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Michael Cabanero
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MA24 - Genomic Evolution, KEAP 3 and More Non-Coding RNA (ID 928)
- Event: WCLC 2018
- Type: Mini Oral Abstract Session
- Track: Biology
- Presentations: 1
- Moderators:
- Coordinates: 9/26/2018, 10:30 - 12:00, Room 205 BD
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MA24.05 - Baseline Spatial Heterogeneity of T790M in Tyrosine Kinase Inhibitor Naïve EGFR-Mutant Lung Adenocarcinomas (ID 14171)
11:00 - 11:05 | Presenting Author(s): Michael Cabanero
- Abstract
- Presentation
Background
Despite a good initial response, most epidermal growth factor receptor EGFR-mutant lung adenocarcinomas develop resistance after treatment with 1st and 2nd generation tyrosine kinase inhibitors (TKIs). Approximately 50-60% of resistance can be attributed to the EGFRT790M mutation, which provides a higher affinity ATP binding site that outcompetes TKIs and restore constitutive kinase function. Although classically thought of as de novoacquisition, the presence of T790M has been shown to exist in some tumors before TKI-therapy. Obtaining a spatial map of T790M in TKI-naïve tumors can provide insight into development of this type of resistance.
a9ded1e5ce5d75814730bb4caaf49419 Method
Eight cases of TKI-naive primary lung adenocarcinoma resections that were later found to be positive for T790M post-treatment with TKI were collected from 2004 to 2012. Initial pre-treatment tumor surgical resections were used for DNA extraction. Two tumor sections per case were divided into equal grid-like regions of approximately 8x8 mm2. The number of grids ranged from 16 to 32 per case, based on tumor size (0.8 cm to 6.5 cm). Digital droplet polymerase chain reaction was used to genotype the sensitizing EGFR-mutations and T790M mutations at each region. Allelic frequencies (AF) of the mutations were measured. Recurrence free interval, defined as surgical resection date to date of recurrence detection, and total duration of TKI-therapy were extracted from medical records.
4c3880bb027f159e801041b1021e88e8 Result
All eight cases of TKI-naïve EGFR-mutant lung adenocarcinomas were positive for T790M at baseline. T790M tumor burden, defined as the mean allelic frequency of T790M, ranged from 0.17% to 40.15% across the tumors. Three main patterns of distribution were observed. In two cases, T790M was present at low level (<1% AF) prevalence throughout the entire tumor. Five cases were characterized by the presence of distinct sub-clonal region, defined as T790M AF high in one or adjacent regions surrounded by regions with low or zero T790M AF. In one case, T790M was the predominant clone with T790M AF closely matching sensitizing EGFR-mutation AF. T790M tumor burden was not associated with either tumor size or recurrence free interval.
8eea62084ca7e541d918e823422bd82e Conclusion
T790M tumor cells exist prior to TKI-therapy in a majority, if not all, EGFR-mutated lung adenocarcinoma that developed T790M mutation as the resistance mechanism to EGFR TKI therapy, rather than by de novo acquisition during TKI-therapy exposure. However, pre-treatment T790M tumor burden did not appear to be associated with recurrence free survival, although this requires more cases for confirmation.
6f8b794f3246b0c1e1780bb4d4d5dc53Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
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MA25 - Oligometastasis: Defining, Treating, and Evaluating (ID 929)
- Event: WCLC 2018
- Type: Mini Oral Abstract Session
- Track: Oligometastatic NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 9/26/2018, 13:30 - 15:00, Room 203 BD
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MA25.11 - Clinical and Molecular Predictors of Outcome in Patients with EGFR mutant NSCLC Brain Metastases treated with RT (ID 14529)
14:40 - 14:45 | Author(s): Michael Cabanero
- Abstract
- Presentation
Background
Brain metastases(BM) develop in ~45% of patients with EGFR mutant(EGFRm) non-small cell lung cancers(NSCLC). There are limited reports on clinical/molecular factors associated with BM outcomes after radiotherapy in EGFRm NSCLC patients.
a9ded1e5ce5d75814730bb4caaf49419 Method
We identified patients with EGFRm NSCLC who presented with or developed BM and had their lung tumor resected. Clinical, demographic and TP53 status were collected from medical/pathology records. Whole-Exome Sequencing of the primary tumor was performed. Overall survival(OS) and intracranial progression(IP) were defined from start of BM treatment and correlated with clinical/molecular features. IP was defined from the date of BM treatment until any brain failure, either local(previously present BM) or distant(development of new BM). Categorical and continuous covariates were tested by Fisher exact or Mann-Whitney test, respectively. OS by Kaplan-Meier with groups compared by log-rank. For each model the Harrell Concordance Index(CI) was performed.
4c3880bb027f159e801041b1021e88e8 Result
From 41 eligible patients with BM, 9 were excluded due to sequencing quality. Of the 32 remaining patients, 20 (62%) had their BM treated with WBI (15 WBI alone and 5 TKIàWBI), 12 (38%) with TKI±SRS (9 TKI àSRS; 2 TKI alone and 1 SRS alone). Median age at BM was 59.5 years(y). Most of the cohort were female(81%), non-smoker(78%), non-Asian(62%) and 50% presented as stage III or higher at diagnosis. An EGFR exon 19 mutation was present in 72% of patients, 25% had 2 or more EGFRm, 15% with additional driver mutations and 53% with TP53 co-mutation. At a median follow-up of 1.21-y, no clinical/molecular factors(treatment, age, gender, ethnicity, smoking status, stage at presentation, EFGR exon 19 versus 21, number of EGFRm, additional driver mutations, TP53 co-mutation) correlated with survival. There was a trend for longer survival for patients treated with TKI±SRS(median 3.4y) compared to WBRT±TKI(median 1.4y); p=0.08 and for age at BM ≤59.5y(median 2.5y) compared to >59.5y (median 1.4y); p=0.2. Higher risk of IP was observed in younger patients (age as continuous variable) with HR of 0.94(95%CI 0.88-1.0), p=0.04; favoring older patients and remained significant after accounting for treatment modality on multivariate analysis p=0.03. No additional clinical/molecular factors correlated with IP.
8eea62084ca7e541d918e823422bd82e Conclusion
In our study, younger age at BM treatment was associated with higher IP. We also observed a trend for longer OS for younger patients(≤59.5y) and for patients treated with TKI±SRS. Our data suggest that younger patients with EGFR BM should undergo close intracranial follow up and that future studies to define the benefit of brain-directed multimodality treatment are warranted.
6f8b794f3246b0c1e1780bb4d4d5dc53Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
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MA27 - Novel Drugs and PDX Models (ID 931)
- Event: WCLC 2018
- Type: Mini Oral Abstract Session
- Track: Targeted Therapy
- Presentations: 2
- Moderators:
- Coordinates: 9/26/2018, 13:30 - 15:00, Room 206 BD
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MA27.01 - Establishment of PDX From Tumors Characterized by EGFR Mutations or ALK Fusion Genes from Resections, Biopsies and Pleural Fluids (ID 12144)
13:30 - 13:35 | Author(s): Michael Cabanero
- Abstract
- Presentation
Background
Patient-derived xenograft (PDX) models allow for cancer tissue expansion, providing an effective method to evaluate tumor biology and mechanisms of response or resistance. Our study aims to establish models in patients enriched for lung adenocarcinoma (LUAD) with EGFR mutations or ALK fusion genes which respond initially to oral targeted therapy, but typically develop resistance and disease relapse within 2 years. The PDXs will be evaluated for their potential to model therapy outcomes, to determine resistance mechanisms and to evaluate novel therapy strategies to overcome resistance.
a9ded1e5ce5d75814730bb4caaf49419 Method
From August 2015 to January 2018, we collected 109 samples from patients with EGFR- or ALK-driven LUAD and from never-smoker LUAD patients with unknown mutation status. Five samples with low tissue viability (i.e. necrotic) or very low tumor content (<100 malignant cells) were excluded. Adequate samples were implanted into the subcutaneous tissue of NOD-SCID mice. At this time, 16 samples have reached the study endpoint (tumor growth ≥1.5cm3) and 60 showed no tumor-growth following implantation (median follow-up: 8m). Results are currently pending for 18 models.
4c3880bb027f159e801041b1021e88e8 Result
Samples were collected from surgical resections (31, 36%), CT-guided biopsies (12, 14%), EBUS (19, 22%) and pleural fluid effusions (24, 28%). Most patients were female (51/86, 59%), never smokers (62/85, 73%), and had stage III or IV cancer (55/79, 70%). Mutations in EGFR and ALK were found in 55/81 (68%) and 12/84 (14%) primary cancers, respectively. Early-passage xenograft engraftment (XG) was observed in only 16 (19%) PDXs, including 9/55 (16%) EGFR- and 1/12 (8%) ALK-mutant cancers. The phenotype and molecular changes (EGFR and ALK) were consistent within the PDX model and its corresponding patient sample. Samples collected from surgical-resection specimens showed a trend towards higher engraftment rates (p=0.084). Conversely, the presence of EGFR or ALK mutations showed a trend towards non-engraftment (noXG, p=0.075). Patient smoking status and tumor stage did not influence engraftment rate. To identify reasons for no tumor-growth, we conducted histological analysis in the subcutaneous fat-pads (nodes in the implant sites) of 28 noXG mice. Interestingly, we identified small non-palpable foci of carcinoma in 8 animals (4 EGFR+ and 2 ALK+).
8eea62084ca7e541d918e823422bd82e Conclusion
Environmental or molecular factors may impair engraftment rates of EGFR+ and ALK+ LUAD samples in PDX models. Nevertheless, these models recapitulate the primary disease and could be useful for population-based drug-screening studies.
6f8b794f3246b0c1e1780bb4d4d5dc53Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
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MA27.03 - Multi-Omic Characterization of TKI-Treated Drug-Tolerant Cell Population in an EGFR-Mutated NSCLC Primary-Derived Xenograft (ID 13370)
13:40 - 13:45 | Author(s): Michael Cabanero
- Abstract
- Presentation
Background
Sixty to eighty percent of advanced stage lung adenocarcinoma patients with epidermal growth factor receptor (EGFR) mutated tumors respond to first generation EGFR tyrosine kinase inhibitors (TKIs). However, cure is not yet achievable with any EGFR TKI monotherapy, as patients eventually progress due to acquired resistance. In vitro evidence suggests that minor populations of epigenetically modified drug tolerant cells (DTCs) may be important for tumor cells surviving TKI. We hypothesize that molecularly characterizing DTCs in vivo and comparing them to the untreated tumor in a patient-derived xenograft (PDX) model may delineate mechanisms of tolerance that closely mimic those occurring in patients.
a9ded1e5ce5d75814730bb4caaf49419 Method
DTCs were produced via chronic exposure to erlotinib in a lung adenocarcinoma PDX harbouring an exon 19 deletion. Histological, genomic, transcriptomic (including single-cell RNA-seq), and epigenetic characterizations were performed on DTCs and compared to untreated baseline (BL) tumors.
4c3880bb027f159e801041b1021e88e8 Result
Compared to BL, DTCs exhibit decreased levels of proliferation (Ki67 by immunohistochemistry (IHC) and increased expression of senescence/quiescence (p21) and anti-apoptosis (BCL-XL) immunohistochemistry (IHC) markers, while maintaining EGFR pathway signaling (pEGFR, pAKT, pERK, pS6 IHC). Whole exome-sequencing provides evidence that DTCs likely do not represent mutationally distinct subclones from the bulk tumor. Instead, DTCs exhibit a number of differentially expressed genes compared to BL tumors that are involved in cell cycle arrest, senescence/quiescence, differentiation, vesicles, and inflammation. Genes with epigenetic differences (chromatin openness and/or promoter methylation) are involved in similar cellular processes. A minor (<2%) subpopulation of transcriptomically-defined DTC-like cells in the BL tumors are very similar to the DTCs, supporting the hypothesis that DTCs may exist prior to treatment. A number of transcription regulators are found to have differential gene expression and epigenetic regulation as well as DNA-binding motifs found in regions of chromatin uniquely open in DTCs or baseline tumors. These transcription regulators are involved in cell maintenance, proliferation, and differentiation, and may play key roles in promoting DTC phenotype.
8eea62084ca7e541d918e823422bd82e Conclusion
In this specific EGFR mutant PDX model sensitive to first generation TKIs, DTC-like cells are found in the BL untreated tumors, and its resultant phenotype after exposure to TKI appears to be involved in cell cycle, differentiation, senescence/quiescence, proliferation and maintenance. PDX models may provide insights into therapeutic strategies to target DTCs, and further improve the survival of EGFR-mutated NSCLC patients.
6f8b794f3246b0c1e1780bb4d4d5dc53Only Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login, select "Add to Cart" and proceed to checkout. If you would like to become a member of IASLC, please click here.
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P1.04 - Immunooncology (Not CME Accredited Session) (ID 936)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall
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P1.04-05 - Elucidating the Role of Leukocyte-Associated Immunoglobin-Like Receptor 2 (LAIR2) in Lung Cancer Development (ID 13859)
16:45 - 18:00 | Author(s): Michael Cabanero
- Abstract
Background
The tumor microenvironment play an important role in shaping cancer development. The contexture of stromal infiltrates have been shown promote or inhibit tumor growth and patient prognosis. In attempts to gain insight into the immune networks that regulate tumorigenesis, we used genome wide expression datasets from patients with resected early stage non-small cell lung cancer (NSCLC) to identify immune-related genes associated with patient survival.
a9ded1e5ce5d75814730bb4caaf49419 Method
Gene expression analysis was conducted on microarray datasets from 128 early-stage NSCLC adenocarcinoma resected tumor samples. Limiting analysis to immune-related genes, we identified a minimum gene set containing LAIR2 that was prognostic for lung adenocarcinoma. Immunohistochemistry and gene ontology analysis were used to determine the function of LAIR2.
4c3880bb027f159e801041b1021e88e8 Result
From the gene signature, the gene encoding the immune collagen receptor LAIR2, was highly expressed within the high-risk patient subgroup (HR = 2.71, 95% CI = 1.49 to 4.90, P = 0.001). Gene ontology analysis revealed that LAIR2 expression correlated with negative immune regulation and associated immune signatures. Immunohistochemistry of resected lung adenocarcinoma revealed heterogeneous expression of LAIR2 within tumor epithelium and stromal immune cells, suggesting specificity and localization. ELISA for LAIR2 suggest that CD4+ Th2 cells maybe a major source of LAIR2 secretion and that recombinant LAIR2 may promote T cell exhaustion by activation of CD8+ T cells and upregulation of PD1 and LAG3.
8eea62084ca7e541d918e823422bd82e Conclusion
Our results suggest that expression of LAIR2 result in poor patient prognosis and is associated with negative immune regulation. An understanding of LAIR2 function will provide insight into factors required during lung cancer progression and targets for intervention.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P2.06 - Mesothelioma (Not CME Accredited Session) (ID 955)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall
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P2.06-38 - Mesothelioma Stem Cells May Be the Critical Factor of Treatment Failure (ID 11344)
16:45 - 18:00 | Author(s): Michael Cabanero
- Abstract
Background
Cancer cell repopulation during treatments of chemotherapy or radiotherapy is a major factor resulting in treatment failure. It has been indicated that cancer stem cells (CSC) may play critical roles during this process. The goal of our study is to characterise mesothelioma stem cells (MSC) and evaluate the prognostic values in those patients with malignant pleural mesothelioma (MPM). The eventual aim would be to design specific target therapy against MSC and develop novel approaches in clinical practice.
a9ded1e5ce5d75814730bb4caaf49419 Method
We have screened a group of genes that are most likely MSC-specific. Further characterization of the selected genes will be of critical importance in tumorigenesis, progression and prognosis. Murine mesothelioma AB12 and RN5 cells treated with either chemotherapy or γ-ray irradiation in culture, were used to compare gene expression profiles. The selected genes were confirmed by real-time PCR, flow cytometry and immunostaining. In vivo models, peritoneal lavage was collected at different time points after RN5 cell injection, to perform magnetic ranking cytometry with antibody-nanoparticle conjugates, and microarray assay. The expression of Tnfsf18 and Ngfr (CD271) genes associated with prognosis was evaluated in tumor tissues from MPM patients treated with SMART vs pre-SMART protocols, as SMART protocol has already shown significant clinical benefit. Image analysis was performed using Apero Imagescope program.
4c3880bb027f159e801041b1021e88e8 Result
The proportion of MSC significantly increased after RN5 parental cells were treated with either chemotherapy, or γ-ray irradiation, or in combination, while MSC showed more resistance to the above treatments, suggesting that chemoradiation resulted in MSC enrichment. Upregulation of genes Tnfsf18, Serpinb9b, Ly6a (Sca-1), Ngf, and Nppb were confirmed. CD271, the receptor of NGF, was shown to be upregulated after chemoradiation, especially after γ-ray radiation with a dose of 10Gy. Mesothelial precursors captured with magnetic nanoparticles conjugated to anti-Msln and trapped in the microfluidic device in the presence of a magnetic field showed an increase over time from 2-8weeks. Image analysis of human section slides indicated that total positive area of CD271 staining was significantly lower in those who were treated with SMART protocol than those with pre-SMART protocol (p<0.0025). Similar results were obtained in the high, medium and low positive areas from the SMART group, and p values are 0.0013, 0.0017 and 0.0035, respectively, when compared with the pre-SMART group.
8eea62084ca7e541d918e823422bd82e Conclusion
MSC-specific genes like CD271 and Tnfsf18 might be used as potential prognostic indicators and therapeutic targets.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P3.03 - Biology (Not CME Accredited Session) (ID 969)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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P3.03-29 - The Prognostic Effect of Tumor Mutation Burden and Smoking History in Resected EGFR Mutant Non-Small Cell Lung Cancer (ID 13199)
12:00 - 13:30 | Author(s): Michael Cabanero
- Abstract
Background
Although EGFRm NSCLC occurs mainly in non-smoking patients, most series report 20%-35% of cases in current or previous smokers. Broad molecular profiling of EGFRm NSCLC in smokers has not been reported.
a9ded1e5ce5d75814730bb4caaf49419 Method
Surgically resected primary EGFR exon 19, 20 and 21 mutated NSCLC tumors from 106 patients were molecularly profiled by whole exome sequencing using the Illumina HiSeq2000 platform. Alignment and variant discovery analysis was performed according to GATK best practices workflow; 74 sequenced to a mean coverage of 65.1x. Demographics and outcomes were compared for smokers and non-smokers (non-S), and by mutation profile.
4c3880bb027f159e801041b1021e88e8 Result
Among 53 non-smokers and 21 smokers (5 current/recent within 10 years), 70% were female, 51% non-Asian, 40.5% >65 years of age and 58.1% had EGFR exon 19. Of the 74 patients, 51% were stage I, 19% stage II and 30% stage III+. Smoking was associated with male sex (p= 0.011) and non-Asian ethnicity (p=0.00002) but not age, stage or EGFR exon 19/20/21 subtype. Multiple “driver” mutations occurred in tumors of 23.8% smokers and 26.4% non-S. TP53/EGFR co-mutation occurred in 52.4% smokers and 47.2% non-S. There was no significant difference seen for TMB in smokers: median TMB in smokers 3(1.4-7.46) versus 2.7(0.96-3.95) in non-S (p=0.11). The strongest prognostic factor for OS and DFS was stage (I, II, III+) (p<0.0001 for each compared to stage I). Smoking history did not have a significant effect on survival: HR 1.61 (CI 0.78-3.32, p=0.2) or probability of relapse: HR 0.9 (CI 0.46-1.77, p=0.77). Smoking within 10 years of NSCLC diagnosis was not associated with shorter OS/DFS. Neither EGFRm subtype nor TP53/EGFR co-mutation was associated with probability of relapse or OS. High TMB was significantly associated with shorter survival: HR above vs below the median 2.37 (CI 1.12-5.01, p=0.024), but not probability of relapse: HR 1.67 (CI 0.88-3.19, p=0.12). A subset analysis found the effect of TMB on survival was significant in patients >65 years (p=0.004), but not in patients <65 years (p=0.95).
8eea62084ca7e541d918e823422bd82e Conclusion
Stage remains the strongest prognostic factor for survival and probability of relapse in completely resected EGFRm NSCLC. TMB appears to have an effect on survival outcomes, unlike smoking status, and this effect may be greater in patients older than 65 years.
6f8b794f3246b0c1e1780bb4d4d5dc53
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P3.16 - Treatment of Early Stage/Localized Disease (Not CME Accredited Session) (ID 982)
- Event: WCLC 2018
- Type: Poster Viewing in the Exhibit Hall
- Track:
- Presentations: 1
- Moderators:
- Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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P3.16-07 - The Impact of Clinical and Molecular Profile of Resected EGFR-Mutant Non-Small Cell Lung Cancer on the Risk of Developing Brain Metastases (ID 13339)
12:00 - 13:30 | Author(s): Michael Cabanero
- Abstract
Background
Brain metastases are common in non-small cell lung cancers (NSCLC) with activating EGFR mutations (EGFRm), occurring in 44%-63% of patients. To date, there are no known clinical or molecular factors to predict the risk of brain metastases in these patients.
a9ded1e5ce5d75814730bb4caaf49419 Method
In this retrospective single-institution study, we identified 106 patients with EGFRm NSCLC who underwent surgery for primary lung tumor. Clinical and demographic data was collected from electronic records. Whole Exome Sequencing (WES) of the primary tumor was performed utilizing the Agilent SureSelect Exome v6+COSMIC baits followed by sequencing on the Illumina HiSeq2500 platform. Development of brain metastases was correlated with clinical/pathologic features, EGFR mutation type, co-mutation of EGFR and other frequently mutated genes; and non-synonymous tumor mutation burden (TMB). Statistical analysis used Fisher exact test for categorical variables, Mann-Whitney test for continuous variables of association with the risk of developing brain metastases, and Gray’s test for the probability of brain metastases over time.
4c3880bb027f159e801041b1021e88e8 Result
Of 106 patients who underwent surgical resection of primary EGFRm NSCLC, WES was successful for 73: 51 (70%) females, 52 (71%) never smokers, 38 (52%) stage I, 14 (19%) stage II and 21 (28%) stage III; 42 (57%) EGFR exon 19 mutation, 30 (41%) exon 21, 1(1%) Exon 20 insertion mutation.
Twenty-five patients (34%) developed brain metastases. Patients with brain metastases were younger (median age 61 vs. 65 years, p=0.021), had more advanced stages (p=0.012), with a trend towards higher rates in females (p=0.066). One patient with brain metastases had de-novo EGFR T790M mutation in the primary tumor. No difference was seen regarding smoking history, EGFR mutation type, TP53 co-mutation, and median TMB. The 5-year probability of brain metastases increased with increasing stage (14% stage I; 43% stage II, [HR=3.00], 44% stage III, [HR=3.13], p=0.03), and a trend towards higher probability among females (33% vs. 19%; HR=0.39 for males, p=0.074), and younger patients (37% <65 years vs. 15% >65, HR=0.37 in older patients, p=0.042). There was no difference in probability of brain metastases based on smoking history, ethnicity, EGFR type (33% exon 19 vs. 22% exon 21, p=0.28), TP53 co-mutation (31% vs. 27% without TP53, p=0.59), or TMB (24% TMB≤2.87 vs. 32% TMB>2.87non-synonymous mutations/Mb, p>0.99).
8eea62084ca7e541d918e823422bd82e Conclusion
While our findings suggest that younger age, advanced stage, and female sex may be associated with the development of BM in EGFRm NSCLC, we could identify no molecular predictor of BM based on EGFR subtype, TP53 co-mutation or TMB.
6f8b794f3246b0c1e1780bb4d4d5dc53
