Adenocarcinoma Lung Cancer Patients Research Articles

Deep sequencing of the TP53 gene reveals a potential risk allele for non-small cell lung cancer and supports the negative prognostic value of TP53 variants.

The TP53 gene remains the most frequently altered gene in human cancer, of which variants are associated with cancer risk, therapy resistance, and poor prognosis in several tumor types. To determine the true prognostic value of TP53 variants in non-small cell lung cancer, this study conducted further research, particularly focusing on subtype and tumor stage. Therefore, we determined the TP53 status of 97 non-small cell lung cancer adenocarcinoma patients using next generation deep sequencing technology and defined the prognostic value of frequently occurring single nucleotide polymorphisms and mutations in the TP53 gene. Inactivating TP53 mutations acted as a predictor for both worse overall and progression-free survival in stage II-IV patients and patients treated with DNA-damaging (neo)adjuvant therapy. In stage I tumors, the Pro-allele of the TP53 R72P polymorphism acted as a predictor for worse overall survival. In addition, we detected the rare R213R (rs1800372, minor allele frequency: 0.0054) polymorphism in 7.2% of the patients and are the first to show the significant association with TP53 mutations in non-small cell lung cancer adenocarcinoma patients (p = 0.003). In conclusion, Our findings show an important role for TP53 variants as negative predictors for the outcome of non-small cell lung cancer adenocarcinoma patients, especially for TP53 inactivating mutations in advanced stage tumors treated with DNA-damaging agents, and provide the first evidence of the R213R G-allele as possible risk factor for non-small cell lung cancer.

MDM2 SNP309 and SNP285 Act as Negative Prognostic Markers for Non-small Cell Lung Cancer Adenocarcinoma Patients.

Objectives: Two functional polymorphisms in the MDM2 promoter region, SNP309T>G and SNP285G>C, have been shown to impact MDM2 expression and cancer risk. Currently available data on the prognostic value of MDM2 SNP309 in non-small cell lung cancer (NSCLC) is contradictory and unavailable for SNP285. The goal of this study was to clarify the role of these MDM2 SNPs in the outcome of NSCLC patients.Materials and Methods: In this study we genotyped SNP309 and SNP285 in 98 NSCLC adenocarcinoma patients and determined MDM2 mRNA and protein levels. In addition, we assessed the prognostic value of these common SNPs on overall and progression free survival, taking into account the TP53 status of the tumor.Results and Conclusion: We found that the SNP285C allele, but not the SNP309G allele, was significantly associated with increased MDM2 mRNA expression levels (p = 0.025). However, we did not observe an association with MDM2 protein levels for SNP285. The SNP309G allele was significantly associated with the presence of wild type TP53 (p = 0.047) and showed a strong trend towards increased MDM2 protein levels (p = 0.068). In addition, patients harboring the SNP309G allele showed a worse overall survival, but only in the presence of wild type TP53. The SNP285C allele was significantly associated with an early age of diagnosis and metastasis. Additionally, the SNP285C allele acted as an independent predictor for worse progression free survival (HR = 3.97; 95% CI = 1.51 - 10.42; p = 0.005).Our data showed that both SNP309 (in the presence of wild type TP53) and SNP285 act as negative prognostic markers for NSCLC patients, implicating a prominent role for these variants in the outcome of these patients.

Prospective Analysis of Patients Treated with Chemotherapy in Metastatic Adenocarcinoma of Lung—Single Centre Experience

Background: Lung cancer is the leading cause of cancer-related death worldwide with an estimated 1.6 million new cases diagnosed each year. According to standard guidelines in NSCLC, the effectiveness of combined chemotherapy regimen comprises of pemetrexed and platinum, and very few reports are available in Indian population. This study shows the experience with pemetrexed and platinum combination chemotherapy in metastatic NSCLC in first line setting. Methods: Total 61 patients with following inclusion criteria were recruited such as: 1) PS of 1 and 2; 2) NSCLC of non-squamous histology; 3) locally advanced or metastatic disease at diagnosis; 4) should have received minimum 3 cycles of pemetrexed and platinum as first line treatment and or continued for 6 cycles; 5) EGFR/ALK mutated or EGFR/ALK unknown patients but must have received upfront chemo. Primary endpoint of the present study is to assess Disease Control Rate (DCR) (CR + PR + SD). Progression Free Survival, OS and Toxicity assessment were secondary endpoints. Results: The mean number of average chemotherapy cycles was found to be 4.38. The range of chemotherapy was 2 - 6 cycles. Disease control rate, defined as (CR + PR + SD), was seen in 44 (72.1%) patients. (PR in 26 (42.62%), SD 18 (29.5%)), Progressive disease (PD) was observed in 17 (27.9%) patients. Overall study showed that patients had PFS of 9.414 months (95% CI 6.709 - 12.120) and OS of 13.437 months (95% CI 10.721 - 16.153). Conclusion: Pemetrexed and platinum combination is effective and well-tolerated chemotherapy regimen in patients with metastatic adenocarcinoma lung cancer patients. Pemetrexed and cisplatin may be more effective in particular. Early switch over to TKIs is preferred immediately after obtaining molecular subtype result.

P1.06-022 Clinical Characteristics of Survival Outliers in Stage IV Adenocarcinoma Lung Cancer Patients

P1.06-022 Clinical Characteristics of Survival Outliers in Stage IV Adenocarcinoma Lung Cancer Patients

P3.02b-056 Survival in EGFR Mutated Advanced Lung Cancer Adenocarcinoma Patients - A National Study: Topic: EGFR Clinical

P3.02b-056 Survival in EGFR Mutated Advanced Lung Cancer Adenocarcinoma Patients - A National Study: Topic: EGFR Clinical

Tumor suppressor candidate 3 as a novel predictor for lymph node metastasis in lung cancer patients.

Tumor suppressor candidate 3 (TUSC3) was recently identified as a potential tumor suppressor gene in several cancer types. However, no data are currently available regarding the expression of TUSC3 in lung cancer. The present study investigated the expression of TUSC3 in patients with lung cancer and determined its association with the clinicopathological parameters of the disease. Cytoplasmic TUSC3 expression was evaluated by immunohistochemistry on tissue microarray slides, which included 35 small cell lung cancer (SCLC) specimens, 80 squamous cell lung cancer specimens (SCC), 80 adenocarcinoma lung cancer (ADC) specimens and 37 normal lung tissue specimens. Analysis showed significantly reduced TUSC3 expression in the SCLC patients, but not in the ADC and SCC patients, as compared with the normal controls. Additionally, TUSC3 expression in the patients with a degree of differentiation of 1–2 (well-moderately differentiated) was significantly higher than that in patients with a differentiation degree of 3–4 (poorly differentiated-undifferentiated). Further analysis showed that TUSC3 expression levels were negatively correlated with the degree of differentiation in the ADC and SCC patients. Notably, a marked decrease in TUSC3 expression was identified in the patients who were lymph node metastasis-positive (LNM+) compared with patients who were LNM−. Further analysis showed that significant differences in TUSC3 expression were identified among the different N stages (LNM status) in the SCLC, ADC and SCC patients. Correlation analysis also identified a negative correlation between TUSC3 expression and LNM in all three pathological types of lung cancer tested. Overall, these results indicated that a reduction in TUSC3 may be associated with a poorly-differentiated grade of lung cancer. Importantly, TUSC3 expression may be a useful predictor of LNM in lung cancer patients. A combined analysis of TUSC3 expression and the clinical variables will aid in predicting the incidence of LNM.

Expression profiling reveals transcriptional regulation by Fbxw7/mTOR pathway in radiation-induced mouse thymic lymphomas

The tumor suppressor gene FBXW7 is deleted and mutated in many different types of human cancers. FBXW7 primarily exerts its tumor suppressor activity by ubiquitinating different oncoproteins including mTOR. Here we used gene transcript profiling to gain a deeper understanding of the role of FBXW7 in tumor development and to determine the influence of mTOR inhibition by rapamycin on tumor transcriptome and biological functions. In comparison to tumors from p53 single heterozygous (p53+/-) mice, we find that radiation-induced thymic lymphomas from Fbxw7/p53 double heterozygous (Fbxw7+/-p53+/-) mice show significant deregulation of cholesterol metabolic processes independent of rapamycin treatment, while cell cycle related genes were upregulated in tumors from placebo treated Fbxw7+/-p53+/- mice, but not in tumors from rapamycin treated Fbxw7+/-p53+/- mice. On the other hand, tumors from rapamycin treated Fbxw7+/-p53+/- mice were enriched for genes involved in the integrated stress response, an adaptive mechanism to survive in stressful environments. Finally, we demonstrated that the Fbxw7 gene signatures identified in mouse tumors significantly overlap with FBXW7 co-expressed genes in human cancers. Importantly these common FBXW7 gene signatures between mouse and human are predictive for disease-free survival in human colon, breast and lung adenocarcinoma cancer patients. These results provide novel insights into the role of FBXW7 in tumor development and have identified a number of potential targets for therapeutic intervention.

BMET-22DIFFERENT SPATIAL DISTRIBUTION OF BRAIN METASTASIS FROM LUNG CANCER DEFINED BY EGFR MUTATION STATUS

PURPOSE: To test this hypothesis that different genetic backgrounds of lung cancers could affect spatial distribution of brain metastasis. EXPERIMENTAL DESIGN: CT or MR images of 200 patients with a total of 1033 treatment naive brain metastases from lung cancer were retrospectively collected. All images were deformed and standardized to MNI 152 standard human brain MRI. Locations of the lesions, depths of the lesions from brain surface, and sizes of the lesions after image standardization were analyzed and compared between histological subtypes of the primary lesion as well as EGRF mutation status. RESULTS: The posterior fossa, the anatomic watershed areas and the grey-white matter junction were confirmed to be predilection areas of lung cancer brain metastasis and brain metastasis with L858R occurred more often in caudate, cerebellum and temporal lobe than those with Ex19Del. Among adenocarcinoma lung cancer patients, depths of the lesions from brain surface were 15.7 ± 9.1mm for Ex19Del, 12.6 ± 8.5mm for L858R and 16.1 ± 8.5mm for WT. The lesions with L858R were located statistically significantly closer to the brain surface than the lesions with Ex19Del or WT (p = 0.0032 and p < 0.0001, respectively). On the other hand, there was no statistically significant difference in tumor size among different EGFR mutation status (p = 0.086). Furthermore, brain metastases of adenocarcinoma lung cancer patients with history of chemotherapy treatment were located statistically significantly deeper from brain surface (p = 0.0002). History of molecular targeted therapy did not have any effect on the depth of the lesion. CONCLUSIONS: This analysis is the first to reveal the relationship between tumor's molecular biological characteristics, namely EGFR mutation status and spatial distribution of brain metastases of lung cancer.

Different spatial distributions of brain metastases from lung cancer by histological subtype and mutation status of epidermal growth factor receptor.

The purpose of this study was to test the hypothesis that the genetic backgrounds of lung cancers could affect the spatial distribution of brain metastases. CT or MR images of 200 patients with a total of 1033 treatment-naive brain metastases from lung cancer were retrospectively reviewed (23 by CT and 177 by MRI). All images were standardized to the human brain MRI atlas provided by the Montreal Neurological Institute 152 database. Locations, depths from the brain surface, and sizes of the lesions after image standardization were analyzed. The posterior fossa, the anatomic "watershed areas," and the gray-white matter junction were confirmed to be more commonly affected by lung cancer brain metastases, and brain metastases with epidermal growth factor receptor (EGFR) L858R mutation occurred more often in the caudate, cerebellum, and temporal lobe than those with exon 19 deletion of EGFR. Median depths of the lesions from the brain surface were 13.7 mm (range, 8.6-21.9) for exon 19 deleted EGFR, 11.5 mm (6.6-16.8) for L858R mutated, and 15.0 mm (10.0-20.7) for wild-type EGFR. Lesions with L858R mutated EGFR were located significantly closer to the brain surface than lesions with exon 19 deleted or wild-type EGFR (P = .0032 and P < .0001, respectively). Furthermore, brain metastases of adenocarcinoma lung cancer patients with a history of chemotherapy but not molecular targeted therapy were located significantly deeper from the brain surface (P = .0002). This analysis is the first to reveal the relationship between EGFR mutation status and the spatial distribution of brain metastases of lung cancer.

Plasma lipid biomarker signatures in squamous carcinoma and adenocarcinoma lung cancer patients

There is a clinical need for reliable biomarkers for lung cancer that permit early diagnosis of the disease and provide prediction of histological phenotype. A prospective study design was used with a study population of patients with suspected lung cancer. Blood samples were collected from 17 patients with histologically confirmed squamous cell lung carcinoma, 17 individuals with adenocarcinoma, and 17 control individuals who did not subsequently have a diagnosis of lung cancer or any other cancer. Blood plasma samples were analysed for their lipid profiles using liquid chromatography coupled with high resolution mass spectrometry. Data were analysed using multivariate statistical methods. There was good separation between histological subtypes and control groups and also between individuals with a subsequent diagnosis of adenocarcinoma and squamous cell carcinoma (sensitivity 80 %, specificity 83 %, Q2 = 0.70). Alterations in the levels of different classes of lipids including triglycerides (TGs), phosphatidylinositols (PIs), phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), free fatty acids, lysophospholipids and sphingolipids were observed in squamous carcinoma and adenocarcinoma lung cancer patients when compared with control patients. In conclusion, this study has identified candidate lipid biomarkers of non-small cell lung cancer patients which may be helpful to indicate the tumour subtype and to differentiate them from patients who do not have lung cancer. Measuring these biomarkers has the potential to improve diagnosis in patients with suspected lung cancer and risk stratification in screening.

A first-in-human study of LOXO-101, a highly selective inhibitor of the tropomyosin receptor kinase (TRK) family.

TPS2624 Background: TheTRK family of neurotrophin receptors, TRKA, TRKB, and TRKC (encoded by NTRK1, NTRK2, and NTRK3 genes, respectively) and their neurotrophin ligands regulate growth, differentiation and survival of neurons. Translocations involving the NTRK1/2/3 kinase domain, mutations involving the TRK ligand-binding site, amplifications of NTRK, TRK splice variants, and autocrine/paracrine signaling have been described in a diverse number of tumor types and may contribute to tumorigenesis. Recently NTRK1 fusions were described in a subset of adenocarcinoma lung cancer patients (Vaishnavi, 2013) and NTRK2 and NTRK3 fusions have been described in multiple tumor types (Skalova, 2014; Ricarte-Filho, 2013; Vaishnavi, 2014). LOXO-101 is a potent, oral, ATP-competitive pan-TRK inhibitor with IC50 values in the low nanomolar range for inhibition of TRK family members in binding and cellular assays, with 100x selectivity over other kinases. LOXO-101 has demonstrated tumor inhibition in preclinical models. M...

A Case Report of a Metastatic Adenocarcinoma of Lung with Dual Positivity for EGFR Mutation and ALK Fusion

Non-small cell lung cancer ranks among the most lethal cancers worldwide. The rate of epidermal growth factor receptor (EGFR) mutations and echinoderm microtubuleassociated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) gene fusion is the most common in younger age, non-smoking Asian adenocarcinoma lung cancer patients. EGFR mutations and ALK gene rearrangements are known to be mutually exclusive and as mutual causes of resistance to EGFR-tyrosine kinase inhibitors (TKIs) or ALK-TKIs. However, rarely such co-alterations do co-exist in some clinical cases. Here we report a 62 year old male, heavy smoker with cough, hemoptysis and fatigue. Histopathological examination of bronchoscopic guided biopsy showed adenocarcinoma histology. Staging evaluation, he was found to have stage IV disease on positron emission tomography-computed tomography scan. The biopsy blocks tested positive for both EGFR mutation and ALK fusion. Patient was initiated on tablet Gefitinib 250 mg once daily. To the best of our knowledge, there has been no report of dual EGFR mutation and ALK fusion positivity from India.

An NMR metabolomics approach for the diagnosis of leptomeningeal carcinomatosis in lung adenocarcinoma cancer patients

Leptomeningeal carcinomatosis (LC) is a metastatic cancer invading the central nervous system (CNS). We previously reported a metabolomic diagnostic approach as tested on an animal model and compared with current modalities. Here, we provide a proof of concept by applying it to human LC originating from lung cancer, the most common cause of CNS metastasis. Cerebrospinal fluid from LC (n = 26) and normal groups (n = 41) were obtained, and the diagnosis was established with clinical signs, cytology, MRI and biochemical tests. The cytology on the CSF, the current gold standard, exhibited 69% sensitivity (~100% specificity) from the first round of CSF tapping. In comparison, the nuclear magnetic resonance spectra on the CSF showed a clear difference in the metabolic profile between the LC and normal groups. Multivariate analysis and cross-validation yielded the diagnostic sensitivity of 92%, the specificity of 96% and the area under the curve (AUC) of 0.991. Further spectral and statistical analysis identified myo-inositol (p < 5 × 10(-14)), creatine (p < 7 × 10(-8)), lactate (p < 9 × 10(-4)), alanine (p < 7.9 × 10(-3)) and citrate (p < 3 × 10(-4)) as the most contributory metabolites, whose combination exhibited an receiver-operating characteristic diagnostic AUC of 0.996. In addition, the metabolic profile could be correlated with the grading of radiological leptomeningeal enhancement (R(2) = 0.3881 and p = 6.66 × 10(-4)), suggesting its potential utility in grading LC. Overall, we propose that the metabolomic approach might augment current diagnostic modalities for LC, the accurate diagnosis of which remains a challenge.

Rash and diarrhea with afatinib treatment in metastatic adenocarcinoma lung cancer patients (pts) unselected for epidermal growth factor receptor (EGFR) mutations: Retrospective study.

e19165 Background: Afatinib (Gilotrif, Giotrif) is an orally administered, irreversible inhibitor of the ErbB family of tyrosine kinases. The drug is approved from june 2013 as front-line therapy f...

Differential proteomic approach for identification and verification of aberrantly glycosylated proteins in adenocarcinoma lung cancer (ADLC) plasmas by lectin-capturing and targeted mass spectrometry

To investigate quantitative differences in aberrant glycosylation of target glycoproteins between noncancerous group and patient group with adenocarcinoma lung cancer (ADLC), differential proteomic approach was developed by cooperatively using comparative lectin-capturing, targeted mass spectrometry (MRM MS), and antibody/lectin sandwich ELISA. Plasma samples comparatively prepared from 3 ADLC patients and 3 controls, with and without lectin-fractionation using fucose-specific Aleuria aurantia lectin (AAL), were trypsin-digested and analyzed for target glycoproteins, alpha-1-acid glycoprotein (AGP) and ceruloplasmin (CP), by MRM MS. From the MRM MS data the abundance levels of AAL-captured glycoforms of both targets were significantly higher in ADLC cases compared to controls, although the levels in total protein abundance were comparable between ADLC and control groups. This difference between ADLC and control groups in the fucosylated glycoform levels was originated mainly from aberrant fucosylation on the targets in ADLC plasmas rather than change in total protein abundance of the targets, and also confirmed by sandwich ELISA. AGP and CP were further verified to be biomarker candidates by MRM-based analysis of AAL-captured plasmas (30 ADLC cases, 30 controls), with AUROC 0.758 and 0.847 respectively. This differential proteomic approach can be useful for identifying and verifying biomarker candidate involved in aberrant protein glycosylation. The present paper introduces an efficient differential proteomic method to investigate quantitative differences in aberrant protein glycosylation of serological glycoproteins between noncancerous group and lung cancer patient group. This differential proteomic approach consisting of the targeted MRM MS of comparatively lectin-captured plasma fractions and the antibody/lectin sandwich ELISA-based assay was evaluated to be useful for identification of aberrantly fucosylated glycoproteins AGP and CP in lung cancer plasmas. In addition, we have demonstrated that the MRM MS-based differential proteomic approach is also useful for high-throughput verification of the aberrantly fucosylated glycoproteins AGP and CP using the large number of individual plasmas. Therefore, the present MRM MS-based differential proteomic strategy with lectin-capturing can be a powerful tool for high-throughput verification of aberrantly glycosylated biomarker candidates, identified preliminary by mass profiling experiments in proteomic fields but requiring further validation using a large number of cohorts.

MiRNA and mRNA cancer signatures determined by analysis of expression levels in large cohorts of patients

Toward identifying a cancer-specific gene signature we applied surprisal analysis to the RNAs expression behavior for a large cohort of breast, lung, ovarian, and prostate carcinoma patients. We characterize the cancer phenotypic state as a shared response of a set of mRNA or microRNAs (miRNAs) in cancer patients versus noncancer controls. The resulting signature is robust with respect to individual patient variability and distinguishes with high fidelity between cancer and noncancer patients. The mRNAs and miRNAs that are implicated in the signature are correlated and are known to contribute to the regulation of cancer-signaling pathways. The miRNA and mRNA networks are common to the noncancer and cancer patients, but the disease modulates the strength of the connectivities. Furthermore, we experimentally assessed the cancer-specific signatures as possible therapeutic targets. Specifically we restructured a single dominant connectivity in the cancer-specific gene network in vitro. We find a deflection from the cancer phenotype, significantly reducing cancer cell proliferation and altering cancer cellular physiology. Our approach is grounded in thermodynamics augmented by information theory. The thermodynamic reasoning is demonstrated to ensure that the derived signature is bias-free and shows that the most significant redistribution of free energy occurs in programming a system between the noncancer and cancer states. This paper introduces a platform that can elucidate miRNA and mRNA behavior on a systems level and provides a comprehensive systematic view of both the energetics of the expression levels of RNAs and of their changes during tumorigenicity.

Surgical treatment of a patient with lung cancer metastasized to the spine with EGFR mutation: A case report

INTRODUCTIONThe prognosis of patients with lung cancer metastasis to the spine is not very promising and a palliative approach is often suggested by scales such as the Tomita score. The choice of surgery for these patients is questionable based on the aggressiveness of the disease. However, certain patient characteristics can be sought out to determine if surgery is indicated. PRESENTATION OF CASEHere, we present a case of a 59 year old male which consulted for back pain, numbness of the upper left thigh, and weakness corresponding to an L2 lesion. It was later discovered that he was suffering from non small cell lung cancer (adenocarcinoma) with a single metastasis to the spine at the level of L2. The patient also presented an EGFR mutation. Thus, the patient presented two good prognosis characteristics: adenocarcinoma and an EGFR mutation. DISCUSSIONAn aggressive treatment was chosen. This included an EGFR inhibitor, surgical treatment, and radiotherapy thereafter. The patient had no complications due to surgery and to date, the patient has survived over 12 months and is free of any symptoms. This case demonstrates that surgical intervention can be considered for certain patients with lung cancer metastasized to the spine. CONCLUSIONThis case demonstrates that surgical intervention can be considered for certain patients with lung cancer metastasized to the spine. We hope spine surgeons in general will start verifying the EGFR mutation status of adenocarcinoma lung cancer patients to determine if surgery is indicated.

P2-020: Genetic characterictics of women lung adenocarcinoma

The incidence of lung cancer has been rapidly increasing in the world and it has been the most frequent malignancy. The most significant carcinogenesis of lung cancer has been smoking. Recently, proportion of adenocarcinoma has been increasing. Asian women adenocarcinoma lung cancer patients show frequently EGFR mutation. These patients show high sensitivity to gefitinib. A considerable proportion of no smoker women have lung cancer, which is a serious problem. We tried to find novel cancer related genes which are different from smoker lung cancer patients. We will perform array comparative genomic hybridization (CGH) with 1,440 human bacterial artificial chromosome (BAC) clones to assess copy number changes in 20 lung cancer samples. These patients received operation in our hospital. Array-CGH methods have been used for genome-wide, high-resolution analysis of chromosomal alterations. All of the patients included had received operation in our hospital. 10 patients are no smoker (No smoker group) and 10 patients were smoker (Smoker group). Potential prognostic variables were comparable between the two groups. In an unsupervised clustering analysis, samples from each group were well separated. The average frequency of copy number changes was similar between the two groups. Our array CGH analysis with BAC clones could detect various genomic alterations in no smoker lung cancers, and no smoker lung cancer samples showed a different pattern of DNA copy number changes than did smoker lung cancer group samples. We have finished 8 no smoker lung cancer samples and 3 smoker lung cancer samples. We will show the array-CGH data about difference between smoker patient pattern and no-smoker. Especially genetic characteritics of adenocarcinoma in women no-smoker patients will be shown.

Human-human hybridomas secreting antibodies specific to human lung carcinoma.

Human Namalwa cells were screened in serum-free medium and in 6-thioguanine, then fused with human lymphocytes from lymph nodes of lung adenocarcinoma cancer patients. Extensive testing using 14 lung cancer cell lines, 11 other cancer cell lines and 4 normal fibroblast lines identified monoclonal antibodies produced by 4 hybridoma clones that reacted specifically with lung adenocarcinoma cells. These monoclonal antibodies also reacted with lung adenocarcinoma tissues and not normal tissues or erythrocytes of any blood type. These hybridoma clones grew and stably secreted the antibodies in serum-free medium as well as in serum-containing medium.