LUNG GROWING INTESTINE?

Document Type

Conference Proceeding

Publication Date

7-17-2025

Publication Title

J Gen Intern Med

Keywords

carboplatin, homeobox protein Nkx 2.1, pembrolizumab, pemetrexed, tumor marker, adult, antineoplastic activity, brush border, cancer inhibition, cell differentiation, conference abstract, coughing, diagnosis, dyspnea, histology, histopathology, human, human tissue, immunofluorescence, immunohistochemistry, intestinal metastasis, laboratory test, lung adenocarcinoma, lymph node metastasis, male, metastatic colon cancer, negative staining, pleura effusion, positron emission tomography, surgery, thoracotomy, upper gastrointestinal tract

Abstract

CASE: A 76-year-old male patient presented with a one-month history of coughing spells, left-sided chest wall pain exacerbated by deep breaths, and worsening dyspnea, notably on exertion. Subsequent CT chest imaging revealed a small left-sided pleural effusion, prompting referral to a pulmonologist. Subsequent management included a leftsided thoracotomy, drainage of serosanguineous fluid, and biopsy of pleural nodules. Further diagnostic workup revealed cytological evidence of adenocarcinoma, prompting consultation with oncology. The positive immunostaining for CK7 and CDX2, along with negative staining for CK20, TTF-1, Calretinin, and D2-40, suggested a pattern consistent with potential primary sites such as the upper gastrointestinal tract. Enteric origin was further suggested by elevated levels of CEA and Ca19/9. PET scan confirmed malignancy in the left pleura and lung, with a likely metastatic lymph node without any gastrointestinal involvement. These findings prompted the diagnosis of enteric-type adenocarcinoma of the lung. Staging classified the cancer as Stage IVA. The patient underwent anti-cancer treatment with pembrolizumab, carboplatin, and pemetrexed. IMPACT/DISCUSSION: Pulmonary enteric adenocarcinoma(PEAC) has a higher propensity to invade the pleura and airways, with a rate of 38.5% and 46.2%, respectively, with our patient having significant involvement of pleural and subpleural tissues. The diagnosis of PEAC may benefit from laboratory testing for tumor biomarkers. A high CEA level was discovered in more than 65% of the patients in the available literature similar to our patient. This marker did not help differentiate PEAC from Metastatic colon cancer (MCC), despite having a high sensitivity and the ability to track the patient's clinical progress. The positive rates for CA19-9 and CA125 were comparatively lower, at 50%. The histopathological features include a tall or oval nucleus, high columnar cells grouped in irregular glandular lumens with central necrosis, brush borders, and irregular necrotic patches. Even though PEAC has unique pathological characteristics, histopathology alone was unable to fully differentiate it from lung MCC. When separating PEAC from normal lung adenocarcinoma and MCC, immunohistochemical markers are crucial. Immunohistochemical markers, including CK20, and CDX2, had far higher positive rates in PEAC than MCC. PEAC can be distinguished from MCC by its elevated CK7. Combining some tumor markers, like CK7+ and CDX2+, increased the sensitivity (71.3%) and specificity (82%) of differentiating PEAC from MCC The chemotherapy regimens for MCC were determined to be unsuitable for PEAC. A patient originally diagnosed with MCC was presented by Lin et al., where no response to MCC chemotherapy was noted. CONCLUSION: PEAC can be easily confused with metastatic intestinal cancer, which has similar histology, molecular profile, and serum markers. The gastrointestinal tract needs to be evaluated to tailor the correct treatment.

Volume

40

First Page

S72

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