Consequences of p16 tumor suppressor gene inactivation in mycosis fungoides and Sezary syndrome and role of the bmi-1 and ras oncogenes in disease …
C Zhang, A Toulev, J Kamarashev, JZ Qin, R Dummer… - Human pathology, 2007 - Elsevier
In examining the expression of oncogenes and tumor suppressor genes in mycosis
fungoides and Sézary syndrome, we found the cell cycle–regulating protein p16 to be
absent in T cells. Immunohistochemical staining with p16-specific antibodies showed that
the number of p16-expressing cells in cutaneous lesions decreases in late stages. The
repression of p16 was not attributable to deletion or methylation of this gene; however, the
Bmi-1 oncogene, a known suppressor of p16, was present in mycosis fungoides and Sézary …
fungoides and Sézary syndrome, we found the cell cycle–regulating protein p16 to be
absent in T cells. Immunohistochemical staining with p16-specific antibodies showed that
the number of p16-expressing cells in cutaneous lesions decreases in late stages. The
repression of p16 was not attributable to deletion or methylation of this gene; however, the
Bmi-1 oncogene, a known suppressor of p16, was present in mycosis fungoides and Sézary …