Words similar to dysplastic
Example sentences for: dysplastic
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Small foci of dysplastic precancers (Class 1) may arise from the diffuse hyperplasias and metaplasias.
In some circumstances, CD4 +and CD8 +T cells were rendered inactive in tumor-bearing hosts [ 8 ] . The inactivation of CD4 +T cells has been attributed either to the tumor cells themselves or to bone marrow-derived cells [ 9 10 11 ] , whereas antigen ignorance or loss of memory have been postulated to underlay that of CD8 +T cells [ 12 13 ] . Other studies have suggested that tumor cells can secrete immunosuppressive factors such as TGF-β or express Fas ligand to induce apoptosis of infiltrating lymphocytes [ 14 15 16 ] . Furthermore, the tumor vasculature appears to be quite different from normal blood vessels, in terms of structural organization, interstitial pressure, and flow patterns [ 17 ] , and in reduced lymphocyte and natural killer cell homing and adhesion [ 18 19 20 21 ] . The existence of significant barriers to effective immunological destruction is further illustrated by a mouse model of concurrent multistage tumorigenesis and anti-oncogene autoimmunity, wherein progenitor dysplastic lesions are infiltrated and disrupted, while solid tumors are not [ 22 ] . The hypothesis is that the microenvironment of certain types of solid tumor can serve to locally suppress T cell infiltration.
However, in both intervention and regression trials, significant CD4 +T cell and CD8 +T cell infiltration into hyperplastic/dysplastic islets and tumors was noted in Rip1-Tag2 mice that had received the combination of sub-lethal radiation and adoptive transfer of TCR splenocytes.
Frequent allelic loss at chromosomal locations 2q, 3p, 4q, 6p, 6q, 8p, 8q, 9p, 11q, 13q, 14q and 17q is observed in head and neck cancer [ 4 8 9 10 11 ] . Molecular studies of hyperplastic, dysplastic, CIS, and invasive head and neck lesions indicate that loss of heterozygosity at chromosomal locations 3p, 9p and 17p are early events in head and neck carcinogenesis [ 4 12 ] . Specific tumor suppressor genes, such as FHIT (3p14.
Several weeks later, a spontaneous autoimmune response to Tag is readily detectable, with significant lymphocyte infiltration of hyperplastic/dysplastic islets.
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