Department of Pathology (Division of Gynecologic Pathology), The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Histopathology. 2013 Jan;62(1):44-58. doi: 10.1111/his.12046.
Traditionally, it was thought that ovarian high-grade serous carcinoma arises from the ovarian surface epithelium and epithelial inclusion glands and that the pathogenesis is de novo; nonetheless, a convincing precursor in the ovary or peritoneum has not been identified to date. During the last few years, however, there has been a dramatic shift in thinking, and a candidate precursor is now recognized in the fallopian tube, especially within the fimbriated end - serous tubal intra-epithelial carcinoma (STIC). Accordingly, STIC is probably the earliest histologically recognizable lesion in the pathogenesis of high-grade serous carcinoma, but steps in this pathway which precede STIC have also been proposed. With subsequent progression, STIC implants onto the ovary and then develops into an invasive high-grade serous carcinoma with rapid tumour growth. For invasive low-grade serous carcinoma, it is well-established that its pathogenesis begins with serous cystadenoma/adenofibroma, which develops sequentially into atypical proliferative serous tumour (typical serous borderline tumour), non-invasive micropapillary (low-grade) serous carcinoma (micropapillary serous borderline tumour) and then invasive low-grade serous carcinoma in a relatively slow stepwise process. It is presumed that cystadenoma/adenofibroma arises from epithelial inclusion glands in the ovary, but recent evidence suggests that epithelial inclusion glands originate in the fallopian tube. Alternatively, it has been proposed that the other early precursors in the low-grade pathway, including serous borderline tumours, non-invasive implants and endosalpingiosis, may also arise directly from tubal mucosa. Therefore, the precursor of most ovarian high-grade serous carcinomas originates in the fallopian tube, and that for low-grade serous tumours may also be derived from the tube. This review paper provides an overview of the fallopian tube's potential role in the pathogenesis of both types of serous neoplasms of the ovary.
传统上，人们认为卵巢高级别浆液性癌起源于卵巢表面上皮和上皮包涵腺体，其发病机制是从头发生；然而，迄今为止尚未在卵巢或腹膜中发现令人信服的前驱病变。然而，在过去的几年中，人们的思维发生了巨大的转变，目前在输卵管中发现了一种候选前驱病变，特别是在输卵管的伞端——输卵管上皮内癌（STIC）。因此，STIC 可能是高级别浆液性癌发病机制中最早在组织学上可识别的病变，但在 STIC 之前的这一途径中的步骤也已经被提出。随着后续的进展，STIC 种植在卵巢上，然后发展为具有快速肿瘤生长的侵袭性高级别浆液性癌。对于侵袭性低级别浆液性癌，其发病机制始于浆液性囊腺瘤/腺纤维瘤，这一过程是逐步发展为非典型增生性浆液性肿瘤（典型浆液性交界性肿瘤）、非浸润性微乳头（低级别）浆液性癌（微乳头浆液性交界性肿瘤），然后是侵袭性低级别浆液性癌，这是一个相对缓慢的逐步过程。人们推测囊腺瘤/腺纤维瘤起源于卵巢上皮包涵腺体，但最近的证据表明上皮包涵腺体起源于输卵管。或者，有人提出，低级别途径中的其他早期前驱病变，包括浆液性交界性肿瘤、非浸润性种植和内输卵管上皮化生，也可能直接来源于输卵管黏膜。因此，大多数卵巢高级别浆液性癌的前驱病变起源于输卵管，而低级别浆液性肿瘤的前驱病变也可能来自于输卵管。这篇综述文章概述了输卵管在卵巢这两种浆液性肿瘤发病机制中的潜在作用。
