Rubio C A
Gastointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and Hospital, 171 76 Stockholm, Sweden.
Anticancer Res. 2003 Jan-Feb;23(1A):347-50.
Much research has centred around the histological characteristics of invasion in colorectal tumors, but the possible mechanisms involved in local tumor progression in individual cases have not been unveiled. We studied large histological sections from 10 consecutive patients operated for a colonic (n = 5) or a rectal (n = 5) carcinoma. Particular attention was paid to the outmost growing tumor-host edge (GT-HE). Results showed that the avant-garde tumor glands (at the GT-HE) had either thinner tumoral epithelium (n = 2), or "pores" (i.e. lacking tumor cells in the deeper portion of the gland), containing either mucin (n = 5), neutrophils or necrotic material (n = 3). The thinner epithelium appears to be a stage preceding the "destruction" of the tumor cells (i.e. glands with "pores"). The progression of colorectal adenocarcinomas at the GT-HE interphase would proceed by the release (free into the host tissues) of mucins, inflammatory cells or necrotic elements through those "pores". The non-neoplastic elements may be "pseudopodial" forerunners (rich in proteolytic enzymes) which permit the local degradation of the tissues of the host. The malignant cells surrounding those glandular "pores" would eventually grow around the secreted products, thus guaranteeing a stepwise but everlasting tumor progression in untreated cases.