Miracle: Patients with advanced lung cancer survive more than 20 years
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Miracle: Patients with advanced lung cancer survive more than 20 years
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Miracle: Patients with advanced lung cancer survive more than 20 years.
Professor Christina Baik, an oncology expert from the University of Washington in the United States, published a particularly valuable case in the top international medical journal “Journal of Thoracic Oncology” .
A patient with advanced non-small cell lung cancer (NSCLC) has benefited from targeted drug therapy for more than 10 years, and the survival period is more than 20 years!
This patient (female, 45 years old) came to the hospital for persistent cough in 1995 (smoking history <1 pack-year). Diagnostic examination showed a solitary infiltrate in the left lower lobe of the lung. Bronchoalveolar carcinoma. The patient underwent left lower lobectomy, and the final pathological stage after treatment was T3N0.
The prognosis of this type of lung cancer is generally poor. Under the treatment of cytotoxic chemotherapy drugs, the 1-year survival rate is only 29%. However, the emergence of EGFR-TKIs inhibitors has significantly improved the treatment situation of some patients.
For advanced NSCLC patients with EGFR mutations, if they received EGFR-TKIs inhibitors, the median overall survival time was more than double that of patients who did not receive the drug treatment (24.3 vs 10.8 months). Patients with metastatic lung adenocarcinoma with EGFR mutations received EGFR-TKIs treatment, and the five-year survival rate reached 14.6%. However, patients with metastatic NSCLC who can achieve long-term survival (>10 years) are rare.
Beginning in 1999, the patient developed recurrent cough, and examination revealed extensive infiltrates on both sides of the lungs. Biopsy confirmed recurrence of bronchioloalveolar carcinoma in the patient. The patient underwent chemotherapy (paclitaxel + capecitabine), and the patient’s tumor focus was controlled. However, in 2003, the patient’s condition began to develop in an unfavorable direction.
In the same year, the US FDA approved the marketing of the world’s first oral targeted drug gefitinib for lung cancer. Patients started to use gefitinib for treatment, and the lesions showed partial remission, and the symptoms improved significantly. The drug had a lasting effect on the tumor, the patient’s lung cancer was under continuous control, and the patient survived another 6 years……
imageSignificant effect of gefitinib treatment
In 2009, the patient’s symptoms worsened again, and disease progression was diagnosed by X-ray examination. The patient has been treated with chemotherapy (pemetrexed) and the EGFR-targeted drug gefitinib, but the disease cannot be controlled.
The doctor decided to try the same generation of EGFR targeting drug Erlotinib again. With erlotinib, the patient once again achieved a sustained anti-tumor response. Until 2012, the patient experienced mild disease progression.
Doctors detected common activating mutations of EGFR by PCR , such as L868R, L861Q, exon 19 deletion, G719X, T790M, S768I, exon 20 insertion and other mutations. However, these mutations were not detected in the patient’s tumor tissue.
The patient continued to use erlotinib until the end of 2014, when the patient’s symptoms worsened. Therefore, this patient will plan to participate in clinical trials of EGFR-TKIs resistance while continuing to use erlotinib.
Physicians evaluate patient samples through high-throughput sequencing (NGS). This test reconfirmed that common activating mutations of EGFR and other known driving factors, including BRAF mutations, and rearrangements of ALK, ROS1, and RET, were indeed absent. However, the physicians found an EGFR kinase domain tandem repeat mutation (exons 18-25) in the patient’s sample.
imageEGFR kinase domain tandem repeat mutation
The doctor also performed NGS evaluation on the patient’s tumor tissue sample operated 20 years ago, and the results suggested that the sample also had a TKD-EGFR mutation (EGFR kinase domain tandem repeat mutation).
Therefore, we have reason to judge that the patient’s tumor treatment status has a significant dependence on EGFR signaling.
In the current case, the patient’s metastatic lung adenocarcinoma was treated with an EGFR-TKI-targeted drug in a barely smoker (low risk) patient who had no known activating EGFR mutations on initial PCR testing Significant disease control effects have been achieved.
What we want to say is that 3%-10% of EGFR wild-type patients (no known activating mutations) can also produce positive results under the treatment of EGFR-TKI targeted drugs.
These patients are usually not given EGFR-TKI targeted drug therapy clinically, so they may lose the chance of effective treatment.
In addition, in anti-tumor treatment, drug resistance is the last thing doctors and patients want to see, which indicates that some tumor patients may not have available drugs.
A number of studies have shown that: ginsenoside Rh2 has obvious drug resistance reverse effect , and it is concentration-dependent.
It can inhibit the function of P-gp overexpressed on the cell membrane of multi-drug resistant tumors, thereby reducing the function of P-gp or Inactivation, ultimately reducing the multidrug resistance of tumor cells.
Ginsenoside Rh2 monomer products have been widely recognized since their launch in 2006.
In order to allow customers to obtain immune-improving products that are truly suitable for them, more customers can experience the value of excellent immune-improving products and improve their own nutritional status and immunity. functions, improve the quality of life, and promote excellent immune-improving products to the public.
Fortunately, United Medical World has initiated the immune reconstruction of tumor patients and love public welfare activities.
References:
[1] Durable Response to Tyrosine Kinase Inhibitor Therapy in a Lung Cancer Patient Harboring Epidermal Growth Factor Receptor Tandem Kinase Domain Duplication
DOI: 10.1097/JTO.0000000000000586
Miracle: Patients with advanced lung cancer survive more than 20 years
(source:internet, reference only)
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