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PubMedDate not supplied

Genomic instability: first step to carcinogenesis.

Multiple genetic alterations are commonly observed in human cancers. It has been suggested that inactivation of DNA repair pathways, which leads to an increased mutation rate and chromosomal instability, can initiate and accelerate the neoplastic process. Such a causality has been shown for DNA mismatch repair and Hereditary Nonpolyposis Colorectal Cancer (HNPCC), and evidence is accumulating that several other DNA repair pathways are frequently inactivated in different cancer types. In addition to genetic alterations, perturbations in DNA methylation patterns (epigenetic changes), which include both local hypermethylation and genome-wide hypomethylation, are frequently observed early in tumorigenesis. Therefore, genomic instability including genetic and/or epigenetic alterations may be the first step in carcinogenesis. Knowledge of these biochemical mechanisms are likely to lead to more effective cancer diagnosis and therapy.

Cell Transformation, Neoplastic↗
PubMed1998

Clonal analysis of renal sporadic angiomyolipomas.

Renal angiomyolipomas are benign tumors composed of variable amounts of mature fat, smooth muscle, and thick-walled blood vessels. They occur either sporadically or in association with tuberous sclerosis. Such tumors are considered as hamartomas, but few data are available concerning their pathogenesis. Indeed, it is not known whether angiomyolipoma is a congenital malformation or a neoplastic process. To answer this question, we assessed the clonality of sporadic angiomyolipomas using molecular analysis. Seven women (mean age, 59 years) with renal angiomyolipomas were included. DNA of the tumor and the normal adjacent kidney was extracted from archival paraffin-embedded tissue. DNA methylation pattern at a polymorphic site on the HUMARA gene was studied by polymerase chain reaction (PCR) amplification after methylation-sensitive enzyme digestion. This procedure enables the differentiation between polyclonal and monoclonal lesions according to their X-chromosome inactivation pattern. Five of the seven women included were informative for the HUMARA gene. The mean size of the angiomyolipomas was 53 mm (range, 18 to 110). In one case, a tumor thrombus was observed in the inferior vena cava. Clonal analysis showed that all of the angiomyolipomas and the tumor thrombus studied were monoclonal. This study shows that sporadic angiomyolipomas are monoclonal lesions consistent with neoplastic disorders. This result strongly supports the hypothesis that angiomyolipomas arise from the clonal proliferation of an uncommited cell, which will further evolve toward different cell types.

Adult↗
PubMed2006

The occipital artery: a microanatomical study.

OBJECTIVE: We performed a systematic microanatomical study of the occipital artery (OA) and its branches to describe the course, diameter, and branches of this vessel as well as the presence and pattern of anastomotic channels between the OA and the vertebral artery. METHODS: Twelve occipital arteries (6 adult cadaveric heads injected with colored latex) were studied using the surgical microscope. Particular attention was given to the course and branching pattern of the artery as well as the presence and type of anastomotic channels between the occipital artery and vertebral artery. RESULTS: Based upon anatomical considerations, the course of the occipital artery was divided into three segments. The first, or digastric segment, extends from the origin to the exit off the occipital groove of the mastoid process. The second segment, or suboccipital, extends from the occipital groove to the superior nuchal line. The third, or terminal segment, corresponds to the subgaleal segment just above the superior nuchal line up to the vertex. Two main descending branches of the second segment or suboccipital were identified. The superficial descending branch (SDB) runs between the splenium capitis and semispinalis capitis while the deep descending branch (DDB) enters the suboccipital triangle. Anastomotic vessels between one of these two descending branches and branches of the vertebral artery were found in 11 out of the 12 OAs dissected (91%). CONCLUSION: Detailed knowledge of the OA anatomy is helpful in choosing this vessel as a donor for extra-intracranial bypasses. More importantly, knowledge and understanding of the type and pattern of anastomoses between the OA and the vertebral artery are critical to avoid disastrous complications (i.e., posterior circulation stroke) during embolization of vascular or neoplastic processes fed by distal OA branches.

Anatomy, Regional↗
PubMed1989

Histomorphometry of bone marrow biopsies in primary osteomyelofibrosis/-sclerosis (agnogenic myeloid metaplasia)--correlations between clinical and morphological features.

Histomorphometry was performed on representative trephine biopsies of the bone marrow on admission of 50 patients (21 male, 29 female - age 67 years) with so-called primary osteomyelofibrosis/-sclerosis (OMF) not preceded by any other subtype of chronic myeloproliferative disorders. This study was firstly aimed at testing correlations between histological features (amount of haematopoiesis, cytological aspects of megakaryocytes, density of reticulin and collagen fibres and degree of osteosclerosis) and laboratory data, as well as spleen size and duration of relevant prediagnostic symptoms. Secondly, we concentrated on a discrimination of OMF patients into two subgroups according to bone marrow morphology and clinical variables. Statistical evaluation of histomorphometric variables and haematological findings disclosed that there was a progressive fibro-osteosclerotic process in the evolution of disease features. Increase in medullary fibrosis was significantly paralleled by an abnormal or pleomorphic megakaryopoiesis in the bone marrow: there was an increase in irregularity of perimeters for megakaryocytes and naked nuclei combined with smaller sizes of these elements including the nuclei. Additionally, there was a greater number of pycnotic bare nuclei. A number of morphometric features (density of fibres, degree of osteosclerosis, amount of haematopoiesis) were associated with corresponding clinical data (spleen size, length of preclinical history). By consideration of a set of basic histomorphometric variables our cohort of 50 patients could be divided into an early hyperplastic subtype with no or minimal medullary reticulin and another group with conspicuous fibrotic and osteosclerotic alterations of the bone marrow. It was noticeable that we found no significant correlation between amount of haematopoiesis or marrow cellularity with splenomegaly. This result suggests that splenic haematopoiesis (myeloid metaplasia) may represent an autonomous or neoplastic process and not only compensation for a failing fibro-osteosclerotic bone marrow.

Aged↗
PubMedDate not supplied

Monoclonal antibodies identify a cell-surface antigen associated with an activated cellular oncogene.

A variety of antigens have been identified on the surface of the malignant cell. However, identical antigens are often found on non-malignant cells of the same or different histological origin, or of a different stage of embryonic development. Many of these tumour-associated antigens appear to be only incidentally expressed on neoplastic cells. Clearly, it would be of great interest to identify cell-surface antigens whose expression is associated specifically with the transformed state and linked directly with the mechanisms responsible for transformation. The detection of activated cellular oncogenes in human and animal cancer cells by the technique of DNA transfection has allowed the isolation of genetic elements which are thought to have a critical role in malignancy. Here, in an effort to identify cell-surface antigens associated with the neoplastic process, we have generated hybridomas which secrete monoclonal antibodies that react specifically with cell-surface determinants found on NIH 3T3 cells transformed by transfection with a group of rat neuroblastoma oncogenes. These antibodies bind to and immunoprecipitate a phosphoprotein of relative molecular mass 185,000 (185 K) from a DNA donor rat neuroblastoma and 13 independent rat neuroblastoma DNA transfectants. There was no antibody reactivity with normal NIH 3T3 cells or with NIH 3T3 cells transformed by various other agents.

Animals↗
PubMed1993

Correlation of proto-oncogene expression and proliferation and meningiomas.

Proliferation and proto-oncogene expression in 19 meningiomas of typical and atypical histology were analyzed in an attempt to understand the mechanism of growth that characterizes the neoplastic process in these tumors. Proliferation was estimated as the proliferative index by the enumeration of S-phase cells in imprints of tumor tissue exposed to bromodeoxyuridine in vitro, and the gene expression of c-myc, c-fos, c-src, c-H-ras, N-myc, acidic and basic fibroblast growth factor, insulin-like growth factors I and II, platelet-derived growth factor-alpha, and epidermal growth factor was quantified by messenger ribonucleic acid dot-blot hybridization assay. Atypical and malignant tumors had significantly higher proliferative indexes than did their nonmalignant counterparts. Levels of c-myc and c-fos messenger ribonucleic acid were elevated more than fivefold in 72 and 78% of the tumors, respectively, relative to the lowest levels detected in the series. Levels of growth factor messenger ribonucleic acid were sporadically elevated; 37 to 44% of tumors had more than fivefold enhanced levels of acidic and basic fibroblast growth factor. Positive correlations between proliferation and proto-oncogene/growth factor expression were found for c-myc in atypical/malignant tumors and for epidermal growth factor in fibroblastic meningiomas. Deregulated expression of c-myc and c-fos common to both typical and atypical tumors suggests that these are early events in the meningioma tumor process that may disturb the control of cell differentiation and together with fibroblast growth factors are likely to endow the transformed cell with a selective growth advantage by reducing the requirement for exogenous mitogens and by providing a niche for the growth of the tumor clone. Positive correlation of c-myc levels with proliferation in atypical/malignant meningiomas implies that this is a feature of malignancy and indicates continued disruption of the negative regulation of proto-oncogene expression, perhaps by tumor suppressor gene losses, during the course of tumor progression.

Cell Division↗
PubMed1996

The role of cell adhesion molecules and proteases in tumor invasion and metastasis.

Over the past 10 years it has become apparent that invasion and metastasis are extremely complex processes; neoplastic cells must escape from the primary tumor, degrade the extracellular matrix, migrate to distant sites, arrest in the capillaries, and migrate through the basement membrane and underlying connective tissue to the metastatic site. Therefore, tumor cells must exhibit considerable flexibility in their adhesive interactions, and this is reflected in a complex and dynamic expression pattern of cell adhesion molecules, proteases, protease inhibitors, motility factors, and growth factors. Despite the recent explosion of information regarding adhesion-related molecules, questions as to their possible roles in normal tissue architecture and as to how alterations in their expression or structure may be responsible for the progression from a single malignant cell to a lethal metastatic disease need further investigation. Moreover, efforts should be made to use the obtained knowledge to contribute to improvements in the clinical management of cancer. In this review the different classes of cell adhesion molecules and proteases are summarized, with special emphasis being placed on molecules that have been shown to correlate with invasion and metastasis. Furthermore, the role of E-cadherin in cell adhesion and invasive processes is discussed in more detail, since E-cadherin may be considered promising as a candidate among cell-adhesion-regulating molecules to be used as a biomarker for malignancy. We also elaborate on the role of the catenins, which associate with and are important for the functioning of E-cadherin.

Animals↗
PubMed1999

Strategies in the development of recombinant vaccines for colon cancer.

A new era involving the evaluation of recombinant vaccines for colon cancer has begun with the concurrent emergence of insights and technologies in the fields of molecular biology and immunology. These advances include (I) the identification and cloning of an array of genes associated with the neoplastic process, such as oncogenes, suppressor genes, genes encoding oncofetal antigens, and tissue lineage determinants; (2) the development of a variety of viral and bacterial vectors to deliver and present gene products; (3) the identification of numerous T-cell costimulatory molecules and the knowledge of their mode of action; (4) the cloning and analysis of the modes of action of an array of cytokines and other immunomodulatory molecules; and (5) a more sophisticated knowledge of the mode(s) of antigen presentation and T-cell activation.

Adjuvants, Immunologic↗
PubMed1990

Different tumor-derived p53 mutants exhibit distinct biological activities.

In its wild-type form, the protein p53 can interfere with neoplastic processes. Tumor-derived cells often express mutant p53. Full-length mutant forms of p53 isolated so far from transformed mouse cells exhibit three common properties in vitro: loss of transformation-suppressing activity, gain of pronounced transforming potential, and ability to bind the heat shock protein cognate hsc70. A tumor-derived mouse p53 variant is now described, whose site of mutation corresponds to a hot spot for p53 in human tumors. While absolutely nonsuppressing, it is only weakly transforming and exhibits no detectable hsc70 binding. The data suggest that the ability of a p53 mutant to bind endogenous p53 is not the sole determinant of its oncogenic potential. The data also support the existence of gain-of-function p53 mutants.

Animals↗
PubMed1992

[Tumor thrombosis in inferior vena cava: diagnostic imaging and therapeutic approximation].

Review of our experience in the diagnosis and treatment of 44 patients with inferior vena cava tumoral thrombosis (IVCTT), associated or not to other neoplastic processes: 34 hypernephroma, 2 cava leiomyosarcoma, 1 paratesticular rhabdomyosarcoma and 1 biphasic synovial sarcoma. Twenty-five patients with hypernephroma and tumor thrombi in the ipsilateral renal vein only were excluded from the analysis since this fact did not change the usual therapeutic approach. In the 19 remaining patients, concomitantly to the primary tumour exeresis a thrombectomy was performed, using cavotomy with proximal and distal clamping in 11 patients and cardiopulmonary by-pass, deep hypothermia and cardiocirculatory arrest in 8 patients. The paper analyzes the radiological investigations performed in order to reach a IVCTT diagnosis, and reviews the related literature.

Humans↗
PubMed2003

Calgranulins in cystic fluid and serum from patients with ovarian carcinomas.

Ovarian cancer remains still associated with poor prognosis because it is diagnosed predominantly at advanced stages. Ovarian-specific tumor markers do not yet exist for early detection of the disease. At the search of diagnostic markers for ovarian cancer, proteomic-based approaches have focused on novel investigations of neoplastic processes in tumor patients. Cystic fluids of malignant and benign ovarian tumors and serum from the corresponding patients were collected and processed for two-dimensional gel electrophoresis. Proteins were visualized on the gels by silver staining. At the low molecular mass level between 10 and 20 kDa, selected protein spots were additionally processed for nanospray mass spectrometry and partial amino acid sequencing. For protein identification, the sequencing results were compared with computer information from a protein data bank. Protein patterns from cystic fluids of ovarian carcinomas differed significantly from those of benign cysts and revealed additional polypeptides at low molecular mass level between 10 and 20 kDa. Protein patterns from serum of patients with malignant ovarian tumors also contained additional polypeptides between 10 and 20 kDa that were not detected in serum from patients with benign cysts. The additional proteins in serum were present in similar electrophoretic positions compared with those found in the cystic fluid of the corresponding ovarian carcinomas. Protein spots in the range of 10-20 kDa were selected for partial amino acid sequencing. Two protein spots were identified as calgranulin A and three spots as calgranulin B. Either both proteins or only calgranulin A or B were present in cystic fluid from ovarian carcinomas and serum of the corresponding patients. These two proteins were absent or not detectable in fluid from benign ovarian cysts and in serum from those patients. Our investigations concerning protein patterns in cystic fluid of malignant and benign ovarian tumors provide new information about alterations in protein synthesis linked to neoplastic events of the ovary. With the proteomic strategy, new tumor markers are characterized and may serve for diagnostic purposes of patients with ovarian cancer.

Adult↗
PubMed1975

In vitro studies on human cervical epithelium, benign and neoplastic.

The early neoplastic lesions of the cervix offer an excellent model to study the neoplastic process in the human; In vitro studies indicate that these lesions are intermediate between normal epithelium and invasive carcinoma in many aspects. More recent studies show that the in vitro cells retain many of the characteristics of their in vivo counterparts. The techniques are available for short-term culture of normal and CIN cells, but no cell lines have been established. Spontaneous transformation of normal cervical epithelial cells in culture has been rare, but planned transformation with chemical carcinogens and HSV-2 has not been successful. Even though much preliminary work has been done, the establishment of a cell line from the human cervix and methods for transforming normal cell in vitro are needed. Studies toward these objectives are continuing in this laboratory.

Adult↗
PubMed1986

Association of human papillomavirus with squamous carcinoma of the uterine cervix.

The frequent association of human papillomavirus infection with preinvasive and invasive cancers of the cervix has led to speculation that the viruses may be involved in the neoplastic process. We have carried out some epidemiological studies of the prevalence of human papillomavirus infection in the female genital tract to evaluate more fully the oncogenic potential of these viruses in the cervix. A non-invasive method of detecting the virus has been developed for this purpose using DNA hybridization of cervical scrapings. The technique has been used to carry out prospective studies of patients with cervical intraepithelial neoplasia (CIN) and to investigate infection in women treated by laser therapy for CIN. We have also studied women with normal cervices to determine the prevalence of human papillomaviruses in the normal population. Further studies have involved the investigation of the effect of interferon on virus replication and epithelial proliferation in women with CIN III.

Carcinoma in Situ↗
PubMed2002

Tenascin and proteoglycans: the role of tenascin and proteoglycans in canine tumours.

Tenascin is a high molecular weight, extracellular matrix glycoprotein, subject to complex spatial and temporal patterns of expression during embryogenesis, wound healing and neoplastic processes. Proteoglycans are complex macromolecules, containing one or more glycosaminoglycans attached to a core protein, which are involved in cell-cell and cell-matrix interaction. Altered expression of both tenascin and proteoglycans has been found in tumours and expression of these two extracellular matrix proteins seems to be modulated in the same way in human and canine tumours. The quantitative and qualitative changes in tenascin and proteoglycan composition may significantly affect behaviour of tumour cells. While tenascin and proteoglycans have many biological functions likely to influence tumour development and progression, their exact role in regulation of tumour cell-cell interaction, proliferation, invasion and metastasis remains to be established. This review focuses on the role of tenascin and proteoglycans in neoplasia and recent developments in canine tumours.

Animals↗
PubMed1995

Highly purified primitive hematopoietic stem cells are PML-RARA negative and generate nonclonal progenitors in acute promyelocytic leukemia.

The hierarchical level of stem cell involvement in acute promyelocytic leukemia (APL) characterized by the pathognomonic PML-RARA fusion gene is unknown. To determine if the cells of the primitive hematopoietic stem cell compartment are involved in the leukemic process, we have used molecular and cell sorting techniques in peripheral blood and bone marrow (BM) cells at diagnosis from three patients with APL and t(15; 17). In two of them, clonality analysis was also possible using the BstXI polymorphic site of the PGK gene. The PML-RARA fusion gene was readily identified by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of BM cells obtained at diagnosis in all three patients. These same samples were then used to sort CD34+ cells and their CD38+ and CD38- subsets by fluorescence-activated cell sorting. In both female patients, CD34+/CD38+ and CD34+/CD38- cell fractions were polyclonal using PCR, whereas a monoclonal pattern was identified at the BM sample obtained at diagnosis either by Southern blotting or by PCR. Because of the high sensitivity of the PCR analysis, the polyclonal pattern of these cell populations could mask the presence of a minor clone. To detect this clone, we preformed RT-PCR analysis for t(15; 17). In one female patient, the abnormal PML-RAR fusion gene was found only in the more mature CD34+/CD38+ cell fraction using a nested PCR approach, whereas the polyclonal CD34+/CD38- fraction was PML-RARA negative. These findings were confirmed in a third patient with APL in whom the PML-RARA transcripts were absent in the CD34+/CD38- cell fraction. To study the clonality at the level of clonogenic progenitors, we used in one patient PGK analysis by PCR of individual burst-forming units-erythroid and colony-forming units-granulocyte-macrophage obtained from the CD34+/CD38- and CD34+/CD38+ cell populations at diagnosis and from the BM sample obtained during remission. The two highly purified cell populations gave rise to morphologically normal colonies clonal for both the BstXI site containing (A) and the BstXI site lacking (B) PGK allelles, indicating their polyclonal content, a pattern that was also found in clonogenic progenitors obtained at remission. These findings strongly suggest that the primitive hematopoietic stem cells as defined by the CD34+/CD38- antigens are not involved by the neoplastic process in APL. These results may have important implications for autografting strategies of retinoic acid/chemotherapy-resistant or relapsed patients.

ADP-ribosyl Cyclase↗
PubMed2000

[Tumor thrombosis of the left renal vein and inferior vena cava secondary to renal cell carcinoma. Findings with ultrasonography, Echo-Doppler, and computerized tomography].

Renal cell carcinoma represents a 2.5-3% of all neoplastic processes, usually seen un patients older than 50 years. 60-75% are resectable at diagnosis, representing local or metastatic advanced disease the rest of them. This tumor tends to spread intravascularly, leading to tumoral thrombosis within the inferior caval vein (ICV) and renal vein 4-10% and 21-35% of cases, respectively. As the only effective treatment is surgical resection, preoperative determining of the thrombus extension is crucial. Thus, an accurate radiological study including ultrasound, doppler sonography, computed tomography and/or Magnetic Resonance, is key for these patients. We present a 49 year-old patient with renal cell carcinoma and associated tumoral thrombosis in inferior caval vein and left renal vein; we provide the most significant figures, explaining its most characteristic radiological findings.

Carcinoma, Renal Cell↗
PubMed2002

High-grade dysplasia in Barrett's esophagus. The case for esophagectomy.

The main principles for optimal management of HGD arising in Barrett's esophagus are that unequivocal diagnosis of HGD is a prerequisite for making the decision of any kind of treatment. HGD must be resected because of the presence of neoplastic cells in the lamina propria in 40% of patients. No reliable endoscopic or endosonographic feature exists that allows accurate prediction of the existence of neoplastic cells within the lamina propria of a patient having HGD in endoscopic biopsy material. Prompt decision to remove an HGD lesion as soon as unequivocal histologic diagnosis has been settled prevents the development of extraesophageal neoplastic spread. Esophagectomy is preferable to endoscopic mucosal excision because approximately 20% of patients who have HGD in preoperative biopsy material carry neoplastic cells beyond the muscularis mucosae. Esophagectomy can be limited to the removal of the esophageal tube without extended lymphadenectomy because 96% of patients who have HGD in endoscopic biopsy samples have a neoplastic process confined to the esophageal wall. Esophageal resection must encompass all the Barrett's area because of the risk for the further development of a second cancer in the metaplastic remnant. Vagus-sparing esophagectomy with colon interposition or elevation of the antrally innervated stomach up to the neck is preferable to conventional esophagectomy with gastric pull up because the former procedure maintains gastric function intact, whereas the latter exposes patients to the risk for the long-term development of reflux esophagitis and even of metaplastic transformation of the proximal esophageal remnant. Subtle details in the understanding of a given patient's clinical course may be critical for making the decision of the most relevant mode of therapy; therefore, patients who have HGD should be treated in dedicated centers, the experience of which offers the best chances of uneventful recovery if the surgical option is retained.

Barrett Esophagus↗
PubMedDate not supplied

[Cesarean hysterectomy im modern obstetrical practice from 1968 to 1993].

A retrospective study of cesarean hysterectomies at the Department of Obstetrics and Gynecology in Novi Sad was conducted for the period 1968-1993. There were 129,127 deliveries, whereas cesarean section was performed in 10,485 (8.12%) cases. There were 55 cesarean hysterectomies (0.042%), while in 0.52% they were performed during cesarean section. Elective hysterectomy was performed in 7 (12.73%) cases because of neoplastic process and uterine myoma, while in 48 (87.27%) cases it was performed for heavy bleeding. Most often bleeding occurred due to complications of placenta previa, uteroplacental apoplexy, premature placental ablation, uterine rupture and atony. Total hysterectomy was performed in 30 (54.54%) cases and subtotal hysterectomy in 25 (45.45%) cases. Bilateral adnexectomy was performed in 3 (5.45%) cases. Urinary bladder injury occurred in 4 (7.27%) patients, wound infection in 11 (20.00%) patients, urinary infection in 3 (5.45%) and pelvic peritonitis in 1 (1.82%) patient. One maternal death (1.82%) occurred due to DIC (disseminated intravascular coagulation). Out of 57 delivered newborns 20 (35.10%) died in the perinatal period. There were 13 stillbirths (22.80%), whereas 7 newborns (12.30%) died in the early neonatal period due to prematurity and RDS (respiratory distress syndrome).

Adult↗