Intestinal type of lung adenocarcinoma (ILADC) was initially described by Tsao and Fraser in 1991. Morphology and immunophenotype of ILADC are the same as in colorectal adenocarcinoma. Rectocolonoscopy must be performed to exclude colorectal origin of adenocarcinoma. Colorectal adenocarcinoma claimed to be genetically similar to an ILADC. Patients. We describe 24- and 26-year-old patients of both genders who went under surgery because of a lung tumor mass detected on CT scan. ILADC was diagnosed on resected lung specimens. According to positivity of Cytokeratin20, CDX-2, and Villin, respectively, and negativity of Cytokeratin7, TTF-1, Napsin-A, SurfactantB, MUC-1, and MUC-2, respectively, ILADC was diagnosed. KRAS mutation was detected in tumor tissue of the male patient. Conclusion. Rectocolonoscopy is the only relevant method for distinguishing the intestinal type of lung adenocarcinoma from metastatic colorectal carcinoma because immunohistochemistry and detection of mutation status are frequently the same in both types of adenocarcinoma. More investigations are needed for further understanding of ILADC in purpose of personalized lung carcinoma therapy particularly introducing detection of mutation status, especially in younger patients. 1. Introduction In the last few decades, adenocarcinoma is the worldwide most common histologic subtype of lung carcinoma. It develops more frequently than any other histologic types of lung carcinoma in no smokers, particular in women. Intestinal type of lung adenocarcinoma ILADC [1, 2] was not mentioned in WHO lung carcinoma classification from 1999 to 2004. In recent years, International Study Group of Lung Carcinoma introduced ILADC in adenocarcinoma classification [3–5], but this variant of lung adenocarcinoma was initially described by Tsao and Fraser in 1991, and it was characterized by a predominant component of malignant tall, stratified columnar, and goblet cells [6]. Immunophenotype of ILADC is the same as in colorectal adenocarcinoma. Malignant cells are positive for Cytokeratin20 and CDX-2 and negative for Cytokeratin7 and TTF-1 [7–9]. Rectocolonoscopy must be performed in order to exclude colorectal origin of adenocarcinoma. Patients reported in the respected literature were older than patients in our study [9]. It is well known that EGFR and KRAS gene mutations act as positive and negative predictors, respectively, of therapeutic response to EGFR targeted therapies in colorectal adenocarcinoma. This tumor claimed to be genetically similar to ILADC [10]. Here we describe 24-year-old and 26-year-old
References
[1]
W. D. Travis, E. Brambilla, H. K. Muller-Hermelink, et al., World Health Organisation Classification of Tumours. Pathology and Genetics of the Lung, Pleura, Thymus and Heart, IARC Press, Lyon, France, 2004.
[2]
W. D. Travis, T. V. Colby, B. Corrin, Y. Shimamoto, E. Brambilla, and L. H. Sobin, World Health Organization International Histological Classification of Tumors, Springer, Berlin, Germany, 1999.
[3]
W. D. Travis, E. Brambilla, M. Noguchi et al., “International association for the study of lung carcinoma/American Thoracic Society/European Respiratory Society international multidisciplinary classification of lung adenocarcinoma,” Journal of Thoracic Oncology, vol. 6, no. 2, pp. 244–285, 2011.
[4]
K. M. Kerr, “Pulmonary adenocarcinomas: classification and reporting,” Histopathology, vol. 54, no. 1, pp. 12–27, 2009.
[5]
W. D. Travis, E. Brambilla, and G. J. Riely, “New pathologic classification of lung carcinoma: relevance for clinical practice and clinical trials,” Journal of Clinical Oncology, vol. 31, no. 8, pp. 992–1001, 2013.
[6]
M.-S. Tsao and R. S. Fraser, “Primary pulmonary adenocarcinoma with enteric differentiation,” Cancer, vol. 68, no. 8, pp. 1754–1757, 1991.
[7]
S. A. Yousem, “Pulmonary intestinal-type adenocarcinoma does not show enteric differentiation by immunohistochemical study,” Modern Pathology, vol. 18, no. 6, pp. 816–821, 2005.
[8]
R. Maeda, N. Isowa, H. Onuma, and H. Miura, “Pulmonary intestinal-type adenocarcinoma,” Interactive Cardiovascular and Thoracic Surgery, vol. 7, no. 2, pp. 349–351, 2008.
[9]
H. C. Li, L. Schmidt, J. K. Greenson, A. C. Chang, and J. L. Myers, “Primary pulmonary adenocarcinoma with intestinal differentiation mimicking metastatic colorectal carcinoma case report and review of literature,” American Journal of Clinical Pathology, vol. 131, no. 1, pp. 129–133, 2009.
[10]
C. García-Inclán, F. López, J. Pérez-Escuredo et al., “EGFR status and KRAS/BRAF mutations in intestinal-type sinonasal adenocarcinomas,” Cellular Oncology, vol. 35, no. 6, pp. 443–450, 2012.
[11]
K. Inamura, Y. Satoh, S. Okumura et al., “Pulmonary adenocarcinomas with enteric differentiation: histologic and immunohistochemical characteristics compared with metastatic colorectal cancers and usual pulmonary adenocarcinomas,” American Journal of Surgical Pathology, vol. 29, no. 5, pp. 660–665, 2005.
[12]
W. D. Travis, E. Brambilla, M. Noguchi et al., “Diagnosis of lung adenocarcinoma in resected specimens. Implications of the 2011 international association for the study of lung Carcinoma/American Thoracic Society/European Respiratory Society Classification,” Archives of Pathology & Laboratory Medicine, vol. 136, pp. 1–23, 2012.
[13]
J. Stojsic, I. Jovanic, J. Markovic, and M. Gajic, “Contribution of immunohistochemistry in differential diagnosis of non-small cell lung carcinomas on small biopsy samples,” Journal of BUON, vol. 18, no. 1, pp. 176–187, 2013.
[14]
S. T. Yuen, H. Davies, T. L. Chan et al., “Similarity of the phenotypic patterns associated with BRAF and KRAS mutations in colorectal neoplasia,” Cancer Research, vol. 62, no. 22, pp. 6451–6455, 2002.
[15]
W. H. Westra, R. J. C. Slebos, G. J. A. Offerhaus et al., “K-ras oncogene activation in lung adenocarcinomas from former smokers: evidence that K-ras mutations are an early and irreversible event in the development of adenocarcinoma of the lung,” Cancer, vol. 72, no. 2, pp. 432–438, 1993.
[16]
C. Oliveira, J. L. Westra, D. Arango et al., “Distinct patterns of KRAS mutations in colorectal carcinomas according to germline mismatch repair defects and hMLH1 methylation status,” Human Molecular Genetics, vol. 13, no. 19, pp. 2303–2311, 2004.