• Cutaneous T-cell Lymphoma
• IL-4/13 inhibitors
• Mycosis fungoides
• microenvironment
• sézary syndrome

• Cell differentiation
• Interleukin-4
• Peptide hydrogel
• Skeletal muscle regeneration
• Stromal derived factor-1

• amniotic membrane
• biomaterials
• canine
• cornea
• tissue proteomics
• wound healing properties

• Animals
• Amnion/chemistry
• Dogs
• Wound Healing
• Proteomics
• Corneal Injuries/veterinary
• Corneal Injuries/therapy
• Proteome
• Tissue Extracts

• GCUGR1125623068D Graduate School, Chulalongkorn University

• VEGFR‐2 inhibitors
• natural products
• phytochemicals
• targeted chemotherapy
• tumour angiogenesis

• Humans
• Biological Products/pharmacology
• Biological Products/therapeutic use
• Neoplasms/drug therapy
• Neoplasms/blood supply
• Neoplasms/pathology
• Neovascularization, Pathologic/drug therapy
• Angiogenesis Inhibitors/pharmacology
• Angiogenesis Inhibitors/therapeutic use
• Animals
• Angiogenesis

• Theophrastus Stiftung, Mühltal, Germany

• Genetic association
• Prostate cancer
• Systematic review

• Humans
• Male
• Prostatic Neoplasms/genetics
• Prostatic Neoplasms/epidemiology
• Prostatic Neoplasms/pathology
• China/epidemiology
• Polymorphism, Single Nucleotide
• Genetic Predisposition to Disease
• Asian People/genetics
• Genetic Association Studies

• 005/2023/SKL The Science and Technology Development Fund, Macau SAR
• MYRG-GRG2023-00087-ICMS The University of Macau

• Anti-CTLA-4
• Anti-PD1
• ICI
• Th subsets
• Tumor immunity

• Humans
• Immune Checkpoint Inhibitors/therapeutic use
• Immune Checkpoint Inhibitors/pharmacology
• Neoplasms/immunology
• Neoplasms/drug therapy
• Tumor Microenvironment/immunology
• Tumor Microenvironment/drug effects
• Animals
• T-Lymphocytes, Helper-Inducer/immunology
• T-Lymphocytes, Helper-Inducer/drug effects
• T-Lymphocyte Subsets/immunology

• Animals
• Humans
• Adipose Tissue/immunology
• Carcinogenesis/immunology
• Carcinogenesis/pathology
• Immunotherapy
• Neoplasms/immunology
• Neoplasms/therapy
• Neoplasms/pathology
• Adaptive Immunity

• Angiogenesis
• Cancer/tumor growth
• Canonical pathway
• Non-canonical pathway
• Sonic hedgehog
• VEGF

• Female
• Humans
• Hedgehog Proteins/metabolism
• Vascular Endothelial Growth Factor A/metabolism
• Phosphatidylinositol 3-Kinases/metabolism
• Placenta Growth Factor
• Signal Transduction/physiology
• Neoplasms

• Angiogenesis
• Cancer-associated fibroblasts
• Hypoxia
• Immune system
• Microfluidic device
• Organ-on-chip
• Organoids
• Renal cell carcinoma
• Screening platform
• Tumor microenvironment
• pH

• Humans
• Carcinoma, Renal Cell/drug therapy
• Endothelial Cells/pathology
• Kidney Neoplasms/drug therapy
• Tumor Microenvironment

• CP: Immunology
• CP: Metabolism
• IL-4Rα signaling
• angiogenesis
• ischemic muscle
• peripheral arterial disease
• type 2 cytokines

• IL-10
• IL-12
• IL-4
• LASIK
• PRK
• corneal wound healing
• excimer laser
• tears

• Angiogenesis
• Breast cancer
• Cellular senescence
• Chromatin
• Immune evasion
• Tumor dormancy
• p53

• Humans
• Neoplasm Recurrence, Local/pathology
• Neoplasms/metabolism
• Phenotype
• Cellular Senescence
• Cytokines/therapeutic use
• Tumor Microenvironment

• R01ES032036 NIH HHS
• R01 CA259001 NCI NIH HHS
• R01CA259001 NIH HHS
• R01 ES032036 NIEHS NIH HHS
• TL1TR003106 NIH HHS

Tumor growth in solid cancers requires adequate nutrient and oxygen supply, provided by blood vessels created by angiogenesis. Numerous studies have demonstrated that this mechanism plays a crucial role in cancer development and appears to be a well-defined hallmark of cancer. This process is carefully regulated, notably by cytokines with pro-angiogenic or anti-angiogenic features. In this review, we will discuss the role of cytokines in the modulation of angiogenesis. In addition, we will summarize the therapeutic approaches based on cytokine modulation and their clinical approval.

During carcinogenesis, tumors set various mechanisms to help support their development. Angiogenesis is a crucial process for cancer development as it drives the creation of blood vessels within the tumor. These newly formed blood vessels insure the supply of oxygen and nutrients to the tumor, helping its growth. The main factors that regulate angiogenesis are the five members of the vascular endothelial growth factor (VEGF) family. Angiogenesis is a hallmark of cancer and has been the target of new therapies this past few years. However, angiogenesis is a complex phenomenon with many redundancy pathways that ensure its maintenance. In this review, we will first describe the consecutive steps forming angiogenesis, as well as its classical regulators. We will then discuss how the cytokines and chemokines present in the tumor microenvironment can induce or block angiogenesis. Finally, we will focus on the therapeutic arsenal targeting angiogenesis in cancer and the challenges they have to overcome.

• angiogenesis
• cancer
• chemokines
• cytokines
• therapy

• eosinophils
• immunotherapy
• melanoma
• prognostic markers

• angiogenesis
• cytokine
• endothelial cell
• hypoxia
• inflammation
• interleukin
• macrophage
• polarization

• Angiogenesis Inhibitors/pharmacology
• Anti-Inflammatory Agents/metabolism
• Anti-Inflammatory Agents/pharmacology
• Anti-Inflammatory Agents/therapeutic use
• Endothelial Cells/metabolism
• Humans
• Inflammation/metabolism
• Interleukins/metabolism
• Ischemia/metabolism
• Neovascularization, Pathologic/metabolism

• HL141108 NIH HHS

• CAR T cells
• T Cell therapy
• cancer
• cytokine receptors
• cytokines
• immunotherapy

• Animals
• Antigens, Neoplasm/immunology
• Cell Engineering
• Cytokines/metabolism
• Hematologic Neoplasms/immunology
• Hematologic Neoplasms/therapy
• Humans
• Immunotherapy, Adoptive/methods
• Neoplasms/immunology
• Neoplasms/therapy
• Receptors, Chimeric Antigen/immunology
• Receptors, Cytokine/metabolism
• Tumor Microenvironment

• F31 CA250401 NCI NIH HHS
• R01 NS106379 NINDS NIH HHS

• adipose tissue
• biomaterial
• inflammation
• insulin resistance
• obesity
• poly(lactide-co-glycolide)

• Adipose Tissue/metabolism
• Animals
• Disease Models, Animal
• Humans
• Implants, Experimental
• Inflammation/genetics
• Inflammation/metabolism
• Interleukin-4/biosynthesis
• Interleukin-4/genetics
• Lentivirus
• Male
• Mice
• Obesity/genetics
• Obesity/metabolism
• Transduction, Genetic

• R01 DK115190 NIDDK NIH HHS
• T32 GM145304 NIGMS NIH HHS
• R01 DK090262 NIDDK NIH HHS
• P30 DK020572 NIDDK NIH HHS
• P30 DK089503 NIDDK NIH HHS
• I01 CX001811 CSRD VA

• endothelium
• extracellular matrix
• fibroblast
• macrophage
• satellite cell

• R01 CA121249 NCI NIH HHS
• R01 CA218578 NCI NIH HHS
• R21 CA231131 NCI NIH HHS
• R41 AT009964 NCCIH NIH HHS

• Keratoconus
• corneae
• cytokines
• human
• inflammation

• Epithelial ovarian cancer
• IGFBP3
• THBS1
• angiogenesis

• Angiogenesis
• Non-clinical toxicity
• Oxidative stress
• Piperine analogue
• Tumor microenvironment.
• Zebrafish

• Breast cancer
• VEGF
• angiogenesis
• anti-angiogenic therapies
• hypoxia
• metastasis
• vascular diseases

• IL-4
• age-related macular degeneration
• angiogenesis
• choroidal neovascularization
• human biology
• medicine
• mouse

• angiogenesis
• biomarker
• cytokines
• endometriosis
• urinary biomarkers

• Cow
• Cystic follicle
• Cytokines
• Follicular fluid
• Ovary

• Cytokines
• FAS
• Lipid content
• Mature SREBP-1
• Sebocytes
• Synergism

Adoptive T cell transfer therapy (ACT) using tumor infiltrating lymphocytes or lymphocytes redirected with antigen receptors (CAR or TCR) has revolutionized the field of cancer immunotherapy. Although CAR T cell therapy mediates robust responses in patients with hematological malignancies, this approach has been less effective for treating patients with solid tumors. Additionally, toxicities post T cell infusion highlight the need for safer ACT protocols. Current protocols traditionally expand T lymphocytes isolated from patient tumors or from peripheral blood to large magnitudes in the presence of high dose IL-2 prior to infusion. Unfortunately, this expansion protocol differentiates T cells to a full effector or terminal phenotype in vitro, consequently reducing their long-term survival and antitumor effectiveness in vivo. Post-infusion, T cells face further obstacles limiting their persistence and function within the suppressive tumor microenvironment. Therapeutic manipulation of T cells with common γ chain cytokines, which are critical growth factors for T cells, may be the key to bypass such immunological hurdles. Herein, we discuss the primary functions of the common γ chain cytokines impacting T cell survival and memory and then elaborate on how these distinct cytokines have been used to augment T cell-based cancer immunotherapy.

• T cell
• TRUCKs
• adoptive cell transfer
• chimeric antigen receptor
• gamma chain cytokines

Genetic redirection of T lymphocytes with chimeric antigen receptors (CARs) has soared from treating cancers preclinically to FDA approval for hematologic malignancies and commercial-grade production scale in under 30 years. To date, solid tumors are less susceptible to CAR therapies and instead have been treated more successfully with immune checkpoint blockade or tumor-infiltrating lymphocyte therapy. Here, we discuss the current challenges in treating solid tumors with CAR T cells, and the obstacles within the host and tumor microenvironment hindering their efficacy. We present a novel three-pronged approach for enhancing the efficacy of CAR T cells whereby a single infusion product can synergize the power of an optimal CAR construct, a highly potent T cell subset, and rejuvenate the endogenous immune response to conquer therapeutically-resistant solid tumors.

• T cell
• adoptive cell transfer
• checkpoint
• chimeric antigen receptor
• solid tumor

Prostate cancer (PCa) is a leading cause of mortality and genetic factors can influence tumour aggressiveness. Several germline variants have been associated with PCa-specific mortality (PCSM), but further replication evidence is needed.

Twenty-two previously identified PCSM-associated genetic variants were genotyped in seven PCa cohorts (12,082 patients; 1544 PCa deaths). For each cohort, Cox proportional hazards models were used to calculate hazard ratios and 95% confidence intervals for risk of PCSM associated with each variant. Data were then combined using a meta-analysis approach.

Fifteen SNPs were associated with PCSM in at least one of the seven cohorts. In the meta-analysis, after adjustment for clinicopathological factors, variants in the MGMT (rs2308327; HR 0.90; p-value = 3.5 × 10⁻²) and IL4 (rs2070874; HR 1.22; p-value = 1.1 × 10⁻³) genes were confirmed to be associated with risk of PCSM. In analyses limited to men diagnosed with local or regional stage disease, a variant in AKT1, rs2494750, was also confirmed to be associated with PCSM risk (HR 0.81; p-value = 3.6 × 10⁻²).

This meta-analysis confirms the association of three genetic variants with risk of PCSM, providing further evidence that genetic background plays a role in PCa-specific survival. While these variants alone are not sufficient as prognostic biomarkers, these results may provide insights into the biological pathways modulating tumour aggressiveness.

Immunotherapy is one of the most recent approaches for controlling and curing malignant tumors. In this paper, we consider a mathematical model of periodically pulsed immunotherapy using CD4⁺ T cells and an antitumor cytokine. Mathematical analyses are performed to determine the threshold of a successful treatment. The interindividual variability is explored by one-, two-, and three-parameter bifurcation diagrams for a nontreatment case. Numerical simulation conducted in this paper shows that (i) the tumor can be regulated by administering CD4⁺ T cells alone in a patient with a strong immune system or who has been diagnosed at an early stage, (ii) immunotherapy with a large amount of an antitumor cytokine can boost the immune system to remit or even to suppress tumor cells completely, and (iii) through polytherapy the tumor can be kept at a smaller size with reduced dosages.

• Biomaterials
• drugs
• macrophage
• repair
• wound

• Animals
• Biocompatible Materials/metabolism
• Biocompatible Materials/pharmacology
• Drug Delivery Systems
• Guided Tissue Regeneration/methods
• Humans
• Immunologic Factors/metabolism
• Immunologic Factors/pharmacology
• Macrophages/drug effects
• Macrophages/physiology

• R01 HL130037 NHLBI NIH HHS

Inflammation represents an important event which facilitates prostate carcinogenesis. Genetic variations in inflammatory response genes could affect the level and function of the protein products, resulting in the differential prostate cancer risk among carriers of different variants. This study attempted to investigate the association of IL-4 rs2243250, IL-6 rs10499563, IL-8 rs4073, as well as NFKBIA rs2233406 and rs3138053 polymorphisms with prostate cancer risk in the Chinese population. Genotyping of the polymorphisms was performed by using polymerase chain reaction-restriction fragment length polymorphism technique on 439 prostate cancer patients and 524 controls, and the association of each polymorphic genotype with prostate cancer risk was evaluated by using logistic regression analysis based on allele, heterozygous, and homozygous comparison models, with adjustment to age and smoking status. We showed that the C allele of IL-4 rs2243250 polymorphism could increase prostate cancer risk (heterozygous comparison model: odds ratio [OR] =1.434, 95% confidence interval [CI] =1.092–1.881, P=0.009; homozygous comparison model: OR =2.301, 95% CI =1.402–3.775, P=0.001; allele comparison model: OR =1.509, 95% CI =1.228–1.853, P<0.001). On the other hand, the C allele of rs10499563 polymorphism could decrease prostate cancer risk (heterozygous comparison model: OR =0.694, 95% CI =0.525–0.918, P=0.010; homozygous comparison model: OR =0.499, 95% CI =0.269–0.926, P=0.028; allele comparison model: OR =0.692, 95% CI =0.553–0.867, P=0.001). No association was observed for the other polymorphisms. In conclusion, IL-4 rs2243250 and IL-6 rs10499563 polymorphisms could serve as potential predictive biomarkers for prostate cancer risk in the Chinese population.

• biomarkers
• inflammation
• logistic regression
• polymorphisms
• prostate neoplasm

• 5-Parameter logistic; SEM
• Cytokine expression profiling; CTL
• Cytokines
• Cytotoxic T lymphocyte
• Interleukin-1 receptor antagonist
• Interleukin-10
• Interleukin-13
• Interleukin-4
• Interleukin; RT
• Multianalyte profiling; CEP
• OSCC
• Oral squamous cell carcinoma; TH1
• Phycoerythrin; 5-PL
• Room temperature; PE
• Salivary proteins
• Squamous cell carcinoma of head and neck
• Standard deviation; xMAP
• Standard error of mean; SD
• T helper 1 lymphocytes; TH2
• T helper 2 lymphocytes; IL

• Antibody-cytokine fusion protein
• Chronic skin inflammation
• Fibronectin
• Interleukin 4
• Psoriasis

• Angiogenesis
• Angiogénesis
• Citocinas
• Cytokines
• Cáncer de pulmón
• Inflamación
• Inflammation
• Lung cancer
• Polimorfismo
• Polymorphism

The progression of head and neck squamous cell carcinoma (HNSCC) is stimulated by various angiogenic peptides and growth factors. A correlation between tumor progression and the secretion of various serological mediators in patients with malignant tumors of the head and neck is of major interest for tumor diagnostics, evaluation of the therapy response and it may predict prognosis by specifying the individual tumor biology. Established chemotherapeutic regimes for head and neck tumors usually consist of platinum-based chemotherapeutic drugs and 5-fluorouracil (5-FU). The present pilot study sought to assess the eligibility of seven serological factors as biomarkers for malignant tumors of the head and neck: Platelet-derived growth factor, vascular endothelial growth factor, epidermal growth factor receptor, osteopontin, granulocyte-colony stimulating factor, interleukin-4 (IL-4) and IL-6. The serum levels of each factor in 20 patients receiving concomitant radiochemotherapy with cisplatin or carboplatin and 5-FU with curative intent were determined prior and subsequent to chemotherapy and were compared with 40 healthy controls. Another aim of the pilot study was to investigate whether the serum of patients showed significant differences in the concentrations of the analyzed factors at the start of concomitant radiochemotherapy compared with the controls, whether those markers indicated a neoplastic process and whether concomitant radiochemotherapy with cisplatin or carboplatin and 5-FU induced significant alterations of concentration compared with pre-therapeutic levels. The included patients were histopathologically diagnosed with HNSCC and the average age was 62.3 years. The serum samples of the patients were obtained during the course of regular pre- and post-chemotherapeutic blood draws one week prior to the start of radiochemotherapy and one week following the completion of chemotherapy. The healthy controls were collected from patients of the Sleep Laboratory of the Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital (Mannheim, Germany) without clinical evidence or laboratory signs of inflammation or history of a malignant disease. The average age was 50.3 years. The serological level of each factor was ascertained by enzyme-linked immunosorbent assay in duplicate. Serum levels of IL-4, IL-6 and osteopontin were significantly increased in patients with HNSCC compared with those in chemotherapy-naive healthy controls. IL-4 and osteopontin showed no significant therapy-associated alterations. Notably, IL-6 levels significantly increased post-therapeutically. Using logistic regression with osteopontin and IL-4, an individual risk-profile for random samples was calculated. IL-4, IL-6 and osteopontin appear to be suitable indicators of the neoplastic process as they are significantly increased in HNSCC patients compared with the control group. With the exception of IL-6, whose levels were in fact increased following therapy, a significant therapy-associated alteration of these factors was missing. Therefore, these serological markers failed to predict the therapy response, but they may be valuable as a screening instrument in primary diagnostics.

• epidermal growth factor receptor
• granulocyte-colony stimulating factor
• head and neck squamous cell carcinoma
• interleukin-4
• interleukin-6
• osteopontin
• platelet-derived growth factor
• serological markers
• vascular endothelial growth factor

• corneal ectasia
• corneal wound healing
• genomics
• keratoconus
• review article

• Animals
• Cornea/metabolism
• Cornea/pathology
• Corneal Injuries/genetics
• Genomics/methods
• Humans
• Wound Healing/genetics