Results 71 to 80 of about 4,921,476 (300)

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

Molecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Metastasis on pause: How dormant tumor cells stay hidden within the tumor microenvironment and evade immune surveillance

Molecular Oncology, EarlyView.
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary, Jose Javier Bravo‐Cordero   +1 more
wiley   +1 more source

Aerosolized BC-819 inhibits primary but not secondary lung cancer growth. [PDF]

, 2011
Despite numerous efforts, drug based treatments for patients suffering from lung cancer remains poor. As a promising alternative, we investigated the therapeutic potential of BC-819 for the treatment of lung cancer in mouse tumor models.
Corinna Pfeifer, Patricia Ohana, Wagner Kai, Carsten Rudolph, Aneja, Manish Kumar, Gilon, Michal, Hochberg, Avraham, Pfeifer, Corinna, Ohana, Patricia, Hasenpusch, Günther, Kai Wagner, Günther Hasenpusch, Gilon Michal, Ohana Patricia, Rudolph, Carsten, Michal Gilon, Hasenpusch Günther, Manish Kumar Aneja, Pfeifer Corinna, Avraham Hochberg, Reinhardt Dietrich, Wagner, Kai, Reinhardt, Dietrich, Aneja Manish Kumar, Hochberg Avraham, Rudolph Carsten, Dietrich Reinhardt   +26 more
core   +2 more sources

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

Molecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska, Stephany Gallardo, Nur S. Zainal, Leena Arora, Matthew Ellis, Maria‐Antoinette Lopez, Judith Austine, Sai Pittla, Serena J Chee, Aiman Alzetani, Emily C Shaw, Christian H Ottensmeier, Gareth J Thomas, Christopher J Hanley   +13 more
wiley   +1 more source

Mesenchymal stem cells as vectors for lung cancer therapy [PDF]

, 2013
Despite recent advances in treatment, lung cancer accounts for one third of all cancer-related deaths, underlining the need of development of new therapies.
Laurent, GJ, Janes, SM, Kolluri, KK
core  

Longer telomere length in peripheral white blood cells is associated with risk of lung cancer and the rs2736100 (CLPTM1L-TERT) polymorphism in a prospective cohort study among women in China. [PDF]

, 2013
A recent genome-wide association study of lung cancer among never-smoking females in Asia demonstrated that the rs2736100 polymorphism in the TERT-CLPTM1L locus on chromosome 5p15.33 was strongly and significantly associated with risk of adenocarcinoma ...
Xiang, Y, Hu W, Ji, BT, Wei Hu, Cai, Q, Chanock, S, Berndt S, Lan Qing, Hosgood, HD, H Dean Hosgood, Hu Wei, Kim Christopher, Cai Qiuyin, Shu X, Richard Cawthon, Barone-Adesi Francesco, Rothman Nathaniel, Cawthon R, Gao, Y, Sonja Berndt, Zheng Wei, Wong-Ho Chow, Chow WH, Stephen Chanock, BARONE ADESI, Francesco, Zheng W, Francesco Barone-Adesi, Bassig B, Yutang Gao, Berndt Sonja, Kim, C, Lan Q, Gao Y, Bryan Bassig, Hu, W, Rothman N., Berndt, S, Cawthon, R, Xiang Yongbin, Kim C, Christopher Kim, Cai Q, Yongbin Xiang, Xiaoou Shu, Bassig, B, Chanock Stephen, Chanock S, Shu Xiaoou, Chow Wong-Ho, Ji Bu-Tian, Barone-Adesi, F, Gao Yutang, Bassig Bryan, Shu, X, Qing Lan, Qiuyin Cai, Zheng, W, Rothman, N, Nathaniel Rothman, Hosgood H. Dean, Wei Zheng, Bu-Tian Ji, Chow, WH, Ji BT, Hosgood HD 3rd, Cawthon Richard, Xiang Y, Lan, Q   +67 more
core   +2 more sources

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

Molecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura, Tadahiro Kuribayashi, Johannes Brägelmann, Sachi Okawa, Masataka Taoka, Shunta Mori, Tomoka Nishimura, Takaaki Tanaka, Go Makimoto, Kiichiro Ninomiya, Kammei Rai, Eiki Ichihara, Ryohei Katayama, Katsuyuki Hotta, Masahiro Tabata, Yosuke Togashi, Yoshinobu Maeda, Martin L. Sos, Katsuyuki Kiura, Kadoaki Ohashi   +19 more
wiley   +1 more source

Multifunctional role of PED/PEA15 in cell death and cell motility in human non small cell lung cancer (NSCLC) [PDF]

, 2009
PED (phosphoprotein enriched in diabetes) is a 15 KDa protein involved in many cellular pathways and human diseases, including type II diabetes and cancer. We recently reported its overexpression in breast and lung cancers, and B-cell chronic lymphocytic
Zanca, Ciro
core   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer [PDF]

Mol Oncol
Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Guerrero‐Alba A, Shacker M, Fleming T, Smith M, Bremner R, Sankpal N.   +5 more
europepmc   +2 more sources