Colorectal cancer--time to reduce the morality.
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Adult↗
Biomedical subjects
J R Jass
Publications and source records attributed to J R Jass.
Predictors of presence, multiplicity, size and dysplasia of colorectal adenomas. A necropsy study in New Zealand.
Three hundred and thirty six forensic necropsy specimens of large bowel were examined in order to identify subject related variables that independently predicted the following adenoma characteristics: presence, size (largest), multiplicity and high grade dysplasia. The variables were age, gender, body mass index, race (European origin versus Maori/Polynesian) and presence of hyperplastic (metaplastic) polyp(s). Subjects included 303 New Zealanders of European origin (M = 185, F = 118) yielding 149 adenomas and 251 hyperplastic polyps and 33 Maori/Polynesians (M = 25, F = 8) yielding five adenomas and one hyperplastic polyp. Independent predictors of adenoma presence as determined by regression analysis were age (p = 0.0001), presence of hyperplastic polyps (p = 0.0001) and male gender (p = 0.05). Models were poor at explaining variation in size, multiplicity, and dysplasia. Larger adenomas occurred more frequently in subjects with multiple adenomas (p = 0.03) and multiple adenomas were probably associated with hyperplastic polyps (p = 0.09) and male gender (p = 0.09) in Europeans. High grade dysplasia was more frequent in women (p = 0.05) and possibly in subjects with hyperplastic polyps (p = 0.2). Body mass index and ethnicity did not predict any adenoma characteristics, but hyperplastic polyp prevalence was influenced by European origin (p = 0.04) and to a lesser extent by body mass index (p = 0.08) as well as presence of adenoma (p = 0.0002) and age ( = 0.005). The association of hyperplastic polyp with presence, multiplicity but not size of adenoma and with a high risk group for colorectal cancer (New Zealanders of European origin) suggests that the hyperplastic polyp serves as a marker for a factor which influences neoplastic evolution at the stages of initiation/transformation but not promotion. Fifty nine per cent of individuals with adenoma(s) did not have hyperplastic polyp(s) emphasising that the last would serve only as a marker of populations and not individuals at high risk of bowel cancer. Low intracolonic butyrate may be the factor linking the expression of the two types of polyp.
Adenoma↗
Proliferation of human gastrointestinal epithelium.
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Adenomatous Polyposis Coli↗
Evolution of hereditary non-polyposis colorectal cancer.
The prevalence of colorectal adenoma in 23 affected patients with hereditary non-polyposis colorectal cancer (HNPCC) was compared with that in an age matched forensic autopsy population. The mean ages at diagnosis of colorectal cancer in men (13) and women (10) were 39 and 37 years respectively. In HNPCC patients who presented below the age of 50 years, at least one adenoma was found in 3 of 10 (30%) men and in 4 of 9 (44%) women. In the age matched autopsy specimens of large bowel, a solitary adenoma was found in 2/42 (5%) men (p = 0.015) and 1/21 (5%) women (p = 0.0075). Of the 11 adenomas from HNPCC patients, nine were greater than 1 cm and six showed a pure villous architecture. Contiguous adenocarcinoma was observed with six adenomas. Adenomas do not occur in large numbers in HNPCC, but develop at a young age, attain a large size, often show a villous configuration, and are more prone to malignant conversion than sporadic adenomas.
Adenocarcinoma↗
Sialic acid and epithelial differentiation in colorectal polyps and cancer--a morphological, mucin and lectin histochemical study.
Loss of O-acetyl substituents from sialic acid expressed in mucin secreted by hyperplastic polyps (21), adenomas (9), a mixed polyp (1) and adenocarcinomas (41) of the colorectum was investigated by mucin histochemistry (diastase PAS and mild PAS) and by lectin histochemistry (Arachis hypogaea or peanut agglutinin) with (nPNA) and without (PNA) prior neuraminidase digestion. Mild PAS and nPNA reactivity were closely correlated, indicating that loss of O-acetyl substituents at C7, C8 and C9 (hence mild PAS positive) and at C4 (hence neuraminidase labile) occur pari passu. These sialic acid alterations were characteristic of mucin secreted by both adenocarcinoma and hyperplastic polyp. The same changes occurred patchily or focally in adenoma. Five "serrated" adenocarcinomas resembled the hyperplastic polyp both morphologically and histochemically. Luminal secretions within cancers were classified as mucin-like (type I) and non-mucin-like (type II). Mild PAS was the most specific technique for mucin-like intraluminal material. However, accumulated luminal secretions (type I or II) and intracytoplasmic lumina were quite specific features of colorectal cancer and could be effectively highlighted by means of dPAS. PNA reactivity without prior neuraminidase digestion showed a distribution unlike nPNA. Whilst PNA expression was more cancer specific than either mPAS or nPNA, it was observed mainly in cancers secreting little or no mucus, thus limiting its value as a tumor marker.
Adenocarcinoma↗
Subsite distribution and incidence of colorectal cancer in New Zealand, 1974-1983.
The purpose of this study was to examine changes in subsite distribution and incidence of colorectal cancer within different age groups. Registration of colorectal cancer by the National Cancer Registry of New Zealand approached 100 percent by 1974. The present study was based on 15,395 individuals aged 25 years and over and registered for colorectal cancer between 1974 and 1983. Subsite distribution (right colon, left colon, rectum) for different age groups (25-49, 50-69, 70+ years) was significantly skewed, with an excess of right colonic cancer in individuals aged 25-49 years and 70+ years. This right colonic excess was accompanied by a relative reduction in left colonic cancer. Age adjusted incidence rates for the periods 1974-78 and 1979-83 were compared and stratified by age group and subsite. Incidence rates increased in all subsites in individuals aged 50+ years. This was particularly evident for right sided cancer in the elderly of both sexes. There was a marked reduction in the incidence of left colonic cancer and rectal cancer in individuals under 50 years. In contrast, the incidence of right colonic cancer remained relatively stable in young individuals. Time trend studies indicate that the skewed subsite distribution of large bowel cancer in different age groups may increase with time and is probably due to varying etiological factors acting on different cohorts.
Adult↗
Ulcerative colitis in the anal canal of patients undergoing restorative proctocolectomy.
The development of stapling instruments has obviated the need to perform anal mucosectomy for ulcerative colitis, but the potential exists for continued inflammation and, perhaps, malignant change. We reviewed the pathology specimens of patients who had had restorative proctocolectomy, to determine the incidence and severity of inflammation in the anal mucosa.
Anal Canal↗
The World Health Organization's histologic classification of gastrointestinal tumors. A commentary on the second edition.
The World Health Organization's (WHO) histologic classification of gastrointestinal tumors has been revised. Although the general basis of classification and the overall outline remain similar to the first edition, advances in the last decade justified changes in classifying certain entities; among them were malignant lymphomas, endocrine tumors, and dysplasias. Several newly recognized entities have also been added.
Carcinoid Tumor↗
Prognostic factors in colorectal cancer.
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Colon↗
Sialic acid histochemistry and the adenoma-carcinoma sequence in colorectum.
A change in sialic acid, notably loss of O acetyl substitution, was studied histochemically in a series of 93 colorectal adenomas that included 14 malignant polyps. Changes in sialic acid were uncommon in adenomas showing mild dysplasia but became increasingly common in moderately and severely dysplastic adenomas and were always present in carcinomatous areas. There was no correlation between a change in sialic acid and either size or villous architecture of benign adenomas. As mucin change often preceded the development of invasive cancer, it could not be used on its own to distinguish between epithelial displacement (pseudoinvasion) and malignant invasion. An abundant luminal accumulation of altered sialic acid in association with an epithelial lining that was non-mucin secreting, however, was specific for cancer. Conversely, the presence of unchanged intracellular or intraluminal O-acetyl sialic acid may help to exclude a diagnosis of malignancy in equivocal cases. The change is not specific for colorectal neoplasms and probably represents a metaplasia to a small intestinal phenotype.
Adenocarcinoma↗
Paget's disease of the anus: a clinicopathological study.
Paget's disease of the anus is a rare disorder of controversial origin and is frequently associated with malignancy. We studied eight patients and carried out immunohistochemical studies to determine whether particular functional profiles might be indicators of a malignant association. One patient presented with synchronous carcinoma and two developed carcinomas 3 and 10 years after excision of Paget's disease. Five patients underwent wide local excision and have not developed cancer (median follow-up 6 years, range 5-13 years). However, four patients developed recurrent Paget's disease. Immunohistochemical studies showed that in general Paget cells stained positively with CAM 5.2 (a cytokeratin marker), gross cystic disease fluid protein (a marker for apocrine cells), human milk fat globule glycoprotein (HMFG 1 and 2) and carcinoembryonic antigen but negatively for PR3A5 (a marker for colonic goblet cells). Three cases had a staining profile which was quite different from that usually observed and these were associated with malignancy. One showed an antigenic profile more typical of a large bowel carcinoma. Paget's disease of the anus appears to run one of two clinical courses: to develop malignancy; or to recur locally, often on repeated occasions. Wide local excision is the treatment of choice but long-term follow-up is necessary because of the cancer risk. An immunohistochemical staining pattern which is different from usual may indicate a higher malignant risk and/or identify some cases of Paget's disease as representing a downward 'pagetoid' extension from a anorectal adenocarcinoma rather than a true epidermotropic apocrine neoplasm of the perianal skin.
Aged↗
A prospective study of the use of 111In-labelled monoclonal antibody against carcino-embryonic antigen in colorectal cancer and of some biological factors affecting its uptake.
This prospective study of radioimmunoscintigraphy using 111In-labelled, C46, a monoclonal antibody against carcino embryonic antigen, CEA, was undertaken in 23 patients with colorectal cancer, 18 with primary carcinomas, 3 with recurrences and 2 with metastases. A sensitivity of 95% and an accuracy of 91% was found. New observations through the use of two administered doses of antibody and the analysis of surgical specimens showed that for the low dose of antibody (average 0.76 mg) tumour uptake was 1.14 x 10(-2)% of the injected dose per gram, whereas on the higher dose (average 4.67 mg) the average tumour uptake was 6.77% (same units) p less than 0.01. Thus a six-fold increase of antibody caused a six-fold increase in tumour uptake, but no change was seen in the tumour to mucosa ratio 4.8 +/- 0.5 (low dose) and 4.0 +/- 1.0 (high dose). A further observation was that well and moderately differentiated tumours took up about four times more than poorly differentiated tumours (p less than 0.05). It was also found that tumour free lymph nodes had a six-fold greater uptake than tumour involved nodes (p less than 0.05) confirming other work with anti-CEA monoclonal antibody. In conclusion, although biological factors influence its efficacy, 111In labelled C46 anti-CEA is a suitable radiopharmaceutical for the radioimmunoscintigraphy of colorectal cancer.
Adult↗
Do aggressive subclones within primary colorectal cancer give rise to liver metastases?
Primary colorectal cancers and hepatic metastases from 24 patients have been compared according to type, grade, DNA content as measured by flow cytometry, and expression of two differentiation antigens and carcinoembryonic antigen (CEA). The primary and secondary tumours were histologically indistinguishable in 23 out of 24 cases. DNA content differed between primary and metastasis in only six cases. Immunohistochemical profiles were usually the same in the primary and metastasis. In particular, heterogeneous expression by the primary was mirrored in the metastasis. In 17 out of 24 (70.1%) patients the primary and metastasis were indistinguishable by all six parameters. In one of these, the liver metastasis had been removed 14 years 10 months after the primary tumour. It is concluded that DNA content as measured by flow cytometry may remain stable for long periods and that the differences shown in this study may simply be due to inadequate sampling of the primary tumour. Phenotypic heterogeneity may be epigenetic and not indicative of genetic instability and cannot be used to track the progression of subclones.
Adenocarcinoma↗
Anal cancer and human papillomaviruses.
Epidemiologic and clinical evidence has suggested a possible association between anal cancer and human papillomavirus (HPV) types that are known to be associated with cervical and other genital cancers. Using Southern blot and dot blot analysis, the authors examined 45 primary anal malignancies for HPV DNA types 6, 11, 16, and 18. HVP 16, DNA was detected in 23 of 41 (56 percent) anal squamous-cell carcinomas (SCC) and in the lymph-node metastases of two of these tumors. In addition, HPV 18 DNA was detected in 2/41 (5 percent) anal SCCs. Anal SCC contained no detectable HPV 6 or 11 DNA. The remaining four primary anal malignancies were not squamous carcinomas and did not contain any detectable HPV DNA. Nonmalignant anal epithelium and malignant rectal mucosa obtained from surgical patients undergoing hemorrhoidectomy and abdominoperineal excision of the rectum did not contain any detectable HPV DNA. HPV 16 DNA in anal cancer was predominantly integrated into the host cell DNA. In situ hybridization was used to demonstrate that HPV 16 DNA in anal SCC tissues is confined to the nuclei of carcinoma cells. The results of this investigation closely parallel similar studies of cervical cancer and lend support to the concept of the involvement of HPV 16 and 18 in the development of anal and genital squamous-cell carcinoma.
Adenocarcinoma↗
Prognostic value of direct spread in Dukes' C cases of rectal cancer.
Seventy-six cancers with involved lymph nodes but with limitation of direct spread in continuity to the bowel wall (Astler-Coller C1 cases) were matched with Astler-Coller C2 cases for clinical variables, macroscopic appearance of tumor, grade of differentiation, and number of positive lymph nodes. Despite this stringent matching, spread was shown to be an important prognostic variable in univariate survival analysis. Estimated five-year survival for Astler-Coller C1 cases was just below 80 percent, equivalent to B2 (Dukes' B) cases. When spread was analyzed in the presence of additional prognostic variables (character of invasive margin and lymphocytic infiltration) by multivariate modeling, its independent prognostic status was maintained. Improved survival for C1 cases was not explained by a lower incidence of local pelvic recurrence. Mechanisms to account for the better prognosis are proposed. This study reaffirms the importance of multivariate techniques of analysis in the assessment of prognosis of patients with rectal cancer.
Follow-Up Studies↗
Observer study of the grading of dysplasia in ulcerative colitis: comparison with clinical outcome.
Patients with extensive ulcerative colitis are entered into surveillance programs that aim to detect premalignant changes. Biopsy specimens have been collected in the St Mark's Hospital (London) surveillance program over a 22-year-period. Specimens from patients reported as having dysplasia were reexamined. A total of 207 biopsy specimens from 86 patients were graded by five experienced pathologists according to the severity of the dysplasia. The overall agreement between the pathologists grading the specimens was poor; each pair agreed on between 42% and 65% of the slides. The best agreement was for slides that were said to show no dysplasia. Comparison with clinical outcome indicated that the pathologists most likely to diagnose dysplasia in patients with carcinoma were also likely to diagnose dysplasia in patients who did not go on to develop carcinoma. Calculating an average grade of dysplasia did not significantly improve diagnostic accuracy. Despite the findings of this interobserver study, dysplasia has been a successful marker in clinical practice. Pathologists should ensure that they have access to previous slides from the same patient and adequate clinical information before reporting biopsies as positive for dysplasia. An additional biopsy should usually be undertaken before surgery is considered.
Biopsy↗