PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “tumor evolution”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,081 records · Page 60Linked to original sources
PubMed2005

[Primary signet ring cell carcinoma of urinary bladder. A case report].

Primary signet ring cell carcinoma of urinary bladder is a rare tumor; accounting for approximately 0.24% of all bladder malignancies. In this study, we report a case of a 58-year old man who consulted for complaints of gross hematuria, the bladder biopsy showed signet ring cell carcinoma; the exploration of gastrointestinal tract did not reveal any other tumor localizations. A total cystoprostatectomy was performed followed by radiotherapy. The aim of this study is to determine the anatomoclinical, therapy and evolution characteristics of this rare tumor.

Carcinoma, Signet Ring Cell↗
PubMed1995

Interconnecting the posterior and middle cranial fossae for tumors that traverse Meckel's cave.

Meckel's cave is an avenue for tumor to spread between the posterior and middle cranial fossae. The most common neoplasms that traverse this channel are trigeminal schwannomas and meningiomas. The classic approach to address disease in both cranial fossae involves separate craniotomies. Recent innovations in skull base surgery have made it possible to perform a single opening with simultaneous exposure of the posterior and middle fossae, without undue brain retraction. Tumors with a large middle fossa component and a smaller posterior fossa portion are exposed via subtemporal craniotomy with petrosectomy and tentorium division. However, tumors with a large posterior fossa component and a smaller middle fossa portion in the setting of serviceable hearing are addressed with retrosigmoid craniotomy and petrosectomy. For bilobed tumors with substantial components in both fossae, subtemporal craniotomy combined with varying degrees of transtemporal petrosectomy and tentorium division is employed. The evolution of techniques to address tumors that traverse Meckel's cave is reviewed and a treatment algorithm is proposed.

Brain Neoplasms↗
PubMed1996

Infrequent alterations of the p15, p16, CDK4 and cyclin D1 genes in non-astrocytic human brain tumors.

While several genetic alterations associated with the evolution of the astrocytomas have been identified, the molecular basis of non-astrocytic brain tumors has remained largely unknown. In this study, p15, p16, CDK4 and cyclin D1 genes were analyzed in 69 nonastrocytic human brain tumors, including 17 oligodendrogliomas, 16 medulloblastomas/primitive neuroectodermal tumors (PNETs), 14 ependymomas and 22 meningiomas. Southern blot analysis of DNA from frozen samples showed no homozygous deletions in p15 or p16 genes in any of these tumors. No mobility shift was found by PCR-single-strand conformation polymorphism (PCR-SSCP) analysis in exons 1 and 2 of the p15 gene and exons 1 and 2 of the p16 genes, except for one oligodendroglioma. Direct sequencing of DNA from this tumor showed a G --> A transition at nucleotide 436 (codon 140) in exon 2 of the p16 gene, which is a common polymorphism. Southern blot analyses revealed no amplification of CDK4 and cyclin D1 genes in any of the neoplasms analyzed. In contrast to astrocytic brain tumors, which show frequent loss of the p16 gene and amplification of the CDK4 gene, alteration of these genes appears to be rare in other neoplasms of the human nervous system.

Astrocytoma↗
PubMed1993

Chromosomal biomarkers in the clonal evolution of head and neck squamous neoplasia.

The biological behavior of any tumor is the result of changes in gene expression caused by mutations accumulated in the carcinogenic process. In squamous carcinoma of the head and neck (SCCHN) there are numerous complex chromosome abnormalities. To make sense of this complexity it is necessary to identify the consistent chromosome changes in a large panel of tumors, to determine if these changes are true representations of the in vivo situation, and to construct a map of gene loci likely to be involved in the development and progression of cancer. Our findings indicate that cultured tumor cells are cytogenetically stable when compared to cells evolving in vivo. We also found that clues to the sequence of events in clonal evolution of individual tumors can be deduced by studying primary and metastatic tumors from the same patient, by examining separate clones within the same tumor, and by analyzing ploidy changes. Furthermore, comparison of the in vitro karyotypes to in situ analysis of the tumor tissue indicates that in vitro cultures are good representations of the in vivo tumor. We conclude that identification of consistent chromosome changes in cultured cells can lead to the loci of genes important in the clinical behavior of individual tumors. The most frequent chromosome abnormalities in SCCHN, found in 40-60% of tumors, are deletions affecting 3p, 5q, 8p, 9p, and 18q. Less common consistent changes found in 30-40% of tumors are gains affecting 3q, 5p, 7p, 8q, and 11q. Preliminary evidence suggests that loss of 18q may be prognostically important and may involve disruption of genes encoding cell adhesion molecules.

Carcinoma, Squamous Cell↗
PubMed1996

Somatic microsatellite mutations as molecular tumor clocks.

Microsatellite (MS) mutations can potentially unravel the past of mutator phenotype tumors, with greater genetic diversity expected in older regions. Rapid clonal expansions of xenografts were characterized by relatively homogenous MS alleles, whereas greater diversity was observed in a colorectal cancer with the greatest variation in its adjacent adenoma. A subcutaneous lung cancer metastasis demonstrated diversity consistent with its one-month clinical duration and evidence of active mitosis during dormancy. The genetic legacy inherent to multistep tumorigenesis provides direct estimates of tumor ages, with up to thousands of cell divisions and high death rates necessary to yield the observed diversities. MS molecular tumor clocks have the unique potential to systematically reconstruct the early and occult evolution of individual human mutator phenotype tumors.

Adenocarcinoma↗
PubMedDate not supplied

[Chondrosarcoma with a myxoid component. Apropos of a "giant" tumor recurrence].

Reporting on a giant tumorous recurrence of a chondrosarcoma with a myxoid component, without perceptible locoregional or general extension, the authors recall the possible long-term evolution of this type of tumor. They underline the difficulty of anatomopathologic diagnosis of tumors with cartilaginous structure, and the necessity for frequent monitoring after exeresis.

Chondrosarcoma↗
PubMed1987

[Mixed carcinoid tumor-adenocarcinoma of the stomach. Review of the literature, apropos of a case].

We report a case of mixed tumor of the stomach with a double histological population: carcinoid and adenocarcinoma. The carcinoid component presented an usual morphological pattern with "atypical" elements, and without argyrophilic cells; the carcinoid cells were exclusively marked by an anti-serotonin serum. The other component was a poorly differentiated carcinoma, with muco secretion, which was not marked by and anti-carcino-embryonic antigen serum. The limit between the two components was sharp. The association of mucin in the carcinoma and serotonin in the carcinoid component was an argument in favour of the diagnosis of mixed tumor carcinoid-adenocarcinoma (composite tumor) of the stomach. The evolution after operation leaded to a local recurrence and to the death 10 months later, in spite of chemotherapy. The existence of composite tumors raises nosological, histogenetical and diagnostic problems, which are discussed in this work. The prognosis of these tumors is unknown and therapeutic possibilities seem to be scanty.

Adenocarcinoma↗
PubMed1997

Deoxyribonucleic acid ploidy and the clinical pattern of grade 2 superficial bladder cancer.

PURPOSE: We attempted to find an objective and quantitative parameter that would enable us to differentiate between aggressive and nonaggressive grade 2 superficial transitional cell carcinoma of the bladder. This type of tumor belongs to a heterogeneous group, 30% of which behave aggressively by invading lamina propria and muscle tissue in the course of the evolution. The remaining 70% of tumors have less aggressive qualities, are nonprogressive and have a low recurrence rate. To date to our knowledge there is no way to differentiate between these 2 subpopulations of tumors. MATERIALS AND METHODS: We performed a retrospective flow cytometric analysis of deoxyribonucleic acid (DNA) ploidy and cell cycle phases on primary and solitary formalin fixed and paraffin embedded tumor tissue. RESULTS: Of the 41 specimens studied 16 were aneuploid and 25 were diploid. Aneuploidy was associated with progressive disease and high mortality rates, particularly in patients who did not receive postoperative adjuvant intravesical instillation. DNA diploidy was equated with lack of mortality and a low progression rate. The use of intravesical bacillus Calmette-Guerin as an adjuvant postoperative treatment was associated with low recurrence rates. In this group elevated G2M percent and S phase fractions correlated with higher recurrence rates. CONCLUSIONS: DNA ploidy was a prognostic factor in stage Ta grade 2 bladder transitional cell carcinoma and should be considered as a complementary test to histopathological analysis. Adjuvant instillation with bacillus Calmette-Guerin is advised after transurethral resection of primary solitary aneuploid stage Ta grade 2 bladder transitional cell carcinomas and of primary solitary diploid tumors with elevated G2M percent and S phase fraction.

Carcinoma, Transitional Cell↗
PubMed1995

The management of synchronous bilateral Wilms tumor.

There has been a distinct evolution in the treatment philosophy for patients with BWT. Initial attempts at radical surgery have given way to the current use of preoperative chemotherapy to preserve as much kidney tissue as possible. With preoperative treatment, usually chemotherapy only, overall survival has become quite favorable in this group of patients, approaching 83% at 2 years. This has facilitated the use of parenchymal-sparing operations, with the potential advantage of decreasing the incidence of end-stage renal disease. The development of renal insufficiency in children with synchronous BWT nonetheless remains a concern. It is important that long-term survivors have systematic follow-up, with measurements of blood pressure, urine protein, serum creatinine, renal clearance, and renal size. Finally, despite the mentioned achievements, the management of children with synchronous BWT still needs standardization. The limited number of patients affected by BWT makes an international effort desirable to address this need.

Diagnostic Imaging↗
PubMed1986

Borderline malignant serous tumors of the ovary maintained on extracellular matrix: evidence for clonal evolution and invasive potential.

Four cases of advanced stage (II or III) and one case of early stage (IC) borderline malignant serous cystadenocarcinomas of the ovary were maintained on culture dishes coated with an extracellular matrix (ECM) produced by bovine corneal endothelial cells. Cells harvested for chromosomal analysis after 2-3 days showed diploid or near-diploid modalities in all cases. Banded chromosome studies in two cases revealed nonrandom clonal abnormalities with trisomy 2, 7, and 12 in seven of 13 metaphases. No structural abnormalities were noted. These cytogenetic findings differ from those found in malignant serous tumors of the ovary. In addition, borderline tumor cells digested the ECM in all cases and formed a cribiform pattern within a few days of primary culture. This study suggests clonal progression from early to advanced stages of borderline malignant serous tumors; readily distinguishable from overtly malignant serous tumors of the ovary. Ability of tumor cells derived from both primary tumors and metastatic implants to digest the ECM implies the possibility that borderline serous tumors have invasive potential.

Adult↗
PubMed2004

Statistical dissection of cytogenetic patterns in lung cancer reveals multiple modes of karyotypic evolution independent of histological classification.

Lung carcinomas are cytogenetically highly complex. In spite of this, patterns of recurrent chromosome aberrations have emerged. Apart from the frequent loss of 3p, losses of 4q, 5q, 8p, 9p, 10q, 13q, and 17p are common and gains often include 1q, 3q, 5p, and 8q. In the present study, we retrieved all aberrant lung carcinoma karyotypes, in total 432 cases, from the Mitelman Database of Chromosome Aberrations in Cancer and identified the most frequent imbalances. Each case was then classified with respect to the presence or absence of these imbalances and the data were statistically analyzed by means of principal component analysis, multidimensional scaling, and hierarchical cluster analysis. The analyses suggest that lung cancer develops through three pathways, initiated by +7, 3p-, and +12, respectively, and that the 3p- pathway is dominated by losses and the +12 pathway by gains. Gain of chromosome 7 was shown to be both important in the 3p- pathway and also forming a group of tumors containing +7 and +20 (with few additional changes). The distribution of the number of imbalances per tumor indicated that the karyotypic evolution might pass through three different phases. Phase I is characterized by tumors with few changes and by well-separated 3p- and +12 pathways. Phase II cases have an increased number of imbalances and exhibit less distinct 3p- and +12 pathways. Phase III tumors are polyploid and highly complex. No marked differences between the karyotypic profiles were found among morphologic subtypes, suggesting that lung cancer morphology is independent of the particular cytogenetic pathway operating in the tumor cells.

Adenocarcinoma↗
PubMed2003

Repeated surgical excision for an unusual variant of nephroblastoma: case report and review of the literature.

Bilateral fetal rhabdomyomatous nephroblastoma is a rare variant of Wilms' Tumor. The authors report the evolution over 48 months of a 10-month-old baby with bilateral nephroblastoma for which a left nephrectomy was initially performed. A right kidney tumor was enucleated preserving the kidney. The transformation of the primary tumor into a completely differentiated cystic nephroblastoma or nephromalike tumor and the appearance of a metachronous lesion was seen. This report emphasizes the role of nephron-sparing surgery in bilateral Wilms' Tumor when a benign transformation occurs under chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

Malignant evolution of choroid plexus papilloma.

Choroid plexus tumors are rare CNS neoplasms. The distinction between choroid plexus papilloma (CPP) and choroid plexus carcinoma (CPC) is made on the basis of clinical and histological criteria. Malignant evolution of CPP may occur, and the presence of mitotic figures in CPP may predict the likelihood of recurrence or malignant evolution. Close surveillance is mandated for these patients. We report on two such cases of CPP that transformed to CPC at the time of recurrence.

Cell Transformation, Neoplastic↗
PubMed1979

[Walker's 256 carcinosarcoma: metastatic dissemination in two cell lines (author's transl)].

Walker's 256 carcinosarcoma a transplantable tumor of the rate changes its behaviour as a consequence of various factors. In this paper we compare the evolution of 2 lines of the tumor: WM 16 (muscular) and Christ Hospital (ascitic) both inoculated intramuscularly. Animals receiving line WM 16 had a severe rapidly progressive evolution dying around day 14 after inoculation with diffuse metastases to lymph nodes (65% of animals), kidneys (53%), spleen (50%), lungs (46.5%), liver (45%), bone marrow (44.8%), in 56% of the animals there were circulating tumoral cells. Animals receiving Christ Hospital line survived up to 40 days, metastases were limited do lungs (48.7%) and lymph nodes (31.7%) and only in 2 of 45 animals circulating tumoral cells were observed.

Animals↗
PubMed1987

Cerebral edema associated with meningiomas.

Fifty patients with intracranial meningiomas have been retrospectively examined, and the cerebral edema on computed tomography scan has been correlated with the clinical evolution, size, location, and histological features of the tumor. The degree of brain edema was found to be related to the clinical evolution and the size of the tumor, whereas the histological features were less significant. These results are discussed after reviewing the data of five other series in the literature of this subject. A correlation between the tumor steroid receptors and edema is suggested.

Adult↗
PubMed2003

[Experimental tumors of the central nervous system: standardisation of a model in rats using the 9L glioma cells].

A number of experimental models have been established during the last decades in order to study tumor biology and the effects of treatment or manipulation of the microenvironment of malignant glial tumors. Even though those models have been well characterised and are, to a certain extent, easily reproducible, there are limitations as to their use and to the interpretation of the results. The aim of this study is to standardize a model of a malignant glial tumor and detect possible events able to modify its development. 9L cells were inoculated intracerebrally in 48 Sprague-Dawley rats; from these, 25 animals were also implanted with a device containing electrodes for the registration of the electroencephalogramm. Animals were daily evaluated by neurologic examination. Twenty four animals developed tumor - 10 animals died either in the immediate pos-operatory period or during evolution; 14 animals did not develop tumor. Macroscopically the tumor was well demarcated from the adjacent brain; by light microscopy the tumor exhibited malignant characteristics as well as extensive infiltration of the brain parenchyma. Diagnosis was that of a malignant astrocytoma. The use of the stereotaxic frame and care to infuse a small volume of liquid containing cells during a period of 120 seconds were the most important procedures to obtain sucess in the model. Additional care should be taken in counting cells in the Neubauer camera and in maintaining cells in constant agitation before injecting the tumor-containing solution. The model here developed was efficient besides being of low cost and of relatively easy execution.

Animals↗
PubMed1986

Eradication of disseminated murine leukemia by treatment with high-dose interleukin 2.

Interleukin 2 (IL 2) in high concentration induces lymphocytes to become nonspecifically cytolytic to a wide variety of tumor targets. We evaluated the therapeutic potential of such lymphokine-activated killer (LAK) cells in vivo and high-dose II 2 in vivo against disseminated murine leukemia. To quantitate the potential anti-leukemia effect of LAK cells in vivo, B6 mice were injected i.p. with graded doses of FBL-3 leukemia cells followed by LAK cells. In this Winn-type assay, 1 X 10(7) LAK cells were able to prevent the outgrowth of 1 X 10(2) FBL-3 cells in only 50% of mice and did not prevent the outgrowth of 1 X 10(6) tumor cells. Thus LAK cells, highly cytolytic to FBL-3 in vitro, mediated only a limited anti-tumor effect when applied directly to leukemia cells in vivo. LAK cells used as an adjunct to chemotherapy induced a small but non-curative effect against FBL-3, however. In this circumstance, LAK cells were markedly less effective than were immune spleen cells from mice previously sensitized to FBL-3. To test the anti-leukemia effect of high-dose IL 2 in vivo, B6 mice were inoculated with 5 X 10(6) FBL-3 cells followed by repeated doses of IL 2 at dose levels shown to induce LAK in vivo. "LAK-inducing" IL 2 doses on days 5 to 9 after FBL-3 inoculation, when tumor was disseminated, cured 50% of the mice. Treatment on days 5 to 9 was far more effective than on days 0 to 4, implying that the evolution of a host-tumor interaction was essential for the therapeutic effect of IL 2. Mice cured of FBL-3 by high-dose IL 2 were found to be immune to FBL-3, suggesting that tumor eradication resulted from a collaboration between LAK activity and tumor-specific immunity.

Animals↗