scholarly journals Bone Metastasis of Non-Small-Cell Lung Cancer Showing Pathological Complete Response to Osimertinib Monotherapy

2021 ◽  
pp. 1876-1881
Author(s):  
Hiroshi Shintani ◽  
Shoji Oura ◽  
Tomoyuki Yamaguchi ◽  
Shinichiro Makimoto
Keyword(s):  
Lung Cancer ◽  
Bone Metastasis ◽  
Lung Adenocarcinoma ◽  
Kinase Inhibitors ◽  
Pathological Complete Response ◽  
Lung Nodule ◽  
Growth Factor Receptor ◽  
Complete Response ◽  
Pathological Examination ◽  
The Right

A 70-year-old man with lung adenocarcinoma had undergone right lower lobectomy and lymph node dissection. Only 6 months later under adjuvant uracil and futraful therapy, the patient developed a solitary bone metastasis in the right 8th rib. Due to positive mutation of epidermal growth factor receptor (EGFR) exon 21 L858R in the primary cancer, the patient received osimertinib monotherapy, leading to massive calcification of the osteolytic bone metastasis with significant decrease of standard uptake value on positron emission tomography. After 12 months of osimertinib monotherapy, slight enlargement of the ground glass nodule, i.e., presumed noninvasive lung cancer, in the right upper lobe, and no further occurrence of metastatic foci made us to resect both the lung nodule and the bone metastasis. Pathological examination showed the lung nodule to be noninvasive adenocarcinoma and the bone metastasis to have no viable cancer cells. The patient was discharged on the 8th postoperative day without any complication. On developing a therapeutic strategy for advanced/recurrent EGFR mutation-positive lung adenocarcinoma, oncologists should note the possibility of pathological complete response to newly developed EGFR tyrosine kinase inhibitors including osimertinib for a presumed cure of oligometastatic lung adenocarcinoma.

scholarly journals Urinary markers in treatment monitoring of lung cancer patients with bone metastasis

2019 ◽  
Vol 34 (3) ◽  
pp. 243-250
Author(s):  
Pei Cheng Jin ◽  
Bo Gou ◽  
Wei Qian
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Bone Metastasis ◽  
Kinase Inhibitors ◽  
Growth Factor Receptor ◽  
Background Level ◽  
Driver Mutations ◽  
Urinary Markers ◽  
Cancer Management ◽  
Non Invasive

Background: Bone metastasis remains critical for advanced stage non-small cell lung cancer (NSCLC)—a disease that is challenging to manage. Urinary markers present opportunities for non-invasive testing. Methods: Urine specimens were collected from patients prior to treatment. Urinary cell-free DNA was subsequently purified from these samples. To address the specificity of the test, driver mutations in epidermal growth factor receptor L858R and L861Q were analyzed. Clinical specificity was established by comparison with healthy volunteers. Regular monitoring was established during treatment with tyrosine kinase inhibitors. The overall survival of patients was correlated with changes in circulating tumor DNA (ctDNA). Results: Baseline clinical correlation of urinary ctDNA and matched tumor specimens achieved 89% concordance. The clinical specificity was 100%. The average background level of urinary ctDNA was 20.7 ng/mL. Comparing patients with and without bone metastasis, the latter had significantly lower baseline levels. During treatment, more pronounced decline in urinary ctDNA was observed in patients without bone metastasis. In our Kaplan–Meier estimator, we observed that patients with a more significant reduction in ctDNA had a better overall survival outcome. Conclusion: Our study demonstrates clear benefits and allows better risk profiling for NSCLC patients with bone metastasis. The non-invasive specimen collection is attractive and complements existing cancer management tools.

scholarly journals Complete Response to Afatinib of an EGFR Exon 18 delE709_T710insD-Mutated Stage IV Lung Adenocarcinoma

2021 ◽  
Author(s):  
Blandine Jelli ◽  
Olivier Taton ◽  
Nicky D'Haene ◽  
Myriam Remmelink ◽  
Zita Mekinda
Keyword(s):  
Lung Adenocarcinoma ◽  
Kinase Inhibitors ◽  
Growth Factor Receptor ◽  
Stage Iv ◽  
Complete Response ◽  
Egfr Mutations ◽  
First Case ◽  
Treatment Interruptions ◽  
Patient Prognosis ◽  
Lung Adenocarcinomas

Introduction: Epidermal growth factor receptor (EGFR) mutations are frequently found in patients with lung adenocarcinomas, 90% being deletions in exon 19 or point mutation in exon 21. Three generations of tyrosine kinase inhibitors (TKIs) targeting EGFR mutations are available and have changed patient prognosis but less data is available on exon 18 mutations and their sensitivity to TKI therapy. Exon 18 delE709_T710insD accounts for 0.06% (16/27,294) of all EGFR mutations and is an oncogenic driver. Several partial responses to afatinib have been described. Case description: We report the first case, to the best of our knowledge, of the complete response to afatinib of a 57-year-old patient with stage IV lung adenocarcinoma with a delE709_T710insD mutation in the EGFR gene detected by next-generation sequencing. Oral afatinib was prescribed and despite treatment interruptions and dosage tapering due to cutaneous adverse events, a complete response was achieved 12 months after treatment initiation and is currently maintained at 17 months. Conclusion: When EGFR mutation is suspected, complete DNA sequencing of exons 18 to 21 should be carried out and we suggest that afatinib should be the first-line treatment for exon 18 delE709_T710insD-mutated advanced lung adenocarcinomas.

scholarly journals Achievement of Cure with Gefitinib in Advanced Lung Adenocarcinoma Harboring an Activating EGFR Mutation: A Case Report

2016 ◽  
Vol 9 (3) ◽  
pp. 565-567 ◽  
Author(s):  
Taiji Kuwata ◽  
Kazue Yoneda ◽  
Kenichi Kobayashi ◽  
Rintarou Oyama ◽  
Hiroki Matumiya ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Kinase Inhibitors ◽  
Growth Factor Receptor ◽  
Complete Response ◽  
Term Survival ◽  
Activating Mutations ◽  
First Case ◽  
Old Japanese ◽  
Gefitinib Treatment ◽  
Activating Egfr Mutation

Tyrosine kinase inhibitors (TKIs) of the epidermal growth factor receptor (EGFR) may achieve long-term survival in selected cases with advanced non-small cell lung cancer harboring activating mutations in the EGFR gene, but a cured case has not been reported yet. Here, we present the first case of EGFR-mutated lung adenocarcinoma cured with an EGFR-TKI, as the 75-year-old Japanese man has achieved complete response with gefitinib treatment and has survived without tumor 10 years after termination of gefitinib treatment.

scholarly journals Genetic Alteration Profiling of Chinese Lung Adenocarcinoma and Its Effect on Targeted Therapy Efficacy

2021 ◽  
Vol 11 ◽  
Author(s):  
Jie Liu ◽  
Wang-yang Xu ◽  
Maosong Ye ◽  
Zilong Liu ◽  
Chun Li
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Lung Adenocarcinoma ◽  
Receptor Tyrosine Kinase ◽  
Targeted Therapies ◽  
Kinase Inhibitors ◽  
Eastern China ◽  
Growth Factor Receptor ◽  
Treatment Decision ◽  
Tyrosine Kinase 2

BackgroundNon-small cell lung cancer (NSCLC) is the most common type of lung cancer and a highly heterogeneous disease with a diversity of phenotypes and genotypes in different populations. The purpose of this study is to investigate oncogenic alterations of lung adenocarcinoma (LUAD) in eastern China and their significance in targeted therapies.MethodsThis study enrolled 101 LUAD patients and used a customized DNA panel to detect molecular alterations. Comprehensive analysis of mutations and clinical application of genomic profiling was carried out.ResultsThe most commonly mutated genes were epidermal growth factor receptor (EGFR) (53%) and tumor protein p53 (TP53) (32%). The less frequently mutated genes were erb-b2 receptor tyrosine kinase 2 (ERBB2) (25%), ATR serine/threonine kinase (ATR) (20%), CCAAT enhancer binding protein alpha (CEBPA) (16%), RB transcriptional corepressor 1 (RB1) (16%), transcription factor 7 like 2 (TCF7L2) (14%), ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) (12%) and spectrin alpha, erythrocytic 1 (SPTA1) (12%). Among them, the frequency of ERBB2, ATR, CEBPA, RB1 and TCF7L2 mutations was much higher than that in the databases. Seventy percent of the patients harbored at least one actionable alteration according to the OncoKB evidence. CEBPA mutations affected the efficacy of EGFR-tyrosine kinase inhibitors. ERBB2, CEBPA and TCF7L2 mutated tumors tend to have higher tumor mutation burden (TMB).ConclusionsLUAD patients from eastern China have a unique profile of mutations. The targeted DNA panel is helpful for personalized treatment decision of LUAD patients, and specific mutations may affect the efficacy of targeted therapies.

scholarly journals Long-lasting response to afatinib that persisted after treatment discontinuation in a case ofEGFR-mutated lung adenocarcinoma

2019 ◽  
Vol 12 (1) ◽  
pp. e227383 ◽  
Author(s):  
Yumie Yamanaka ◽  
Yoshitaka Seki ◽  
Takeo Ishikawa ◽  
Kazuyoshi Kuwano
Keyword(s):  
Kinase Inhibitors ◽  
Growth Factor Receptor ◽  
Complete Response ◽  
Middle Lobe ◽  
Japanese Woman ◽  
Old Japanese ◽  
Exon 19 Deletion ◽  
History Of ◽  
Epidermal Growth ◽  
The Right

It is unknown whether tyrosine kinase inhibitors targeting epidermal growth factor receptor (EGFR) can be discontinued in patients in whomEGFR-mutated lung cancer has well stabilised. We present a case of a 73-year-old Japanese woman with no history of smoking. Right pulmonary lower lobectomy, lymph node dissection and segmental resection of the right middle lobe were performed. Additionally, she underwent adjuvant chemotherapy for stage IIIB adenocarcinoma harbouring anEGFRexon 19 deletion. Afatinib was administered for liver metastases after 15 months. A complete response of metastatic disease was achieved for 2 years. However, afatinib was unavoidably discontinued due to splenectomy for the treatment of idiopathic thrombocytopenic purpura. Although afatinib was not resumed, due to the abscess formation as surgery complication, a drug-free complete response was sustained for over 18 months. The present case suggests that exceptional and durable responses to afatinib can be achieved in individual cases.

Re-use of erlotinib in a patient using osimertinib after erlotinib, case report

2021 ◽  
pp. 107815522110191
Author(s):  
Pinar Gursoy
Keyword(s):  
Lung Cancer ◽  
Case Report ◽  
Treatment Options ◽  
Resistance Mutation ◽  
Growth Factor Receptor ◽  
Complete Response ◽  
Egfr Mutations ◽  
T790m Mutation ◽  
Development Of Resistance ◽  
Exon 19

Introduction Most patients with non-small-cell lung cancer tumors that have epidermal growth factor receptor (EGFR) mutations have deletion mutations in exon 19 or exon 21, or both.In recent years, targeted therapies in lung cancer have increased survival, but the development of resistance to these drugs poses a major problem. Thesubstitution of methionineforthreonine at position 790 (T790M) mutation,is primarily responsible for this resistance. However, after osimertinib used in T790M positivepatients treatment options are generally limited to chemotherapy. Case report We reported the efficacy of erlotinib, which we reapplied due to the disappearance of the resistance mutation after osimertinib in a 68-year-old patient using osimertinib after erlotinib. Management and outcome: In the patient using erlotinib due to exon 19 deletion when progression was observed and T790M positivity was detected, osimertinib treatment was initiated. However, when T790M was found to be negative with rebiopsy in progression after osimertinib, a complete response was achieved by restarting erlotinib. Discussion The strategy of restarting erlotinib treatment with negative T790M mutation detected in biopsies of patients with osimertinib resistance may be an acceptable treatment option.

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