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At least 757 records · Page 42Linked to original sources
PubMed1976

The role of vascular proliferation in the growth of brain tumors.

The formation of new blood vessels, i.e., angiogenesis, is a critical step in the evolution of a brain tumor from the earliest avascular phase to the clinically overt, vascular stage. For cerebral astrocytomas, intense capillary proliferation is a poor prognostic sign, associated with rapidly growing tumors. The in vivo production of a vasoformative substance can be demonstrated by transplanting human and experimental gliomas to the rabbit cornea. Intense neovascularization is elicited by the tumor and not by control tissues. If the same tumor is transplanted to the vitreous, thereby interrupting the vasoformative signal, the tumor remains in a dormant state for a prolonged period of time, despite its malignant potential. Inhibition of angiogenesis would be an important adjunct to the surgical treatment of gliomas.

Animals↗
PubMed1981

Evidence that there exist four classes of RNA tumor viruses which encode proteins with associated tyrosine protein kinase activities.

The transforming protein of Rous sarcoma virus, p60src, the Abelson virus protein, p120, and the Y73 virus protein, p90, all have associated tyrosine protein kinase activities in vitro. Possible structural homology between these functionally related proteins was investigated by two-dimensional analysis of both methionine-containing and phosphate-containing tryptic peptides derived from biosynthetically labeled proteins. Marked differences were found between the maps of both [35S]methionine-labeled and 32P-labeled tryptic peptides. This suggests that the transforming gene of Rous sarcoma virus and the putative transforming genes of Abelson virus and Y73 virus are different. In addition, each of these genes has been shown previously to be unrelated to the putative transforming gene of Fujinami sarcoma virus, another virus which encodes a protein with associated tyrosine protein kinase activity. Therefore, it appears that there exist at least four distinct classes of functionally related RNA tumor viruses. Analysis of phosphorylated tryptic peptides did, however, reveal homology between one of the two phosphotyrosine-containing tryptic peptides of p90 of Y73 virus and the single phosphotyrosine-containing tryptic peptide of p60src of Rous sarcoma virus. Comigration of these two peptides in several different buffers and the identical mobility of their phosphorylated cleavage products after secondary digestion with protease V8 of Staphylococcus aureus indicated that p60src and p90 contain an identical site of tyrosine phosphorylation in vivo. The results are discussed with respect to the evolution of RNA tumor viruses which encode proteins with associated tyrosine protein kinase activities and the limitations of analysis of detecting homology between genes by both molecular hybridization and peptide mapping.

Abelson murine leukemia virus↗
PubMed1988

Genetic tagging of tumor cells with retrovirus vectors: clonal analysis of tumor growth and metastasis in vivo.

Retrovirus vector infection was used to introduce large numbers of unique genetic markers into tumor cell populations for the purpose of analyzing comparative changes in the clonal composition of metastatic versus that of nonmetastatic tumors during their progressive growth in vivo. The cell lines used were SP1, a nonmetastatic, aneuploid mouse mammary adenocarcinoma, and SP1HU9L, a metastatic variant of SP1. Cells were infected with delta e delta pMoTN, a replication-defective retrovirus vector which possesses the dominant selectable neo gene and crippled long terminal repeats. G418r colonies were obtained at a frequency of 4 x 10(-3). Southern blot analysis of a number of clones provided evidence of random and heritable integration of one or two copies of the proviral DNA. Clonal evolution of primary tumor growth and the nature of lineage relationships among spontaneous metastases and primary tumors were analyzed by subcutaneously injecting 10(5) cells from a pooled mixture of 3.6 x 10(2) G418r SP1HU9L or 10(4) G418r SP1 colonies into syngeneic CBA/J mice. The most striking finding was the relative clonal homogeneity of advanced primary tumors; they invariably consisted of a small number (less than 10) of distinct clones despite the fact that hundreds or thousands of uniquely marked clones had been injected. In the case of the metastatic SP1HU9L cells, the nature of these "dominant" clones varied from one tumor to another. Analysis of a number of lung metastases revealed that a proportion of them were derived from dominant primary tumor clones and were composed of one, and sometimes two, distinct progenitors. In some animals, all the lung metastases were derived from a common progenitor clone, whereas in others, each metastatic nodule had a different progenitor. The results show the following. (i) Retrovirus vector infection can be used to introduce large numbers of unique and stable clonal markers into tumor cell populations. (ii) The progeny of a very limited number of clones dominate in advanced primary tumors. (iii) Mammary carcinoma metastases are of mono- or biclonal origin. The significance of the results is discussed.

Adenocarcinoma↗
PubMed2006

Methylation of RASSF1A and TRAIL pathway-related genes is frequent in childhood intracranial ependymomas and benign choroid plexus papilloma.

Ependymomas (EP) represent the third most frequent type of central nervous system (CNS) tumor of childhood, after astrocytomas and medulloblastomas. No prognostic biological markers are available, and differentiation from choroid plexus papilloma (CPP) is difficult. The present objective was, for a sample of 27 children with intracranial EP and 7 with CPP, to describe and compare the methylation status of 19 genes (with current HUGO symbol, if any): p15INK4a (CDKN2B), p16INK4a and p14ARF (both CDKN2A), APC, RB1, RASSF1A (RASSF1), BLU (ZMYND10) FHIT, RARB, MGMT, DAPK (DAPK1), ECAD (CDH1), CASP8, TNFRSF10C, TNFRSF10D, FLIP (CFLAR), INI1 (SMARCB1), TIMP3, and NF2. Three adult corteses were used as a control. We detected a similar percentage of methylated tumors in both groups (71% in CPP and 77% in EP). No gene was methylated in that control group. RASSF1A was the most frequently methylated gene in both benign tumors (66%) and EP (56%). The genes associated with apoptosis were methylated in both groups of tumors. The percentages of TRAIL pathway genes (CASP8, TFRSF10C, and TFRSF10D) methylated were 30, 9.5, and 36.4%, respectively, in ependymomas and 50, 50, and 16.7%, respectively, in choroid plexus papillomas. No other gene was methylated in the benign tumors, whereas FHIT was methylated in 22%, RARB in 14.8%, BLU in 13.6%, p16INK4a in 11.1%, TNFRSF10C in 9.5%, and DAPK in 7.4% of ependymomas. Although we did not observe a statistical relationship between methylation and clinical outcome, the methylation pattern does not appear to be randomly distributed in ependymoma and may represent a mechanism of tumor development and evolution.

Adolescent↗
PubMed1976

Morphological and clinical observations of patients with early bladder cancer treated with total cystectomy.

In 21 cases, early bladder cancer was detected by urine cytology, although not by cystoscopy, and was treated by total cystectomy. The neoplasms, all transitional cell carcinomas of moderate to high degrees of anaplasia, were entirely in situ in 17 of the 21 patients; in 4, although mainly in situ, the tumors showed additional minimal microinvasion. Widespread mucosal involvement was demonstrated in every case by step-sectioning, and extension into the prostatic ducts occurred in 7 of the 19 male patients and into the mucosa of one or both distal ureters in 12 patients. Premalignant atypia of the mucosa was also widespread and direct intramucosal spread of cancer cells was a significant factor, particularly along the prostatic ducts and ureters. The duration of significant symptoms (follow-up for 9 years before cystectomy in several cases and for 8 years in 1 histologically proved case) suggests that the evolution of these tumors may be considerably longer than previously documented.

Aged↗
PubMedDate not supplied

Hormonal regulation of MUC1 expression.

Several circulating mucinous markers, including CA 15.3, MCA, CA 459, CASA, and Truquant BR, are secreted products of the polymorphic MUC1 gene, and are used as diagnostic tools in patients with breast cancer. In clinical practice the measurement of the levels of these markers in the blood can give important information on the tumor's response to treatment and its biological behavior during disease monitoring. Since the marker levels reflect the activity of the tumor, it is important to know all factors influencing the production/secretion and the blood concentrations of MUC1 mucin. Recent findings suggest that MUC1 gene expression is regulated by steroid hormones and other substances present in the serum. Such observations are very important not only because of their biological significance but also for their clinical implications, as one approach to breast cancer therapy is based on chemical hormone manipulation. Nevertheless, we have preliminarily demonstrated that endocrine treatment in breast cancer patients does not influence the circulating CA 15.3 serum levels, so changes in marker levels are related only to the clinical evolution of the tumor.

Biomarkers, Tumor↗
PubMed1994

[Predictive signs of cancers in dermatomyositis. Study of 29 cases].

Dermatomyositis (DM) is characterized by an inflammatory myopathy and typical cutaneous lesions. In a retrospective study, 29 adult cases without overlap syndrome were reviewed. Our aim was to define predictive signs of cancer. Ten (four women, six men) of the 29 patients (35%) had DM associated with malignancy. The diagnosis of cancer was made concomitantly in six cases, more than year after (two cases), more than year prior to (two cases) the occurrence of DM. No extensive diagnosis procedures were necessary for identifying the tumors. A paraneoplasic evolution was certain for any patient, probable for six, improbable for fourth. For the group with malignancy: age was higher (P = 0.01), albumin lower (P = 0.04), C reactive protein higher (P = 0.0061). These parameters seem to have predictive value for the presence of malignancy.

Adult↗
PubMed1999

Sequential accumulation of K-ras mutations and p53 overexpression in the progression of pancreatic mucinous cystic neoplasms to malignancy.

OBJECTIVE: Pancreatic mucinous cystic neoplasms (MCNs) provide a spectrum of neoplastic changes ranging from benign to malignant. The authors have correlated K-ras mutations and p53 overexpression with the evolution of these tumors. METHODS: Areas of mild, moderate, or severe dysplasia were microdissected from paraffin-embedded tissue sections of 28 different MCNs (10 benign, 9 borderline, 9 malignant). Nonneoplastic pancreatic ducts were also microdissected from tissues adjacent to the tumors. Ten serous cystadenomas served as negative controls. K-ras codon 12 mutations were identified by a mutant-enriched nested polymerase chain reaction-restriction fragment length polymorphism assay and confirmed by sequencing. p53 overexpression was demonstrated by immunohistochemistry. RESULTS: K-ras mutations were detected in 20% of benign, 33% of borderline, and 89% of malignant MCNs. Histologically, mutations were found in 26% (7/27) of MCN epithelia with mild dysplasia, 38% (5/13) of MCN epithelia with moderate dysplasia, and 89% (8/9) of MCN epithelia with severe dysplasia or carcinoma. Ten percent (4/39) of nonneoplastic pancreatic ducts at the margins of MCN harbored mutations, all associated with borderline or malignant tumors. Overexpression of p53 occurred in none of the benign or borderline MCNs but in 44% (4/9) of the malignant tumors (p = 0.006 benign/borderline vs. malignant). p53 immunoreactivity was concentrated in areas of severe dysplasia/carcinoma or invasion, where K-ras mutation had been detected. CONCLUSION: These findings demonstrate a sequential accumulation of genetic changes in the carcinogenesis of MCN. K-ras mutations appear early and increase in proportion with increasing dysplasia. Overexpression of p53 is a late finding observed only in carcinomas, and in combination with mutated K-ras genes. The presence of K-ras mutations in nonneoplastic ducts supports formal pancreatic resection over enucleation for treatment. Mucinous cystic neoplasms may be a useful model to study the evolution of pancreatic ductal adenocarcinomas, in which precursor lesions remain unknown.

DNA Mutational Analysis↗
PubMed2000

Time-lapse video reveals immediate heterogeneity and heritable damage among human ileocecal carcinoma HCT-8 cells treated with raltitrexed (ZD1694).

BACKGROUND: Cellular heterogeneity in drug response has important clinical implications, and is believed to develop over many generations during clonal evolution in human tumors. The purpose of this study was to determine the level of heterogeneity exhibited by sister cells soon after their birth. METHODS: Human ileocecal carcinoma cells (HCT-8) were followed up to 11 days in vitro after a 2-h exposure to 1 microM raltitrexed (IC(95)) in a time-lapse video system. RESULTS: Over five experiments, 414 cells were followed after exposure to raltitrexed. Immediate sterility occurred in 74% of treated cells. Only 6% of cells could produce more than two generations of offspring, and heterogeneity in drug response was seen. Comparing sister cells < 24 h old, the more proliferative sibling produced up to 73 times more offspring, with a median ratio of 9.0 (control median = 1.19). Offspring of prolific drug-treated cells had a decreased probability of division (68% compared with 92%) and an increased average interdivision time (19.0 h compared with 15.1 h). CONCLUSIONS: Short-term exposure to raltitrexed resulted in increased interdivision times and production of sterile offspring extending seven generations. Cellular heterogeneity (difference in proliferation potential comparing drug-treated sister cells) was evident without a period of clonal evolution.

Aged↗
PubMed2000

Molecular evolution of multiple recurrent cancers of the bladder.

We describe the reconstruction of bladder tumor development in individual patients spanning periods of up to 17 years. Genomic alterations detected in the tumors were used for hierarchical cluster analysis of tumor subclones. The cluster analysis highlights the clonal relationship between tumors from each patient. Based on the cluster data we were able to reconstruct the evolution of tumors in a genetic tree, where tumors with few aberrations precede those with many genetic insults. The sequential order of the tumors in these pedigrees differs from the chronological order in which the tumors appear. Thus, a tumor with few alterations can be occult for years following removal of a more deranged derivative. Extensive genetic damage is seen to accumulate during the evolution of the tumors. To explain the type and extent of genetic damage in combination with the low stage and grade of these tumors, we hypothesize that in bladder cancer pathogenesis an increased rate of mitotic recombination is acquired early in the tumorigenic process.

Evolution, Molecular↗
PubMed1992

The ultrastructure of peripheral neurofibroma: the role of mast cells and their interaction with perineurial cells.

The authors analyze the ultrastructure of mast cells and perineurial cells when both are present in neurofibroma of the nerve sheath. Samples of pathologic tissue taken from three patients with neurofibroma of a peripheral nerve sheath were analyzed by light and transmission electron microscopy. The observations document the characteristics of the tumor cells (Schwann cells and perineurial cells) as well as the presence of numerous mast cells, typically in close contact with the perineurial cells and never with the Schwann cells. Many electron-dense vesicles were found between the cells; these vesicles are created when the cell membrane of the mast cell buds, and then they come into contact with the adjacent perineurial cell. Endocytosis vesicles are often present in the cytoplasm of perineurial cells. Analysis of these observations led the authors to assume the existence of a metabolic interaction between the two cell type in contact with each other and an active role of the mast cells in the evolution of the tumor. The following two theories are plausible: either the mast cells actively stimulate tumor growth, or they alter the phenotype of the tumor cell. These findings could have interesting clinical applications. The use of treatment protocols which inhibit mast cell activity could, in theory, stop either the proliferation of the neurofibroma or its malignant transformation.

Cell Division↗
PubMedDate not supplied

[Dysembryoplastic neuroepithelial tumors. A benign tumor cause of partial epilepsy in young adults].

Dysembryoplastic neuroepithelial tumor (DNT) is a newly recognized brain lesion first reported in 1988 by Daumas-Duport et al. The authors described five cases of DNT, that occurred in young people and were characterized by partial seizures. Seizures could become intractable and secondary generalised. Usually, the interictal neurological examination was normal. In most cases, computed tomography showed a supratentorial, "pseudocystic" low density appearance associated in some cases with calcific hyperdensity or focal contrast enhancement. Magnetic resonance imaging demonstrated a predominantly intracortical lesion. Common features included low signal intensity on T1-weighted images and high signal on T2-weighted images. Temporal and frontal lobes were mainly involved. Dysembryoplastic origin explained the clinical and radiological stability and the benign evolution of this tumor. Tumor resection was required only when epilepsy was intractable or when there was intracranial hypertension. Earlier intervention can prevent the physical and psychosocial damage resulting from chronic seizures and can improve the prognosis for these young patient. Histologically, DNT have been incorporated amond the category of neuronal and mixed neuronoglial tumors. Three patterns are described: a simple form with a unique glioneuronal element, a complex form with specific glioneuronal element, nodules being made of multiple variants looking like astrocytomas, oligodendrogliomas or oligo-astrocytomas, foci of dysplastic cortical disorganisation, and a non specific form. When specific glioneuronal composant is absent (50% of cases), the identification of DNT has therapeutic and prognostic implications because aggressive therapy may be avoided, sparing these young patients the long term effects of radio-or chemotherapy.

Adult↗
PubMed2006

Expression and clinical signification of cytosolic hyaluronan levels in invasive breast cancer.

BACKGROUND: Hyaluronic acid (HA), a high-molecular weight glycosaminoglycan, has been considered to be involved in the growth and progression of malignant tumors in several experimental studies. The objective of this work was to evaluate the cytosolic HA content in breast cancer, its possible relationship with clinicopathological tumor parameters and steroid receptor status, as well as its potential prognostic significance. METHODS: Cytosolic HA levels were examined by means of immunoradiometric techniques in 850 patients with invasive breast cancer. The mean follow-up period for these patients was 55.1 months. RESULTS: Cytosolic HA levels ranged widely in tumors (4-59767 ng/mg protein; median: 4960). Statistical analysis showed that HA levels were significantly higher in younger patients (p=0.0001), as well as in premenopausal than in postmenopausal patients (p=0.001). HA levels were also significantly higher in ductal or lobular histological type than in other histological types (coloid, medullar or papillar types) (p=0.0001). Likewise, HA correlated significantly and positively with tumoral levels of PgR (r sub S: 0.11; p=0.001) in the all group of patients. In the subgroup of patients with ductal invasive type, HA levels were also significantly higher in well differentiated tumors and in diploid tumors. In addition, in this latter group of patients, HA levels in tumors correlated also positively and significantly with the either estrogen-inducible proteins: PgR (r sub S: 0.11; p=0.001), pS2 (r sub S: 0.117; p=0.008) and tPA (r sub S: 0.314; p=0.0001). On the other hand, significant association between HA intratumoral levels and relapse-free survival and overall survival in the overall group of patients was not found. However, high HA intratumoral levels were significantly associated with longer relapse-free survival in the subgroup of patients with ductal histological type tumors (p=0.01), as well as in those patients without any type of systemic adjuvant treatment (p=0.01). CONCLUSIONS: Our results suggest that high intratumoral levels of HA may be associated with tumors of favorable evolution in certain subgroups of patients with breast cancer. Thus, HA may provide additional prognostic information to that given by other biochemical markers currently used in breast cancer.

Breast Neoplasms↗
PubMed1995

Acquired deficiency in C1-inhibitor associated with signet ring cell gastric adenocarcinoma: a probable connection of antitumor-associated antibodies, hemolytic anemia, and complement turnover.

BACKGROUND: Acquired deficiency in C1-inhibitor (C1-INH) associated with malignancy is often asymptomatic because clinical manifestations are not dependent on a critical complement threshold (in contrast to hereditary C1-INH deficiency). Increased complement consumption involving different kinds of antibodies is the postulated mechanism for this disease, but other factors must play an important role. CASE REPORT: A 76-year-old woman with unremarkable medical history experienced three episodes of angioedema over 6 months. Investigations revealed a complement profile characteristic of acquired deficiency in C1-INH, a hemolytic anemia, and a signet ring cell adenocarcinoma (linitis plastica). A gastrectomy and a splenectomy were performed. The postoperative course was characterized by a complete disappearance of the symptoms of angioedema and hemolytic anemia. A local recurrence of the tumor 5 months later could not be resected. The patient died 17 months after the initial surgery was performed. RESULTS: Quantitative and functional analyses of the complement factors showed persistent excessive complement consumption. Markers of hemolytic anemia disappeared after tumor removal but recurred in the second part of the disease evolution. Immunohistochemical findings in tumor tissue showed loss of normal blood group antigens but expression of Lea antigen, as well as C1q deposition. CONCLUSION: To explain the whole clinical and laboratory picture, we hypothesize a connection between tumor immunohistochemical profile, complement consumption, and hemolytic anemia. Tumor cell surface antigens might lead to a permanent but asymptomatic complement consumption that is worsened and becomes clinically manifest by superimposed hemolytic anemia caused by cross-reactive antibodies to newly expressed blood group antigens on tumor cells. This hypothesis should be confirmed by other observations.

Aged↗
PubMed1995

[Calcifying odontogenic epithelial tumor (Pindborg's tumor). Review of a case with maxillary localization].

We report a case of maxillary sitting of a calcifying odontogenic epithelial tumor (Pindborg's tumor). It is a benign tumor with similar microscopical findings with the ameloblastoma although its natural evolution is different. The tumor has an actodermal odontogenic origin. The stem cell from which it develops and its growth stimulus are unknown. Although the intermediary stratum of the enamel producing organ has been incriminated. A swelling of the maxillae or a casual finding--as the case reported--are the most common manifestations at beginning of these cases. The differential diagnosis depends on the radiological pattern we may find. Various surgical procedures may be considered optional. It could vary from enucleation to complete resection of the affected structure. Aggressive surgery is not indicated.

Adolescent↗
PubMed1981

Defective function of granulocytes in patients with cancer.

Mobilization of granulocytes into a serum-filled chamber, histochemical nitroblue tetrazolium (NBT) reduction tests, and phagocytosis were performed in 11 patients with solid tumors treated with surgical excision and chemotherapy and in 22 untreated or surgically treated patients. The results revealed a decreased mobilization (p less than 0.001) and an impaired capability of neutrophils to reduce NBT after stimulation (p less than 0.05) in both groups of patients. The decrease in the values in the stimulated reduction of NBT was more pronounced in untreated patients than in treated ones. At the same time the phagocytic activity of neutrophils on Candida albicans, which was decreased (p less than 0.01) in untreated patients, was normal in those who had been treated with chemotherapy. There were no distinctive correlations between circulating immune complexes and granulocyte function. We propose that this newly demonstrated defect in neutrophil mobilization and low median C. albicans-stimulated NBT reduction contributes more in the evolution of the tumor than in the pathogenesis of infections and that chemotherapy seems to restore a better granulocyte function.

Adult↗
PubMed2006

[Clinicopathological study of incidental cancer prostate in patients undergoing surgery for symptomatic diagnosis of BPH].

UNLABELLED: OBJECTIVES-INTRODUCTION: Retrospective study of a series of patients with prostate surgery (suprapubic prostate adenomectomy -APS-, and prostate transurethral resection -RTU-P-) for presumed BPH symptomatic non-respondent to the conservative medical treatment. Analysis of prevalence, incidence, clinical-pathological, treatment, tumor progression and evolution of the patients with incidental prostate cancer (CPI) detected. MATERIAL AND METHODS: 1593 patients with prostate surgery (APS and RTU-P) during 6 years (1996-2001) were revised. APS 35%, RTU-P 65%. Revision of all pathological anatomy of surgical specimens and the evolutions of the patients with CPI. RESULTS: 78 CPI; Prevalence 4,89%; Incidence 13 cases/year. Mean age 73.6 years. Digital rectal examination was normal in 100%, mean PSA 6 ng/ml (0.5-30). Group APS: 25 CPI (32%); prevalence 4.55%; incidence 4 cases/year; mean PSA 7.7 ng/ml (2.8-30); mean weight resection 65 gs. Group RTU-P: 53 CPI (68%); prevalence 5,07%; incidence 9 cases/year; mean PSA 5.2 ng/ml (0,5-29); mean weight resection 20 gs. 22% biopsy previously by high PSA, mean PSA 14 ng/ml (4,8-30). Gleason average 5 (mean 4.8), rank 3-8. pTla 66%, pTlb 33%. TREATMENT: 57% follow-up watched without treatment (wait and see); 18% hormonal treatment; 3% finasteride; 9% Radical Prostatectomy; 9% radiotherapy. Follow Lost 4%. Mean follow-up 47.19 months (12-96). Tumor progression 13.3% (10 patients). Specific CPI mortality 2.6% (2 patients). CONCLUSIONS: We didn't observe significant differences between the prevalence of CPI in both groups (APS and RTU-P). The detected tumours were mainly well differentiated and in stage pTla. In more than half of the cases an expectant attitude without treatment was decided. 13,3% of tumor progression after 47.19 months of follow mean and specific CPI mortality 2.6%.

Aged↗
PubMedDate not supplied

Pediatric cancer: environmental and genetic aspects.

One in 600 children 0-16 years of age develop cancer, and 60% to 70% of them are cured. Projection of the data indicates that by the turn of the century, 1 of every 900 individuals between the ages of 16 and 44 years will be a cancer survivor. In the adult population, carcinogens and irradiation play a major role in oncogenesis. In the pediatric population other factors are probably dominant. Children of low socioeconomic groups, with nutritional deficiencies, are more exposed to viral infections at a very early age and have a greater chance of developing tumors such as Burkitt lymphoma or mixed cellularity Hodgkin disease. Other factors such as hormone-assisted conception or in vitro fertilization may have carcinogenic potential, although this has yet to be determined. Maternal diet during pregnancy, especially low folic acid consumption periconception, may have bearing on the fetus's risk of developing malignancy. The hazards of exposure to electric and magnetic fields from high-voltage transmission lines, home electric appliances, video display terminals, or residence near nuclear plants, although very doubtful, are included in the list of cancer promoters in children. Activated oncogenes, mutated suppressor genes, mismatch repair genes, nucleotide excision genes, and loss of imprinting genes are beginning to evolve as important factors in carcinogenesis. The more in-depth information on genetic and environmental factors should provide new data on the evolution of pediatric tumors and possibly on their prevention.

Adolescent↗