Figure 1:
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Figure 3:
![The Cross-talk of AR and ErbB2 pathways In Naderi's study, the function of ERK1/2, testosterone, and Heregulin can be suppressed by both AR and ErbB2 pathways. Anti-ErB2 and anti-androgen therapy can inhibit the function of testosterone and ErbB2 and further cause the phosphorylation of ERK1/2, followed by negative regulation of cell growth. [52]](https://sciendo-parsed.s3.eu-central-1.amazonaws.com/6471cdf2215d2f6c89db169a/j_fco-2023-0007_fig_003.jpg?X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Content-Sha256=UNSIGNED-PAYLOAD&X-Amz-Credential=ASIA6AP2G7AKGINON56A%2F20260315%2Feu-central-1%2Fs3%2Faws4_request&X-Amz-Date=20260315T024706Z&X-Amz-Expires=3600&X-Amz-Security-Token=IQoJb3JpZ2luX2VjEOn%2F%2F%2F%2F%2F%2F%2F%2F%2F%2FwEaDGV1LWNlbnRyYWwtMSJGMEQCIGkmX5txNwu%2F%2FTC4lyZx18F99y3uXdHcnSlzTsTfBu%2FOAiBpdrXxhq%2BnVRE%2ByP0wUlgsMS6dOE19TwNwVZU87h0r6irFBQiy%2F%2F%2F%2F%2F%2F%2F%2F%2F%2F8BEAIaDDk2MzEzNDI4OTk0MCIMsQ9qt9tnF5C4ECnTKpkF8NnHttQGoV8R99CL%2B%2B6DyVOvEx5qdIJcbHbeKoDB1%2FQ8v8Q7xIOa1GovtChUpAzgyuAVKRUgT%2BGST5kwOuGlpTkLc2R3jkGYtFdLdhhZsgH%2B07EQ44QsUvPA9pq28IkGsjXsgAZ5nfxkL%2FgokZuxxMVRfJoBqT4wgX%2F1Xokc2UsEyKOGF1nz%2B7gPCdklEaDgtfgSUUe19OL9Skr%2FpVcEFD83loQW%2B3k9REXpXig1ax9KI0KDEbVk2ypEZGTnuQtoWZLKajENCmboZvDcHXf9a4EJ2lq0WD0yH9daRaIE3TVBR%2F4YGZeJ0tDH6PuzrOHRpHLMPQQJC4ApBtLe%2FBudfob0ncGq%2Fa3WYTu1sKLfsWC7o82WKdzmqI7gyOaHyy8HSw4UPhlppJzgy%2F0qwNHcorWRUb8VcvaYglJ8OqL8pmDNXbtFZIAyOEC2AX5lNuCvja0a6teow5jd6Ek009H%2FjCJxM%2BV%2FhwaN5JDLIOlaqjjEUscnYmMRX%2BmFkJNuAc1SKnoc9CSMSmPpa3LWCkL7LiKL7caIqwO3zwJWoQA%2BlOHttlIqd6g%2FCFiWnHEbCowPzMvPOxafrw1lW0cNn8frYJHZeELc0j6Ep3J67s43fsYM4gDp0mf3Gyjv8%2FXvYaUzP7U1wp2eipk2ijyeM33zGnwG6FkzGfisJZ3amtMHh112uKD%2FJbasVJkJ7kl4ON%2ForIWOz0q12K1ytI2bgygt6Uhj6D0iU8vTIhPmr922Hm9rGMnwXOdL9pjcvulyNbSVmP%2FE0vumkS908uHbUmpkqzD3lPhcOMZyONO20AiK%2BP847%2BiWwVST2y3QYP5TwRw5wlemLts6jw1lAwxeeDzqGx9GMcLjvMdiCsKKjodwPh0v6DpsmcrxgWkwpfvXzQY6sgESDOG%2BrQBodfr8tmScfEbftZL3qHBzfZdQVAiz6Gj52y1%2Bt9ZJRyc%2FXMMZ0FOWt3KSSfRKt8zjc0nExa6kFDZVpsfghFzMoGleNYrWVuuwuvPwFv5IR2ax4ih52Qc2QEJPsEE6a85N3sHFwziNtWmz8M2Gk%2Bd%2FSbdPnzxJ798YNQwO1t0HYZmh8NL7x5E65UVWD0tzIak9jTHob31kAEyGWH%2BDdAiTUpnn%2FwLGEOy6Wveo&X-Amz-Signature=e31aa5d54ff464f8d952d273778861cf66f526f6cc74ffca35e2b6e27f5e6c01&X-Amz-SignedHeaders=host&x-amz-checksum-mode=ENABLED&x-id=GetObject)
Treatment recommendation from the literature review_
| CLASSIFICATION | INTERVENTION |
|---|---|
| ATYPICAL APOCRINE LESIONS (AA) | No intervention +− Core needle biopsy |
| APOCRINE DCIS (ADCIS) | Mastectomy or conservative surgery +/− adjuvant radiation therapy |
| APOCRINE CARCINOMA | Neoadjuvant chemotherapy + surgery +/− radiation therapy + anti-androgen therapy (if AR+) + anti-HER2 antibodies (if HER2+) +/− PI3 kinase inhibition and CDK4/6 inhibitors (if biomarkers detected) |
Immunohistology characteristics of ADCIS and pure apocrine carcinoma_
| IMMUNOHISTOLOGY MARKERS | PURE APOCRINE CARCINOMA | ADCIS | INVOLVING PATHWAY |
|---|---|---|---|
| ER, PR (−), AR (+) | 100% strictly match to AR (+,) ER(−), PR (−) criteria | >90% | AR pathway |
| HER-2 | 1/3 positive, 2/3 negative | 47.1% | HER2 signaling pathway |
| GCDFP-15 | 75% | 96.4% | AR pathway |
| AMACR | > 90% | > 90% | Oxidative degradation pathways |
| ER-A36 | 94.7% | 94.7% (classified with pure apocrine carcinoma) | MAPK/ERK signaling pathway EGFR/Src/ERK signaling pathway |
| PIK3CA | >80% | 100% | PI3K/mTOR pathway |
| P53 | 46–50% | 61.8% | PI3K/mTOR/p53 pathway |
| PD-L1 | 10–40% | N/A | PD-1/PD-L1 pathway |
| AR-V7 | 57% | N/A | AR pathway |