Biomedical subjects

C A Rubio

Publications and source records attributed to C A Rubio.

At least 235 records · Page 13Linked to original sources

PubMedDate not supplied

Further studies on the histological characteristics linked to local tumour invasion in colorectal carcinomas.

Cross-sectional slicing of the specimen (large histological sections) from 112 consecutive surgical specimens having a colonic (n = 79) or a rectal (n = 33) adenocarcinoma were reviewed. Neoplastic glands with a thin layer of neoplastic cells were present at the growing tumour edge in 32.8% of the colonic carcinomas and in 35.7% of the rectal carcinomas. Glands lacking part of the neoplastic epithelium at the growing edge (i.e. with glandular "pore" formation) were found in 80.5% of the colonic carcinomas and in 85.7% of the rectal carcinomas. The possibility that the thin layer of tumour cells in neoplastic glands antedated the formation of glandular "pores" was entertained. From the results it would appear that at the growing edge of colorectal carcinomas, neoplastic glands usually develop epithelial "pores". The contents of those neoplastic glands, namely mucin, inflammatory cells and/or necrotic material, are released through those "pores" into the surrounding host tissues. Those materials, rich in proteolytic enzymes, would encourage the degradation of the juxtaposed matrix of the host. To restore the continuity of those incomplete glands, new cancer cells would grow around the mucin "lakes" or the inflammatory-necrotic aggregates free in the stroma. This mechanism guarantees a lifelong tumour progression in untreated patients. Since preoperative irradiation was administered only to patients carrying rectal tumours, it is apparent that the histological features here described are neither evoked nor abrogated by irradiation.

Adenocarcinoma↗

PubMedDate not supplied

Histological features pertinent to local tumour progression in Barrett's adenocarcinoma.

Sections from 18 resected esophagi having a Barrett's adenocarcinoma were reviewed. Particular attention was paid to the neoplastic glands at the tumour-host tissue interphase (T/HI). In 3 (17%) of the 18 adenocarcinomas, the glands at the T/HI displayed a thinner layer of tumour cells. In 13 (72%) of the 18 adenocarcinomas, the glands at the T/HI showed a partial loss of tumour cells; that phenomenon was denominated glandular pore formation. The thinner epithelium appears to be a stage preceding the focal destruction of the tumour cells leading to pore formation. Through those glandular pores, cell-free mucin, inflammatory cells or necrotic elements were released into the surrounding host tissues. It is conceivable that those non-neoplastic "pseudopodial" forerunners, rich in proteolytic enzymes, encourage the disintegration of the surrounding host tissues. From the tip of the glandular pores malignant cells will grow around the secreted products to restore glandular continuity. The remodelling of the glands will guarantee a stepwise but everlasting tumour progression deeper into the host. The remaining 2 (11%) of the 18 Barrett's adenocarcinomas were of signet ring cell type. The presence of cell-free mucin "lakes" within the tissues of the host in signet ring cell Barrett's adenocarcinomas suggest a similar mechanism of tumour progression.

Adenocarcinoma↗

PubMedDate not supplied

Cell proliferation of the normal esophagus of mice harbouring a squamous cell neoplasia in the uterine cervix.

Some human tumors have been found to induce proliferative lesions in the squamous epithelium in organs remote from the primary tumor. This phenomenon was explored in the present animal model. After a single injection of 3H-thymidine, the proportion of DNA synthesizing basal and parabasal esophageal cells as well as the pace of intraepithelial cell migration was assessed in 124 C57Bl mice. The uterine cervix of 57 animals had been painted topically with 3,4 benzo(a)pyrene for 5 months, or with the vehicle acetone (44 animals), while 23 animals remained untreated. Groups of animals were killed from 8 hours to 10 days following a single pulse labelling. The proportion of DNA synthesizing basal and parabasal esophageal cells and of their daughter cells (as deduced by observations at various time intervals) was similar in animals harbouring neoplasias of the uterine cervix, in those treated with benzo(a)pyrene but having histologically normal cervical epithelium, in acetone treated as well as in untreated controls. Thus, in the model used herein, we failed to demonstrate increased cell proliferation in the esophageal mucosa of animals having a squamous cell neoplasia in the uterine cervix. The method appears, however, sensitive enough to register ongoing cell proliferation patterns and will be applied to the study of other experimentally induced tumors.

Animals↗

PubMedDate not supplied

Adenocarcinoma in inflammatory colorectal disease. Histological features pertinent to local tumour progression.

Histological sections of 65 surgical specimens from patients with inflammatory colonic disease (ICD) and a colorectal carcinoma, were reviewed. Twenty-five specimens had ulcerative colitis, 35 Crohn's colitis and 2 indeterminate colitis. The presence of neoplastic glands at the tumour front having: a) retained mucin, inflammatory cells and/or necrotic material, b) neoplastic glands with a thin layer of tumour cells, c) neoplastic glands lacking a group of tumour cells (i.e. glandular pore formation) and d) neoplastic glands in which the intraglandular retained mucin, inflammatory cells and/or necrotic material were seen discharged through the glandular pores into the juxtaposed matrix, were recorded. Of the 58 specimens with gland-forming adenocarcinomas, 17 (29.3%) had at the invading front neoplastic glands with a thin layer of tumour cells and 56 (96.6%) neoplastic glands with pores. The material discharged through those pores into the surrounding matrix was mucin (n = 46), inflammatory cells -mainly granulocytes- and/or necrotic material (n = 10). It was assumed that the thin layer of tumour cells in neoplastic glands antedated glandular "pore" formation. Through those "pores" mucin, inflammatory cells and/or necrotic material were subsequently released into the surrounding host tissues. Those products, rich in proteolytic enzymes, would encourage the degradation of the juxtaposed normal tissues, thus facilitating local tumour growth. To restore the continuity of those incomplete glands, new cancer cells would grow around mucin "lakes" or inflammatory-necrotic aggregates in the stroma. This mechanism will guarantee a life-long tumour progression in untreated patients.

Adenocarcinoma↗

PubMedDate not supplied

Colorectal adenomas produce lysozyme.

Lysozyme is an innate non-immunologic antibacterial enzyme produced by the Paneth cells of the upper intestinal tract. Lysozyme is not normally secreted in the lower intestinal tract. Previous reports indicate, however, that lysozyme may be secreted by colorectal neoplasias. The aim was to audit lysozyme expression in colorectal diseases including neoplasias. For that purpose, sections were stained with lysozyme (Muramidase), Ki67 (MIB1) and CD 68. Intense lysozyme overexpression (+++) was compared among 177 colorectal tissues: 35 having normal mucosa, 20 regenerative mucosa in inflammatory bowel disease (IBD), 2 inflammatory polyps, 3 collagenous colitis, 2 melanosis coli, 21 hyperplastic polyps, 42 tubular adenomas, 9 serrated adenomas, 30 villous adenomas and 13 invasive carcinomas. Intense lysozyme overexpression (+++) was found in 9.5% of the hyperplastic polyps, in 97.6% of the tubular adenomas, in 88.9% of the serrated adenomas, in 93.3% of the villous adenomas, in 76.9% of the carcinomas, but in none of the other tissues investigated. Neoplastic colorectal cells may acquire the capacity to produce lysozyme. The presence of that enzyme may not be a haphazard, capricious event in mutated colorectal epithelial cells but part of a more elaborate molecular behavior, not necessarily antibacterial. Recently, it was demonstrated that patients having lysozyme-secreting breast carcinomas were associated with a favorable prognosis. Whether lysozyme expression has any bearing on the biological behavior of colorectal carcinomas remains to be elucidated. Lysozyme overexpression (+++) also occurred in 2 of the 21 hyperplastic polyps, suggesting that intense lysozyme production might herald a possible dysplastic evolution in some hyperplastic polyps.

Adenocarcinoma↗

PubMedDate not supplied

The chronological appearance of flat colonic neoplasias in rats.

Following weekly s.c. injections of the colonotropic carcinogen 1,2-dimethylhydrazine (DMH), we investigated the occurrence of flat and protruding neoplasias in the colon of rats at various time intervals. Forty-seven DMH-treated rats were sacrificed at the 13th, 15th, 19th, 21st and 22nd weeks. A total of 88 tumors evolved in 35 of the 47 DMH-treated rats. The number of neoplasias/animal was 0.3 at week 13, 1.2 at week 15, 2.0 at week 19, 2.5 at week 21 and 4.0 at week 22. In the right colon, although the percent of flat adenomas was lower than of protruding adenomas, the percent of flat carcinomas was significantly higher than of protruding carcinomas, indicating that flat adenomas progress more rapidly to invasive carcinoma than protruding adenomas in the right colon. The opposite was recorded in the left colon where the percent of protruding adenomas was lower than of flat adenomas, but the percent of protruding carcinomas was higher than of flat carcinomas. During the last experimental week as many as 63% of the protruding carcinomas occurred but only 25% of the flat carcinomas. These experimental results seem to substantiate previous observations in humans suggesting that, in the colonic mucosa, flat and protruding adenomas follow different pathways of neoplastic transformation.

Adenocarcinoma↗

PubMedDate not supplied

Histological changes pertinent to local tumor progression in hereditary nonpolyposis colorectal cancer (HNPCC). A preliminary report.

While the genetic profiles of hereditary colorectal tumors are being unravelled, the mechanisms implicated in their local progression remain to be deciphered. In this work histological features occurring at the invading tumor front were investigated in ten hereditary non-polyposis colorectal cancers (HNPCC). Of eight moderately-differentiated (i.e. gland-forming) adenocarcinomas, six had dilated glands with a thin layer of tumor cells and all eight had dilated glands in which a group of cells was lacking, i.e. with a glandular pore. It was apparent that the thin glandular epithelium was a stage preceding pore formation. In glands with pores, the contents of the neoplastic glands--rich in proteolytic enzymes--were extruded directly into the extracellular matrix (ECM), leading to the local destruction of the juxtaposed matrix. It was assumed that to restore the continuity of the glands new cancer cells would grow from the tip of the free borders of the pore into the damaged ECM, thus guaranteeing a stepwise, but everlasting, tumor progression in untreated patients.

Adaptor Proteins, Signal Transducing↗

PubMedDate not supplied

Possible mechanism pertinent to mucosal invasion in sporadic colonic adenomas.

Colorectal adenomas are foci of dysplastic mucosa that may antedate the development of a colorectal cancer. In this work we investigated 62 colonic polyps. A close examination revealed that in some adenomatous glands facing the muscularis mucosa a group of dysplastic cells were missing. Those glandular defects were connoted as glandular pores. Many glands with pores were dilated and had retained mucin, inflammatory cells and/or necrotic material. Those products were often released through the pores into the surrounding lamina propria. Glandular pores were recorded in 25% (3/12) of the tubular adenomas, in 33% (2/6) of the serrated adenomas, in 50% (4/8) of the tubulo-villous adenomas and in 67% (14/21) of the villous adenomas. None of the 14 hyperplastic polyps had glandular pores. While cell locomotion is considered to be the most important parameter accountable for the local progression of tumors, the present results may offer an alternative view to the cell-migration theory (as the sole pathway of invasion). The release of proteolytic secretions through glandular pores in some colonic adenomas disrupt the surrounding matrix, a mechanism that would facilitate neoplastic cell penetration into the lamina propria.

Adenoma↗

PubMedDate not supplied

Serrated adenomas of the cardia.

Adenomas of the stomach are histologically classified into tubular and villous adenomas, mixed (tubulovillous) and papillary phenotypes being also recognized. They are localized in the antrum and the body. In a previous work we reported a case of serrated adenoma of the cardia having, at the time of diagnosis, an invasive growth. In this communication we report five newly identified cases of serrated adenomas of the cardia. The five neoplasias were characterized by serrated indentations furnished with dysplastic epithelium. Five out of six serrated adenomas--including the previously reported case--had, in addition, an invasive or a suspected invasive carcinoma. The latter case had at the time of diagnosis lung and liver metastasis. Metastases were also demonstrated in two additional cases. In similarity with other adenoma phenotypes, serrated adenomas of the cardia have a propensity to evolve into invasive carcinoma, a phenomenon that appears to be size-dependent.

Adenoma↗

PubMedDate not supplied

Ciliated cells in papillary adenocarcinomas of Barrett's esophagus.

Eighteen surgical specimens having an adenocarcinoma arising in Barrett's esophagus were reviewed, and special attention was paid to the presence of ciliated cells. The tumors were classified as glandular (9), papillary (4), diffuse (3) and mixed (2) types. Ciliated cells were observed in one specimen, in cystically dilated glands in Barrett's mucosa adjacent to a papillary adenocarcinoma. Ciliated tumor cells were found in three of the four papillary adenocarcinomas. The fourth papillary tumor, 1 mixed papillary-diffuse adenocarcinoma and the remaining 13 adenocarcinomas had no ciliated cells. Thus, the presence of cilia in exfoliated tumor cells from the esophagus should raise the suspicion of a papillary adenocarcinoma arising in Barrett's mucosa.

Adenocarcinoma, Papillary↗

PubMedDate not supplied

Extended intestinal metaplasia. A survey of 1392 gastrectomies from dwellers of the Pacific basin.

BACKGROUND: To assess the extent of gastric intestinal metaplasia (IM) in gastrectomy specimens in populations of the Pacific basin having different incidence of gastric carcinoma. MATERIALS AND METHODS: One thousand three hundred and nine-two gastrectomies were investigated: 1088 had a gastric carcinoma and 304 miscellaneous gastric diseases. Twenty-one thousand three hundred and fourteen histological sections were reviewed under low-power (4X). IM was either spotty (SIM) or extended (EIM= encompassing one or more entire low-power fields/section). Widespread IM (WIM) was regarded as EIM if present in > or =5 histological sections. RESULTS AND CONCLUSION: The percent of gastrectomies harboring a carcinoma increased significantly with increasing age more notably in those with diffuse carcinomas (DC) than in those with intestinal carcinomas (IC). The percent of gastrectomies with EIM was significantly higher in specimens with IC than with DC, particularly among elderly patients, and in specimens from countries with a high cancer incidence. The percent of gastrectomies with WIM was higher in specimens having IC than in those having DC. Migration per se did not influence the frequency of specimens with EIM in elderly Japanese patients: Japanese migrants to Hawaii had a similarly high frequency of EIM as those dwelling in Japan. Japanese patients with a gastric carcinoma showed atypical mitoses in areas with EIM far from the tumor, suggesting that cellular mutation(s) play a role in the evolution of EIM towards gastric dysplasia and carcinoma in that ethnic group. The drawback of gastric biopsies in assessing the extent of gastric intestinal metaplasia and, thereby, estimating possible cancer risk in long-term studies has been stressed.

Age Factors↗

PubMedDate not supplied

Paneth cell adenoma of the ileum.

A Paneth cell adenoma of the ileum was recently found in a 47-year-old male with familial adenomatous polyposis (FAP). The patient had years previously been subjected to a total proctocolectomy. Following surgery, endoscopical biopsies were obtained from the duodenum (10 biopsies) in four instances and from the ileal pouch (6 biopsies) in three. All biopsies were taken between 1988 and 2003. Hematoxylin and eosin (H&E) sections from all those 16 biopsies were reviewed. In one biopsy from the ileal pouch, a tubular adenoma carrying 92% dysplastic Paneth cells was found. Paneth cells were more easily singled out when H&E sections were observed in a fluorescent microscope than when using conventional transmitted light, or lysozyme immunostain. Despite a wide distribution of Paneth cells in mucosas with intestinal metaplasia (e.g. Barrett's esophagus and gastric intestinal metaplasia), in the normal small intestine and in the large intestine with chronic inflammatory diseases only a few Paneth cell neoplasias have been reported in the GI tract. The cause of the apparent natural resistance of these specialized cells provided with anti-microbial and growth factors to undergo neoplastic transformation deserve further investigation. A review of the literature indicates that this is the first reported case of Paneth cell adenoma of the small intestine.

Adenomatous Polyposis Coli↗

PubMedDate not supplied

Bronchogenic gastric cyst. A case report.

A case of congenital bronchogenic cyst in the gastric mucosa is presented. The cyst was lined by pseudostratified epithelium and covered with ciliated cells. Congenital bronchogenic cysts should be differentiated from acquired gastric cysts lined with ciliated metaplastic cells that evolve as a result of environmental factors.

Adult↗

PubMedDate not supplied

Serrated and microtubular colorectal adenomas in Italian patients. A 5-year survey.

Colorectal adenomas from 1552 Italian patients were histologically classified into tubular (TAs), tubulo-villous (TVAs), villous (VAs), serrated (SAs) and microtubular (MTAs). The purpose was to compare the results to those in 3135 colorectal adenomas from Swedish patients. Of the 1552 adenomas, 827 (53%) were TAs, 352 (23%) TVAs, 196 (12%) VAs, 102 (7%), SAs and 14 (0.9%) MTAs. The remaining 61 (4%) were of combined phenotypes (COMBAs). The percentage of VA (considered as the most important dysplastic precursor of colorectal cancer) was higher in Florence than in Stockholm. Notably, the incidence of colorectal cancer in males was also higher in Florence (78.6/10(5)) than in Stockholm (57.2/10(5)). Notwithstanding, the highest rate of submucosal invasion (7%) was found among SAs. The diameter of the largest section was used to define the size of the largest adenoma in individual patients. Of the 1380 neoplasias measuring < or =12 mm, only 0.9% (n=13) had invasive carcinomas, but as many as 8.1% (n=14) of the 172 neoplasias measuring > or =13 mm. SAs and MTAs are special adenoma phenotypes with particular morphological and cell proliferative attributes at variance from those of TAs, VAs or TVAs. In the light of the present results, it is proposed that SAs and MTAs are included in future reports of colorectal adenomas in order to compare their frequency worldwide.

Adenoma↗

PubMedDate not supplied

Possible mechanism connected with the progression of submucosal invasion in colorectal neoplasias.

Previous studies in human and in experimentally-induced colorectal carcinomas showed that the material retained in dilated glands at the growing tumour edge was directly released into the peritumoral extracellular matrix (ECM) through glandular faults called glandular pores. In this work, the characteristics of the glands at the growing edge in adenomas with submucosal invasion were investigated in 56 patients. Sections (stained with hematoxylin-eosin, and MNF 116) from 56 colonic adenomas with submucosal invasion were reviewed. Pore formation was defined as a glandular defect characterised by lack of a group of epithelial cells in the deeper portion of the glands. Numerous dilated submucosal glands with pores were found in 46 (82%) of the 56 neoplasias. Through those pores retained mucin, neutophils and/or necrotic material, containing proteolytic enzymes, were siphoned off into the surrounding tissues, causing disruption of the paratumoral ECM and facilitating host penetration by neoplastic cells. Glandular continuity seems to be restored by the proliferation of malignant cells from the tip of the free borders of the pores into the disrupted ECM. The sealing of the glandular flaws would permit the re-accumulation of intraglandular proteolytic material, a mechanism that would replicate a new wave of host invasion, thus ensuring a stepwise, but continual, tumour progression at the growing edge in untreated patients.

Adenoma↗

PubMedDate not supplied

Intraductal serrated adenoma of the pancreas. A case report.

CASE REPORT: A 48-year-old male with known hypothyreosis consulted his physician for symptoms compatible with TIA (transient ischemic attacks). Computer tomography (CT) in December 2001 revealed an irregular, lobulated mass in the processus uncinatus of the pancreas head. A CT examination 14 months later revealed status quo. In July 2004, a new CT showed an increase in size of the expansive pancreatic mass. The patient was operated on in August 2004 with a preliminary diagnosis of incidentaloma of the pancreas. The pathological examination showed a 4 x 3.5 x 2.5 cm large tumour. Histology revealed an intraductal serrated adenoma. The epithelial fronds had sawtooth-like configurations. An area with early invasive carcinoma was found. The tumour had progressed slowly during the 2.7 years of surveillance. Serrated neoplasia in the duodenum may result in similar cases in the future.

Adenoma↗

PubMedDate not supplied

Macrophage-associated chronic diarrhea of unknown origin. Preliminary observations.

The distribution of macrophages in the colonic mucosa was investigated in 13 patients with chronic diarrhea. Group I consisted of 5 patients; both colonoscopy and colonic biopsies were reported as normal. Group II included 5 patients with normal colonoscopy, but with collagenous colitis or lymphocytic colitis at histology. Group III consisted of 3 patients with mucosal inflammation at both colonoscopy and histology. Immunostain with CD68 (a macrophage marker) revealed, in all patients from Group I, a linear accumulation of CD68+ macrophages at the top of the lamina propria. In contrast, sections from patients in Groups II and III showed a random distribution of CD68+ macrophages. Since all three groups of patients here investigated had chronic diarrhea, it goes without saying that the linear recruitment of macrophages in Group I may not be the direct cause of chronic diarrhea, as no similar linear recruitment of macrophages was demonstrated in patients with collagenous colitis or with chronic inflammation. Although the cause(s) of chronic diarrhea in patients of Group I remain to be elucidated, it would appear that the recruitment of macrophages along the superficial aspect of the lamina propria mucosa (lpm) is a characteristic cellular response in patients with this subtype of chronic diarrhea.

Adult↗

PubMedDate not supplied

Mott cell (Russell bodies) Barrett's oesophagitis.

The first case of Barrett's oesophagus with chronic inflammation having predominantly (> 50%) Mott cells, i.e. plasma cells with stored immunoglobulins, known as Russell bodies, is reported. Biopsies from two oesophagoscopies revealed similar changes, suggesting that the predominance of Mott cells is not a fortuitous event but a more long-lasting microscopic process. Periodic acid-Schiff (PAS) stain ruled out Candida albicans and immunostains, plasma cell neoplasia. Mott cells were not present in biopsies from the gastric mucosa or the urinary bladder, suggesting that this phenomenon was not widespread but localized to the Barrett's mucosa. The retention of immunoglobulins (Russell bodies) suggests that the mechanism of protein transport in those plasma cells is incompetent, and that the proteins are neither degraded nor secreted, but remain stored in dilated cisternae. Increased awareness of the existence of this subgroup of Barrett's oesophagitis may result in similar cases being reported in the future.

ADP-ribosyl Cyclase 1↗