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At least 379 records · Page 21Linked to original sources
PubMed1985

[Is iatrogenic vesico-renal reflux a negligible factor in the evolution of recurrent superficial tumors of the bladder?].

The electrocoagulation and resection of superficial tumors of the bladder leads to iatrogenic refluxes. The frequency of subsequent vesical recurrences may thus favor tumoral grafts in the upper urinary tract. Fives cases illustrate this risk. They were treated by ureteral resections and by one bilateral, and two unilateral nephroureterectomies. Should these refluxes be ignored or treated surgically in the event of repeated papillomatous recurrences?

Aged↗
PubMed1983

Genotypic and phenotypic evolution of a murine tumor during its progression in vivo toward metastasis.

To follow the cellular progeny of the multiple-drug-marked benign murine tumor cell line MDW4 during its progression in vivo toward metastatic spread in DBA/2 mice, the following parameters were analyzed: retention of the drug-resistant markers ouabain resistance (OuaR) and thioguanine resistance (ThgR), lectin-resistance pattern (WGAR), and the karyotype of cell populations (and clones derived from these cells) removed at intervals from the solid tumor growing at the site of inoculation, as well as distant metastatic nodules. It was determined that the initially homogeneous inoculum composed of OuaR, ThgR, and WGAR hypotetraploid cells (mode: 68 +/- 2 chromosomes) was gradually overgrown and replaced by a new population of cells that were either OuaR or ouabain-sensitive but that became thioguanine-and lectin-sensitive and hyperploid (mode: 95 +/- 5). Regardless of the composition of the individual drug marker combinations, only cells with high chromosome contents were found to be able to disseminate to distant visceral organs and to rapidly produce metastases upon sc or iv reinjection. The presence of the same number of metacentric chromosomes in metastatic cells as in MDW4 and the coextinction of two recessive drug-resistant markers (WGAR and ThgR) suggested that cells endowed with invasive-metastatic potential represent the product of spontaneous somatic hybridization between the original nonmetastatic MDW4 cells and normal host cells of unknown origin. Such a fusion was followed by more or less extensive chromosome segregation that accounts for the karyotype mosaicism and the occasional drug marker heterogeneity identified in cell populations of metastatic nodules.

Animals↗
PubMed1997

Common patterns of genetic evolution in human solid tumors.

Human solid tumors develop multiple genetic evolutionary abnormalities as they evolve. Studies that have focused primarily on early colorectal cancer have suggested that genetic instability is a prominent feature of preinvasive disease. At least two separate mechanisms for the generation of genetic instability have been identified. The first, which involves widespread microsatellite instability in near-diploid cells, affects less than one-fifth of colon cancers. The second form of genetic instability is characterized by the development of p53 gene abnormalities that result in gross aneuploidy and multiple structural chromosomal changes. p53/aneuploidy affects most colon cancers, breast cancers, and many other solid tumors. This genetic evolutionary change commonly occurs at the interface between severe dysplasia and invasive disease. Specific post-aneuploid sequences of genetic changes that are relevant to tumor progression often involve the accumulation of multiple gain-of-function abnormalities in individual cells. The co-occurrence of Her-2/neu overexpression and EGF receptor overexpression in the same aneuploid cells defines an adeno/squamous genetic evolutionary sequence that is common to ductal breast cancers, non-small cell lung cancers, and other solid tumors. Later steps in this sequence include ras and c-myc overexpression. The neuroendocrine genetic evolutionary sequence is a separate branch of the p53/aneuploidy sequence with distinctive features that include loss of Rb and raf1 overexpression. Her-2/neu overexpression is not characteristic of this sequence; c-myc amplification/overexpression is common to both p53-associated sequences. The neuroendocrine sequence is found in small cell carcinoma of the lung and in minor proportions of other solid tumors, including breast cancer. Multiparameter cell-based methods are especially well suited for elucidation in human solid tumors of the genetic evolutionary sequences that could provide a rational scientific basis for determining prognosis and for optimizing therapy in individual cancer patients.

Aneuploidy↗
PubMed1988

Prescheduling graphic displays for optimal cancer therapies to reveal possible tumor regression or stabilization.

The paper describes an adaptive control approach to the problem of the treatment of solid tumors. The evolution with time t of the state of a tumor is modelled by a two-compartment system, governed by two differential equations forming an autonomous system under therapy control u, (formula; see text) where y1 and y2 are the number of proliferating and nonproliferating cells, respectively. The output is analyzed in the phase plane y1y2. The control problem is that of restricting the tumor state to a predetermined region of the plane by selecting a suitable change in therapy control u, e.g., modality and dosage, when the state solution intersects the boundary of this region and the ratio y1/y2 of proliferating to nonproliferating cells is displayed together with an elapsed time scale. Then, consequent selection of a suitable therapeutic sequence may be assisted by the use of a data base as part of an expert system. The process is repeated at each intersection of the prescribed boundary. Such sequences may lead to stabilization of the system through the appearance on a computer display screen of a stable equilibrium point or a limit cycle.

Cell Division↗
PubMed2004

Molecular cytogenetic characterization shows higher genetic homogeneity in conventional renal cell carcinoma compared to other kidney cancers.

In this study seven primary kidney tumors out of 13 were cytogenetically characterized by comparative genomic hybridization (CGH) on the surgical specimens as well as by spectral karyotyping (SKY) analysis after short-term culturing. In two of the seven cases only a normal karyotype was identified. Non-clonal aberrations were observed in four of the seven cases. Overall numerical alterations were more frequent than structural changes. The two structural alterations identified constituted of a deletion of the short arm of chromosome 3 in a conventional renal cell carcinoma (RCC), and a ring chromosome derived from chromosome 8 in a papillary RCC. By CGH gains of copy number were revealed on chromosomes 3, 5, 7, 8q, and 20, while the losses encompassed 3p and 17p. In the papillary RCCs only gains were found. Comparison between SKY and CGH data suggests that the conventional RCCs are genetically more homogeneous than the other types of kidney cancer. In the two papillary RCCs, trisomies of chromosomes 7 and 17 were typical findings. In the transitional cell carcinoma different findings by CGH and SKY would suggest that these tumors constitute a heterogeneous population of tumor cells which could represent different steps of somatic evolution of tumors.

Adult↗
PubMed1999

Non-linear model of cancer growth and metastasis: a limiting nutrient as a major determinant of tumor shape and diffusion.

A new approach for modelling the spatio-temporal evolution of tumors is presented. To test its validity, a very basic model is considered, which, in spite of its simplicity, is capable of generating a multiplicity of morphologies and growth and migration rates. From an in-vivo scenario of basic life processes, cancer cell proliferation is described as a competition for basic nutrients. The chosen mathematical treatment and simulation techniques permit a direct implementation of the local nonlinear couplings existing between the various cell populations and the free and bound nutrient concentration. A discussion of the results and proposed improvements and applications of the model is also presented.

Cell Division↗
PubMedDate not supplied

Treatment of mice bearing a Krebs ascitic tumor by means of a protocol based on radioactive copper (64Cu). IV. Consequences of the nature of cancer: tumor-resistant mice.

In the efficient treatment described (Anticancer Research 9: 941-946, 1989) some compounds (64Cu and thioproline) act against the malignant genomes, and other components (metal ions, amino acids, vitamin D2, thyroxine and chelating substances) act against the functioning of the host cells having the cancer functioning (cancer cells). The experiments described show that this treatment developed with mice injected on day zero with 5 x 10(5) Krebs ascitic cells, is also efficient for mice bearing a spontaneous malignant tumor even if it is not an ascitic tumor. After the decrease in weight due to the loss of the tumor, a typical weight evolution was observed characterized by a second weight increase followed by a decrease leading to normal weight. This last weight remained stable. This typical weight evolution in tumor-free mice (after spontaneous tumor or experimental Krebs ascitic tumor) was related to the age of the tumor at the beginning of the treatment, that is, according to our hypothesis (Anticancer Res 9:955-960, 1989) to the cancer evolution emphasizing the great importance of all physiological phenomena related to this cancer course. To test the consequence of this treatment, some of these tumor-free mice were injected with 5 x 10(5) ascitic cells. No tumor developed in these tumor-free mice meaning that they also were tumor-resistant. This last result is in agreement with the forecast of the systemic analysis on which the efficient treatment was based.

Animals↗
PubMed2003

Evidence emerges for early metastasis and parallel evolution of primary and metastatic tumors.

Tumor progression to metastasis usually is assumed to occur through clonal genomic and epigenetic evolution. However, present evidence that challenges this paradigm. They show that genomic aberrations in tumor cells disseminated in the bone marrows of patients with no clinical evidence of metastasis generally do not resemble the aberrations in the primary tumors from which they arose. They interpret this to mean that tumor cells disseminate very early and evolve to metastatic disease independent from the primary tumor. Their model suggests that adjuvant therapies should be targeted to lesions in the disseminated cells rather than lesions found in primary tumors.

Animals↗
PubMed1996

Gains and losses of DNA sequences in malignant mesothelioma by comparative genomic hybridization.

The molecular basis of malignant mesothelioma is poorly known. We examined genetic changes in 11 mesothelioma specimens by comparative genomic hybridization (CGH). Five DNA specimens originated from uncultured tumor tissues and six from cell lines established from the same patients. Findings from the classical karyotypic characterization of both primary tumors and cell lines have been reported previously. In the CGH analyses the most common genetic alterations in the 11 mesothelioma specimens were losses of chromosomal regions in 1p, 8p, 14q, and 22q and gains of 5p, 6p, 8q, 15q, 17q, and 20. The cell lines had on average a much higher total number of genetic changes than the uncultured tumor specimens. Clonal relationship between the cell lines and the uncultured tissue specimens could not usually be demonstrated even though they originated from the same patient. The observed differences may partly be due to high frequency of chromosomal rearrangements, which CGH cannot detect, partly due to contamination of tumor specimens with normal tissue, and partly due to genetic evolution in tumor cell lines.

Chromosome Aberrations↗