We further suggest that, through the use of TPA, various stages associated with cancer development in humans, i.e., initiation through promotion and progression, can be identified in vitro.
It is possible that the expression of malignancy in Burkitt lymphoma is caused by immunoglobulin V region gene translocation resulting in activation of a gene on the long arm of human chromosome 8.
An analysis of over 30 polymorphic genetic markers for possible genetic linkage to a gene increasing susceptibility to cancer revealed positive LOD scores to markers within or near the major histocompatibility complex [HLA-A,B (0.639), properdin B (Bf) (0.162), glyoxylase-1 (GLO-1) (0.166)] as well as to acid phosphatas (0.566) and MNSs (0.449).
However, the ADA activity and/or the ADA/PNP ratio were consistently higher in the cells from the patients with chronic T gamma lymphocytosis than in those with chronic T malignancy.
An analysis of over 30 polymorphic genetic markers for possible genetic linkage to a gene increasing susceptibility to cancer revealed positive LOD scores to markers within or near the major histocompatibility complex [HLA-A,B (0.639), properdin B (Bf) (0.162), glyoxylase-1 (GLO-1) (0.166)] as well as to acid phosphatas (0.566) and MNSs (0.449).
In Burkitt lymphoma the c-myc gene, the cellular homologue of the viral oncogene v-myc, has been implicated in the aetiology of this human B-cell malignancy.
Recent clinical studies suggest a relationship between high AHH activity and lung cancer associated with cigarette smoking (Kouri, R.E., McKinney, C.E., Slomiany, D.J., Snodgrass, D.R., Wray, N.P., and McLemore, T.L.Cancer Res.42: 5030-5037, 1982).
Nine genomic-DNA samples were digested with each of 23 restriction endonucleases and probed with human P1-450 cDNA fragments; restriction fragment length polymorphisms are detected, although it remains to be seen whether such a recombinant DNA test will be useful in determining individuals at increased risk for cigarette smoking-induced cancer and toxicity.
Southern blot analysis showed close similarity of the restriction patterns of the rat c-erbB-2 gene and the rat neu oncogene, suggesting possible involvement of c-erbB-2 in human cancer.
Furthermore, the concentration of 5'-NPD was found to be five times higher in the G2/M cells of the cancer specimens than that in the noncancer specimens.
Free E2 and SHBG were also measured in the serum of (e) postmenopausal patients having breast cancer (n = 38) and (f) matched control cancer patients (n = 67).
To determine whether the c-mos oncogene has been translocated in AML-M2 with this translocation and to isolate DNA sequences and genes from these two chromosomes that may be important in malignancy, we constructed somatic cell hybrids between a Chinese hamster ovary cell (CHO) mutant defective in glycine metabolism and myeloblasts with an 8;21 translocation from a patient with AML.
We emphasize the need for more thorough documentation of family histories and cancer association in this cancer-associated genodermatosis in order to clarify hereditary syndrome identification, and to improve cancer control through employment of cutaneous signs as a beacon for highly targeted forms of visceral cancer.
These results suggest that genotype analysis of the c-Ha-ras-1 locus, in combination with other clinical parameters, may be of prognostic value in assessing the potential for cancer.