NCT06369181
Neuroendocrine Transformation in RB1/TP53 Inactivated NSCLC
Recruiting · Not specified · Fudan University · registry updated 2024-04-23
Inclusion and exclusion lines below are quoted from ClinicalTrials.gov. No match score is shown, because a score needs a person's age, biomarkers, and treatment dates. Confirm the record with the study team.
Histology transformation from non-small cell lung cancer (NSCLC) to neuroendocrine carcinomas (NEC), especially from epidermal growth factor receptor (EGFR) mutant lung adenocarcinoma (LADC) to small cell lung cancer (SCLC), is widely recognized as a rare mechanism for NSCLC to confer tyrosine kinase inhibitors (TKIs) resistance. The probability of its occurrence is about 3-14% in NSCLC patients who are resistant to TKI treatment. In addition to EGFR mutations, NSCLC patients carrying ALK/ROS1 mutations and receiving corresponding TKI treatment may also experience NEC transformation(NET). In a previous study \[Pubmed ID: 35609408\], the investigators demonstrated that NET also develops in NSCLCs without TKI targets or treatments. This phenomenon could be under-recognized, because re-biopsy was less frequently performed in these patients. The investigators had also shown that p53/Rb inactivation might correlated with NET and should be considered for NET risk prediction....
Inclusion
- Age ≥ 18 years old;
- ECOG function status score 0-2 points;
- Pathological diagnosis of stage III-IV non neuroendocrine non-small cell lung cancer;
- RB1/TP53 gene/protein testing (IHC, NGS, or other techniques are acceptable) has been completed and confirmed to be dual inactivation of RB1/TP53;
- For patients with baseline pathology of adenocarcinoma, complete driver gene testing (including at least EGFR and ALK);
- The patient undergoes at least one systemic treatment (chemotherapy, targeted drug therapy, immunotherapy, etc.) and receives regular follow-up;
Exclusion
- Baseline pathological examination reveals neuroendocrine components (including any percentage of small cell carcinoma, large cell carcinoma, differentiated neuroendocrine carcinoma, etc);
- Unable to perform RB1/TP53 testing ;
- Patients with baseline pathology of adenocarcinoma and inability to perform driver gene testing (including at least EGFR, ALK);
- Symptomatic interstitial lung disease or active infection/non infectious pneumonia;
- History of other malignant tumors;
- Physical examination or clinical trial findings that researchers believe may interfere with the results or increase the risk of treatment complications for patients, or other uncontrollable diseases