The Importance of Distinguishing Mucinous and Nonmucinous Bronchioloalveolar Carcinomas

Introduction

The first published case of bronchioloalveolar carcinoma (BAC) was in 1876 by Louis Charles Malassez, Associate Director of Histological Laboratories of the Collège de France.1 However, it was Abraham Liebow, in 1960, who first called attention to the fact that there seemed to be two cytological types of BAC,2 later called “Type 1” and “Type 2,” by Manning et al in 1984.3 Although more type 1's were mucinous and type 2's were nonmucinous, there was considerable overlap in their presentation and clinical course. In addition, up to 15% of tumors had a mixture of both.4–6 To that end, comment and concern were voiced regarding the many apparent ways in which what the entity called BAC presented.7

Abstract

The bronchioloalveolar carcinomas (BAC) refer to peripheral lung adenocarcinomas characterized by their lepidic pattern of growth. They encompass a spectrum of tumors, including in situ adenocarcinomas, as well as minimally invasive and invasive adenocarcinomas but also having two different cytological subtypes: nonmucinous and mucinous. This spectrum of tumors shares certain characteristics: less smoking exposure, less male predominance, presentation as a solitary ground-glass/subsolid nodule/mass or multifocal air-space consolidation (or both), significantly fewer extrathoracic metastases, and a better prognosis than other adenocarcinomas. However, it has become increasingly evident that the nonmucinous and mucinous cytological subtypes are two separate diseases, mostly because of molecular characteristics as well as differing therapeutic results. This general review aims to clarify the new pathological classification, imaging, molecular biology, prognostic, and therapeutic features of BAC relating to their two different cytological subtypes.

Keywords

Mucinous bronchioloalveolar, nonmucinous, K-ras mutations, EGFR mutations, lepidic, lung adenocarcinoma, Clara cell