Invasive Adenocarcinoma (invasive + adenocarcinoma)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


Oesophageal resection for high-grade dysplasia in Barrett's oesophagus

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 8 2000
Dr G. Zaninotto
Background The aims of this study were to evaluate the prevalence of invasive cancer in patients with high-grade dysplasia in Barrett's oesophagus and to verify whether a second endoscopy with multiple biopsies could improve the accuracy of preoperative diagnosis. In addition, the mortality, morbidity and survival rates in patients with high-grade dysplasia having oesophageal resection were recorded. Methods Fifteen patients were observed from 1982 to 1998; the first seven patients were offered primary oesophageal resection after diagnosis. The other eight patients underwent a second endoscopy with a median of 12 biopsies examined. All later underwent oesophageal resection. Results Invasive adenocarcinoma was found in five patients, with a minimal difference between the first and second periods (two of seven versus three of eight). There were no perioperative deaths. Early morbidity was observed in eight patients and late morbidity in four. The actuarial survival rate was 79 per cent at 5 years. The Karnofsky status was unchanged from preoperative values in 13 of 15 patients after a median follow-up of 46 months. Conclusion These patients with high-grade dysplasia had a 33 per cent probability of harbouring invasive oesophageal carcinoma but even a second endoscopy failed to identify patients with invasive tumour. Oesophagectomy was performed with no deaths and remains a rational treatment in patients fit for surgery. © 2000 British Journal of Surgery Society Ltd [source]


Critical reappraisal of current surveillance strategies for Barrett's esophagus: analysis of a large German Barrett's database

DISEASES OF THE ESOPHAGUS, Issue 8 2008
B. H. A. Von Rahden
SUMMARY Endoscopic surveillance is recommended for patients with Barrett's esophagus (BE). Based on a large database, gathered from predominantly community-based practices in Germany, we aimed to investigate the time-course of malignant progression and apply these findings to current clinical practice. Data of 1438 patients with BE from a large German BE database were analyzed. Patients with at least one follow-up endoscopy/biopsy were included. Detection of ,malignant Barrett' (either high-grade intra-epithelial neoplasia or invasive adenocarcinoma) was considered as study end-point. Of 1438 patients with BE, 57 patients had low-grade intra-epithelial neoplasia (LG-IN) on initial biopsy and 1381 exhibited non-neoplastic BE. ,Malignant Barrett' was detected in 28 cases (1.9%) during a median follow-up period of 24 months (1,255), accounting for an incidence of 0.95% per patient year of follow-up. The frequency of ,malignant Barrett' was significantly higher (P < 0.001, ,2 -test) in the LG-IN group (n = 11, 19.3%) compared with the non-neoplastic BE group (n = 17, 1.2%). In the non-neoplastic BE group, ,malignant Barrett' was predominantly found during re-endoscopy within the first year of follow-up (12 of 17; 70.6%), in contrast to the LG-IN group, in which ,malignant Barrett' was observed predominantly after a time exceeding 12 months (8 of 11, 72.7%; P = 0.05, Fisher's exact test). Initial endoscopic evaluations seem to play the most crucial role in managing BE. After 1 year of follow-up, endoscopic surveillance should be focused on patients with LG-IN. In patients with repeatedly proven non-neoplastic BE, elongation of the follow-up intervals to the upper limit of current guidelines, that is, 5 years, might be justified. [source]


Changing role of in vivo models in columnar-lined lower esophagus

DISEASES OF THE ESOPHAGUS, Issue 4 2002
Y. Koak
SUMMARY. Columnar-lined lower esophagus (CLE) or Barrett's esophagus (BE) is caused by chronic reflux of the gastrointestinal tract and can progress to invasive adenocarcinoma. However, the pathophysiology, cell of origin, and management of this condition is incompletely understood. This review evaluates the role of in vivo models in resolving these debates. A search was performed on the Ovid and Pub Medline for 1964,2001 and Cochrane Collaboration. The keywords used were adenocarcinoma, animal model, Barrett's esophagus, columnar-lined esophagus, eosophageal neoplasms, and esophageal carcinogenesis. All relevant papers were scrutinized and an attempt at tabulation was made. In vivo models have been used at several stages of debate on the pathophysiology of BE. They provide conclusive evidence for its acquired nature secondary to duodenogastroesophageal reflux. The cell of origin of experimental BE may arise from adjacent columnar epithelium, basal layer multipotent cells, or esophageal glands. Experimental work on BE is lacking in assessing therapeutic modalities. [source]


Striving for a better operative outcome: 101 Pancreaticoduodenectomies

HPB, Issue 6 2008
A.W.C. Kow
Abstract Pancreaticoduodenectomy (PD), once carried high morbidity and mortality, is now a routine operation performed for lesions arising from the pancreatico-duodenal complex. This study reviews the outcome of 101 pancreaticoduodenectomies performed after formalization of HepatoPancreatoBiliary (HPB) unit in the Department of Surgery. A prospective database comprising of patients who underwent PD was set up in 1999. Retrospective data for patients operated between 1996 and 1999 was included. One hundred and one cases accrued over 10 years from 1996 to 2006 were analysed using SPSS (Version 12.0). The mean age of our cohort of patients was 61±12 years with male to female ratio of 2:1. The commonest clinical presentations were obstructive jaundice (64%) and abdominal pain (47%). Majority had malignant lesions (86%) with invasive adenocarcinoma of the head of pancreas being the predominant histopathology (41%). Median operative time was 315 (180,945) minutes. Two-third of our patients had pancreaticojejunostomy (PJ) while the rest had pancreaticogastrostomy (PG). There were five patients with pancreatico-enteric anastomotic leak (5%), three of whom (3%) were from PJ anastomosis. Overall, in-hospital and 30-day mortality were both 3%. The median post-operative length of stay (LOS) was 15 days. Using logistic regressions, the post-operative morbidity predicts LOS following operation (p<0.005). The strategy in improving the morbidity and mortality rates of pancreaticoduodenectomies lies in the subspecialization of surgical services with regionalization of such complex surgeries to high volume centers. The key success lies in the dedication of staffs who continues to refine the clinical care pathway and standardize management protocol. [source]


Comparison of risk factors for invasive squamous cell carcinoma and adenocarcinoma of the cervix: Collaborative reanalysis of individual data on 8,097 women with squamous cell carcinoma and 1,374 women with adenocarcinoma from 12 epidemiological studies

INTERNATIONAL JOURNAL OF CANCER, Issue 4 2007
Article first published online: 27 NOV 200
Abstract Squamous cell carcinomas account for about 80% of cancers of the uterine cervix, and the majority of the remainder are adenocarcinomas. There is limited evidence on the extent to which these histological types share a common etiology. The International Collaboration of Epidemiological Studies of Cervical Cancer has brought together and combined individual data on 8,097 women with invasive squamous cell carcinoma, 1,374 women with invasive adenocarcinoma and 26,445 women without cervical cancer (controls) from 12 epidemiological studies. Compared to controls, the relative risk of each histological type of invasive cervical cancer was increased with increasing number of sexual partners, younger age at first intercourse, increasing parity, younger age at first full-term pregnancy and increasing duration of oral contraceptive use. Current smoking was associated with a significantly increased risk of squamous cell carcinoma (RR = 1.50, 95% CI: 1.35,1.66) but not of adenocarcinoma (RR = 0.86 (0.70,1.05)), and the difference between the two histological types was statistically significant (case-case comparison p < 0.001). A history of screening (assessed as having had at least one previous nondiagnostic cervical smear) was associated with a reduced risk of both histological types, but the reduction was significantly greater for squamous cell carcinoma than for adenocarcinoma (RR = 0.46 (0.42,0.50) and 0.68 (0.56,0.82), respectively; case,case comparison, p = 0.002). A positive test for cervical high-risk HPV-DNA was a strong risk factor for each histological type, with 74% of squamous cell carcinomas and 78% of adenocarcinomas testing positive for HPV types 16 or 18. Squamous cell and adenocarcinoma of the cervix share most risk factors, with the exception of smoking. © 2006 Wiley-Liss, Inc. [source]


Reproducibility of the diagnosis of small adenocarcinoma of the lung and usefulness of an educational program for the diagnostic criteria

PATHOLOGY INTERNATIONAL, Issue 1 2005
Masayuki Noguchi
Using 32 small adenocarcinomas of the lung including bronchioloalveolar carcinoma (BAC), the reproducibility of diagnosis by the modified diagnostic criteria for small adenocarcinoma (Cancer 75; 2844, 1995) and the effectiveness of an educational program for 27 volunteer general pathologists were examined. The average coincidence rate of the diagnosis before and after the program was 42.4% and 56.6%, respectively. The coincidence rate after the program was significantly higher than that before the program (P < 0.05). In contrast, the average coincidence rate of six lung cancer specialists was 71.4%, and this was significantly higher than that for general pathologists after the program (P < 0.05). When the cases were divided into two groups (in situ adenocarcinoma (BAC and BAC with alveolar collapse) and early invasive adenocarcinoma), the average coincidence rate for the general pathologists after the program increased to 85.3%, which was significantly higher than that before the program (80.3%; P < 0.05). The rate for the specialists was 89%, which was higher than that for the general pathologists after the program but not significantly so. This trial was thought to provide a theoretical background for the histological diagnosis of peripheral type adenocarcinoma of the lung and to justify the existing diagnostic criteria. [source]


Hepsin cooperates with MYC in the progression of adenocarcinoma in a prostate cancer mouse model

THE PROSTATE, Issue 6 2010
Srinivas Nandana
Abstract BACKGROUND Hepsin is a cell surface protease that is over-expressed in more than 90% of human prostate cancer cases. The previously developed Probasin-hepsin/Large Probasin-T antigen (PB-hepsin/LPB-Tag) bigenic mouse model of prostate cancer demonstrates that hepsin promotes primary tumors that are a mixture of adenocarcinoma and neuroendocrine (NE) lesions, and metastases that are NE in nature. However, since the majority of human prostate tumors are adenocarcinomas, the contribution of hepsin in the progression of adenocarcinoma requires further investigation. METHODS We crossed the PB-hepsin mice with PB-Hi-myc transgenic mouse model of prostate adenocarcinoma and characterized the tumor progression in the resulting PB-hepsin/PB-Hi-myc bigenic mice. RESULTS We report that PB-hepsin/PB-Hi-myc bigenic mice develop invasive adenocarcinoma at 4.5 months. Further, histological analysis of the 12- to 17-month-old mice revealed that the PB-hepsin/PB-Hi-myc model develops a higher grade adenocarcinoma compared with age-matched tumors expressing only PB-Hi-myc. Consistent with targeting hepsin to the prostate, the PB-hepsin/PB-Hi-myc tumors showed higher hepsin expression as compared to the age-matched myc tumors. Furthermore, endogenous expression of hepsin increased in the PB-Hi-myc mice as the tumors progressed. CONCLUSIONS Although we did not detect any metastases from the prostates in either the PB-hepsin/PB-Hi-myc or the PB-Hi-myc mice, our data suggests that hepsin and myc cooperate during the progression to high-grade prostatic adenocarcinoma. Prostate 70: 591,600, 2010. © 2009 Wiley-Liss, Inc. [source]


HP37 PROGNOSTIC FACTORS IN OESOPHAGEAL CANCER: NUMBER OF LYMPH NODES AND EXTRACAPSULAR LYMPH NODE INVASION , AN INTERIM ANALYSIS

ANZ JOURNAL OF SURGERY, Issue 2007
S. K. Thompson
Purpose Controversy exists over the 2nd edition of the TNM staging system introduced by the American Joint Committee in Cancer in 1988, and revised in 2002. Prognostic pathological factors such as the number of positive lymph nodes and any extracapsular lymph node invasion may refine this current staging system and optimize patient treatment. Methodology All patients who underwent surgical resection for oesophageal cancer were identified in a prospectively-maintained database. Patients without invasive adenocarcinoma or squamous cell cancer were excluded. Pathology slides were reviewed by a single pathologist. Survival data was calculated using Kaplan-Meier curves, and prognostic factors were examined using the log rank test. Results 235 surgical specimens met inclusion criteria, and 95 specimens have been reviewed so far. The 5-yr overall survival rate was 43% (median 31.4 months). Subdividing pN-stage into 1,2 positive nodes and >2 positive nodes showed significant differences in 5-yr survival between both groups: 41% vs. 6.0%, respectively (P = 0.0003). Similarly, including absence and presence of extracapsular lymph node invasion into our pathology review showed significant differences in 5-yr survival: 40% vs. 7.8%, respectively (P < 0.01). A negative circumferential margin, and the absence of both vascular and perineural invasion were also found to significantly improve survival rates. Conclusions The number and characteristics of metastatic invasion of lymph nodes should be included in current oesophageal cancer staging systems. Clinicians will then have more accurate prognostic information, and treatment can be better tailored to patients' needs. [source]


Contrast-enhanced colour Doppler-targeted vs a 10-core systematic repeat biopsy strategy in patients with previous high-grade prostatic intraepithelial neoplasia

BJU INTERNATIONAL, Issue 12 2010
Michael Mitterberger
Study Type , Diagnosis (case series) Level of Evidence 4 OBJECTIVE To compare the results of contrast-enhanced colour Doppler (CECD)-targeted prostate biopsy with a systematic 10-core grey-scale biopsy scheme in patients initially diagnosed with high-grade prostatic intraepithelial neoplasia (HGPIN), as although HGPIN is thought to be a precursor to invasive adenocarcinoma, its diagnosis is no longer considered an indication for repeat prostate biopsy and patients should be followed by prostate-specific antigen levels and a digital rectal examination. PATIENTS AND METHODS In all, 104 patients (aged 45,78 years) diagnosed with HGPIN on initial prostate needle biopsy were referred for a repeat biopsy within 6 months. Two independent examiners evaluated each patient; one used CECD-targeted biopsy (up to five cores) into hypervascular regions in the peripheral zone only, and subsequently the second took a systematic 10-core grey-scale biopsy. Cancer detection rates of both techniques were compared. RESULTS Overall, 26 of the 104 men (25%) had prostate cancer in the repeated biopsy. Using the CECD technique cancer was detected in 21% (22 of 104). The positive re-biopsy rate using the systematic technique was 9.6% (10 of 104; P < 0.001). The total incidence of HGPIN with no evidence of tumour on re-biopsy was 8.7% (nine of 104). The Gleason score in all 22 cancers detected with the CECD technique varied between 6 and 8. The systematic technique detected cancers with Gleason scores of 6 or 7. There were no adverse events or complications. CONCLUSION CECD increased the detection rate of prostate cancer, and using fewer biopsy cores than the systematic biopsy technique in patients previously diagnosed with HGPIN. [source]


Frequent aberrant methylation of the promoter region of sterile , motif domain 14 in pulmonary adenocarcinoma

CANCER SCIENCE, Issue 11 2008
Weihong Sun
Aberrant methylation of promoter CpG islands is known to be a major inactivation mechanism of tumor-suppressor and tumor-related genes. In order to identify novel hypermethylated genes in early stage lung adenocarcinoma, we carried out methylated CpG island amplification, modified suppression subtractive hybridization, and methylation-specific polymerase chain reaction to identify aberrant methylation of CpG islands in the A/J mouse lung adenoma model, which histologically mimics the early stage of human pulmonary adenocarcinoma. Through methylated CpG island amplification, suppression subtractive hybridization, and differential screening, we detected five genes, three of which have human homologs. Two of them showed downregulation of their expression in human lung adenocarcinoma. Of these two genes, we selected sterile , motif domain 14 (SAMD14) and further analyzed its methylation status and expression level by methylation-specific polymerase chain reaction and quantitative real-time polymerase chain reaction. Most of the lung adenocarcinoma cell lines showed suppressed expression of SAMD14 together with hypermethylation at the promoter region, although an immortalized bronchial epithelium cell line (PL16B) did not show hypermethylation and did express SAMD14. The expression of SAMD14 in A549 was rescued by treatment with the demethylation agent 5-aza-2,-deoxycytidine. These data indicate that hypermethylation of the SAMD14 gene promoter region is associated with silencing of its expression. Hypermethylation at the CpG site of the SAMD14 promoter region was detected frequently in early invasive adenocarcinoma (8/24, 33.3%) but not in in situ adenocarcinoma (0/7, 0%) or normal lung tissue (0/31, 0%). Hypermethylation of the SAMD14 gene is a specific event in pulmonary adenocarcinogenesis and malignant progression. (Cancer Sci 2008; 99: 2177,2184) [source]


Bottom-up cell proliferation with cyclin A and p27Kip1 expression in ulcerative colitis-associated dysplasia

PATHOLOGY INTERNATIONAL, Issue 1 2006
Tetuo Mikami
To analyze the cell kinetics of ulcerative colitis (UC)-associated dysplasia, cyclin A, cyclin D1, cyclin E, cdk2, cdk4, p21Waf1, and p27Kip1 were immunohistochemically examined, in comparison with sporadic tubular adenomas. Immunohistochemical labeling indices for each marker in formalin-fixed paraffin-embedded tissue sections were assessed in a total of 23 low-grade dysplasias, 27 high-grade dysplasias, and 14 invasive adenocarcinomas associated with UC. For comparison, 21 sporadic tubular adenomas with low-grade dysplasia, 33 with high-grade dysplasia, and 21 invasive adenocarcinomas were also examined. In UC-associated dysplasias, cyclin A and p27Kip1 were located in the lower parts of the crypts and p21Waf1 in the upper regions. In tubular adenomas, cyclin A, cdk4, p27Kip1, and p21Waf1 were all expressed in the upper parts of the crypts. The expression levels of cyclin D1, cyclin E, and cdk2 were low. The cell proliferation zone in UC-associated dysplasia is located towards the bases of the crypts with the strong expression of cyclin A and p27Kip1, in contrast to tubular adenomas, which have their cell proliferation zone in the upper parts of neoplastic crypts. It is considered that tumorigenesis with UC-associated dysplasia is of the bottom-up type, related to altered expression of cyclin A and p27Kip1. [source]


Expression of double-stranded RNA-activated protein kinase in small-size peripheral adenocarcinoma of the lung

PATHOLOGY INTERNATIONAL, Issue 11 2005
Mee Sook Roh
The authors investigated the protein expression of double-stranded RNA-activated protein kinase (PKR), which was identified by using a previous cDNA microarray study, to discover PKR's correlations with several pathological parameters and to elucidate its role in neoplastic transformation and progression of lung adenocarcinomas. Immunohistochemistry for PKR was performed and a semiquantitative scoring method was calculated based on staining intensity and percentage of immunoreactive tumor cells (high vs low) for one bronchioloalveolar carcinoma (BAC), 16 adenocarcinomas consisting of BAC and invasive carcinoma (mixed) and 21 invasive adenocarcinomas without BAC (invasive). The BAC had high-grade expression and the mixed type tended to more frequently show high-grade expression than the invasive type (P = 0.028). There were no significant associations with age, tumor size, lymph node metastasis, lymphovascular invasion or the pathological stage. The Kaplan,Meier survival curves demonstrated that the patients with high-grade PKR expression had significantly shorter survival periods than those patients with low-grade PKR expression (P = 0.018). These results do not support the concept of PKR as a tumor suppressor in small-size peripheral adenocarcinomas of the lung. [source]