Figure 1:
Figure 2:
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=ASIA6AP2G7AKN6TPEW4I%2F20260315%2Feu-central-1%2Fs3%2Faws4_request&X-Amz-Date=20260315T012631Z&X-Amz-Expires=3600&X-Amz-Security-Token=IQoJb3JpZ2luX2VjEOj%2F%2F%2F%2F%2F%2F%2F%2F%2F%2FwEaDGV1LWNlbnRyYWwtMSJFMEMCIFXGBFEobVntozF2KrkZLftUlepuPCpTQOyLye9CWWCbAh9z2ju7P%2Fnog8kF%2F2YiM%2B0t7vHsu7ymZYYBbWQVxMYsKsQFCLH%2F%2F%2F%2F%2F%2F%2F%2F%2F%2FwEQAhoMOTYzMTM0Mjg5OTQwIgx3p1Zk7pvZuEiJkOQqmAV5UkLThlSW%2BVEg%2F4X0qe9oGYYdVdxcH6OXbWiVPMkPfres1eW2%2BuztyV5uIO73DWC81o03XBNHv%2BI8%2BhFZGrWfXadqplwrSpiSZQjMp24%2BC5T0CrgRto5OYJ4gnkRKf4v9TKR0miSojO8m%2FHlgTGz8k07Lk9boYjgYxAO0KW7lrnWVLbNkHgYVf8qRi%2BNW2kD8SkYuAb3Sk0xolmhFJuXAMhdWsfI3NOW3BpiOYnwKHiXuMEn6HM9q0Nzh%2FmK9Bqs04LSP4QseB5BX7u6Qz5cMSmtPJqcnQmjOYddIVK%2FyRjGcEgejKNZzFoPoTQGy74wXA5n0JzcdWR5P8qCiCkA7Igf4TcRlnREpVWTEhdT4vrtYFZ%2BwhI7xK0D198Zl7ZtrVJXkqnpAlJC35zEsA2OJGVWvKt6XRGpxlyUNgHw2jRZS1Phe47RDp962Ckl4s6Nwqe0HzIGBIEyMYtyf9oUIsUeQEsV%2BmwPh%2FwCgc0XJtLgmoEzeYWADl3E3bkTE7a2wYcZ6NH0VEdlcPa%2BmS%2Bn87XBt5DNTS4YZCCRk5ixJLIwhGZTQmR69OBgn2G9H7jCRVqkdmuFFxHNpsz3JtdY%2FP7ggqOtbJcf%2F6kQ1vasGcHz9UAjuYTt2i4gPf%2BPxxZimjdaI%2BBWcFXMFSXtr5ZTcBIyjBx9j57CuF9fWBb01ImtsfrpzgBO%2BeGkw2f1ep%2FOCwxdYs7BUIsajDdw2Uk4JGxs8vS6h3x5U9nXTZJzkP97hqJHx1DyRpHxQXC7LvmtAdcI%2B7paMnbJaFOFLFiNEWJC0JlLbIIj5gAxOGiqdqKJru%2FfZGAmP%2FK%2FDrH02k4ja0nchv6qumwGdql9%2Bh43IG8NoE8Dm77yGW3DOhFStUdLdzKO0IINMMO%2F0180GOrMB4o3kEXuOka2TWqm%2Fd%2F6PPS4Dzi%2FxMZXEaZwy5XjCfdxZWXOlthA%2FY41RyDH%2Bp9MEmrv5cVy6V7QASckO32NHIzPEYvR1Uo2yIvWH1UO73rc%2FmbEsIZWFyAKl2tMiw6CSYpolLACyAlBvgxJx6ZIk%2FkhR44SOntvXioFp9ZWHyRrJf5F0XGamMqqsnU1jN6yrZjHZGPrKbBjh531MzCITrnOX74EcrkCves9mPGopKC%2BwBqc%3D&X-Amz-Signature=f0871bd584a360939efc4b97f40dda7513791af2251dc316e62d30a28072e8db&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 |