Breast metastasis from EGFR-mutated lung adenocarcinoma: A case report and review of the literature.
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ABSTRACT:
SUBMITTER: Ota T
PROVIDER: S-EPMC6098998 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:EGFR mutation has been detected in more than half of non-small cell lung cancer (NSCLC) patients in Asia. Lung cancer is the main cause of malignant tumor-related death worldwide. Although distant metastases often occurs in patients with advanced NSCLC, uterine cervical metastasis is rare. Here, we report a case of EGFR-mutated lung adenocarcinoma with cervical metastasis. A 63-year-old female with known lung adenocarcinoma was found to have abnormal vaginal bleeding during osimertinib follow-up visits. Immunohistochemical (IHC) staining and next-generation sequencing (NGS) of the biopsy sample from the uterine cervical tumor confirmed metastatic dissemination from the primary lung malignancy. NGS assisted the diagnosis of uterine cervical metastasis from the primary lung. This is another major clinical application of NGS in addition to medication guidance and identification of drug resistance mechanisms.
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Project description:Somatic mutations in the EGFR proto-oncogene occur in ~15% of human lung adenocarcinomas and the importance of EGFR mutations for the initiation and maintenance of lung cancer is well established from mouse models and cancer therapy trials in human lung cancer patients. Recently, we identified DOK2 as a lung adenocarcinoma tumor suppressor gene. Here we show that genomic loss of DOK2 is associated with EGFR mutations in human lung adenocarcinoma, and we hypothesized that loss of DOK2 might therefore cooperate with EGFR mutations to promote lung tumorigenesis. We tested this hypothesis using genetically engineered mouse models and find that loss of Dok2 in the mouse accelerates lung tumorigenesis initiated by oncogenic EGFR, but not that initiated by mutated Kras. Moreover, we find that DOK2 participates in a negative feedback loop that opposes mutated EGFR; EGFR mutation leads to recruitment of DOK2 to EGFR and DOK2-mediated inhibition of downstream activation of RAS. These data identify DOK2 as a tumor suppressor in EGFR-mutant lung adenocarcinoma.
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Project description:Introduction: Small cell lung cancer (SCLC) transformation represents a mechanism of resistance to osimertinib in EGFR-mutated lung adenocarcinoma, which dramatically impacts patients' prognosis due to high refractoriness to conventional treatments. Case Description: We present the case of a patient who developed a SCLC phenotypic transformation as resistance mechanism to second-line osimertinib for T790M-positive EGFR-mutated NSCLC. Our patient received platinum-etoposide doublet following SCLC switch and achieved a modest clinical benefit which lasted 4 months. NGS and IHC analyses for p53 and Rb were performed on subsequent liver biopsies, revealing baseline TP53 mutation and complete absence of p53 and Rb expression. Primary cell cultures were established following a liver biopsy at the time of SCLC transformation, and drug sensitivity assays showed meaningful cell growth inhibition when osimertinib was added to platinum-etoposide compared with control (p < 0.05). A review of the current literature regarding SCLC transformation after failure of osimertinib was performed. Conclusions: Based on retrospective data available to date, platinum-etoposide chemotherapy is the preferred treatment choice in the occurrence of SCLC transformation after osimertinib failure. The extension of osimertinib in combination with chemotherapy in the occurrence of SCLC transformation as resistance mechanism to osimertinib is a matter of debate. The combination of osimertinib and platinum-etoposide was effective in inhibiting cell growth in our primary cell cultures. Clinical studies are needed to further explore this combination in the occurrence of SCLC transformation as a resistance mechanism to osimertinib.
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Project description:RATIONALE:Anlotinib has been proved to be effective in advanced refractory non-small cell lung cancer. PATIENT CONCERNS:A 47-year-old female non-smoker was admitted due to persistent chest tightness for a month. DIAGNOSES:Epidermal growth factor receptor (EGFR) wild-type advanced primary lung adenocarcinoma without brain or bone metastasis. INTERVENTIONS:The patient failed 2 lines of pemetrexed/docetaxel plus carboplatin and third-line erlotinib. Fourth-line anlotinib was administered thereafter. OUTCOMES:The pulmonary lesions showed partial remission 5 months after anlotinib monotherapy. The patient demonstrated a progression-free survival of more than 7 months and an overall survival of >12 months. The adverse events including hypertension and fatigue were well-tolerated. LESSONS:Salvage anlotinib might be a reasonable choice in EGFR wild-type lung adenocarcinoma after failure of chemotherapy. Further well-designed trials are warranted to verify this occasional finding.
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