Pathology and genetic markers of colorectal cancer in Lynch syndromes I and II

Henry T. Lynch, T. Smyrk, Stephen J. Lanspa, J. N. Marcus, B. M. Boman, P. Watson, J. F. Lynch, C. R. Boland, H. Appelman, G. Cristofaro, P. Bufo, P. Mingazzini, E. DiGiulio, A. V. Tauro

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Approximately 6% of the total colorectal cancer burden is accounted for by hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndromes I and II. The Lynch syndrome II gene is tentatively located on chromosome 18q11-q21, as a result of significant linkage to JK (Kidd blood group). However, no specific biomarkers are available for diagnosis or screening. Thus, family history remains the key. Biomolecular studies have shown chromosomes 5, 17, and 18 to be important areas for allelic loss in colorectal cancer. A Lynch syndrome patient recently showed allelic loss on chromosome 5 polyps, while a separately arising colonic cancer showed allelic loss on chromosome 18 and not on chromosome 5. Colon cancer pathology in HNPCC has been characterized by increased mucinous adenocarcinoma, which is more poorly differentiated, with possibly increased signet cell carcinomas. Adenomas in this disease show significantly more moderate or severe dysplasia with villous features. Flat adenomas have been recently identified in HNPCC. Biochemical data has shown significantly less binding by the lectins peanut agglutinin and Dolichos biflorous agglutinin (DBA) in HNPCC. This is important in that dysplastic flat mucosa and adenomas in patients with FPC showed significantly decreased binding with DBA. In vitro cell labeling of rectal colonic mucosa by [3H]-thymidine in patients with HNPCC has shown increased uptake in the distal crypt compartment. It is clear that many gaps remain in our knowledge of genetic defects that contribute to colorectal cancer. The Lynch syndromes need to be assessed with basic pathology and the newly emerging biomolecular techniques.

Original languageEnglish
Pages (from-to)341-350
Number of pages10
JournalJournal of Tumor Marker Oncology
Volume3
Issue number4
StatePublished - 1988

Fingerprint

Lynch Syndrome II
Hereditary Nonpolyposis Colorectal Neoplasms
Genetic Markers
Colorectal Neoplasms
Pathology
Chromosomes, Human, Pair 5
Loss of Heterozygosity
Dolichos
Adenoma
Chromosomes, Human, Pair 18
Agglutinins
Colonic Neoplasms
Mucous Membrane
Peanut Agglutinin
Mucinous Adenocarcinoma
Chromosomes, Human, Pair 17
Blood Group Antigens
Polyps
Lectins
Thymidine

All Science Journal Classification (ASJC) codes

  • Cancer Research

Cite this

Lynch, H. T., Smyrk, T., Lanspa, S. J., Marcus, J. N., Boman, B. M., Watson, P., ... Tauro, A. V. (1988). Pathology and genetic markers of colorectal cancer in Lynch syndromes I and II. Journal of Tumor Marker Oncology, 3(4), 341-350.

Pathology and genetic markers of colorectal cancer in Lynch syndromes I and II. / Lynch, Henry T.; Smyrk, T.; Lanspa, Stephen J.; Marcus, J. N.; Boman, B. M.; Watson, P.; Lynch, J. F.; Boland, C. R.; Appelman, H.; Cristofaro, G.; Bufo, P.; Mingazzini, P.; DiGiulio, E.; Tauro, A. V.

In: Journal of Tumor Marker Oncology, Vol. 3, No. 4, 1988, p. 341-350.

Research output: Contribution to journalArticle

Lynch, HT, Smyrk, T, Lanspa, SJ, Marcus, JN, Boman, BM, Watson, P, Lynch, JF, Boland, CR, Appelman, H, Cristofaro, G, Bufo, P, Mingazzini, P, DiGiulio, E & Tauro, AV 1988, 'Pathology and genetic markers of colorectal cancer in Lynch syndromes I and II', Journal of Tumor Marker Oncology, vol. 3, no. 4, pp. 341-350.
Lynch, Henry T. ; Smyrk, T. ; Lanspa, Stephen J. ; Marcus, J. N. ; Boman, B. M. ; Watson, P. ; Lynch, J. F. ; Boland, C. R. ; Appelman, H. ; Cristofaro, G. ; Bufo, P. ; Mingazzini, P. ; DiGiulio, E. ; Tauro, A. V. / Pathology and genetic markers of colorectal cancer in Lynch syndromes I and II. In: Journal of Tumor Marker Oncology. 1988 ; Vol. 3, No. 4. pp. 341-350.
@article{d91aad6e4cde41da86d8ba9754ccdc79,
title = "Pathology and genetic markers of colorectal cancer in Lynch syndromes I and II",
abstract = "Approximately 6{\%} of the total colorectal cancer burden is accounted for by hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndromes I and II. The Lynch syndrome II gene is tentatively located on chromosome 18q11-q21, as a result of significant linkage to JK (Kidd blood group). However, no specific biomarkers are available for diagnosis or screening. Thus, family history remains the key. Biomolecular studies have shown chromosomes 5, 17, and 18 to be important areas for allelic loss in colorectal cancer. A Lynch syndrome patient recently showed allelic loss on chromosome 5 polyps, while a separately arising colonic cancer showed allelic loss on chromosome 18 and not on chromosome 5. Colon cancer pathology in HNPCC has been characterized by increased mucinous adenocarcinoma, which is more poorly differentiated, with possibly increased signet cell carcinomas. Adenomas in this disease show significantly more moderate or severe dysplasia with villous features. Flat adenomas have been recently identified in HNPCC. Biochemical data has shown significantly less binding by the lectins peanut agglutinin and Dolichos biflorous agglutinin (DBA) in HNPCC. This is important in that dysplastic flat mucosa and adenomas in patients with FPC showed significantly decreased binding with DBA. In vitro cell labeling of rectal colonic mucosa by [3H]-thymidine in patients with HNPCC has shown increased uptake in the distal crypt compartment. It is clear that many gaps remain in our knowledge of genetic defects that contribute to colorectal cancer. The Lynch syndromes need to be assessed with basic pathology and the newly emerging biomolecular techniques.",
author = "Lynch, {Henry T.} and T. Smyrk and Lanspa, {Stephen J.} and Marcus, {J. N.} and Boman, {B. M.} and P. Watson and Lynch, {J. F.} and Boland, {C. R.} and H. Appelman and G. Cristofaro and P. Bufo and P. Mingazzini and E. DiGiulio and Tauro, {A. V.}",
year = "1988",
language = "English",
volume = "3",
pages = "341--350",
journal = "Journal of Tumor Marker Oncology",
issn = "0886-3849",
publisher = "International Academy of Tumor Marker Oncology",
number = "4",

}

TY - JOUR

T1 - Pathology and genetic markers of colorectal cancer in Lynch syndromes I and II

AU - Lynch, Henry T.

AU - Smyrk, T.

AU - Lanspa, Stephen J.

AU - Marcus, J. N.

AU - Boman, B. M.

AU - Watson, P.

AU - Lynch, J. F.

AU - Boland, C. R.

AU - Appelman, H.

AU - Cristofaro, G.

AU - Bufo, P.

AU - Mingazzini, P.

AU - DiGiulio, E.

AU - Tauro, A. V.

PY - 1988

Y1 - 1988

N2 - Approximately 6% of the total colorectal cancer burden is accounted for by hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndromes I and II. The Lynch syndrome II gene is tentatively located on chromosome 18q11-q21, as a result of significant linkage to JK (Kidd blood group). However, no specific biomarkers are available for diagnosis or screening. Thus, family history remains the key. Biomolecular studies have shown chromosomes 5, 17, and 18 to be important areas for allelic loss in colorectal cancer. A Lynch syndrome patient recently showed allelic loss on chromosome 5 polyps, while a separately arising colonic cancer showed allelic loss on chromosome 18 and not on chromosome 5. Colon cancer pathology in HNPCC has been characterized by increased mucinous adenocarcinoma, which is more poorly differentiated, with possibly increased signet cell carcinomas. Adenomas in this disease show significantly more moderate or severe dysplasia with villous features. Flat adenomas have been recently identified in HNPCC. Biochemical data has shown significantly less binding by the lectins peanut agglutinin and Dolichos biflorous agglutinin (DBA) in HNPCC. This is important in that dysplastic flat mucosa and adenomas in patients with FPC showed significantly decreased binding with DBA. In vitro cell labeling of rectal colonic mucosa by [3H]-thymidine in patients with HNPCC has shown increased uptake in the distal crypt compartment. It is clear that many gaps remain in our knowledge of genetic defects that contribute to colorectal cancer. The Lynch syndromes need to be assessed with basic pathology and the newly emerging biomolecular techniques.

AB - Approximately 6% of the total colorectal cancer burden is accounted for by hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndromes I and II. The Lynch syndrome II gene is tentatively located on chromosome 18q11-q21, as a result of significant linkage to JK (Kidd blood group). However, no specific biomarkers are available for diagnosis or screening. Thus, family history remains the key. Biomolecular studies have shown chromosomes 5, 17, and 18 to be important areas for allelic loss in colorectal cancer. A Lynch syndrome patient recently showed allelic loss on chromosome 5 polyps, while a separately arising colonic cancer showed allelic loss on chromosome 18 and not on chromosome 5. Colon cancer pathology in HNPCC has been characterized by increased mucinous adenocarcinoma, which is more poorly differentiated, with possibly increased signet cell carcinomas. Adenomas in this disease show significantly more moderate or severe dysplasia with villous features. Flat adenomas have been recently identified in HNPCC. Biochemical data has shown significantly less binding by the lectins peanut agglutinin and Dolichos biflorous agglutinin (DBA) in HNPCC. This is important in that dysplastic flat mucosa and adenomas in patients with FPC showed significantly decreased binding with DBA. In vitro cell labeling of rectal colonic mucosa by [3H]-thymidine in patients with HNPCC has shown increased uptake in the distal crypt compartment. It is clear that many gaps remain in our knowledge of genetic defects that contribute to colorectal cancer. The Lynch syndromes need to be assessed with basic pathology and the newly emerging biomolecular techniques.

UR - http://www.scopus.com/inward/record.url?scp=0024213158&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024213158&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0024213158

VL - 3

SP - 341

EP - 350

JO - Journal of Tumor Marker Oncology

JF - Journal of Tumor Marker Oncology

SN - 0886-3849

IS - 4

ER -