Patterns of DNA‐ploidy in operable colorectal carcinoma: A prospective study of 100 cases

Russo, Antonio; Bazan, Viviana; Plaja, Sergio; Leonardi, Patricia I.; Bazan, P

doi:10.1002/jso.2930480103

Cited by 14 publications

(7 citation statements)

References 30 publications

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“…2,3 Abnormal nuclear DNA content can be found in adenomas a well as carcinomas of the colorectum. [4][5][6] Aneuploidy occurs in approximately 60 per cent per cent) of colorectal cancers [7][8][9] and has been reported in as many as 8-35 per cent of adenomas. [10][11][12] The majority of these studies were performed retrospectively on archival material using flow cytometry.…”

Section: Introductionmentioning

confidence: 99%

Genetic heterogeneity in sporadic colorectal adenomas

Saraga¹,

Bautista²,

Dorta

et al. 1997

J. Pathol.

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The majority of colorectal cancers develop from adenomatous polyps under the influence of factors that are still poorly understood. Tumourigenesis is generally considered a multistep process in which multiple genetic alterations occur, eventually reflected in abnormalities of the cellular DNA content. Macroscopical features such as tumour size and tumour architecture (tubular, tubulovillous, or villous) are correlated wit the chance of malignancy in the lesion. Grade of dysplasia can be considered an indicator for the level of progression of the adenoma towards invasive carcinoma. These characteristics were correlated with the presence or absence of K‐ras mutations and the DNA ploidy in a prospective study performed on 46 large sporadic colorectal adenomas resected by endoscopy. DNA ploidy and K‐ras mutations were analysed in two samples taken at distant sites in the adenomas. Aneuploidy was present in 12 adenomas (26 per cent) and K‐ras mutations occurred in 26 (57 per cent). A highly significant correlation was found between aneuploidy and adenoma size, architecture, and grade of dysplasia. The presence of K‐ras mutations was significantly correlated only with the size of the adenomas. The proportion of adenomas with aneuploidy and/or a K‐ras mutation increased when two samples were analysed instead of one. This observation suggests that the prevalence of genetic mutations and of aneuploidy is probably underestimated, as generally only one sample is investigated. No correlation was observed between K‐ras mutations and ploidy. This study demonstrates the presence of genetic heterogeneity in colorectal adenomas and supports the notion that K‐ras mutation is an early event, while aneuploidy is a late event in the adenoma–carcinoma sequence. © 1997 John Wiley & Sons, Ltd.

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Section: Introductionmentioning

confidence: 99%

Genetic heterogeneity in sporadic colorectal adenomas

Saraga¹,

Bautista²,

Dorta

et al. 1997

J. Pathol.

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“…Several recently performed studies have shown that FCM DNA analysis provides useful information regarding diagnosis, prognosis, and therapeutic response in neoplastic lesions [Badalament et al, 1988;Russo et al, 1991;Williams and Daly, 1990;Greenebaum et al, 1985;Briffod et al, 19891. Several reports have proved the feasibility of FCM DNA analysis on fine-needle aspiration (FNA) samples from breast tumours [Levack et al, 1987;., 19871 and from other solid neoplasias [Azavedo et a] it is known that samples however preserved (fresh, frozen, and paraffin-embedded) from hepatic tumours are suitable for FCM DNA analysis [Salmon et al, 1988;Tsushima et al, 1987;Frankfurt et a1 . , 19841.…”

Section: Introductionmentioning

confidence: 99%

Flow cytometric DNA analysis of hepatic tumours on ultrasound‐guided fine‐needle aspirates

Russo

Bazan

Plaja

et al. 1992

Journal of Surgical Oncology

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A study was performed on a nonconsecutive series of 51 patients in order to assess the feasibility, reliability, and usefulness of flow cytometric (FCM) DNA analysis of samples obtained from benign and malignant hepatic tumours by means of ultrasound-guided fine-needle aspiration (UG-FNA). Cytological and often histological confirmation of the nature of the lesion was obtained in all cases from an expert pathologist. For FCM DNA analysis in 32 cases, it was also possible to use samples obtained at surgery from the actual tumours. There were no post UG-FNA complications, either early or late. It was possible to perform FCM DNA analysis on 6/7 (85.7%) of the benign tumour aspirates and all 44 (100%) coming from the malignant tumours. All the benign tumours showed a DNA-diploid pattern, while the DNA content was aneuploid in 91% of the malignant tumours. Apart from one case, the results of the FCM DNA analysis of the samples removed at surgery were the same as those obtained from the aspirates (97%). FCM DNA analysis on UG-FNA samples from hepatic tumours is a fairly simple, reproducible, well-tolerated technique; it does not involve risks if performed by skilled operators and, since it can be easily repeated even on small tumours, it is a suitable method for monitoring hepatic metastases during chemotherapy.

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“…Tumors were clinically staged according to the Dukes' classification as modified by Turnbull et al [10,11], Broders' [12] classification was used for histological grading. DNA ploidy was assessed on nuclei obtained from frozen tissues and stained with propidium iodide as previously reported [9]. Proliferative activity was expressed as the fraction of cells in the S phase of the cell cycle (FCM-S).…”

Section: Patient Features and Tissue Handlingmentioning

confidence: 99%

“…Proliferative activity was expressed as the fraction of cells in the S phase of the cell cycle (FCM-S). Median FCM-S values were taken as a cutoff point and tumors were accordingly classified into 'high' and 'low' S phase tumors [9].…”

Section: Patient Features and Tissue Handlingmentioning

confidence: 99%

“…Multiple tumor samples were taken from at least 5 different areas avoiding grossly necrotic tissues [9], Matched paired sets of tumor and normal mucosa samples were divided into aliquots and stored at -8 0°C . Tumors were clinically staged according to the Dukes' classification as modified by Turnbull et al [10,11], Broders' [12] classification was used for histological grading.…”

Section: Patient Features and Tissue Handlingmentioning

confidence: 99%

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Cathepsin D Content in Colorectal Cancer

Tumminello¹,

Gebbia²,

Pizzolanti³

et al. 1995

Oncology

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Cathepsin D content and activity were determined in matched paired sets of colorectal tumor tissue and normal mucosa and correlated with a number of biological and clinical parameters. Significantly higher cathepsin D activity was measured in tumor cytosol compared to paired normal mucosa (p < 0.02), in Dukes’ stage A tumors compared to Dukes’ B and C (p < 0.05), in tumors < 5 cm compared to those > 5 cm, or in tumors with a low proliferation rate compared to those with a high proliferation rate (p < 0.05). Moreover, significant differences in enzyme activity between tumor tissue and paired normal mucosa were observed in node-positive and G2 tumors (p < 0.05). No significant correlation between cathepsin D activity and other biological parameters was found. Further, no differences in cathepsin D content between tumor tissue and paired normal mucosa were observed except in Dukes’ stage A tumors (p < 0.02). A significantly increased cathepsin D content was also observed in tumors > 5 cm compared to tumors < 5 cm (p < 0.01). No relationship between tumor cathepsin D content and clinical stage was detected. However, a significant correlation (p < 0.05) was observed between the tumor-specific content of this enzyme and tumor grade. Finally, there was no relationship between tumor-specific cathepsin D activity and content (r = –0.27, p = 0.23). These data suggest that cathepsin D activity rather than content correlates with the malignant progression of colorectal cancer. This phenomenon should be taken into consideration when clinical studies are undertaken to assess the potential prognostic value of proteolytic enzymes involved in tumor progression.

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Patterns of DNA‐ploidy in operable colorectal carcinoma: A prospective study of 100 cases

Cited by 14 publications

References 30 publications

Genetic heterogeneity in sporadic colorectal adenomas

Genetic heterogeneity in sporadic colorectal adenomas

Flow cytometric DNA analysis of hepatic tumours on ultrasound‐guided fine‐needle aspirates

Cathepsin D Content in Colorectal Cancer

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