Table 4.
Coexpression analysis of AP‐1, NF‐кB, and STAT3 members in oral cancer lesions and their association with the HPV status
| Category | HPV+ve (n = 16) | HPV‐ve (n = 45) | P value |
|---|---|---|---|
| AP1− NF‐кB− STAT3– | 1 | 0 | 0.524 |
| AP1+ NF‐кB− STAT3– | 1 | 5 | 0.997 |
| AP1− NF‐кB+ STAT3– | 0 | 0 | 0 |
| AP1− NF‐кB− STAT3+ | 0 | 0 | 0 |
| AP1+ NF‐кB+ STAT3– | 10 | 5 | 0.0002 ** |
| AP1+ NF‐кB− STAT3+ | 0 | 0 | 0 |
| AP1− NF‐кB+ STAT3+ | 0 | 4 | 0.571 |
| AP1+ NF‐кB+ STAT3+ | 4 | 31 | 0.005 ** |
Each member of AP‐1 (JunB, JunD, and c‐Fos), NF‐κB (p50 and p65), and STAT3 (Total STAT3 and phosphorylated STAT3) were scored 0 for Nil/Weak expression and 1 for Moderate/Strong expression). Any marker in category AP‐1/NF‐κB/STAT3 if scored as 1 in immunohistochemical analysis, indicated involvement of respective category of the transcription factor. Based on the presence or absence of each class (AP‐1/NF‐κB/STAT3) of transcription factor, individual tumor tissues were segregated in different categories and their distribution was evaluated by Fisher's Exact Test. **Highly significant correlation.