Never-smoking women with lung cancer from the Spanish WORLD07 database.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 1531-1531 ◽  
Author(s):  
Dolores Isla ◽  
Mariano Provencio ◽  
Margarita Majem ◽  
Enriqueta Felip ◽  
Nuria Vinolas ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Contraceptive Use ◽  
Previous History ◽  
Stage Iv ◽  
Egfr Mutations ◽  
Malignant Tumours ◽  
Treatment Data ◽  
History Of ◽  
Egfr Tki ◽  
History Of Cancer

1531 Background: Gender differences in lung cancer (LC) have been reported, but with many unresolved issues yet. Tobacco causes the majority of women lung cancer (WLC), although the rate of never-smoking WLC is higher than in men. Several factors may play etiologic roles, and an in-depth understanding is needed. Methods: WORLD07 is a Spanish prospective, multicenter, epidemiologic female-specific LC database sponsored by ICAPEM, a professional association committed with WLC research. In order to improve the knowledge on never-smoking WLC, information has been extracted from WORLD07 database. Results: From October/2007 to October/2011, 1371 newly diagnosed WLC were included in an e-database from 32 centers, 539 (39.3%) never-smoking. Patient (p) characteristics: median age 71.1 years(y); median age of menarche 13y.; motherhood 91.2% (median 2.3 children, median age at first child 26.4y); oral contraceptive use 11.9%; postmenopausal 88.9% (median age of menopause 49y); HRT 5.2%; second-hand smokers 40% (work-exposure 17.1%, home-exposure 88.8%); obesity 16.3%; familiar history of cancer 39.9% (LC 29.8%); previous history of cancer 13% (breast/lung/cervix: 41.4/5.7/2.9%); current LC histology(%): adenocarcinoma/SqCC/LCC/SCLC: 83.4/6.2/5.5/3.9; EGFR mut+ (268 p analyzed): 55.5% (exon 19/20/21(%): 61.1/7.4/36.9); TNM NSCLC I/II/III/IV(%): 14/3.3/19.8/60.3. Treatment: EGFR-TKI in p EGFR mut+, stage IV(1st-/2nd-line)(%): 51.7/15.4; stage IV NSCLC (1st-line/2nd-line): platinum-based CT 42.5%, EGFR-TKI 33.5%, combinations with bevacizumab 2.9% / EGFR-TKI 15.8%. Overall survival: median 27 months(m), 1/2-y(%) 74.8/55.2; stage IV NSCLC: median 20.5m, 1/2-y(%) 67/46; EGFR-mut+ p: median 27.3m, 1/2-y(%) 75/54.3. Conclusions: According to our e-database, WLC showed high rates of never-smokers (39.3%), and of relatives diagnosed with malignant tumours (39.9%, ≅1/3 LC). Adenocarcinoma was the most frequent histology (76.1%), and more than half of the cases analyzed harboured EGFR mutations. Although 40% were second-hand smokers, further investigations are warranted. Survival outcomes remain satisfactory, as expected from this selected subgroup of p. Additional epidemiologic and treatment data will be presented.

Lung cancer in women: The Spanish female-specific database WORLD 07

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 8084-8084 ◽  
Author(s):  
N. Vinolas ◽  
M. Magem ◽  
P. Garrido ◽  
A. Artal ◽  
J. De Castro ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Smoking Habit ◽  
Previous History ◽  
Stage Iv ◽  
Large Cell ◽  
Egfr Mutations ◽  
Passive Smoker ◽  
History Of ◽  
Female Specific ◽  
History Of Cancer

8084 Background: Lung cancer is the leading cause of cancer mortality among women in many countries. Gender differences have been reported, most of them based on retrospective analysis. Methods: WORLD07 is a prospective, multicenter, epidemiologic female-specific lung cancer database developed by the Spanish Lung Cancer Group. Data on demographics, previous cancer history, reproductive and hormonal status, diet, alcohol, tobacco, and occupational information are being collected just as histology, stage, treatment and survival. Results: From October 2007 to Nov 2008, 342 female newly diagnosed of lung cancer were collected in an e-database in 20 Spanish centers. Patients (p) characteristics are: median age 61.7 years (y) (range: 36 - 87); Caucasian: 98.2%; Marital status (%): married 67.7, unmarried 11.2, divorced 7.1, widow 14. Educational level (%): basic 57.4, secondary 29.1, university 13.5. Median age of menarche 12.7 y. Children: 79.4% (median: 2); Median age of first child 27 y. Oral contraceptive: 30.6%. Pre-menopausal 15.4%,postmenopausal 84.6%. Median age of menopause 46.7 y. HRT: 5.3%. Median duration of HRT: 4.4 y. Obesity: 11.3%. Smoking habit (%): never (passive smoker/no exposition)/former/current smokers: 42 (42.8/57.2) /19 /39; Median packs/year 72.4. Former smokers: 1–5/5–10/10–15/>15 y (%): 51/11.8/7.8/29.4. Work exposure 3.5%. Alcohol consumption 3.2%. Familial history of cancer: 45.5% (lung cancer 29.7%). Previous history of cancer 13.8% (breast 33.3%). Current lung cancer histology (%): adenocarcinoma/BAC/squamous/large cell/NOS: 70.4/5.7/10.4/7.9/5.7. SCLC 11.8%. TNM I/II/III/IV (%): 16/3.9/28.7/51.4. Surgical treatment 24.7 % (lobectomy/pneumonectomy/exploratory: 85.5/9.2/5.3%). Available data of 122 stage IV NSCLC p: 74.6% receive chemotherapy, 92.3% of them two drugs and 68.9 % platinum-based (59% cisplatin). EGFR mutations analysis 7.9%. Conclusions: According this series, 42% of Spanish lung cancer women are never smokers and 70.4% have adenocarcinoma. Other collected information, choice of treatment and survival outcomes will be also analyzed. No significant financial relationships to disclose.

scholarly journals Lung Cancer Screening in Patients With a Previous History of Cancer

CHEST Journal ◽  
2016 ◽  
Vol 150 (4) ◽  
pp. 701A
Author(s):  
Joshua Lopez ◽  
Leanne Goldstein ◽  
Brian Tiep ◽  
Argelia Sandoval ◽  
Arnold Rotter ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Screening ◽  
Previous History ◽  
Lung Cancer Screening ◽  
History Of ◽  
History Of Cancer

Drug Combinatorial Therapies for the Treatment of KRAS Mutated Lung Cancers

2019 ◽  
Vol 19 (23) ◽  
pp. 2128-2142 ◽  
Author(s):  
Hao He ◽  
Chang Xu ◽  
Zhao Cheng ◽  
Xiaoying Qian ◽  
Lei Zheng
Keyword(s):  
Lung Cancer ◽  
Adjuvant Therapy ◽  
Combination Therapy ◽  
Clinical Benefit ◽  
Poor Prognosis ◽  
Egfr Mutations ◽  
Kras Mutations ◽  
Lung Cancers ◽  
Egfr Tki ◽  
Egfr Tkis

: KRAS is the most common oncogene to be mutated in lung cancer, and therapeutics directly targeting KRAS have proven to be challenging. The mutations of KRAS are associated with poor prognosis, and resistance to both adjuvant therapy and targeted EGFR TKI. EGFR TKIs provide significant clinical benefit for patients whose tumors bear EGFR mutations. However, tumors with KRAS mutations rarely respond to the EGFR TKI therapy. Thus, combination therapy is essential for the treatment of lung cancers with KRAS mutations. EGFR TKI combined with inhibitors of MAPKs, PI3K/mTOR, HDAC, Wee1, PARP, CDK and Hsp90, even miRNAs and immunotherapy, were reviewed. Although the effects of the combination vary, the combined therapeutics are one of the best options at present to treat KRAS mutant lung cancer.

scholarly journals Post-Progression Survival after EGFR-TKI for Advanced Non-Small Cell Lung Cancer Harboring EGFR Mutations

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0135393 ◽  
Author(s):  
Yoshihito Kogure ◽  
Hideo Saka ◽  
Masahide Oki ◽  
Toshiki I. Saito ◽  
Shimaa Nour Moursi Ahmed ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Egfr Mutations ◽  
Small Cell Lung ◽  
Egfr Tki

scholarly journals Global proteome and phosphoproteome alterations in third generation EGFR TKI resistance reveal drug targets to circumvent resistance

2020 ◽  
Author(s):  
Xu Zhang ◽  
Tapan K. Maity ◽  
Karen E. Ross ◽  
Yue Qi ◽  
Constance M. Cultraro ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Signaling Pathways ◽  
Egfr Mutations ◽  
Altered Expression ◽  
Mesenchymal Transition ◽  
Tki Resistance ◽  
Egfr Tki ◽  
Egfr Tkis ◽  
Resistant Cells

AbstractLung cancer is the leading cause of cancer mortality worldwide. The treatment of lung cancer patients harboring mutant EGFR with orally administered EGFR TKIs has been a paradigm shift. Osimertinib and rociletinib are 3rd generation irreversible EGFR TKIs targeting the EGFR T790M mutation. Osimertinib is the current standard care for patients with EGFR mutations due to increased efficacy, lower side effects, and enhanced brain penetrance. Unfortunately, all patients develop resistance. Genomic approaches have primarily been used to interrogate resistance mechanisms. Here, we have characterized the proteome and phosphoproteome of a series of isogenic EGFR mutant lung adenocarcinoma cell lines that are either sensitive or resistant to these drugs. To our knowledge, this is the most comprehensive proteomic dataset resource to date to investigate 3rd generation EGFR TKI resistance in lung adenocarcinoma. We have interrogated this unbiased global quantitative mass spectrometry dataset to uncover alterations in signaling pathways, reveal a proteomic signature of epithelial mesenchymal transition (EMT) and identify kinases and phosphatases with altered expression and phosphorylation in TKI resistant cells. Decreased tyrosine phosphorylation of key sites in the phosphatase SHP2 suggests its inhibition resulting in inhibition of RAS/MAPK and activation of PI3K/AKT pathways. Furthermore, we performed anticorrelation analyses of this phosphoproteomic dataset with the published drug-induced P100 phosphoproteomic datasets from the Library of Integrated Network-Based Cellular Signatures (LINCS) program to predict drugs with the potential to overcome EGFR TKI resistance. We identified dactolisib, a PI3K/mTOR inhibitor, which in combination with osimertinib overcomes resistance both in vitro and in vivo.One Sentence SummaryGlobal quantitative proteome and phosphoproteome analyses to examine altered signaling pathways in isogenic 3rd generation EGFR TKI sensitive and resistant cells.

scholarly journals 1730P Cancer long survivor artificial intelligence follow-up (CLARIFY): Family history of cancer and lung cancer

2021 ◽  
Vol 32 ◽  
pp. S1198-S1199
Author(s):  
V. Calvo ◽  
E. Niazmand ◽  
E. Carcereny ◽  
S. Jozashoori ◽  
D. Rodriguez ◽  
...  
Keyword(s):  
Artificial Intelligence ◽  
Lung Cancer ◽  
Family History ◽  
Family History Of Cancer ◽  
History Of ◽  
History Of Cancer

scholarly journals Concurrent Genetic Alterations and Other Biomarkers Predict Treatment Efficacy of EGFR-TKIs in EGFR-Mutant Non-Small Cell Lung Cancer: A Review

2020 ◽  
Vol 10 ◽  
Author(s):  
Yijia Guo ◽  
Jun Song ◽  
Yanru Wang ◽  
Letian Huang ◽  
Li Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Treatment Efficacy ◽  
Genetic Alterations ◽  
Small Cell ◽  
Egfr Mutations ◽  
Small Cell Lung ◽  
Egfr Mutant ◽  
Egfr Tki ◽  
Egfr Tkis ◽  
Gene Alterations

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) greatly improve the survival and quality of life of non-small cell lung cancer (NSCLC) patients with EGFR mutations. However, many patients exhibit de novo or primary/early resistance. In addition, patients who initially respond to EGFR-TKIs exhibit marked diversity in clinical outcomes. With the development of comprehensive genomic profiling, various mutations and concurrent (i.e., coexisting) genetic alterations have been discovered. Many studies have revealed that concurrent genetic alterations play an important role in the response and resistance of EGFR-mutant NSCLC to EGFR-TKIs. To optimize clinical outcomes, a better understanding of specific concurrent gene alterations and their impact on EGFR-TKI treatment efficacy is necessary. Further exploration of other biomarkers that can predict EGFR-TKI efficacy will help clinicians identify patients who may not respond to TKIs and allow them to choose appropriate treatment strategies. Here, we review the literature on specific gene alterations that coexist with EGFR mutations, including common alterations (intra-EGFR [on target] co-mutation, TP53, PIK3CA, and PTEN) and driver gene alterations (ALK, KRAS, ROS1, and MET). We also summarize data for other biomarkers (e.g., PD-L1 expression and BIM polymorphisms) associated with EGFR-TKI efficacy.

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