The nonsmokers' and smokers' pathways in lung adenocarcinoma: Histological progression and molecular bases.
Reads0
Chats0
TLDR
In this paper, the authors describe the two pathways with special reference to potential relationships between histological subtypes, malignant grades, and driver mutations, and show that the non-smokers' pathway is mostly driven by EGFR mutations, whereas in the smokers' pathway, approximately one-quarter of LADCs have KRAS mutations, but the other three-quarters have no known driver mutations.Abstract:
There could be two carcinogenetic pathways for lung adenocarcinoma (LADC), that are, the non-smokers' pathway and the smokers' pathway. This review article describes the two pathways with special reference to potential relationships between histological subtypes, malignant grades, and driver mutations. The lung is composed of two different tissue units, the terminal respiratory unit (TRU) and the central airway compartment (CAC). In the non-smokers' pathway, LADCs develop from the TRU, and their histological appearances change from lepidic to micropapillary during the progression process. In the smokers' pathway, LADCs develop from either the TRU or the CAC, and their histological appearances vary among cases in the middle of the progression process, but they are likely converged to acinar/solid at the end. On a molecular genetic level, the non-smokers' pathway is mostly driven by EGFR mutations, whereas in the smokers' pathway, approximately one-quarter of LADCs have KRAS mutations, but the other three-quarters have no known driver mutations. p53 mutations are an important factor triggering the progression of both pathways, with unique molecular alterations associated with each, such as MUC21 expression, chromosome 12p13-21 amplification in the non-smokers' pathway, and HNF4α expression and TTF1 mutations in the smokers' pathway. However, investigation into the relationship between histological progression and genetic alterations is in its infancy. Tight cooperation between traditional histopathological examinations and recent molecular genetics can provide valuable insight into better understanding the nature of LADCs.read more
Citations
More filters
Journal ArticleDOI
Crosstalk between H1975 tumor cells and platelets to induce the proliferation, migration and tube formation of vascular endothelial cells.
TL;DR: In this paper, the authors investigated the impact of H1975 cell crosstalk with activated platelets (PLTs) on the proliferation, migration and tube formation of HUVECs and concluded that tumor cells interacting with PLTs may play an important role in tumor angiogenesis by affecting or mediating changes in the properties of vascular endothelial cells.
Journal ArticleDOI
Chronic Progression of Lung Cancer Recurrence After Surgery: Warning Role of Postoperative Pneumonia
Dong-qi Lin,Jin-guo Zhu,Xiao-hua Xu,Ke Xiao,Xu-qing Wen,Qi-fa Zheng,Yu-hua Zhou,Xin-ying Cai +7 more
TL;DR: Postoperative pulmonary inflammation assessed 4 months post-surgery also significantly influenced LRO development, indicating a need for close follow-up of lung inflammatory conditions to improve patient outcomes.
Journal ArticleDOI
Ttc39c is a potential target for the treatment of lung cancer
TL;DR: In this article , the effect of tetratricopeptide repeat domain 39 C (Ttc39c) gene subtraction on lung adenocarcinoma was investigated. And the authors found that Ttc39C strongly regulates the proliferation and metastasis of lung cancer cells.
Journal ArticleDOI
Constructing a Prognostic Gene Signature for Lung Adenocarcinoma Based on Weighted Gene Co-Expression Network Analysis and Single-Cell Analysis
TL;DR: Wang et al. as mentioned in this paper used WGCNA to identify the most relevant modules and important cell subpopulations (clusters) in lung adenocarcinoma (LUAD) tissues, and constructed molecular subtypes by unsupervised consensus clustering based on genes in key modules.
Journal ArticleDOI
Anoikis-related genes combined with single cell sequencing: Insights into model specification of lung adenocarcinoma and applicability for prognosis and therapy
Yiyi Zhou,Zhenli Hu +1 more
TL;DR: In this paper , the authors used anoikis and bioinformatics to construct a prognostic model for lung adenocarcinoma and explore new therapeutic strategies.
References
More filters
Journal ArticleDOI
Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer
Manabu Soda,Young Lim Choi,Munehiro Enomoto,Shuji Takada,Yoshihiro Yamashita,Shunpei Ishikawa,Shin-ichiro Fujiwara,Hideki Watanabe,Kentaro Kurashina,Hisashi Hatanaka,Masashi Bando,Shoji Ohno,Yuichi Ishikawa,Hiroyuki Aburatani,Toshiro Niki,Yasunori Sohara,Yukihiko Sugiyama,Hiroyuki Mano +17 more
TL;DR: It is shown that a small inversion within chromosome 2p results in the formation of a fusion gene comprising portions of the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene in non-small-cell lung cancer (NSCLC) cells.
Journal ArticleDOI
Tracking the Evolution of Non–Small-Cell Lung Cancer
Mariam Jamal-Hanjani,Gareth A. Wilson,Nicholas McGranahan,Nicolai Juul Birkbak,Thomas B.K. Watkins,Selvaraju Veeriah,Seema Shafi,Diana Johnson,Richard Mitter,Rachel Rosenthal,Max Salm,Stuart Horswell,Mickael Escudero,Nik Matthews,Andrew Rowan,Tim Chambers,David A. Moore,Samra Turajlic,Hang Xu,Siow Ming Lee,Martin Forster,Tanya Ahmad,Crispin T. Hiley,Christopher Abbosh,Mary Falzon,Elaine Borg,Teresa Marafioti,David Lawrence,Martin Hayward,Shyam Kolvekar,Nikolaos Panagiotopoulos,Sam M. Janes,Ricky Thakrar,Asia Ahmed,Fiona H Blackhall,Yvonne Summers,Rajesh Shah,Leena Dennis Joseph,Anne Marie Quinn,Phil Crosbie,Babu Naidu,Gary Middleton,Gerald Langman,Simon Trotter,Marianne Nicolson,Hardy Remmen,Keith Kerr,Mahendran Chetty,Lesley Gomersall,Dean A. Fennell,Apostolos Nakas,Sridhar Rathinam,Girija Anand,Sajid A. Khan,Peter Russell,Veni Ezhil,Babikir Ismail,Melanie Irvin-Sellers,Vineet Prakash,Jason F. Lester,Malgorzata Kornaszewska,Richard Attanoos,Haydn Adams,Helen Davies,Stefan C. Dentro,Philippe Taniere,Brendan O'Sullivan,Helen Lowe,John A. Hartley,Natasha Iles,Harriet Bell,Yenting Ngai,Jacqui Shaw,Javier Herrero,Zoltan Szallasi,Roland F. Schwarz,Aengus Stewart,Sergio A. Quezada,John Le Quesne,Peter Van Loo,Caroline Dive,Allan Hackshaw,Charles Swanton +82 more
TL;DR: Intratumor heterogeneity mediated through chromosome instability was associated with an increased risk of recurrence or death, a finding that supports the potential value of chromosome instability as a prognostic predictor.
Journal ArticleDOI
Mutations of the Epidermal Growth Factor Receptor Gene in Lung Cancer Biological and Clinical Implications
Takayuki Kosaka,Yasushi Yatabe,Hideki Endoh,Hiroyuki Kuwano,Takashi Takahashi,Tetsuya Mitsudomi +5 more
TL;DR: Exons 18–21 of the tyrosine kinase domain of the epidermal growth factor receptor(EGFR) gene define a distinct subset of pulmonary adenocarcinoma without KRAS mutations, which is not caused by tobacco carcinogens.
Journal ArticleDOI
KIF5B-RET fusions in lung adenocarcinoma.
Takashi Kohno,Hitoshi Ichikawa,Yasushi Totoki,Kazuki Yasuda,Masaki Hiramoto,Takao Nammo,Hiromi Sakamoto,Koji Tsuta,Koh Furuta,Yoko Shimada,Reika Iwakawa,Hideaki Ogiwara,Takahiro Oike,Masato Enari,Aaron J. Schetter,Hirokazu Okayama,Aage Haugen,Vidar Skaug,Suenori Chiku,Itaru Yamanaka,Yasuhito Arai,Shun-ichi Watanabe,Ikuo Sekine,Seishi Ogawa,Curtis C. Harris,Hitoshi Tsuda,Teruhiko Yoshida,Jun Yokota,Tatsuhiro Shibata +28 more
TL;DR: In-frame fusion transcripts of KIF5B (the kinesin family 5B gene) and the RET oncogene are identified and a RET tyrosine kinase inhibitor, vandetanib, suppresses the fusion-induced anchorage-independent growth activity of NIH3T3 cells.
Journal ArticleDOI
ALK Rearrangements Are Mutually Exclusive with Mutations in EGFR or KRAS: An Analysis of 1,683 Patients with Non–Small Cell Lung Cancer
Justin F. Gainor,Anna M. Varghese,Sai-Hong Ignatius Ou,Sheheryar Kabraji,Mark M. Awad,Ryohei Katayama,Amanda C. Pawlak,Mari Mino-Kenudson,Beow Y. Yeap,Gregory J. Riely,A. John Iafrate,Maria E. Arcila,Marc Ladanyi,Jeffrey A. Engelman,Dora Dias-Santagata,Alice T. Shaw +15 more
TL;DR: Functional ALK rearrangements were mutually exclusive with EGFR and KRAS mutations in a large Western patient population, and this lack of overlap was also observed in ALK-positive cancers with acquired resistance to crizotinib.