BRIIL-2 is a clinical study for evaluation of efficacy and toxicity of third line treatment of pulmonary metastasis from renal cancer and melanoma with flexible bronchoscopic istillation of IL-2. Moreover, we evaluate local (BALT) and peripheral lymphocytic activation during this IL-2 administration. Up today we enrolled two patients with pulmonary metastasis from renal cancer already treated with two lines of molecular therapy, chemotherapy or systemic immunotherapy. Regarding to immunologic stimulation, lymphocytic fraction decreased from 21 to 2% in the first and from 10.5 to 6% in the second patient, indicating lymphocytic enrollment for activation, while TCD4/CD8 ratio is stable. In both patients we also observed a significant increase of HLA-DR in T lymphocytes (CD3) either in BAL or in peripheral blood. No significant major toxicities were observed after broncho-istillation, even if the dose was progressively increased. Thus IL-2 broncho-istillation could represent a valid administration modality to obtain an effective immunologic stimulation either local or systemic.

Download full-text PDF

Source

Publication Analysis

Top Keywords

pulmonary metastasis
12
metastasis renal
12
renal cancer
12
bronchoscopic istillation
8
treatment pulmonary
8
immunologic stimulation
8
[il-2 bronchoscopic
4
istillation immune
4
immune cell
4
cell activation
4

Similar Publications

Targeting the ERK1/2 and p38 MAPK pathways attenuates Golgi tethering factor golgin-97 depletion-induced cancer progression in breast cancer.

Cell Commun Signal

January 2025

Department of Cell and Molecular Biology, College of Medicine, Chang Gung University, 259 Wen-Hwa 1 road, Guishan District, Taoyuan, Taiwan.

Background: The Golgi apparatus is widely considered a secretory center and a hub for different signaling pathways. Abnormalities in Golgi dynamics can perturb the tumor microenvironment and influence cell migration. Therefore, unraveling the regulatory network of the Golgi and searching for pharmacological targets would facilitate the development of novel anticancer therapies.

View Article and Find Full Text PDF

[Savolitinib Induced Pathological Complete Response in Non-small Cell Lung Cancer with MET Amplification: A Case Report].

Zhongguo Fei Ai Za Zhi

November 2024

Department of Pulmonary Oncology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin 300000, China.

Mesenchymal-epithelial transition factor (MET) gene mutation is a large class of mutations commonly seen in non-small cell lung cancer (NSCLC). MET mutation includes subtypes such as MET exon 14 skipping mutation (METex14m) and MET amplification (METamp). For advanced NSCLC with METex14m, Savolitinib has a high sensitivity as a member of tyrosine kinase inhibitors (TKIs).

View Article and Find Full Text PDF

Background: The early stages of tumor bone metastasis are closely associated with changes in the vascular niche of the bone microenvironment, and abnormal angiogenesis accelerates tumor metastasis and progression. However, the effects of lung adenocarcinoma (LUAD) cells reprogrammed by the bone microenvironment on the vascular niche within the bone microenvironment and the underlying mechanisms remain unclear. This study investigates the effects and mechanisms of LUAD cells reprogrammed by the bone microenvironment on endothelial cells and angiogenesis, providing insights into the influence of tumor cells on the vascular niche within the bone microenvironment.

View Article and Find Full Text PDF

Pralsetinib demonstrated impressive improvement of survival in non-small cell lung cancer (NSCLC) patients harbored de novo RET fusion. However, the efficacy in patients with acquired RET fusion after resistance to EGFR/ALK-TKIs has only been reported on a case-by-case basis, and the strategy for overcoming the acquired RET fusion has not been fully investigated. This multicenter, real-world analysis enrolled 32 patients with unresectable NSCLC harbored acquired RET fusion after resistance to EGFR/ALK-TKIs in 23 centers across China from July 1, 2018 to Nov 23, 2022.

View Article and Find Full Text PDF

Mycobacterium tuberculosis (M. tuberculosis) bacteria can cause oxidative stress and the production of inflammatory cytokines, creating an environment that enhances tumour formation, progression and metastasis. Epidemiological studies have found a link between lung cancer and tuberculosis (TB), but the cellular mechanism is still unclear.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!