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Results for “tumor evolution”

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At least 523 records · Page 29Linked to original sources
PubMedDate not supplied

[Malignant liver hemangiopericytoma ruptured after an abdominal traumatism].

This paper reports a case of malignant liver hemangiopericytoma broken after an abdominal traumatism which revealed that the patient has this disease. This case is interesting because the abdominal traumatism gave us the opportunity of making a precocious diagnosis. The clinical and paraclinical signs of acute abdomen fastened surgery. The paper reviews the medical literature linked to these rare tumors. The paper also describes morphological features typical for these vascular tumors, whose evolution is unpredictable.

Abdominal Injuries↗
PubMed2002

[In silico cloning of evolutionarily conserved mouse F-LANa].

Differentially expressed genes between normal liver and hepatocellular carcinomas were investigated using differential display. In previous study, human F-LANa was identified as a differentially expressed gene, up-regulated in hepatocellular carcinoma. In this study, we developed an in silico cloning approach to rapidly and accurately characterize the mouse ortholog of the human F-LANa. Mouse F-LANa encodes a 239 aa protein exhibiting 97.9% similarity to the human ortholog gene. Homology analysis was carried out in various species and showed that F-LANa was evolutionarily conserved from yeast to human. Based on the alignment results, phylogenetic tree was established here.

Animals↗
PubMed2003

New late-intensification schedules for cancer treatments.

The nonlinear Gompertz equation that describes the evolutions of tumors under different treatments was investigated. It was shown that late logarithmic intensification asymptotically reduces the tumor cell population to zero. Using the same total amount of therapy, the schedule following a logarithmic function produces a larger reduction of tumor cell population than the schedule using a therapy with constant intensity. On the other hand, a logarithmic intensification should be more tolerable by the patients than a faster temporal growth therapy. We have shown that during the treatment the dose intensity should not be decreased at any time while the therapy is applied, because this will allow the tumor to relapse. The therapy intensity should be continuously increased as possible. We have solved an optimization problem for several late intensification treatments by the constraints of the total dose and the maximum individual (or daily) dose. Based on our results, we have designed new chemotherapy and radiotherapy treatments.

Algorithms↗
PubMed1991

Genetic analysis of germ cell tumors: current progress and future prospects.

Cytogenetic analysis of germ cell tumors (GCTs) has identified i(12p) as a specific cytogenetic abnormality identified in more than 80% of GCTs, present in all histologies, in primary and metastatic lesions, in testicular and extragonadal presentations, and in ovarian and sex cord stromal tumors. Other nonrandom numeric and structural chromosomal abnormalities have also been identified. Oncogene studies suggest a potential role for n-ras mutations in GCT transformation. The role of loss of tumor suppressor genes and increased genomic dosage of growth promoter genes remain areas of great interest. Leukemias and differentiated malignancies that arise in the setting of GCT appear to be clonally derived from GCT cells, with evidence of karyotypic progression and acquisition of other tumor-specific cytogenetic markers. Identification of i(12p) in poorly differentiated midline carcinomas of uncertain histogenesis can assist in the diagnosis of GCT. The presence of three or more copies of 12p may predict resistance to chemotherapy and portend a higher likelihood of treatment failure. Future cytogenetic studies in GCT promise to provide insight into the biology and treatment of all solid tumors, because GCTs are a model of chemotherapeutic responsiveness, cellular differentiation, and tumor clonal evolution.

Cell Differentiation↗
PubMedDate not supplied

[Is the bladder localization of urothelial transitional carcinoma a nosologic entity different from tumors appearing in the upper urinary tract?].

This study was undertaken in 69 patients with transitional cell carcinoma of the upper urinary tract. In 31, bladder tumor was diagnosed prior to (35.5%), concomitant with (38.5%), and after treatment of the upper urothelial tumor. Localization in the bladder more commonly involved the ipsilateral left or right lateral aspect and less frequently involved the trigone. It is difficult to predict the nature of the bladder tumor from the upper urinary tract tumor. However, we have observed that excision of the upper tract tumor favourably affects the evolution of the bladder tumor diagnosed prior to or concomitant with treatment of the upper tract tumor.

Carcinoma, Transitional Cell↗
PubMed1988

[Risk factors for the recurrence of spinocellular epithelioma. Study of 650 cases].

An evaluation is made of the clinical and histological parameters of 650 cases of spinocellular epithelioma. The statistical analysis shows tumor relapse to be related to tumor size, evolution time, relapse following previous treatments, earlier cutaneous lesions, Broders' grading, acantholysis, inflammatory infiltrate and type of treatment applied.

Biopsy↗
PubMed1988

Chromosomal translocations and gene rearrangements in non-Hodgkin lymphomas.

Unlike other types of malignancy, non-Hodgkin lymphomas have a specific reciprocal chromosomal translocation as a genomic hallmark in most patients. Among the more prevalent B-cell lymphomas, 65% of patients show a 14q + chromosome with rearrangement of the heavy-chain immunoglobulin genes at band 14q32.3, whereas the less common T-cell lymphomas typically have a selective rearrangement of the alpha T-cell receptor genes involving band 14q11.2. The presence of additional recurrent chromosomal defects in several subgroups of lymphomas is associated with tumor phenotype, evolution, and response to therapy.

Chromosomes, Human, Pair 14↗
PubMed1980

An evolution of malignant mixed müllerian tumor.

In an unusual example of malignant mixed müllerian tumor, a tumor originated in the uterine corpus as an endometrial carcinoma consisting of ordinary endometrial adenocarcinoma, papillary adenocarcinoma, mucinous adenocarcinoma, and squamous cell carcinoma. Following hysterectomy, the tumor recurred at the vaginal vault as poorly differentiated papillary adenocarcinoma. During the second recurrence as a pelvic tumor about 3 years after hysterectomy, the tumor evolved into a malignant mixed müllerian tumor with predominance of sarcomatous element. The latter included undifferentiated sarcoma, endometrial stromal sarcoma, fibromyxosarcoma, leiomyosarcoma and rhabdomyosarcoma. These findings support the contention of Sternberg et al. that a malignant mixed müllerian tumor may exceptionally originate in an endometrial carcinoma.

Adenocarcinoma↗
PubMed1998

Intracellular coexpression of epidermal growth factor receptor, Her-2/neu, and p21ras in human breast cancers: evidence for the existence of distinctive patterns of genetic evolution that are common to tumors from different patients.

Multiparameter flow cytometry studies were performed on cells from the primary tumors of 94 patients with breast cancer. Correlated cellular measurements of cell DNA content, Her-2/neu, epidermal growth factor receptor (EGFR), and p21ras levels were performed on each of 5,000 to 100,000 cells from each tumor. When criteria for positivity were matched with those in common use for immunohistochemical studies, 28 of 94 (30%) breast cancers were classified as positive for Her-2/neu overexpression. When similar criteria were applied to the EGFR measurements, 23 of 94 (24%) cases were classified as positive for EGFR overexpression. Similarly, 23 of 94 (24%) cases were classified as positive for p21ras overexpression. By conventional flow cytometric criteria for DNA ploidy, 24 cases were diploid, 28 were tetraploid, and 42 were aneuploid. When the measurements were treated as separate sets of data, the only statistically significant correlations noted were the high frequency of diploid tumors, which did not overexpress any of the three oncogenes studied (P < 0.05), and an association between Her-2/neu overexpression and aneuploidy (P < 0.03). When the data were treated as correlated intracellular measurements, 90 of the 94 tumors studied contained a population of cells in which the intracellular levels of Her-2/neu expression were directly correlated with the levels of EGFR expression in the same cells. The ratio of Her-2/neu molecules to EGFR molecules in the same cells exceeded 1 in the majority of tetraploid and aneuploid cases and was close to or less than 1 in the majority of diploid cases. In nearly all tumors, p21ras overexpression was observed only in cells that overexpressed Her-2/neu, EGFR, or both, and p21ras levels per cell were more closely correlated with levels of EGFR per cell in the same cells than with Her-2/neu levels per cell. The data are consistent with a model in which heterodimerization of Her-2/neu and EGFR in individual cells is achieved by one of several genetic evolutionary pathways, all of which commonly lead to p21ras overexpression. The two major genetic evolutionary pathways identified in this study are an aneuploid, Her-2/neu overexpression-driven pathway seen in 59 of 94 tumors, and a diploid, EGFR overexpression-driven pathway seen in 19 of 94 tumors. All tumors with Her-2/neu:EGFR ratios greater than 2 contained an infiltrating ductal carcinoma component, whereas all infiltrating pure lobular carcinomas had Her-2/ neu:EGFR ratios that were less than 2. All of the genetic evolutionary pathways identified in this study were represented among the 11 tumors from patients who experienced early tumor recurrences.

Analysis of Variance↗