Mucinous lung adenocarcinoma, particularly referring to <i>EGFR</i>‐mutated mucinous adenocarcinoma

Wakejima, Ryo; Inamura, Kentaro; Ninomiya, Hironori; Nagano, Hiroko; Mun, Mingyon; Okumura, Sakae; Okubo, Kan; Ishikawa, Yuichi

doi:10.1111/pin.12879

Cited by 13 publications

(7 citation statements)

References 24 publications

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“…These mucin core proteins are also expressed in nonmucinous lung adenocarcinoma as well as in IMA, and their expression patterns are diverse. 16,17 Nonterminal respiratory unit (TRU)-type adenocarcinoma, which may originate from bronchial surface epithelial and glandular cells, 18 correlates with the expression of MUC5AC and MUC5B. 19,20 It indicates that the precursor cells may influence the expression patterns of secretory mucins in lung neoplasms.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive clinicopathological characteristics and mucin core protein expression profiles of bronchiolar adenoma

et al. 2022

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Aims Bronchiolar adenoma (BA) is a novel entity in the 2021 WHO classification of lung tumours. The expression profile of mucin core proteins in BAs is not clear. The aim of this study was to clarify the expression profiles of mucins and to validate the clinicopathologic and molecular features of BAs. Methods and results We examined the clinicopathological, immunohistochemical, and molecular features of 20 BAs. Our cohort comprised 10 proximal and 10 distal BAs. Only seven of 18 patients (39%) were accurately diagnosed with BA at the time of intraoperative consultation. The frequent genetic alterations were BRAF V600E (35%) and KRAS (30%) mutations, which were mutually exclusive. The expression of MUC1, MUC4, and MUC5B was observed in all cases and that of MUC5AC and MUC6 was observed in nine (45%) and five (25%) cases, respectively. MUC4 was diffusely expressed in 18 cases. In contrast, MUC1, MUC5AC, MUC5B, and MUC6 displayed a patchy expression pattern. These expression patterns were similar to that of bronchiolar epithelium in normal lung tissue. In addition, overexpression of MUC1 and MUC4 on the entire cell surface was not observed in any of the BAs, suggesting their benign nature. Conclusion BA commonly exhibits diffuse MUC4 and patchy MUC1 and MUC5B expression. Its unique expression pattern is probably attributed to mucin expression specific to the bronchiolar epithelium. These results confirm the clinicopathologic and molecular characteristics of BA, including the difficulty in intraoperative frozen section diagnosis and the broad morphologic spectrum of BA derived from the bronchiolar epithelium.

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Section: Discussionmentioning

confidence: 99%

Comprehensive clinicopathological characteristics and mucin core protein expression profiles of bronchiolar adenoma

et al. 2022

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“…Although we did observe an improved PFS from 1st line targeted therapies among our current patients, these treatments were not found to be associated with the IMA prognosis in our multivariate analysis. The distinct characteristics of EGFR mutations that have been found to have no female predominance and operate in a different tumorigenic pathway in IMA could have impacted on these targeted treatment responses [ 42 ]. Finally, PD L-1 expression was not examined in all the patients in our cohort.…”

Section: Discussionmentioning

confidence: 99%

Optimizing palliative chemotherapy for advanced invasive mucinous adenocarcinoma of the lung

et al. 2021

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Background A primary pulmonary invasive mucinous adenocarcinoma (IMA) is a rare subtype of invasive adenocarcinoma of the lung. The prognosis of advanced IMA depending on chemotherapy regimen has not been fully investigated. Here, we compared the clinical outcomes of patients with advanced IMA treated with different palliative chemotherapies that included novel therapeutics. Methods This single-center retrospective study included a total of 79 patients diagnosed with IMA and treated with palliative chemotherapy. The primary outcome was the comparison of overall survival according to palliative chemotherapy type. Risk factors associated with death were evaluated as a secondary outcome. Results The study cohort of 79 patients comprised 27 progressive or recurrent cases and 52 initial metastatic patients. Thirteen patients (16.5%) received targeted therapy and 18 cases (22.8%) received immunotherapy. When we compared the survival outcomes of the different treatment regimens, patients with IMA treated by immunotherapy (undefined vs. non-immunotherapy 17.0 months, p < 0.001) had better overall survival rates. However, there was no difference in the prognosis between the cases treated with a targeted therapy (35.6 vs. non-targeted therapy 17.0 months, p = 0.211). None of the conventional regimens produced a better outcome. By multivariable analysis, immunotherapy (HR 0.28; 95% CI 0.11–0.74; P = 0.008) was found to be an independent prognostic factor for death. Conclusions This study suggests that immunotherapy for patients with advanced IMA may provide favorable outcomes than other chemotherapy options.

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“…34,35 Parenthetically, KRAS is the most common mutated gene in MACs, as well as GNAS and EGFR mutations in the latter neoplasm. [36][37][38][39] One can argue as to the nature of the MCC and its relationship to MAC, but several studies have reported an association between CPAM type 1 and MAC with KRAS. [40][41][42] Because the clinical outcome is so favorable in the cases of putative MAC in CPAM type 1, Nelson et al 43 have questioned whether these lesions only "mimic adult MAC.…”

Section: Cpam and Distinct Mutationsmentioning

confidence: 99%

Congenital Pulmonary Airway Malformations With a Reconsideration and Current Perspective on the Stocker Classification

2023

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Congenital cystic pulmonary lesions (CCPLs) are represented by the following entities: congenital pulmonary airway malformation (CPAM), formerly congenital cystic adenomatoid malformation, extra- and intralobar sequestration (EIS), congenital lobar emphysema (overexpansion), and bronchogenic cyst. The developmental model of CPAM histogenesis by Stocker proposed perturbations designated as CPAM type 0 to type 4 without known or specific pathogenetic mechanisms along the airway from the bronchus to the alveolus. This review highlights mutational events either at the somatic level in KRAS (CPAM types 1 and possibly 3) or germline variants in congenital acinar dysplasia, formerly CPAM type 0, and pleuropulmonary blastoma (PPB), type I, formerly CPAM type 4. The potential for overt malignant progression exists in the case of PPB type I and CPAM type 1 in some cases to well-differentiated mucinous adenocarcinoma. On the other hand, CPAM type 2 is an acquired lesion resulting from interruption in lung development secondary to bronchial atresia. The latter is also regarded as the etiology of EIS whose pathologic features are similar, if not identical, to CPAM type 2. These observations have provided important insights into the pathogenetic mechanisms in the development of the CPAMs since the Stocker classification.

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Mucinous lung adenocarcinoma, particularly referring to EGFR‐mutated mucinous adenocarcinoma

Cited by 13 publications

References 24 publications

Comprehensive clinicopathological characteristics and mucin core protein expression profiles of bronchiolar adenoma

Comprehensive clinicopathological characteristics and mucin core protein expression profiles of bronchiolar adenoma

Optimizing palliative chemotherapy for advanced invasive mucinous adenocarcinoma of the lung

Congenital Pulmonary Airway Malformations With a Reconsideration and Current Perspective on the Stocker Classification

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