Institution
University of Texas System
Education•Austin, Texas, United States•
About: University of Texas System is a education organization based out in Austin, Texas, United States. It is known for research contribution in the topics: Cancer & Population. The organization has 13901 authors who have published 10925 publications receiving 319328 citations. The organization is also known as: UT System.
Topics: Cancer, Population, Antigen, Gene, Antibody
Papers published on a yearly basis
Papers
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TL;DR: A model for generating cellular phenotypic diversity based on the proposed mechanism for rapid generation of immunoglobulin molecular diversity in B cells may be applicable to malignant cells and to cells in general.
Abstract: The emergence of diversified tumor cell subpopulations in malignant neoplasms accounts for their heterogeneous cellular phenotypes and virtually ensures that some tumor cells will ultimately evolve with the most favorable properties for their enhanced abilities to survive, grow, invade and metastasize (tumor progression). The rates of cellular phenotypic diversification appear to vary greatly among different tumors and within the same tumor, and they are probably controlled, at least in part, by cellular instability due to chromosomal defects and random somatic mutational events, the rates of which are known to be higher in more malignant cells, and by epigenetic events, which may vary widely depending on the nature of the tumor cells and their microenvironments. As tumor progression proceeds, the most malignant cell subpopulations appear to lose their responsiveness to changes in tumor microenvironment while maintaining their high rates of phenotypic diversification. Tumor and normal cell-cell and cell-extracellular matrix interactions, as well as tumor cell nutrients, oxygen, hormones, growth factors, inducers and other regulatory molecules provide individual malignant cells with microenvironmental signals that could act through epigenetic cellular modifications, such as DNA methylation, and transcriptional, posttranscriptional, translational and posttranslational controls, or combinations of these. In addition, integration of viral gene sequences or viral modification of host DNA in critical regions could affect phenotypic stability. Finally, manipulation of tumor cells by antitumor therapy can also have profound effects on the rates of phenotypic diversification of the surviving tumor cells. A model for generating cellular phenotypic diversity based on the proposed mechanism for rapid generation of immunoglobulin molecular diversity in B cells may be applicable to malignant cells and to cells in general. In this model the expression and activity of gene products from multigene families are affected by a variety of genetic and epigenetic controlling mechanisms, and alterations in regulatory genes caused by recombination, methylation, mutation, or other changes could lead to differences in gene expression, resulting in widespread quantitative (and perhaps some qualitative) changes in particular gene products or their activities. As they proceed down different pathways of gene expression, each cell would be exposed to continual host selection pressures creating diverse, ever-changing malignant cell-populations.
169 citations
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TL;DR: Stromal overgrowth is a significant histologic indicator of malignant behavior in cystosarcoma phyllodes and was significant at P levels of 0.0014 and 0.02, respectively.
Abstract: Twenty-six cases of cystosarcoma phyllodes diagnosed at M. D. Anderson Hospital were reviewed. The following criteria were evaluated for possible correlation with local recurrence, uncontrolled local recurrence, metastasis, and tumor death: tumor size, stromal overgrowth, tumor necrosis, mitotic rate, stromal cellularity, nuclear size and pleomorphism, the presence of specialized stroma, and initial therapy. Of the 26 tumors, seven caused death. Five patients developed metastatic spread, and all of them died of tumor. Five patients had local recurrence, which was uncontrolled in three (two patients died with uncontrolled recurrence alone, and one with uncontrolled recurrence and metastasis). Stromal overgrowth was present in eight cases. Six of the seven patients who died of tumor had stromal overgrowth, including all five with metastasis. Correlation of stromal overgrowth with meta static spread and tumor death was significant at P levels of 0.0014 and 0.02, respectively. It is concluded that stromal overgrowth is a significant histologic indicator of malignant behavior in cystosarcoma phyllodes.
169 citations
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169 citations
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TL;DR: Analysis of differences in 10‐year survival rates from breast cancer among white, black, and Hispanic women controlling for the effects of age, socioeconomic status, stage of disease, and delay suggests ethnic differences in breast cancer survival are not mediated by differences in delay in seeking treatment for breast cancer symptoms.
Abstract: This study examined differences in 10-year survival rates from breast cancer among white, black, and Hispanic women controlling for the effects of age, socioeconomic status (SES), stage of disease, and delay in seeking treatment for symptoms. Breast cancer patients (n = 1983) treated at M. D. Anderson Hospital and Tumor Institute in Houston, Texas between 1949 and 1968, were followed for 10 years. Ethnicity, SES, stage of disease, and delay were all found to affect survival when considered separately. Black patients were less likely to survive than either white or Hispanic patients whose survival experience appeared to be similar. Multivariate analysis that used a Cox regression technique showed that ethnic differences remained when age, SES, stage, and delay were included in the model. In contrast, the authors could not detect an effect of delay on survival when ethnicity and all other variables were included. These data suggest that ethnic differences in breast cancer survival are not mediated by differences in delay in seeking treatment for breast cancer symptoms.
169 citations
Authors
Showing all 13902 results
Name | H-index | Papers | Citations |
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Yi Chen | 217 | 4342 | 293080 |
Joseph L. Goldstein | 207 | 556 | 149527 |
Eric N. Olson | 206 | 814 | 144586 |
Hagop M. Kantarjian | 204 | 3708 | 210208 |
Thomas C. Südhof | 191 | 653 | 118007 |
Gordon B. Mills | 187 | 1273 | 186451 |
Michael S. Brown | 185 | 422 | 123723 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Russel J. Reiter | 169 | 1646 | 121010 |
John D. Minna | 169 | 951 | 106363 |
Timothy A. Springer | 167 | 669 | 122421 |
Gabriel N. Hortobagyi | 166 | 1374 | 104845 |
Rodney S. Ruoff | 164 | 666 | 194902 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Ronald A. DePinho | 160 | 486 | 104039 |