Risultati per: Scoperta una nuova molecola anti-cancro

This qualitative study assesses the association of anti-Asian hate with older Asian individuals’ health and the clinician’s role in addressing hate incidents.

New England Journal of Medicine, Volume 390, Issue 23, Page 2178-2190, June 20, 2024.

Background
Primary dysmenorrhoea occurs in up to 50% of menstruating females. Non-steroidal anti-inflammatory drugs (NSAIDs) are the most commonly used therapeutic remedies for dysmenorrhoea in Uganda. However, NSAIDs are associated with a 3–5 fold increase in the risk of gastrointestinal (GI) adverse drug effects.

Objectives
We aimed to determine the prevalence and associated factors of self-reported NSAID-related GI adverse effects in female students who use NSAIDs in managing dysmenorrhoea-associated pain at Makerere University.

Design
A cross-sectional study.

Setting
Makerere University’s main campus, situated North of Kampala, Uganda.

Participants
314 female students pursuing an undergraduate programme at Makerere University and residing in different halls of residence and hostels.

Outcomes
Social demographic data, menstrual history and treatment data.

Results
Overall, 314 valid responses were received from female students with a median age of 22 years (IQR: 18–29 years). The median age at menarche was 13 years (IQR: 9–18 years). 41% (n=129/314) of the respondents had used medication for dysmenorrhoea and 32% (n=41/129) of whom reported NSAID-associated GI adverse effects with nausea being the most frequently reported (44%, n=18/41)
Factors independently associated with GI adverse effects were: age at menarche (p=0.026), duration of menstruation (p=0.030) and use of ibuprofen (p=0.005). Females taking ibuprofen for dysmenorrhoea were about four times as likely to have NSAID-associated GI adverse effects (adjusted OR 3.87, 95% CI 1.51 to 9.91) than those who did not receive ibuprofen. Logistic regression was used to determine factors associated with self-reported adverse effects of NSAIDs among the female students. A p

This cohort study describes the clinical features, patient characteristics, and treatment of anti-melanoma differentiation–associated gene 5 (MDA5) dermatomyositis.

Il farmaco semaglutide è la punta dell’iceberg che potrebbe funzionare anche sulle patologie del fegato e dei reni, fino all’Alzheimer. Allo studio c’è anche l’insulina smart e termostabile

Ecco come cambiano i multipli del settore in Borsa: gli analisti guardano al futuro dei prodotti per l’oncologia in un mercato da 440 miliardi

A distanza di un mese l’uno dall’altro, due centri di ricerca britannici hanno identificato un serie di proteine nel sangue che segnalano in anticipo la diagnosi di tumore

A distanza di un mese l’uno dall’altro, due centri di ricerca britannici hanno identificato un serie di proteine nel sangue che segnalano in anticipo la diagnosi di tumore

New England Journal of Medicine, Volume 390, Issue 19, Page 1827-1829, May 16/23, 2024.

Objective
The gain of function (GOF) CTNNB1 mutations (CTNNB1 GOF ) in hepatocellular carcinoma (HCC) cause significant immune escape and resistance to anti-PD-1. Here, we aimed to investigate the mechanism of CTNNB1 GOF HCC-mediated immune escape and raise a new therapeutic strategy to enhance anti-PD-1 efficacy in HCC.

Design
RNA sequencing was performed to identify the key downstream genes of CTNNB1 GOF associated with immune escape. An in vitro coculture system, murine subcutaneous or orthotopic models, spontaneously tumourigenic models in conditional gene-knock-out mice and flow cytometry were used to explore the biological function of matrix metallopeptidase 9 (MMP9) in tumour progression and immune escape. Single-cell RNA sequencing and proteomics were used to gain insight into the underlying mechanisms of MMP9.

Results
MMP9 was significantly upregulated in CTNNB1 GOF HCC. MMP9 suppressed infiltration and cytotoxicity of CD8+ T cells, which was critical for CTNNB1 GOF to drive the suppressive tumour immune microenvironment (TIME) and anti-PD-1 resistance. Mechanistically, CTNNB1 GOF downregulated sirtuin 2 (SIRT2), resulting in promotion of β-catenin/lysine demethylase 4D (KDM4D) complex formation that fostered the transcriptional activation of MMP9. The secretion of MMP9 from HCC mediated slingshot protein phosphatase 1 (SSH1) shedding from CD8+ T cells, leading to the inhibition of C-X-C motif chemokine receptor 3 (CXCR3)-mediated intracellular of G protein-coupled receptors signalling. Additionally, MMP9 blockade remodelled the TIME and potentiated the sensitivity of anti-PD-1 therapy in HCC.

Conclusions
CTNNB1 GOF induces a suppressive TIME by activating secretion of MMP9. Targeting MMP9 reshapes TIME and potentiates anti-PD-1 efficacy in CTNNB1 GOF HCC.