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PubMed1997

Stromelysin-3 expression in early (pT1) carcinomas and pseudoinvasive lesions of the colorectum.

Pseudoinvasion in colorectal adenomas is often difficult to distinguish from invasive carcinoma. Previous studies have indicated that expression of stromelysin-3 (ST-3), one of the metalloproteinase family of enzymes, may be useful for the identification of early invasive carcinoma. The goal of our study was to detect ST-3 expression in colorectal adenomatous polyps to see if it could be helpful for the differential diagnosis of pseudoinvasion vs. true invasion. We studied 25 polypectomy specimens which were divided histologically into 2 groups; the first consisted of 15 adenomas with invasive carcinoma, 8 of these carcinomas were more diffusely infiltrative (pT1), and 7 tended to be expansively invasive. The second group was composed of 10 adenomas with pseudoinvasion. A 35S labelled cDNA probe was used for in situ hybridization (ISH) and a monoclonal antibody (5ST-4A9) for immunohistochemistry (IHC). The distribution of ST-3 expression as detected by IHC and ISH was identical. All diffusely infiltrative carcinoma cases showed ST-3 expression, but only focally in 2 cases with marked lymphocytic infiltration. None of the expansive carcinoma or pseudoinvasion cases showed ST-3 expression. ST-3 expression seems to be an indicator of invasion, but a negative reaction for ST-3 does not rule out an expansive invasive neoplasm or a diffusely infiltrative invasive tumour with a dense lymphocytic reaction.

Adenomatous Polyps↗
PubMed2000

Outcome after surgical resection of intraductal papillary and mucinous tumors of the pancreas.

OBJECTIVE: Treatment of intraductal papillary and mucinous tumors of pancreas (IPMT) usually requires surgery. The objective of this study was to evaluate the risk of recurrence in patients after surgery according to the histological nature of the neoplasm and the type of surgery. METHODS: The outcome of 45 patients who underwent partial pancreatectomy (n = 35) or total pancreatectomy (n = 10) for IPMT was studied according to the nature of the neoplasm (invasive carcinoma or noninvasive neoplasm), type of surgery (partial or total pancreatectomy), and lymph nodes status. RESULTS: The overall 3-yr actuarial survival rate was 83%. Death occurred in seven of 20 (35%) patients with invasive carcinoma and in one of 26 (4%) patients with noninvasive tumors (p<0.05). There were two recurrences in the seven patients with noninvasive neoplasm who underwent partial pancreatectomy with involved resection margins, and none in the 13 patients with disease-free margins. In patients with invasive carcinoma, there was one recurrence after total pancreatectomy, six after partial pancreatectomy with disease-free margins and six after partial pancreatectomy with involved margins. In patients with invasive carcinoma, total pancreatectomy and the absence of lymph nodes involvement were independently associated with a low risk of recurrence. CONCLUSIONS: IPMT may be managed as follows: 1) in patients with noninvasive neoplasms, partial pancreatic resection should be guided by frozen section examination until disease-free margins are obtained; and 2) in patients with invasive carcinoma, total pancreatectomy seems most likely to cure the patient, but should be discussed according to the general status and the age.

Actuarial Analysis↗
PubMed1998

Cell proliferative activity in intraductal papillary-mucinous neoplasms and invasive ductal adenocarcinomas of the pancreas: an immunohistochemical study.

OBJECTIVE: To evaluate cell proliferative activity and expression of cytokeratins (CKs) and epithelial membrane antigen (EMA) in intraductal papillary-mucinous neoplasm of the pancreas (IPNP). METHODS: We examined cell proliferative activity in normal pancreatic ducts, IPNP, and invasive ductal adenocarcinoma of the pancreas by immunohistochemistry for proliferating cell nuclear antigen (PCNA) and Ki67 antigen. Expression of CKs and EMA was also examined immunohistochemically. RESULTS: In normal pancreas (n = 5), PCNA- or Ki67-positive ductal epithelia were not found. Cytokeratins (polyclonal, CAM5.2, CK-7, CK-8, CK-18, and CK-19) were expressed in the ducts and ductules but not in the acinus, and EMA expression was noted in the acinus but rarely in the ducts. In IPNP (n = 9) and invasive ductal adenocarcinoma (n = 6) of the pancreas, the overall PCNA-labeling index (PCNA-LI) was 3.2 +/- 4.1 and 16.0 +/- 7.2, respectively, and overall Ki67-LI was 2.2 +/- 2.6 and 14.5 +/- 6.3, respectively. In IPNP, the PCNA-LI and Ki67-LI were low in adenoma areas (PCNA-LI = 0.9 +/- 0.7), intermediate in dysplastic areas (PCNA-LI = 3.7 +/- 2.4), and rather high in carcinoma in situ areas (PCNA-LI = 11.5 +/- 8.4). Both CKs and EMA were noted in tumor cells. CONCLUSIONS: The data suggest that cell proliferative activity is low in IPNP compared to invasive ductal adenocarcinoma, that cell proliferative activity increases with the grade of cell atypia in IPNP, and that CK expression is not changed during the neoplastic change, but EMA is newly expressed or overexpressed during the neoplastic change.

Aged↗
PubMed1991

Comparison of peroxidase-labeled DNA probes with radioactive RNA probes for detection of human papillomaviruses by in situ hybridization in paraffin sections.

A study comparing in situ hybridization using nonradioactive DNA probes directly conjugated with horseradish peroxidase (HRP), and 35S-labeled antisense RNA probes for human papillomavirus (HPV) types 6/11, 16, and 18 was performed on formalin-fixed, paraffin-embedded tissue from 34 lesions of the cervix and vulva. These lesions included exophytic condylomas and intraepithelial and invasive neoplasms. HPV 6/11 was detected in two of four condylomata acuminata by both in situ techniques. HPV 16 was detected in 13 of 30 cases of intraepithelial and invasive neoplasms by both methods. Discordance between the two methods occurred in two instances. The radiolabeled probe but not the HRP probe detected HPV 16 in one case of cervical intraepithelial neoplasia (CIN 3), whereas the converse occurred in one case of vulvar intraepithelial neoplasia (VIN 3). HPV 18 was not detected in any of the specimens by either method. This study demonstrates that nonradioactive HRP-labeled probes for the detection of specific HPV types are as sensitive as the more laborious and potentially hazardous radioactive probes.

DNA Probes, HPV↗
PubMedDate not supplied

Invading basal cell carcinoma of the jaw: an under-evaluated complex entity.

Basal cell carcinoma (BCC) is a locally invasive neoplasm, rarely metastatic, yet capable of significant local destruction and disfigurement. Invasion into the bone is uncommon and only a few cases of invasion into facial bones, but never to the mandible or maxilla, have been described. We report three patients with BCC lesions invading their jaws, as a consequence of which either their mandible or maxilla had to be partially resected. This resulted in facial mutilation which required comprehensive multi-disciplinary therapy to restore function and esthetics. Such therapy requires a combination of modalities offered by both plastic and maxillofacial surgeons, as well as oral and dental rehabilitators.

Adult↗
PubMed2000

Histopathologic analysis of chromosome aneuploidy in ductal carcinoma in situ.

Formalin-fixed, paraffin-embedded sections from 28 cases of ductal carcinoma in situ (DCIS; 12 with coexisting invasive neoplasm) were analyzed for numerical alterations of chromosomes 7, 8, 16, and 17 by performing fluorescence in situ hybridization (FISH) using centromeric (alpha-satellite) probes. Based on signal counts in 200 to 300 nuclei, each hybridization was classified as disomic (copy loss in <40%, copy gain in < 10%), monosomic (copy loss in at least 50% of nuclei, partial if 40% to 49%) or trisomic/polysomic (copy gain in at least 20% of nuclei, partial if 10% to 19%). Grade I lesions were characterized by complete lack of significant chromosome gain, but 29% showed partial (focal) monosomy. Grade III lesions, in contrast, showed partial or complete trisomy/polysomy in 88% of hybridizations versus monosomy in only 4%. Grade II DCIS exhibited a mixed pattern of chromosome aneuploidy: 38% hybridizations were disomic, 36% trisomic/polysomic, and 26% monosomic (8 of 10 hybridizations showing complete monosomy occurred in grade II lesions). Disomic hybridizations exhibiting rare cells (5% to 10%) with copy gain were more frequent in tumors with coexisting invasive neoplasm (5 of 17 v 2 of 33, P = .02). In morphologically heterogeneous lesions, higher-grade foci were characterized by chromosome copy gain relative to corresponding lower-grade areas in 17 of 22 (77%) hybridizations. These results show the presence of multiple (at least 3) distinct chromosome aneuploidy patterns in DCIS, in keeping with divergent mechanisms of genetic alteration. Degree of chromosomal instability, moreover, may correlate with progression of DCIS to invasive growth, implying that genetic instability is a parameter that impacts the likelihood of early breast carcinoma progression.

Aneuploidy↗
PubMedDate not supplied

Sequence variations of the late upstream region of HPV16 in cervical intraepithelial neoplasm and invasive carcinoma.

HPV16 is the most common type of human papillomavirus (HPV) seen in cervical squamous cell carcinoma. A 78-bp promotor element at nt 4118-4196 called late upstream region (LUR), critical for the expression of late genes, has been identified recently. Late genes encode viral capsid proteins that coat viral DNA to form particles and serve as antigen. To elucidate whether there are any sequence variations within LUR of HPV16 and any difference of these sequence variations between cervical invasive squamous cell carcinoma (CIC) and cervical intraepithelial neoplasia (CIN), we sequenced HPV16 LUR from 50 cases of HPV16-positive CIC and CIN. We found that variation frequency in the late upstream region ranged from 0 to 4.2 except for two cases in which variation frequency was as high as 22.8%. Eight of 24 CINs and 17 of 26 CICs contained two or more variations (33% vs. 65%, P < 0.025). The results suggested that the sequence variations occurred more often in LUR of HPV16 than in other regions of HPV16 and the variations in HPV16 LUR might play a role in the process of carcinogenesis of cervical carcinoma.

Base Sequence↗
PubMed1992

Differences in the integration pattern and episomal forms of human papillomavirus type 16 DNA found within an invasive cervical neoplasm and its metastasis.

Human papillomavirus (HPV) type 16 DNA was found in three separate neoplastic lesions within a female patient. The physical state of the viral DNA in each lesion was determined by two-dimensional agarose gel electrophoresis. The primary cervical tumor contained large amounts of several distinct episomal forms as well as integrated HPV DNA. Metastatic tumor tissue found in the vagina had greatly reduced levels of episomal DNA and a viral DNA integration pattern that was different from that of the primary tumor. The vulvar carcinoma in situ had what appears to be free and integrated forms of viral DNA. The results show that although metastatic tissue retained HPV DNA, further rearrangements of the integrated viral DNA pattern found in the primary tumor may occur with a dramatic decrease of episomal forms during malignant progression.

Carcinoma, Squamous Cell↗
PubMed1999

[Integrated colposcopy and phase contrast microscopy for diagnosis of squamous intraepithelial lesions and invasive cervical neoplasms].

Colposcopy or cytology examinations alone allows to obtain diagnostic concordance with histopathological examination between 74-89% and 68-86%, respectively in SIL and cervical cancer detection. Both methods used simultaneously allow increase concordance with histopathology up to 95-100%. Cytological examination may be used simultaneously with colposcopy when Ph microscopy is used. The aim was to estimate benefits of conjunction of colposcopy and Ph cytology in SIL and cervical cancer detection in daily gynecological practice. Integrated colposcopy and cytology examinations were performed in 200 patients. Cervico-vaginal smears were obtained from the patient before Acetic-Acid Test and Lugol-Solution-Test were performed. Wet smears (Ph) were made. Results of integrated colposcopy and cytology were verified by histopathological examination. Diagnostic specificity, sensitivity, and Youden's value were estimated for Ph cytology, H-E cytology, and colposcopy alone and for integrated colposcopy and Ph cytology. Simultaneous colposcopy and Ph cytology reveal specificity 97.1% sensitivity 94.6% and Youden's value 91.8% thus provide fast, reliable and comprehensive information for accurate diagnosis in daily gynecological practice.

Carcinoma, Squamous Cell↗
PubMed1985

Basement membranes in cancer.

Basement membranes are ubiquitous tissue constituents which occur as supportive structure adjacent to epithelium, endothelium, mesothelium and also around smooth as well as striated muscle cells, Schwann cells and fat cells. In various types of cancer, basement membranes have been extensively studied by electron microscopy. Often basement membrane interruptions were seen in invasive neoplasms but in some tumors the neoplastic cells were surrounded by a continuous basal lamina. Recent immunocytochemical studies have shown that in invasive carcinomas the neoplastic cells often lack a continuous basement membrane. This may be caused by catabolic activity of invasive tumor cells, which have been shown to produce specific collagenases, or by insufficient production and/or extracellular assembly of basement membrane components by the neoplastic epithelial cells. In diagnostic histopathology, immunocytochemical staining of basement membrane components such as type IV collagen and laminin may help to distinguish between noninvasive (benign or in situ) and invasive lesions. Furthermore, in carcinomas the extent of the expression of basement membrane components may be correlated with the degree of differentiation of the neoplastic cells. Finally, in soft tissue tumors, basement membrane staining may be helpful for the differentiation of basement membrane producing neoplasms (e.g. of vascular, neural, smooth muscle or striated muscle origin) from non-basement membrane producing neoplasms (e.g. of fibroblastic origin).

Basement Membrane↗
PubMed2005

Epidermal growth factor mediates detachment from and invasion through collagen I and Matrigel in Capan-1 pancreatic cancer cells.

BACKGROUND: Pancreatic adenocarcinoma is a highly invasive neoplasm. Epidermal growth factor (EGF) and its receptor are over expressed in pancreatic cancer, and expression correlates with invasion and metastasis. We hypothesized that EGF receptor and integrin signalling pathways interact in mediating cellular adhesion and invasion in pancreatic cancer, and that invasiveness correlates temporally with detachment from extracellular matrix. METHODS: We tested this hypothesis by investigating the role of EGF in mediating adhesion to and invasion through collagen I and Matrigel in the metastatic pancreatic adenocarcinoma cell line Capan-1. Adhesion and invasion were measured using in vitro assays of fluorescently-labeled cells. Adhesion and invasion assays were also performed in the primary pancreatic adenocarcinoma cell line MIA PaCa-2. RESULTS: EGF inhibited adhesion to collagen I and Matrigel in Capan-1 cells. The loss of adhesion was reversed by AG825, an inhibitor of erbB2 receptor signalling and by wortmannin, a PI3K inhibitor, but not by the protein synthesis inhibitor cycloheximide. EGF stimulated invasion through collagen I and Matrigel at concentrations and time courses similar to those mediating detachment from these extracellular matrix components. Adhesion to collagen I was different in MIA PaCa-2 cells, with no significant change elicited following EGF treatment, whereas treatment with the EGF family member heregulin-alpha elicited a marked increase in adhesion. Invasion through Matrigel in response to EGF, however, was similar to that observed in Capan-1 cells. CONCLUSION: An inverse relationship exists between adhesion and invasion capabilities in Capan-1 cells but not in MIA PaCa-2 cells. EGF receptor signalling involving the erbB2 and PI3K pathways plays a role in mediating these events in Capan-1 cells.

Biocompatible Materials↗
PubMed1998

Establishment of ameloblastoma cell line, AM-1.

Ameloblastomas are slowly growing, locally invasive neoplasms with a potentially destructive behaviour. The molecular mechanisms that regulate the cell growth and invasion of ameloblastoma cells are unknown. Because ameloblastoma cells placed in culture have a very limited lifespan, the establishment of immortalized clones of ameloblastoma cells would aid its study. We produced an immortalized ameloblastoma cell line (AM-1) using human papillomavirus type-16. This cell line maintains epithelial cell morphology and expresses cytokeratins K8, K14, K18, K19. Furthermore, bcl-2 protein, which prevents apoptosis, is expressed. We investigated the behaviour of these cells on a collagen matrix in vitro. These cells grew in a monolayer over foci of collagen degradation and could invade the collagen gel at such sites. Since the behavior of cell line AM-1 mimics the behavior of ameloblastoma in vivo, it may be a valuable model for the study of these neoplasms.

Ameloblastoma↗
PubMed2005

Inhibition of Rho-kinase affects astrocytoma morphology, motility, and invasion through activation of Rac1.

Malignant astrocytomas are highly invasive neoplasms infiltrating diffusely into regions of normal brain. Whereas the molecular and cellular mechanisms governing astrocytoma invasion remain poorly understood, evidence in other cell systems has implicated a role for the Rho-GTPases in cell motility and invasion. Here, we examine how the inhibition or activation of Rho-kinase (ROCK) affects astrocytoma morphology, motility, and invasion. ROCK was inhibited in astrocytoma cells by using 5 to 100 mumol/L of Y27632 or by expressing the dominant-negative ROCK mutant, RB/PH TT. ROCK activation was achieved by expressing a constitutively active mutant, CAT. ROCK inhibition led to morphologic and cytoskeletal alterations characterized by an increase in the number and length of cell processes, increased membrane ruffling, and collapse of actin stress fibers. Using two-dimensional radial migration and Boyden chamber assays, we show that astrocytoma migration and invasion were increased at least 2-fold by ROCK inhibition. On the contrary, ROCK activation significantly inhibited migration and invasion of astrocytoma cells. Furthermore, using a Rac-GTP pull-down assay, we show that Rac1 is activated as a consequence of ROCK inhibition. Finally, we show that treatment of astrocytoma cells with small interfering RNA duplexes specific for Rac1-reversed stellation, prevented membrane ruffling formation and abrogated the increased motility observed following treatment with Y27632. Our data show that Rac1 plays a major role in astrocytoma morphology, motility, and invasion. These findings warrant further investigation to determine precisely how the modulation of Rac1 and ROCK can be exploited to inhibit glioma invasion.

Actins↗
PubMed1999

Middle ear adenocarcinoma with intracranial extension. Case report.

Middle ear adenocarcinoma is a very rare, locally invasive neoplasm assumed to arise from the middle ear mucosa. Although endolymphatic sac tumor (aggressive papillary middle ear tumor) and jugulotympanic paraganglioma may show brain invasion, intracranial extension of histologically confirmed middle ear adenocarcinoma has not been previously reported. The authors describe a 53-year-old man who suffered from otalgia and tinnitus for more than 10 years and from neurological deficits for 1 year due to a large temporal bone tumor that invaded the temporal lobe. A combined neurosurgical and otolaryngological resection was performed. Pathological analysis revealed a low-grade adenocarcinoma of a mixed epithelial-neuroendocrine phenotype, which showed a close histological similarity to, and topographical relationship with, middle ear epithelium. The authors conclude that middle ear adenocarcinoma belongs to the spectrum of extracranial tumors that have possible local extension to the brain.

Adenocarcinoma↗