Results 101 to 110 of about 2,086,066 (301)

Keratin 19 as a prognostic marker and contributing factor of metastasis and chemoresistance in high‐grade serous ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Keratin 19 (KRT19) is overexpressed in high‐grade serous ovarian cancer with high levels of Kallikrein‐related peptidases (KLK) 4–7 and is associated with poor survival. In vivo analyses demonstrate that elevated KRT19 increases peritoneal tumour burden.
Sophia Bielesch   +13 more
wiley   +1 more source

Vascular Niche in Lung Alveolar Development, Homeostasis, and Regeneration

open access: yesFrontiers in Bioengineering and Biotechnology, 2019
Endothelial cells (ECs) constitute small capillary blood vessels and contribute to delivery of nutrients, oxygen and cellular components to the local tissues, as well as to removal of carbon dioxide and waste products from the tissues.
Akiko Mammoto   +2 more
doaj   +1 more source

Establishment of a humanized patient‐derived xenograft mouse model of high‐grade serous ovarian cancer for preclinical evaluation of combination immunotherapy

open access: yesMolecular Oncology, EarlyView.
We have established a humanized orthotopic patient‐derived xenograft (Hu‐oPDX) mouse model of high‐grade serous ovarian cancer (HGSOC) that recapitulates human tumor–immune interactions. Using combined anti‐PD‐L1/anti‐CD73 immunotherapy, we demonstrate the model's improved biological relevance and enhanced translational value for preclinical ...
Luka Tandaric   +10 more
wiley   +1 more source

Differential and Temporal Immunomodulation of alpha4 Integrins on CD4+ Memory Cells by Bordetella pertussis and Bordetella parapertussis [PDF]

open access: yes, 2012
Pertussis, caused by Bordetella pertussis (B. pertussis), is reemerging worldwide due to vaccine inefficacy. The hallmarks of infection are extreme lymphocytosis and delayed recovery, which are partially associated with pertussis toxin.
Ravindra, Dipti
core   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov   +3 more
wiley   +1 more source

Persistent lineage plasticity driving lung cancer development and progression

open access: yesClinical and Translational Medicine
Background Lung cancer, a leading cause of cancer death, displays profound histologic and molecular heterogeneity across adenocarcinoma, squamous, and small‐cell types. Clinically, tumours can shift between these states, reflecting lineage plasticity—the
Fanchen Meng   +7 more
doaj   +1 more source

Estimating The Annual Cost of Smoking-Related Diseases in Indonesia [PDF]

open access: yes, 2009
Background: Smoking plays a role in the development of chronic diseases and causes substantial negative economic consequences. This study was carried out to estimate the annual cost of smoking-related cardio-cerebrovascular and pulmonary diseases in ...
Hudoyo, Ahmad   +6 more
core   +1 more source

CD47 promotes mitogen‐activated protein kinase and epithelial‐to‐mesenchymal transition molecular programs to drive prometastatic phenotypes in non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Beyond its role in immune evasion, this study identified that CD47 drives tumor‐intrinsic signaling in non‐small cell lung cancer (NSCLC). Transcriptomic profiling and functional studies revealed that CD47 regulates cell adhesion, migration, and metastasis through an ERK–EMT signaling axis.
Asa P.Y. Lau   +8 more
wiley   +1 more source

Chronic obstructive pulmonary disease: a complex comorbidity of lung cancer [PDF]

open access: yes
Chronic obstructive pulmonary disease (COPD) is a major burden throughout the world. It is associated with a significantly increased incidence of lung cancer and may influence treatment options and outcome.
Grose, Derek, Milroy, Robert
core   +2 more sources

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

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