Quantitative analysis of CEA expression in colorectal adenocarcinoma and serum: Lack of correlation

Abstract

Tissues and sera from 110 patients diagnosed with colorectal primary carcinoma, 20 patients with benign colorectal diseases and 31 healthy donors were subjected to quantitative CEA analysis. Multiple samples from tumor lesions and autologous histologically normal mucosa (10 cm from the tumor) were obtained at the time of surgery (cancer patients) or endoscopy (benign patients and healthy volunteers). CEA content was measured in protein extracts obtained from these tissues using a quantitative RIA method. A limit of normality for CEA content was established as 300 ng/mg of protein. When this was taken as cut‐off, 104 of 110 (94.5%) tumor lesions and 51 of 110 (46.4%) autologous histologically normal colonic mucosa from cancer patients had elevated CEA levels. No correlation with stage of disease was found, while a correlation was observed with degree of tumor differentiation. A statistically significant difference between CEA content in tumor lesions and in histologically normal mucosa from cancer patients was observed (p = −0.001). Moreover, CEA content was statistically higher in the normal mucosa from cancer patients than in that from healthy donors (p = 0.005). CEA content in tissue specimens from benign lesions differed significantly from that in tissue from healthy donors (p = 0.005) and in carcinoma lesions (p < 0.001). The highest CEA content was observed in benign lesions with severe dysplasia. No statistical correlation between CEA content in carcinoma tissues and serum CEA levels (r = 0.195, p = .13) was found. Therefore, in considering diagnosis or therapy with anti‐CEA MAbs for colorectal‐carcinoma patients, or potential therapies with anti‐CEA recombinant vaccines, serum CEA levels should not be taken as indicating CEA expression in tumor lesions. Int. J. Cancer 72:949–954, 1997. © 1997 Wiley‐Liss, Inc.

Tumour CEA as predictor of better outcome in squamous cell carcinoma of the lung

“…We also found, in agreement with Okamura et al [7], but in contrast to a study on colon cancer [9], a significant association between S-and T-CEA. Nevertheless, this effect persisted only for ADK after stratifying by histology.…”

“…However, S-CEA is not always present in lung cancer patients with positive T-CEA [8]. Lack of a close correlation between T-and S-CEA has also been reported in colorectal carcinoma [9]. These findings suggest the possibility that T-CEA expression might be a more useful prognostic indicator than S-CEA.…”

Chemoprevention by cyclooxygenase-2 inhibition reduces immature myeloid suppressor cell expansion

“…The mice received celecoxib as a dietary supplement at 1000 parts per million, a dose estimated to be 140 mg/kg per day, which is similar to the clinical dose of 300-400 mg per day when corrected for skin surface area [21,37]. Clinically, this dose has been shown to result in celecoxib serum levels comparable with those observed in FAP patients treated with celecoxib [13]. A similar median number of tumors/ animal in the untreated mice with 1,2-DMH-induced tumors was found at each of the three time points examined, ranging from 26 weeks post initiation of carcinogenesis to terminal necropsy (medians of 286 and 309 days post initiation of tumor induction with 1,2-DMH).…”

“…Further, COX-2 inhibitors alter the balance of immunosuppressive and immunostimulatory cytokines [9] and reduce PGE-2 suppression of dendritic cell (DC) and monocyte differentiation and maturation [10,11], allowing more effective augmentation of antitumor immune responses International Immunopharmacology 7 (2007) 140 -151 www.elsevier.com/locate/intimp [12]. COX-2 is over-expressed in human colorectal tumors [1,13] and in chemically-induced [14][15][16] and transgenic rodent colon tumors [17][18][19][20][21]. The inhibition of COX-2 activity has been shown to suppress intestinal carcinogenesis in experimental models [14][15][16][17][19][20][21] and patients with familial adenomatous polyposis (FAP) [2].…”

Real-time reverse transcription PCR and the detection of occult disease in colorectal cancer

“…However, only approximately half of colorectal cancers shed CEA in levels sufficient for their detection in monitoring therapy and there is no correlation between the level of CEA expression in tumour biopsies and the presence of CEA protein in the serum (Guadagni et al, 1997). Consequently, CEA was an early marker used to target tumour cells, initially in LN (Mori et al, 1995) followed by its detection in peripheral blood (Mori et al, 1996).…”