Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 14 de 14
Filter
Add more filters










Publication year range
2.
Nat Commun ; 12(1): 2582, 2021 05 11.
Article in English | MEDLINE | ID: mdl-33976133

ABSTRACT

Immune checkpoint blockers (ICBs) have failed in all phase III glioblastoma (GBM) trials. Here, we show that regulatory T (Treg) cells play a key role in GBM resistance to ICBs in experimental gliomas. Targeting glucocorticoid-induced TNFR-related receptor (GITR) in Treg cells using an agonistic antibody (αGITR) promotes CD4 Treg cell differentiation into CD4 effector T cells, alleviates Treg cell-mediated suppression of anti-tumor immune response, and induces potent anti-tumor effector cells in GBM. The reprogrammed GBM-infiltrating Treg cells express genes associated with a Th1 response signature, produce IFNγ, and acquire cytotoxic activity against GBM tumor cells while losing their suppressive function. αGITR and αPD1 antibodies increase survival benefit in three experimental GBM models, with a fraction of cohorts exhibiting complete tumor eradication and immune memory upon tumor re-challenge. Moreover, αGITR and αPD1 synergize with the standard of care treatment for newly-diagnosed GBM, enhancing the cure rates in these GBM models.


Subject(s)
Antineoplastic Combined Chemotherapy Protocols/pharmacology , Drug Resistance, Neoplasm/drug effects , Glioblastoma/drug therapy , Glucocorticoid-Induced TNFR-Related Protein/agonists , T-Lymphocytes, Regulatory/drug effects , Animals , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Cell Line, Tumor/transplantation , Cellular Reprogramming/drug effects , Cellular Reprogramming/immunology , Disease Models, Animal , Female , Glioblastoma/immunology , Humans , Immune Checkpoint Inhibitors/pharmacology , Immune Checkpoint Inhibitors/therapeutic use , Immunologic Memory/drug effects , Male , Mice , Mice, Knockout , Programmed Cell Death 1 Receptor/antagonists & inhibitors , T-Lymphocytes, Cytotoxic/immunology , T-Lymphocytes, Regulatory/immunology , T-Lymphocytes, Regulatory/metabolism
3.
Rev Med Suisse ; 17(723): 201-205, 2021 Jan 27.
Article in French | MEDLINE | ID: mdl-33507661

ABSTRACT

The COVID-19 pandemic that has swept around the world in early 2020 has changed our daily practice and habits. Fortunately, however, 2020 also brings its share of new approaches and therapeutic combinations as well as new therapies. These advances are improving the outcomes and quality of life of our patients across the spectrum of oncological diseases. This article summarises the latest oncological advances and novelties for 2020 in the following tumor entities : lung, breast, digestive, gynecological, urological and ENT.


La pandémie de Covid-19 survenue début 2020 dans le monde entier aura bouleversé notre pratique quotidienne et nos habitudes. Heureusement, sur le plan thérapeutique, l'année 2020 apporte également son lot de nouvelles approches et combinaisons thérapeutiques ainsi que l'introduction de nouvelles molécules, permettant d'améliorer le pronostic vital et la qualité de vie de nos patients, dans de nombreux domaines. Cet article résume les dernières avancées et nouveautés oncologiques de l'année 2020 dans les domaines suivants : poumon, sein, sphère digestive, gynécologique, urologique et ORL.


Subject(s)
COVID-19 , Pandemics , Humans , Medical Oncology , Neoplasms , Quality of Life , SARS-CoV-2
4.
Nat Biomed Eng ; 3(3): 230-245, 2019 03.
Article in English | MEDLINE | ID: mdl-30948807

ABSTRACT

The compression of brain tissue by a tumour mass is believed to be a major cause of the clinical symptoms seen in patients with brain cancer. However, the biological consequences of these physical stresses on brain tissue are unknown. Here, via imaging studies in patients and by using mouse models of human brain tumours, we show that a subgroup of primary and metastatic brain tumours, classified as nodular on the basis of their growth pattern, exert solid stress on the surrounding brain tissue, causing a decrease in local vascular perfusion as well as neuronal death and impaired function. We demonstrate a causal link between solid stress and neurological dysfunction by applying and removing cerebral compression, which respectively mimic the mechanics of tumour growth and of surgical resection. We also show that, in mice, treatment with lithium reduces solid-stress-induced neuronal death and improves motor coordination. Our findings indicate that brain-tumour-generated solid stress impairs neurological function in patients, and that lithium as a therapeutic intervention could counter these effects.


Subject(s)
Brain Neoplasms/drug therapy , Brain Neoplasms/physiopathology , Lithium/therapeutic use , Stress, Physiological , Animals , Brain/diagnostic imaging , Brain/pathology , Brain/physiopathology , Brain Neoplasms/blood supply , Brain Neoplasms/diagnostic imaging , Cell Line, Tumor , Humans , Mice, Nude , Neurons/drug effects , Neurons/pathology , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Perfusion
5.
Proc Natl Acad Sci U S A ; 115(37): E8717-E8726, 2018 09 11.
Article in English | MEDLINE | ID: mdl-30150398

ABSTRACT

Blood-brain/blood-tumor barriers (BBB and BTB) and interstitial transport may constitute major obstacles to the transport of therapeutics in brain tumors. In this study, we examined the impact of focused ultrasound (FUS) in combination with microbubbles on the transport of two relevant chemotherapy-based anticancer agents in breast cancer brain metastases at cellular resolution: doxorubicin, a nontargeted chemotherapeutic, and ado-trastuzumab emtansine (T-DM1), an antibody-drug conjugate. Using an orthotopic xenograft model of HER2-positive breast cancer brain metastasis and quantitative microscopy, we demonstrate significant increases in the extravasation of both agents (sevenfold and twofold for doxorubicin and T-DM1, respectively), and we provide evidence of increased drug penetration (>100 vs. <20 µm and 42 ± 7 vs. 12 ± 4 µm for doxorubicin and T-DM1, respectively) after the application of FUS compared with control (non-FUS). Integration of experimental data with physiologically based pharmacokinetic (PBPK) modeling of drug transport reveals that FUS in combination with microbubbles alleviates vascular barriers and enhances interstitial convective transport via an increase in hydraulic conductivity. Experimental data demonstrate that FUS in combination with microbubbles enhances significantly the endothelial cell uptake of the small chemotherapeutic agent. Quantification with PBPK modeling reveals an increase in transmembrane transport by more than two orders of magnitude. PBPK modeling indicates a selective increase in transvascular transport of doxorubicin through small vessel wall pores with a narrow range of sizes (diameter, 10-50 nm). Our work provides a quantitative framework for the optimization of FUS-drug combinations to maximize intratumoral drug delivery and facilitate the development of strategies to treat brain metastases.


Subject(s)
Antineoplastic Combined Chemotherapy Protocols/administration & dosage , Blood-Brain Barrier/drug effects , Brain Neoplasms/drug therapy , Drug Delivery Systems/methods , Ado-Trastuzumab Emtansine , Animals , Antineoplastic Combined Chemotherapy Protocols/pharmacokinetics , Blood-Brain Barrier/metabolism , Brain/diagnostic imaging , Brain/metabolism , Brain/pathology , Brain Neoplasms/metabolism , Brain Neoplasms/secondary , Breast Neoplasms/drug therapy , Breast Neoplasms/metabolism , Breast Neoplasms/pathology , Cell Line, Tumor , Doxorubicin/administration & dosage , Doxorubicin/pharmacokinetics , Humans , Maytansine/administration & dosage , Maytansine/analogs & derivatives , Maytansine/pharmacokinetics , Mice , Microbubbles , Trastuzumab/administration & dosage , Trastuzumab/pharmacokinetics , Ultrasonography/methods , Xenograft Model Antitumor Assays
6.
Cancer Cell ; 33(5): 874-889.e7, 2018 05 14.
Article in English | MEDLINE | ID: mdl-29681511

ABSTRACT

Gliomas comprise heterogeneous malignant glial and stromal cells. While blood vessel co-option is a potential mechanism to escape anti-angiogenic therapy, the relevance of glial phenotype in this process is unclear. We show that Olig2+ oligodendrocyte precursor-like glioma cells invade by single-cell vessel co-option and preserve the blood-brain barrier (BBB). Conversely, Olig2-negative glioma cells form dense perivascular collections and promote angiogenesis and BBB breakdown, leading to innate immune cell activation. Experimentally, Olig2 promotes Wnt7b expression, a finding that correlates in human glioma profiling. Targeted Wnt7a/7b deletion or pharmacologic Wnt inhibition blocks Olig2+ glioma single-cell vessel co-option and enhances responses to temozolomide. Finally, Olig2 and Wnt7 become upregulated after anti-VEGF treatment in preclinical models and patients. Thus, glial-encoded pathways regulate distinct glioma-vascular microenvironmental interactions.


Subject(s)
Brain Neoplasms/blood supply , Glioma/blood supply , Oligodendrocyte Transcription Factor 2/metabolism , Oligodendroglia/microbiology , Wnt Proteins/metabolism , Animals , Bevacizumab/pharmacology , Blood-Brain Barrier/metabolism , Brain Neoplasms/drug therapy , Brain Neoplasms/metabolism , Cell Line, Tumor , Gene Expression Regulation, Neoplastic/drug effects , Glioma/drug therapy , Glioma/metabolism , Humans , Mice , Neoplasm Transplantation , Oligodendrocyte Transcription Factor 2/genetics , Temozolomide/pharmacology , Tumor Cells, Cultured , Tumor Microenvironment , Wnt Proteins/genetics , Wnt Signaling Pathway/drug effects
7.
Nat Rev Clin Oncol ; 15(5): 325-340, 2018 05.
Article in English | MEDLINE | ID: mdl-29508855

ABSTRACT

Immunotherapy has emerged as a major therapeutic modality in oncology. Currently, however, the majority of patients with cancer do not derive benefit from these treatments. Vascular abnormalities are a hallmark of most solid tumours and facilitate immune evasion. These abnormalities stem from elevated levels of proangiogenic factors, such as VEGF and angiopoietin 2 (ANG2); judicious use of drugs targeting these molecules can improve therapeutic responsiveness, partially owing to normalization of the abnormal tumour vasculature that can, in turn, increase the infiltration of immune effector cells into tumours and convert the intrinsically immunosuppressive tumour microenvironment (TME) to an immunosupportive one. Immunotherapy relies on the accumulation and activity of immune effector cells within the TME, and immune responses and vascular normalization seem to be reciprocally regulated. Thus, combining antiangiogenic therapies and immunotherapies might increase the effectiveness of immunotherapy and diminish the risk of immune-related adverse effects. In this Perspective, we outline the roles of VEGF and ANG2 in tumour immune evasion and progression, and discuss the evidence indicating that antiangiogenic agents can normalize the TME. We also suggest ways that antiangiogenic agents can be combined with immune-checkpoint inhibitors to potentially improve patient outcomes, and highlight avenues of future research.


Subject(s)
Neoplasms/drug therapy , Neovascularization, Pathologic/drug therapy , Vascular Endothelial Growth Factor A/immunology , Vesicular Transport Proteins/immunology , Angiogenesis Inhibitors/therapeutic use , Humans , Immunotherapy/trends , Neoplasms/immunology , Neovascularization, Pathologic/immunology , Tumor Microenvironment/drug effects , Tumor Microenvironment/immunology , Vascular Endothelial Growth Factor A/therapeutic use , Vesicular Transport Proteins/therapeutic use
8.
Cell Res ; 28(2): 221-248, 2018 Feb.
Article in English | MEDLINE | ID: mdl-29086765

ABSTRACT

The cerebral cortex is essential for integration and processing of information that is required for most behaviors. The exquisitely precise laminar organization of the cerebral cortex arises during embryonic development when neurons migrate successively from ventricular zones to coalesce into specific cortical layers. While radial glia act as guide rails for projection neuron migration, pre-formed vascular networks provide support and guidance cues for GABAergic interneuron migration. This study provides novel conceptual and mechanistic insights into this paradigm of vascular-neuronal interactions, revealing new mechanisms of GABA and its receptor-mediated signaling via embryonic forebrain endothelial cells. With the use of two new endothelial cell specific conditional mouse models of the GABA pathway (Gabrb3ΔTie2-Cre and VgatΔTie2-Cre), we show that partial or complete loss of GABA release from endothelial cells during embryogenesis results in vascular defects and impairs long-distance migration and positioning of cortical interneurons. The downstream effects of perturbed endothelial cell-derived GABA signaling are critical, leading to lasting changes to cortical circuits and persistent behavioral deficits. Furthermore, we illustrate new mechanisms of activation of GABA signaling in forebrain endothelial cells that promotes their migration, angiogenesis and acquisition of blood-brain barrier properties. Our findings uncover and elucidate a novel endothelial GABA signaling pathway in the CNS that is distinct from the classical neuronal GABA signaling pathway and shed new light on the etiology and pathophysiology of neuropsychiatric diseases, such as autism spectrum disorders, epilepsy, anxiety, depression and schizophrenia.


Subject(s)
Cerebral Cortex/embryology , Endothelial Cells/metabolism , GABAergic Neurons/physiology , Interneurons/physiology , gamma-Aminobutyric Acid/metabolism , Animals , Behavior, Animal , Cell Movement , Cerebral Cortex/blood supply , Cerebral Cortex/cytology , Female , Gene Expression Profiling , Male , Mice , Mice, Knockout , Mice, Transgenic , Models, Animal , Neurodevelopmental Disorders/etiology , Neurodevelopmental Disorders/physiopathology , Neurogenesis/physiology , Phenotype , Pregnancy , RNA/genetics , Receptors, GABA-A/physiology , Vesicular Inhibitory Amino Acid Transport Proteins/metabolism
9.
Article in English | MEDLINE | ID: mdl-29119058

ABSTRACT

For in vivo imaging, the short-wavelength infrared region (SWIR; 1000-2000 nm) provides several advantages over the visible and near-infrared regions: general lack of autofluorescence, low light absorption by blood and tissue, and reduced scattering. However, the lack of versatile and functional SWIR emitters has prevented the general adoption of SWIR imaging by the biomedical research community. Here, we introduce a class of high-quality SWIR-emissive indium-arsenide-based quantum dots (QDs) that are readily modifiable for various functional imaging applications, and that exhibit narrow and size-tunable emission and a dramatically higher emission quantum yield than previously described SWIR probes. To demonstrate the unprecedented combination of deep penetration, high spatial resolution, multicolor imaging and fast-acquisition-speed afforded by the SWIR QDs, we quantified, in mice, the metabolic turnover rates of lipoproteins in several organs simultaneously and in real time as well as heartbeat and breathing rates in awake and unrestrained animals, and generated detailed three-dimensional quantitative flow maps of the mouse brain vasculature.

10.
Sci Transl Med ; 9(391)2017 05 24.
Article in English | MEDLINE | ID: mdl-28539475

ABSTRACT

Although targeted therapies are often effective systemically, they fail to adequately control brain metastases. In preclinical models of breast cancer that faithfully recapitulate the disparate clinical responses in these microenvironments, we observed that brain metastases evade phosphatidylinositide 3-kinase (PI3K) inhibition despite drug accumulation in the brain lesions. In comparison to extracranial disease, we observed increased HER3 expression and phosphorylation in brain lesions. HER3 blockade overcame the resistance of HER2-amplified and/or PIK3CA-mutant breast cancer brain metastases to PI3K inhibitors, resulting in marked tumor growth delay and improvement in mouse survival. These data provide a mechanistic basis for therapeutic resistance in the brain microenvironment and identify translatable treatment strategies for HER2-amplified and/or PIK3CA-mutant breast cancer brain metastases.


Subject(s)
Brain Neoplasms/metabolism , Breast Neoplasms/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Receptor, ErbB-3/metabolism , Animals , Antineoplastic Agents/therapeutic use , Brain Neoplasms/drug therapy , Brain Neoplasms/secondary , Breast Neoplasms/complications , Breast Neoplasms/drug therapy , Female , Mice , Phosphoinositide-3 Kinase Inhibitors , Protein Kinase Inhibitors/therapeutic use , Receptor, ErbB-3/antagonists & inhibitors , Receptor, ErbB-3/genetics
11.
Proc Natl Acad Sci U S A ; 113(16): 4470-5, 2016 Apr 19.
Article in English | MEDLINE | ID: mdl-27044097

ABSTRACT

Glioblastomas (GBMs) rapidly become refractory to anti-VEGF therapies. We previously demonstrated that ectopic overexpression of angiopoietin-2 (Ang-2) compromises the benefits of anti-VEGF receptor (VEGFR) treatment in murine GBM models and that circulating Ang-2 levels in GBM patients rebound after an initial decrease following cediranib (a pan-VEGFR tyrosine kinase inhibitor) administration. Here we tested whether dual inhibition of VEGFR/Ang-2 could improve survival in two orthotopic models of GBM, Gl261 and U87. Dual therapy using cediranib and MEDI3617 (an anti-Ang-2-neutralizing antibody) improved survival over each therapy alone by delaying Gl261 growth and increasing U87 necrosis, effectively reducing viable tumor burden. Consistent with their vascular-modulating function, the dual therapies enhanced morphological normalization of vessels. Dual therapy also led to changes in tumor-associated macrophages (TAMs). Inhibition of TAM recruitment using an anti-colony-stimulating factor-1 antibody compromised the survival benefit of dual therapy. Thus, dual inhibition of VEGFR/Ang-2 prolongs survival in preclinical GBM models by reducing tumor burden, improving normalization, and altering TAMs. This approach may represent a potential therapeutic strategy to overcome the limitations of anti-VEGFR monotherapy in GBM patients by integrating the complementary effects of anti-Ang2 treatment on vessels and immune cells.


Subject(s)
Antibodies, Neoplasm/pharmacology , Glioblastoma , Macrophages , Neoplasm Proteins , Neoplasms, Experimental , Neovascularization, Pathologic , Quinazolines/pharmacology , Receptors, Vascular Endothelial Growth Factor , Ribonuclease, Pancreatic , Animals , Cell Line, Tumor , Drug Screening Assays, Antitumor , Glioblastoma/drug therapy , Glioblastoma/metabolism , Glioblastoma/pathology , Macrophages/metabolism , Macrophages/pathology , Mice , Neoplasm Proteins/antagonists & inhibitors , Neoplasm Proteins/metabolism , Neoplasms, Experimental/drug therapy , Neoplasms, Experimental/metabolism , Neoplasms, Experimental/pathology , Neovascularization, Pathologic/drug therapy , Neovascularization, Pathologic/metabolism , Neovascularization, Pathologic/pathology , Receptors, Vascular Endothelial Growth Factor/antagonists & inhibitors , Receptors, Vascular Endothelial Growth Factor/metabolism , Ribonuclease, Pancreatic/antagonists & inhibitors , Ribonuclease, Pancreatic/metabolism
12.
Proc Natl Acad Sci U S A ; 113(16): 4476-81, 2016 Apr 19.
Article in English | MEDLINE | ID: mdl-27044098

ABSTRACT

Inhibition of the vascular endothelial growth factor (VEGF) pathway has failed to improve overall survival of patients with glioblastoma (GBM). We previously showed that angiopoietin-2 (Ang-2) overexpression compromised the benefit from anti-VEGF therapy in a preclinical GBM model. Here we investigated whether dual Ang-2/VEGF inhibition could overcome resistance to anti-VEGF treatment. We treated mice bearing orthotopic syngeneic (Gl261) GBMs or human (MGG8) GBM xenografts with antibodies inhibiting VEGF (B20), or Ang-2/VEGF (CrossMab, A2V). We examined the effects of treatment on the tumor vasculature, immune cell populations, tumor growth, and survival in both the Gl261 and MGG8 tumor models. We found that in the Gl261 model, which displays a highly abnormal tumor vasculature, A2V decreased vessel density, delayed tumor growth, and prolonged survival compared with B20. In the MGG8 model, which displays a low degree of vessel abnormality, A2V induced no significant changes in the tumor vasculature but still prolonged survival. In both the Gl261 and MGG8 models A2V reprogrammed protumor M2 macrophages toward the antitumor M1 phenotype. Our findings indicate that A2V may prolong survival in mice with GBM by reprogramming the tumor immune microenvironment and delaying tumor growth.


Subject(s)
Antibodies, Bispecific/pharmacology , Antibodies, Neoplasm/pharmacology , Antineoplastic Agents/pharmacology , Glioblastoma/drug therapy , Macrophages/metabolism , Neoplasm Proteins/antagonists & inhibitors , Neoplasms, Experimental/drug therapy , Ribonuclease, Pancreatic/antagonists & inhibitors , Vascular Endothelial Growth Factor A/antagonists & inhibitors , Vesicular Transport Proteins/antagonists & inhibitors , Animals , Cell Line, Tumor , Glioblastoma/metabolism , Glioblastoma/pathology , Humans , Macrophages/pathology , Mice , Neoplasm Proteins/metabolism , Neoplasms, Experimental/metabolism , Neoplasms, Experimental/pathology , Ribonuclease, Pancreatic/metabolism , Vascular Endothelial Growth Factor A/metabolism , Vesicular Transport Proteins/metabolism , Xenograft Model Antitumor Assays
13.
J Natl Cancer Inst ; 108(2)2016 Feb.
Article in English | MEDLINE | ID: mdl-26547932

ABSTRACT

BACKGROUND: Central nervous system (CNS) metastases represent a major problem in the treatment of human epidermal growth factor receptor 2 (HER2)-positive breast cancer because of the disappointing efficacy of HER2-targeted therapies against brain lesions. The antibody-drug conjugate ado-trastuzumab emtansine (T-DM1) has shown efficacy in trastuzumab-resistant systemic breast cancer. Here, we tested the hypothesis that T-DM1 could overcome trastuzumab resistance in murine models of brain metastases. METHODS: We treated female nude mice bearing BT474 or MDA-MB-361 brain metastases (n = 9-11 per group) or cancer cells grown in organotypic brain slice cultures with trastuzumab or T-DM1 at equivalent or equipotent doses. Using intravital imaging, molecular techniques and histological analysis we determined tumor growth, mouse survival, cancer cell apoptosis and proliferation, tumor drug distribution, and HER2 signaling. Data were analyzed with one-way analysis of variance (ANOVA), Kaplan-Meier analysis, and Coefficient of Determination. All statistical tests were two-sided. RESULTS: T-DM1 delayed the growth of HER2-positive breast cancer brain metastases compared with trastuzumab. These findings were consistent between HER2-driven and PI3K-driven tumors. The activity of T-DM1 resulted in a survival benefit (median survival for BT474 tumors: 28 days for trastuzumab vs 112 days for T-DM1, hazard ratio = 6.2, 95% confidence interval = 6.1 to 85.84, P < .001). No difference in drug distribution or HER2-signaling was revealed between the two groups. However, T-DM1 led to a statistically significant increase in tumor cell apoptosis (one-way ANOVA for ApopTag, P < .001), which was associated with mitotic catastrophe. CONCLUSIONS: T-DM1 can overcome resistance to trastuzumab therapy in HER2-driven or PI3K-driven breast cancer brain lesions due to the cytotoxicity of the DM1 component. Clinical investigation of T-DM1 for patients with CNS metastases from HER2-positive breast cancer is warranted.


Subject(s)
Antibodies, Monoclonal, Humanized/pharmacology , Antineoplastic Agents/pharmacology , Biomarkers, Tumor/analysis , Brain Neoplasms/drug therapy , Brain Neoplasms/secondary , Breast Neoplasms/pathology , Maytansine/analogs & derivatives , Receptor, ErbB-2/analysis , Ado-Trastuzumab Emtansine , Animals , Antibodies, Monoclonal, Humanized/administration & dosage , Antineoplastic Agents/administration & dosage , Apoptosis/drug effects , Blotting, Western , Brain Neoplasms/chemistry , Breast Neoplasms/chemistry , Cell Proliferation/drug effects , Drug Administration Schedule , Drug Resistance, Neoplasm , Female , Gene Expression Profiling , Kaplan-Meier Estimate , Maytansine/administration & dosage , Maytansine/pharmacology , Mice , Mice, Nude , Microarray Analysis , Microscopy, Electron , Odds Ratio , Trastuzumab , Xenograft Model Antitumor Assays
14.
J Plast Reconstr Aesthet Surg ; 61(10): 1170-6, 2008 Oct.
Article in English | MEDLINE | ID: mdl-18639513

ABSTRACT

BACKGROUND: A lack of scientific data about the complex three dimensional changes in relation to the rest of the face is the reason for the multitude of rejuvenation approaches to the aging upper lip. In this study the underlying anatomic changes and facial proportions of the senile upper lip are scientifically evaluated for the first time. METHODS: (1) In 182 standardized subject photographs proportions of the upper lip were measured, compared to facial dimensions and correlated to age. (2) In cranial MRI scans of 30 women aged 20-35 and 30 women aged 65-80 relevant anatomical dimensions were measured. RESULTS: Both studies showed a statistically significant lengthening of the aging upper lip. The photomorphometric study further shows an increase of prolabium skin at the cost of a decreasing visible upper lip vermilion. The MRI scans showed a decrease in thickness. A loss of volume could not be shown. CONCLUSION: Isolated volume augmentation is not a causal method of upper lip rejuvenation and it may therefore rather lead to an unnatural 'blown up' look.


Subject(s)
Aging/physiology , Lip/anatomy & histology , Skin Aging/physiology , Adolescent , Adult , Aged , Aged, 80 and over , Anthropometry , Child , Child, Preschool , Face/anatomy & histology , Female , Humans , Image Processing, Computer-Assisted , Magnetic Resonance Imaging , Male , Middle Aged
SELECTION OF CITATIONS
SEARCH DETAIL
...