-2↓,
Bcl-xL↓,

1169-

Bos,

Boswellic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in Orthotopic Mouse Model By Downregulating Inflammatory, Proliferative, Invasive, and Angiogenic Biomarkers

in-vivo,

CRC,

50-200 mg/kg

mice

TumCG↓,
TumVol↓,
Weight∅, without significant decreases in body weight
ascitic↓,
TumMeta↓,
Ki-67↓,
CD31/PECAM-1↓,
NF-kB↓,
COX2/PTGS2↓,
Bcl-2↓,
Bcl-xL↓,
IAP1↓,
survivin↓,
cycD1/CCND1↓,
ICAM-1↓,
MMP9↓,
CXCR4↓,
VEGF↓,

7174-

CHA,

Inhibition of SUV39H1 reduces tumor angiogenesis via Notch1 in oral squamous cell carcinoma

vitro+vivo,

OS,

OS-RC-2

nude mice without thymus (18–20 g;

SUV39H↓, The effect of SUV39H1 inhibition on OSCC was investigated in vivo by chaetocin treatment.
TumCG↓, In vivo experiment chaetocin treatment significantly inhibit the growth of tumor, and reduce SUV39H1, Notch1, CD31 expression.
NOTCH1↓,
CD31/PECAM-1↓,
VEGF↓, lead to the decreased expression of Notch1 and VEGF proteins, as well as the decreased migration and tube formation ability of vascular endothelial cells
toxicity↓, Treatment doses of Chaetocin has no obvious toxicity in mice
Ki-67↓, groups treated Chaetocin, SUV39H1, Notch1, CD31, Ki67 staining intensity is lower than the control group
angioG↓, These results further suggest that inhibition of SUV39H1 may reduce tumor angiogenesis.

465-

CUR,

Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues

vitro+vivo,

Liver,

HepG2

1.2, 2.4, 4.8 and 9.6 µg/mL, 24 and 48 h; 120 and 240 mg/kg/day, 15 days

vitro+vivo,

Liver,

HUH7

vitro+vivo,

Liver,

MHCC-97H

TumCG↓,
MDSCs↓,
TLR4↓,
NF-kB↓,
IL6↓,
IL1↓, IL-1β
PGE2↓,
COX2/PTGS2↓,
GM-CSF↓,
angioG↓,
VEGF↓,
CD31/PECAM-1↓,
GM-CSF↓,
α-SMA↓,
p‑IKKα↓, p-IKKα, p-IKKβ
MyD88↓,

6211-

CUR,

The effect of curcumin on hypoxia in the tumour microenvironment as a regulatory factor in cancer

Review,

Var,

HIF-1↓, Curcumin, the major component of the rhizomes of Curcuma longa L., reduces HIF-1 levels and function, inhibiting the production of vascular endothelial growth factor (VEGF).
VEGF↓, Curcumin suppresses the HIF-1 pathway under hypoxia, which decreases VEGF expression in both tumour and stromal cells and suppresses angiogenesis.
angioG↓, curcumin efficiently inhibits the angiogenesis of vascular endothelial cells triggered by hypoxia.
RadioS↑, continued interest in curcumin is the molecules’ modulation of initiation, promotion, and progression stages of cancer while concomitantly acting as a radiosensitizer and chemosensitizer for tumours.
ChemoSen↑, Combining cisplatin with curcumin promotes cell apoptosis through the YWHAG pathway and its interaction with HIF-1α, affecting the pentose phosphorylation pathway [
other↝, Cancer patients with hypoxia in their tumours have a poorer prognosis and are at greater risk of metastasis
Apoptosis↑, Curcumin exerts its unique anti-tumour efficacy primarily via pleiotropic functions resulting in apoptosis and decreased tumour cell growth and metastasis
TumCG↓,
TumMeta↓,
BioAv↓, However, due to its low water solubility and low chemical stability, curcumin’s use is limited.
COX2/PTGS2↓, abrogate the proliferation of pancreatic cancer cells through inhibition of COX-2, CD-31, VEGF, and IL-8 and suppression of TGF-β via NF-κB and HIF-1α downregulation
CD31/PECAM-1↓,
IL8↓,
TGF-β↓,
NF-kB↓,
JAK2↓, Curcumin application reduced tumourspheres of H460 cells via inhibition of the JAK2/STAT3 signalling pathway
STAT3↓,

7008-

Fuc,

Ten Years of Research on Fucoidan and Cancer: Focus on Its Antiangiogenic and Antimetastatic Effects

Review,

Var,

antiOx↑, anti-oxidant, antiviral, immunoregulatory, anti-coagulant, anti-thrombotic, anti-lipidemic, anti-diabetic, anti-tumor, anti-metastatic, and anti-angiogenic properties
AntiViral↑,
Imm↝,
*AntiThr↑,
*AntiDiabetic↑,
AntiTum↑,
TumMeta↑,
angioG↓,
Hif1a↓, ↓ HIF-1α and VEGF in hypoxic-like conditions
VEGF↓,
MMPs↓, ↓ MMPs
EMT↓, ↓ EMT (↓ N-cadherin; ↑ E-cadherin)
N-cadherin↓,
E-cadherin↑,
TIMP1↑, ↑ TIMP
PI3K↓, ↓ PI3K/Akt/mTOR
Akt↓,
mTOR↓,
MMP2↓, ↓ MMP-2, 9
ChemoSen↑, available findings indicate that oral intake of fucoidan as dietary supplement in combination with conventional adjuvant chemotherapy can prolong survival time, decrease some adverse effects (e.g., fatigue)
OS↑,
fatigue↓,
CD31/PECAM-1↓, fig 2

801-

GAR,

Cisplatin,

Garcinol sensitizes human head and neck carcinoma to cisplatin in a xenograft mouse model despite downregulation of proliferative biomarkers

in-vivo,

HNSCC,

0.5 mg/kg

mouse

Apoptosis↑, enhanced the apoptotic effect of cisplatin
cycD1/CCND1↓,
Bcl-2↓,
survivin↓,
VEGF↓,
TumCG↓,
Ki-67↓, index (Ki-67) and microvessel density (CD31) were downregulated in tumor tissues by the combination of cisplatin and garcinol.
CD31/PECAM-1↓,

7365-

HibSad,

Insight into the molecular evidence supporting the remarkable chemotherapeutic potential of Hibiscus sabdariffa L

Review,

Var,

chemoPv↑, Both crude extracts and pure compounds of the plant were reported to induce chemoprevention, selective cytotoxicity, cell cycle arrest, apoptosis, autophagy and anti-metastasis effects in varied types of human cancer cells.
selectivity↑,
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumMeta↓,
ATG5↑, figure 3
Beclin-1↑,
LC3II↑,
MMP2↓,
MMP9↓,
CD31/PECAM-1↓,
VEGF↓,
uPA↓,
TIMP2↑,
NF-kB↓,
p38↑,
P53↑,
Casp3↑,
Casp8↑,
Casp9↑,
Bcl-2↓,
BAX↑,
Cyt‑c↑,
TNF-α↑,
Fas↑,
FasL↑,
JNK↑,
cJun↑,
angioG↓,
VEGFR2/KDR/Flk1↓,
PCNA↓,
CCN2/CTGF↓,
RAGE↓,

7691-

IP6,

Inositol Hexaphosphate Suppresses Growth and Induces Apoptosis in Prostate Carcinoma Cells in Culture and Nude Mouse Xenograft: PI3K-Akt Pathway as Potential Target

vitro+vivo,

Pca,

PC3

in-vitro,

Pca,

C4-2B

TumCP↓, IP6 treatment of cells suppressed proliferation, induced apoptosis along with caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and inhibited constitutive activation of Akt and its upstream regulators PI3K,
Apoptosis↑, IP6 inhibits growth and induces apoptosis in PC-3 cells
Casp3↑,
cl‑PARP↑,
Akt↓, IP6 decreases phosphorylation or expression of signaling molecules in PI3K-Akt axis
PI3K↓,
p‑GSK‐3β↓, Downstream of Akt, IP6 inhibited the phosphorylation of glycogen synthase kinase 3 (GSK-3) α/β at Serine21/9 and consequently reduced Cyclin D1 expression.
cycD1/CCND1↓,
TumVol↓, Efficacy studies employing PC-3 tumor xenograft growth in nude mice showed that 2% IP6 (weight/volume) feeding in drinking water inhibits tumor growth and weight by 52–59%
TumW↓,
PCNA↓, IP6 significantly reduces the expression of molecules associated with cell survival/proliferation (ILK1, phospho-Akt, Cyclin D1, PCNA) and angiogenesis (PECAM-1 or CD31, VEGF, eNOS, hypoxia-inducible factor-1α (HIF-1α),
angioG↓,
CD31/PECAM-1↓,
ILK↓,
VEGF↓,
eNOS↓,
Hif1a↓,

972-

MAG,

Magnolol suppresses hypoxia-induced angiogenesis via inhibition of HIF-1α/VEGF signaling pathway in human bladder cancer cells

vitro+vivo,

Bladder,

T24/HTB-9

angioG↓,
VEGF↓,
H2O2↓,
Hif1a↓,
VEGFR2/KDR/Flk1↓,
Akt↓,
mTOR↓,
P70S6K↓,
4E-BP1↓,
TumCG↓,
CD31/PECAM-1↓,
CA↓, carbonic anhydrase IX

4968-

PSO,

Psoralidin: emerging biological activities of therapeutic benefits and its potential utility in cervical cancer

in-vitro,

Cerv,

45–60 µM

*Inflam↓, showing anti-inflammatory, anti-oxidant, estrogenic, neuroprotective, anti-diabetic, anti-depressant, antimicrobial, and anti-tumor activities substantiate its promising biological effects.
*antiOx↑,
*neuroP↑,
*AntiDiabetic↑,
*Bacteria↓,
AntiTum↑,
CSCs↓, Its capacity to effectively target cancer stem cells (CSCs) in general adds to its therapeutic potential.
ROS↑, Psoralidin carries out its anti-cancer activity by inducing oxidative stress, autophagy, and apoptosis.
TumAuto↑,
Apoptosis↑,
ChemoSen↑, This unique characteristic suggests its potential to be used as an adjunct molecule in combination with existing treatment to enhance the efficacy of chemo/radiotherapy for treating CaCx.
RadioS↑,
BioAv↓, low bioavailability and intestinal efflux limit the use of psoralidin in clinical applications
*cardioP↑, Psoralidin demonstrated cardioprotective effects.
*ROS↓, Furthermore, psoralidin administration resulted in a decrease in ROS levels and lactate dehydrogenase (LDH) release, indicating reduced oxidative stress and cellular damage in the heart.
*LDH↓,
TumCP↓, LNCaP Induction of apoptosis ↓Cell proliferation ↑TRAIL
TRAIL⇅,
TumCMig↓, PC-3, PzHPV-7, C4-2B 5–20 µM ↓Cell proliferation, ↓Migration, Invasion ROS generation
EMT↓, RWPE-1, xenograft mice 4 µM ↓Cell proliferation, Induction of apoptosis, Autophagy induction, EMT Inhibition ↓NF-кB signaling
NF-kB↓,
P53↑, HepG2 64 µM Induction of apoptosis ↑p53
Casp3↑, figure 4
NOTCH↓,
CSCs↓, Anti-CSC activity
angioG↓, Anti-angiogenesis
VEGF↓, it inhibited angiogenesis by downregulating the expression of pro-angiogenic molecules VEGF, Ki67, and CD31
Ki-67↓,
CD31/PECAM-1↓,
TRAILR↑, psoralidin treatment induced the activation of death receptors 1 (DR 1) and DR 2 after 48 h of treatment
MMP↓, Psoralidin significantly increased the loss of ΔΨm, affecting a large percentage of cancer cells (58.38% ± 1.41%) and causing a major disruption of the mitochondrial membrane potential.
BioAv↓, hydrophobic nature, inadequate pharmacokinetic profile of psoralidin, and intestinal efflux, which hampers its clinical application
BioAv↑, bioavailability of psoralidin significantly improved with a value of 339% w.r.t to reference through its nanoencapsulation (NCs) using chitosan and Eudragit S100

3288-

SIL,

Silymarin in cancer therapy: Mechanisms of action, protective roles in chemotherapy-induced toxicity, and nanoformulations

Review,

Var,

Inflam↓, Silymarin, a milk thistle extract, has anti-inflammatory, immunomodulatory, anti-lipid peroxidative, anti-fibrotic, anti-oxidative, and anti-proliferative properties.
lipid-P↓,
TumMeta↓, Silymarin exhibits not only anti-cancer functions through modulating various hallmarks of cancer, including cell cycle, metastasis, angiogenesis, apoptosis, and autophagy, by targeting a plethora of molecules
angioG↓,
chemoP↑, but also plays protective roles against chemotherapy-induced toxicity, such as nephrotoxicity,
EMT↓, Figure 2, Metastasis
HDAC↓,
HATs↑,
MMPs↓,
uPA↓,
PI3K↓,
Akt↓,
VEGF↓, Angiogenesis
CD31/PECAM-1↓,
Hif1a↓,
VEGFR2/KDR/Flk1↓,
Raf↓,
MEK↓,
ERK↓,
BIM↓, apoptosis
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Casp↑,
MAPK↓,
P53↑,
LC3II↑, Autophagy
mTOR↓,
YAP/TEAD↓,
*BioAv↓, Additionally, the oral bioavailability of silymarin in rats is only 0.73 %
MMP↓, silymarin treatment reduced mitochondrial transmembrane potential, leading to an increase in cytosolic cytochrome c (Cyt c), downregulating proliferation-associated proteins (PCNA, c-Myc, cyclin D1, and β-catenin)
Cyt‑c↑,
PCNA↓,
cMyc↓,
cycD1/CCND1↓,
β-catenin/ZEB1↓,
survivin↓, and anti-apoptotic proteins (survivin and Bcl-2), and upregulating pro-apoptotic proteins (caspase-3, Bax, APAF-1, and p53)
APAF1↑,
Casp3↑,
MDSCs↓, ↓MDSCs, ↓IL-10, ↑IL-2 and IFN-γ
IL10↓,
IL2↑,
IFN-γ↑,
hepatoP↑, Moreover, in a randomized clinical trial, silymarin attenuated hepatoxicity in non-metastatic breast cancer patients undergoing a doxorubicin/cyclophosphamide-paclitaxel regimen
cardioP↑, For example, Rašković et al. studied the hepatoprotective and cardioprotective effects of silymarin (60 mg/kg orally) in rats following DOX
GSH↑, silymarin could protect the kidney and heart from ADR toxicity by protecting against glutathione (GSH) depletion and inhibiting lipid peroxidation
neuroP↑, silymarin attenuated the neurotoxicity of docetaxel by reducing apoptosis, inflammation, and oxidative stress

7942-

TQ,

Thymoquinone inhibits inflammation, neoangiogenesis and vascular remodeling in asthma mice

in-vitro,

Asthma,

asthma mice in vivo

*IL4↓, TQ inhibited the production of inflammatory factors interleukin-4/-5 (IL-4/-5) by enzyme-linked immunesorbent assay (ELISA).
*IL5↓,
*CD31/PECAM-1↓, platelet endothelial cell adhesion molecule-1, which is also known as CD31 and α-smooth muscle actinalpha (α-SMA) expression in asthma mice challenged by OVA was suppressed by TQ.
*VEGFR2/KDR/Flk1↓, TQ suppressed the activation of VEGFR2-PI3K-Akt pathway and up-regulated the expression of Slit glycoprotein-2 (Slit-2) both in vivo and in vitro
*PI3K↓,
*Akt↓,
*SLIT2↑,
*Inflam↓, Our study demonstrates that TQ attenuated the inflammatory reaction by antagonizing IL-4/-5 while the anti-neoangiogenesis effect of TQ is mediated by inhibition of vascular endothelial growth factor (VEGF)
*VEGF↓,

2411-

UA,

Ursolic acid in health and disease

Review,

Var,

Inflam↓, UA because of its beneficial effects, which include anti-inflammatory, anti-oxidant, anti-apoptotic, and anti-carcinogenic effects
antiOx↑,
NF-kB↓, Colon cancer HCT116, HT29 20 μM for 8 hour ↓ NF-kB, Bcl-xL, Bcl-2, and cyclin D1
Bcl-xL↓,
Bcl-2↓,
cycD1/CCND1↓,
Ki-67↓, ↓ Ki67, CD31, STAT3, and EGFR, ↑ p53 and p21 mRNA expression
CD31/PECAM-1↓,
STAT3↓,
EGFR↓,
P53↑,
P21↓,
HK2↓, MCF-7, MDA-MB-231 20 μM for 24 hours ↓ HK2, PKM2, ATP, and lactate ↓ pERK1/2, and depolarization of mitochondrial membrane potential, ↑ Nitric oxide and ATM
PKM2↓,
ATP↓,
lactateProd↓,
p‑ERK↓,
MMP↓,
NO↑,
ATM↑,
Casp3↑, T24 cancer cells ↑ Caspase 3 activity ↑ AMPK activation ↑ JNK activation
AMPK↑,
JNK↑,
FAO↑, 80 μM UA reduces triglyceride (TG) and cholesterol levels by increasing fatty acid oxidation and decreasing fatty acid synthesis in hepatocytes
FASN↓,
*GSH↑, ↑ Vitamin C, E, GSH, SOD, CAT, GPx, GST, and GR in heart
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
neuroP↑, This demonstrates that UA has a protective effect against various inflammatory conditions of the brain.

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,
Total Targets: 145

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

SLIT2↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1, Catalase↑, 1, GPx↑, 1, GSH↑, 1, GSTs↑, 1, ROS↓, 1, SOD↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

LDH↓, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PI3K↓, 1,

Migration(tgid=13) ⓘ

CD31/PECAM-1↓, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1, VEGFR2/KDR/Flk1↓, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL4↓, 1, IL5↓, 1, Inflam↓, 2,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2, BioAv↑, 1,

Clinical Biomarkers(tgid=22) ⓘ

LDH↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 2, cardioP↑, 1, neuroP↑, 1,

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,
Total Targets: 25

Scientific Paper Hit Count for: CD31/PECAM-1, platelet endothelial cell adhesion molecule-1 (PECAM-1)

2 Boswellia (frankincense)
2 Curcumin
1 Artemisinin
1 chaetocin
1 Fucoidan
1 Garcinol
1 Cisplatin
1 Hibiscus sabdariffa
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
1 Magnolol
1 Psoralidin
1 Silymarin (Milk Thistle) silibinin
1 Thymoquinone
1 Ursolic acid

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#:295  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

CD31/PECAM-1 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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