Results 91 to 100 of about 53,346 (263)

Complicações em reconstrução mamária total em pacientes mastectomizadas por câncer de mama: análise comparativa de longo prazo quanto a influência de técnica, tempo de cirurgia, momento da reconstrução e tratamento adjuvante

open access: yesRevista Brasileira de Cirurgia Plástica
INTRODUÇÃO: Algumas técnicas de reconstrução total de mama, independentemente de sua complexidade, apresentam complicações específicas, com diferentes graus de morbidade.
Francisco Claro Jr.   +3 more
doaj   +1 more source

Antigen Spreading via Localized Administration Enhances Adoptive TCR‐T Cell Therapy in Pancreatic Cancer

open access: yesAdvanced Science, EarlyView.
Cancer vaccines face limitations in pancreatic cancer due to insufficient tumor antigens. This ionic liquid ILvax via local tumor delivery triggers robust cDC1‐dependent systemic anti‐tumor immunity. It boosts endogenous CD8+ T cells and optimizes adoptive TCR‐T function, providing a promising synergistic therapeutic strategy.
Junming Huang   +11 more
wiley   +1 more source

Aumento mamário por meio da incisão da abdominoplastia: estudo prospectivo de 100 casos

open access: yesRevista Brasileira de Cirurgia Plástica
INTRODUÇÃO: A gravidez e a obesidade causam distensão da parede abdominal e também produzem mudanças na forma e no tamanho das mamas. Assim, não é incomum a necessidade de melhoria estética da área abdominal, coincidindo com o desejo de aumento de mama ...
Gal Moreira Dini   +6 more
doaj   +1 more source

Breast implant illness after reconstruction with silicone breast implants

open access: yesJNCI: Journal of the National Cancer Institute
Abstract Background “Breast implant illness” (BII) is a constellation of non-specific constitutional, rheumatologic, mental, and cognitive symptoms reported increasingly by women carrying silicone breast implants (SBIs).
Jonathan Spoor   +18 more
openaire   +7 more sources

Single‐Cell RNA Editing Identifies T Cell ADAR1 as a Key Regulator of Immune Exhaustion and Anti‐PD‐1 Resistance in Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
Single‐cell RNA editing analysis identifies ADAR1 as a regulator of dysfunctional T cell states in colorectal cancer. Elevated ADAR1 activity promotes T cell exhaustion and impairs antitumor immunity partly through TGF‐β‐SMAD signaling, contributing to anti‐PD‐1 resistance and highlighting T cell ADAR1 as a potential therapeutic target and biomarker ...
Da Kang   +10 more
wiley   +1 more source

Inhibition of KDEL Receptors Remodels the Tumor Microenvironment for T Cell Independent Tumor Regression

open access: yesAdvanced Science, EarlyView.
Inhibition of KDELR2 in a small fraction of tumor cells generates sustainable immunogenic cell death conditions within the tumor microenvironment. These conditions promote the regression of tumors in a T cell independent manner. During regression, macrophages prime T cells that subsequently provide systemic protection against recurrence. The potency of
Shakti P Pattanayak   +6 more
wiley   +1 more source

Neuron‐Derived MIF Engages VCAM1 to Fuel a Self‐Amplifying CXCL8 Loop That Drives Perineural Invasion and Metastasis in Gastric Cancer

open access: yesAdvanced Science, EarlyView.
Neuron‐derived MIF binds VCAM1 on gastric cancer cells and activates ERK/STAT3 signaling, leading to CXCL8 transcription and secretion. Tumor‐derived CXCL8 subsequently stimulates neuronal CXCR2 to enhance MIF production, establishing a self‐amplifying MIF–VCAM1–CXCL8 positive‐feedback loop that promotes perineural invasion, tumor progression, and ...
Xunjun Li   +13 more
wiley   +1 more source

RBM12 Maintains Glioma Stem Cells by Activating Amino Acid‐Dependent mTORC1 Signaling via SLC7A5 mRNA Stabilization

open access: yesAdvanced Science, EarlyView.
This study shows that in glioma stem cells (GSCs), RBM12 recruits ALKBH5 to remove m6A from SLC7A5 transcripts, thereby enhancing mRNA stability, which elevates large neutral amino acid (LNAA) levels and activates mTORC1, promoting GSC proliferation, self‐renewal, and tumor growth.
Hong Lei   +18 more
wiley   +1 more source

DHODH Drives Sunitinib Resistance Via a Non‐Enzymatic Mechanism by Inhibiting TRIM28 Ubiquitination and Consequent VEGFA Activation in RCC

open access: yesAdvanced Science, EarlyView.
This non‑enzymatic function of DHODH drives sunitinib resistance by competing with TRIM37 to block TRIM28 ubiquitination, thereby stabilizing TRIM28 and activating VEGFA transcription. Disrupting the DHODH–TRIM28 interaction with lisaftoclax restores drug sensitivity.
Shijie Qian   +10 more
wiley   +1 more source

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