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 »  Abstract
 » Introduction
 » Subjects and Methods
 » Results
 » Discussion
 » Conclusion
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  Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 55  |  Issue : 3  |  Page : 273-275
 

Clinicopathological profile of lung cancer at a tertiary care center


Department of Medical Oncology, Omega Hospitals, Hyderabad, Telangana, India

Date of Web Publication28-Jan-2019

Correspondence Address:
Dr. Satya Palanki Dattatreya
Department of Medical Oncology, Omega Hospitals, Hyderabad, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijc.IJC_455_17

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 » Abstract 


BACKGROUND: Lung cancer is one of the most common malignancies with high morbidity and mortality. Nonsmall cell lung cancer (NSCLC) accounts for majority of cases. AIMS: This study aims to study the clinical and pathological features of lung cancer patients treated at our institute between January 2011 and December 2016. SUBJECTS AND METHODS: It is a retrospective study. 446 patients of lung cancer were retrospectively analyzed for demographic data, history of smoking, histological type, and presence of epidermal growth factor receptor (EGFR) mutation/anaplastic lymphoma kinase (ALK) mutations. RESULTS: Of the 446 patients analyzed, 304 (68%) were males and 142 (32%) were females, with the ratio being 2:1. Most of our patients had a lesion localizing to the right side (45.7%) than left (37.8%). NSCLC was reported in 81.1% of our patients. EGFR mutation was found in 60 (24%) patients, the most common mutation being the deletion of exon 19 (73%) followed by L858R mutation (21.6%). CONCLUSIONS: EGFR and ALK mutation testing of all the lung cancer patients is to be encouraged as these mutations form druggable targets.


Keywords: Adenocarcinoma, epidermal growth factor receptor, lung cancer


How to cite this article:
Dattatreya SP, Bansal R, Vamsy M, Vaniawala S, Nirni S S, Dayal M, Sharma R. Clinicopathological profile of lung cancer at a tertiary care center. Indian J Cancer 2018;55:273-5

How to cite this URL:
Dattatreya SP, Bansal R, Vamsy M, Vaniawala S, Nirni S S, Dayal M, Sharma R. Clinicopathological profile of lung cancer at a tertiary care center. Indian J Cancer [serial online] 2018 [cited 2019 Apr 26];55:273-5. Available from: http://www.indianjcancer.com/text.asp?2018/55/3/273/250890





 » Introduction Top


Lung cancer is the leading cause of death among the cancer patients worldwide. The major risk factor has been attributed to the prevalent habit of smoking tobacco. Its incidence seems to be rising in India and world over, despite several smoking cessation programs, thus indicating that several other factors contribute to its pathogenesis. The ICMR cancer registry reported 57,795 cases in 2010, which is expected to rise by 2020 to an annual incidence of 67,000 new cases.[1] Globocan estimate of lung cancer in India would indicate that the age-standardized incidence of lung cancer in India is 6.9/100,000 of our population.[2] Majority of the patients present at an advanced stage of the disease, which makes management of these patients challenging. Despite advances in detection and management, the overall 5-year survival in lung cancer remains low at 15%.[3]

Our knowledge of lung cancer has expanded, and we are moving from histological classification to molecular classification. Driver mutations and new molecular targets are being identified.[4] The tyrosine kinase domain of epidermal growth factor receptor (EGFR) undergoes activating mutation and is a target for therapy. Mutation in exons 18–21 of the tyrosine kinase domain of the gene for EGFR correlates with high likelihood of response to EGFR tyrosine kinase inhibitors. A fusion gene between echinoderm microtubule-associated protein-like 4 (EML 4) and intracellular domain of anaplastic lymphoma kinase (ALK) called EML4-ALK has been identified in a subset, commonly in nonsmall cell lung cancer (NSCLC).[5],[6] Different incidence rates of these mutations have been reported. These mutations are mutually exclusive. With the advent of molecularly targeted agent, the median survival has improved from 12–14 months to 24–36 months.

The histological subtypes of lung cancer, namely, small cell lung cancer (SCLC) and the NSCLC, exhibit varying epidemiological patterns.


 » Subjects and Methods Top


A retrospective analysis of all the histopathologically proven primary lung cancer patients diagnosed and treated at our center over the period of January 2011–December 2016 was carried out. Patients with secondary lung cancer, lymphoproliferative disease, malignant pleural effusion with an unknown primary, and other rare histologies were excluded from the study. A note was made of the demographical data, along with the histological subtype, side of the tumor, EGFR mutation testing, and ALK rearrangement analysis. Data were entered and analyzed.


 » Results Top


A retrospective analysis of 446 patients of lung cases registered between January 2011 and December 2016 at our institute was studied. Patients ranged in age from 29 to 87 years. Majority of the patients were in the age group of 40–60 years (49.1%), with the median age of 60. Of the 446 patients analyzed, 304 (68%) were males and 142 (32%) were females, with the ratio being 2:1. Most of our patients had a lesion localizing to the right side (45.7%) than left (37.8%). NSCLC was reported in 81.1% of our patients. Adenocarcinoma was the most common histological subtype (66%). Squamous cell carcinoma was present in 11.6% patients, adenosquamous in 3.5% patients, and large cell in 0.5% patients. Small cell carcinoma was seen in 2.9% patients, while 15.5% of patients had undifferentiated histology. EGFR testing was performed on 250 patients and ALK testing was done on 238 patients. EGFR mutation was found in 60 (24%) patients, the most common mutation being the deletion of exon 19 (73%) followed by L858R mutation (21.6%). Other rare mutations seen were L861Q (2 patients) and S720P (1 patient). ALK rearrangement was seen in five patients (2.1%). None of the samples showed a concomitant mutation.


 » Discussion Top


The gender distribution of the patients in our study reflects the rising trend of lung cancer in women. The male to female ratio was 2:1 in this study. This may be explained by the fact that more and more urban women are now resorting to smoking as a habit. The median age of diagnosis in our study was 60 years, with 49.1% patients in the age group of 40–60 years. Noronha et al.[7] studied 489 lung cancer patients treated over a period of an year and reported a median age of 56 years with a male to female ratio of 3.5:1. A retrospective analysis of metastatic lung cancer patients carried out at Kidwai institute found 55.6% patients in the age group of 41–60 years.[8]

In this study, we found that 69% of patients were smokers (current or reformed). A study from Kolkata at a tertiary medical care center reported a high incidence of smoking of 81.2%.[9] Babu et al.[8] found that of the 304 patients in their study, 63.5% were smokers. The cause of occurrence of lung cancer in nonsmokers remains elusive. In nonsmokers, the attributable risk factors include secondhand smoke;[10],[11] environmental exposures including asbestos,[12],[13] arsenic, and radon;[14] viruses like human papillomavirus;[15] lung diseases such as idiopathic pulmonary fibrosis;[16] and indoor air pollutants like fumes and smoke emitted from coal stove.[17]

Over the past four decades, there has been a shift in the pathologic distribution of NSCLC. In the study, NSCLC (81.1%) constituted the major histological type, with adenocarcinoma being most commonly found in 66% of patients. In the study by Noronha et al. conducted at Tata Memorial Hospital on 489 patients, they showed 92% had NSCLC histology, with adenocarcinoma constituting 43.8%. We found squamous cell carcinoma in 11.6% of the patients, while Noronha et al. found squamous cell histology in 26.2% of the patients. This is in contrast to the findings reported by Babu et al.[8] who found an equal distribution of adenocarcinoma and squamous cell carcinoma. Kumar et al.[9] reported squamous cell carcinoma to be the common histological type in their study of 266 patients at a tertiary center in Kolkata.

We found the right lung to be more commonly involved than the left and so was seen by Mohan et al. (52.3%)[18] and Kumar et al. (65.79%) in their studies.

Various studies on NSCLC patients of Indian ethnicity have reported the presence of EGFR mutations in the range of 23%–44%.[19] We found EGFR mutation testing to be positive in 24% of our patients who underwent EGFR testing, while ALK-1 gene rearrangement was seen in only 2.1% of the patients who underwent the testing. These findings were similar to the ones found by the observational study carried out across various locations all over the country involving a cohort of 3351 patients of NSCLC. About 28.19% of patients were positive for the presence of EGFR mutation, with exon 19 mutation being found in 72.99%. They found ALK gene rearrangement in 2.53% patients. Kalal Iravathy et al.[20] found EGFR mutation in 20.59% of 267 lung cancer patients at a tertiary health center in Hyderabad, with exon 19 mutation being the most common (56%). We found exon 19 deletion in 73% of the cases with EGFR mutation. We found ALK gene rearrangement in 2.1% cases, while Kalal Iravathy et al. reported it at a frequency of 4.11%. The EGFR mutations and ALK rearrangements occur independent of each other, i.e. they are mutually exclusive, and this was observed in our study too.


 » Conclusion Top


The detection of these as molecular targets for therapy has revolutionized the treatment of lung cancer. The targeted agents, namely, erlotinib, gefitinib, and crizotinib, are now category 1 recommendation for treatment of metastatic lung cancer and with their use, the progression-free survival of up to 24–36 months have been reached when compared to 8.7 months with the use of systemic chemotherapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

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Takiar R, Nadayil D, Nandakumar A. Projections of number of cancer cases in India (2010-2020) by cancer groups. Asian Pac J Cancer Prev 2010;11:1045-9.  Back to cited text no. 1
    
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Available from: http://www.globocan.iarc.fr/Pages/fact_sheets_ cancer.aspx. [Last accessed on 2016 Feb 20].  Back to cited text no. 2
    
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Jemal A, Siegel R, Ward E, Hao Y, Xu J, Murray T, et al. Cancer statistics, 2008. CA Cancer J Clin 2008;58:71-96.  Back to cited text no. 3
    
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Pao W, Girard N. New driver mutations in non-small-cell lung cancer. Lancet Oncol 2011;12:175-80.  Back to cited text no. 4
    
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Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature 2007;448:561-6.  Back to cited text no. 5
    
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Zhang X, Zhang S, Yang X, Yang J, Zhou Q, Yin L, et al. Fusion of EML4 and ALK is associated with development of lung adenocarcinomas lacking EGFR and KRAS mutations and is correlated with ALK expression. Mol Cancer 2010;9:188.  Back to cited text no. 6
    
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Noronha V, Dikshit R, Raut N, Joshi A, Pramesh CS, George K, et al. Epidemiology of lung cancer in India: Focus on the differences between non-smokers and smokers: A single-centre experience. Indian J Cancer 2012;49:74-81.  Back to cited text no. 7
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8.
Babu G, Lakshmaiah KC, Kamath M, Lokanath D. Metastatic lung cancer at a tertiary cancer centre in South India. J Thorac Oncol 2017;12 (Suppl):S484-S5.  Back to cited text no. 8
    
9.
Kumar BS, Abhijit M, Debasis D, Abinash A, Ghoshal AG, Kumar DS, et al. Clinico-pathological profile of lung cancer in a tertiary medical centre in India: Analysis of 266 cases. J Dent Oral Hygiene 2011;3:30-3.  Back to cited text no. 9
    
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Brennan P, Buffler PA, Reynolds P, Wu AH, Wichmann HE, Agudo A, et al. Secondhand smoke exposure in adulthood and risk of lung cancer among never smokers: A pooled analysis of two large studies. Int J Cancer 2004;109:125-31.  Back to cited text no. 10
    
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Vineis P, Airoldi L, Veglia F, Olgiati L, Pastorelli R, Autrup H, et al. Environmental tobacco smoke and risk of respiratory cancer and chronic obstructive pulmonary disease in former smokers and never smokers in the EPIC prospective study. BMJ 2005;330:277.  Back to cited text no. 11
    
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van Loon AJ, Kant IJ, Swaen GM, Goldbohm RA, Kremer AM, van den Brandt PA, et al. Occupational exposure to carcinogens and risk of lung cancer: Results from the Netherlands cohort study. Occup Environ Med 1997;54:817-24.  Back to cited text no. 12
    
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Chen CL, Hsu LI, Chiou HY, Hsueh YM, Chen SY, Wu MM, et al. Ingested arsenic, cigarette smoking, and lung cancer risk: A follow-up study in arseniasis-endemic areas in Taiwan. JAMA 2004;292:2984-90.  Back to cited text no. 13
    
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Darby S, Hill D, Auvinen A, Barros-Dios JM, Baysson H, Bochicchio F, et al. Radon in homes and risk of lung cancer: Collaborative analysis of individual data from 13 European case-control studies. BMJ 2005;330:223.  Back to cited text no. 14
    
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Ciotti M, Giuliani L, Ambrogi V, Ronci C, Benedetto A, Mineo TC, et al. Detection and expression of human papillomavirus oncogenes in non-small cell lung cancer. Oncol Rep 2006;16:183-9.  Back to cited text no. 15
    
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Hubbard R, Venn A, Lewis S, Britton J. Lung cancer and cryptogenic fibrosing alveolitis. A population-based cohort study. Am J Respir Crit Care Med 2000;161:5-8.  Back to cited text no. 16
    
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Yu IT, Chiu YL, Au JS, Wong TW, Tang JL. Dose-response relationship between cooking fumes exposures and lung cancer among Chinese nonsmoking women. Cancer Res 2006;66:4961-7.  Back to cited text no. 17
    
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Mohan A, Latifi AN, Guleria R. Increasing incidence of adenocarcinoma lung in India: Following the global trend? Indian J Cancer 2016;53:92-5.  Back to cited text no. 18
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Doval D, Prabhash K, Patil S, Chaturvedi H, Goswami C, Vaid A, et al. Clinical and epidemiological study of EGFR mutations and EML4-ALK fusion genes among Indian patients with adenocarcinoma of the lung. Onco Targets Ther 2015;8:117-23.  Back to cited text no. 19
    
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Kalal Iravathy G. Molecular diagnosis of lung cancers. Mol Enzymol Drug Targets 2015;1:1-8.  Back to cited text no. 20
    




 

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