Angiosarcoma associated with lymphedema is a rare soft tissue malignancy that occurs owing to chronic lymphedema, primarily following breast cancer surgery. We present a case of an 83-year-old female who developed angiosarcoma 14 years after undergoing breast cancer surgery. Diagnosis was confirmed through excisional biopsy, histopathological evaluation, and imaging. Computed tomography and magnetic resonance imaging revealed diffuse dermal thickening with an enhanced subcutaneous nodular lesion on the right arm. This unusual case emphasizes the importance of vigilant monitoring in patients with chronic lymphedema post-breast cancer surgery, as early radiologic and clinical detection can facilitate timely intervention and improve outcomes.

Purpose: The incidence of breast cancer in older females is increasing with increased life expectancy. This study analyzed tumor characteristics and oncological outcomes in patients aged ≥ 70 years compared to patients in a younger postmenopausal group, in conjunction with their adherence to treatment guidelines. Methods: Patients aged ≥ 50 years, newly diagnosed with breast cancer, were divided into two age categories: ≥ 70 years and 50–69 years. All patients underwent curative surgery at Korea University Guro Hospital between January 2009 and December 2019. Clinical data on tumor subtype, histopathological grade, and clinical stage, along with treatment details were collected. Disease-free survival, distant recurrence-free survival, and breast cancer-specific survival rates were determined. Results: Of 1,199 patients, 166 (13.8%) were ≥ 70 years at the time of surgery. The diseasefree, distant recurrence-free, and breast cancer-specific survival rates were significantly lower in patients aged ≥ 70 years (p < 0.05). In a subgroup analysis, human epidermal growth factor receptor 2-positive tumors were the only subtype with a statistically significant difference in survival outcomes, and adherence to the guidelines was strongly linked to a better prognosis. Conclusion Patients aged ≥ 70 years had lower disease-free, distant recurrence-free, and breast cancer-specific survival rates compared to younger postmenopausal patients aged 50–69 years. With the continuous increase in life expectancy and advances in healthcare, it is critical to optimize treatment strategies for older patients with breast cancer to improve survival outcomes and enhance their quality of life.

Purpose: Zinc finger protein 639 (ZNF639) is often found within the overlapping amplicon of PIK3CA, and previous studies suggest its involvement in the pathogenesis of esophageal and oral squamous cell carcinomas. However, its expression and significance in breast cancer remain uncharacterized. Methods: Immunohistochemical analysis of ZNF639 was performed using tissue microarrays.Functional studies, including colony formation, Transwell cell migration, and in vivo metastasis, were conducted on breast tumor cells with ZNF639 knockdown via small interfering RNA transfection. Results: Reduced ZNF639 immunoreactivity was observed in 82% of the breast cancer samples, independent of hormone receptor and human epidermal growth factor receptor 2 status. In multivariate Cox regression analyses, ZNF639 expression was associated with favorable survival outcomes, including recurrence-free survival (hazard ratio, 0.35; 95% confidence interval [CI], 0.14–0.89) and overall survival (hazard ratio, 0.41; 95% CI, 0.16– 1.05). ZNF639 knockdown increased clonogenicity, cell motility, and lung metastasis in NOD/ SCID mice. Following the ZNF639 knockdown, the expression of Snail1, vimentin, and C-C chemokine ligand 20 (CCL20) was upregulated, and the changes in cell phenotype mediated by ZNF639 were reversed by the subsequent knockdown of CCL20. Conclusion Low ZNF639 expression is a novel prognostic factor for recurrence-free survival in patients with breast cancer.

Purpose: Breast cancer (BC) is a predominant malignancy globally, surpassing lung cancer in terms of diagnostic frequency, with an escalating incidence rate in recent decades.Recent studies have investigated the role of protein kinase C zeta (PRKCZ) in diverse cellular processes in cancer biology. In this study, we evaluated the association between PRKCZ and deleterious outcomes in BC and elucidated the mechanisms underlying its expression in breast carcinoma. Methods: The correlation between PRKCZ and survival rates of patients with BC was investigated using The Cancer Genome Atlas database. The methylation status of the PRKCZ promoter was analyzed using the UALCAN database. Furthermore, we investigated the mechanisms underlying PRKCZ inactivation in BC by treatment with transferase inhibitors, methylation-specific polymerase chain reaction (PCR) analysis, western blotting, and luciferase reporter gene assays. The degree of methylation and expression levels of PRKCZ, as regulated by DNA methyltransferase 1 (DNMT1), were quantified using quantitative PCR and western blotting. Results: Our analysis revealed that decreased expression of PRKCZ in BC was significantly correlated with poor clinical prognosis. Furthermore, we observed that hypermethylation of the PRKCZ promoter contributed to its reduced expression in BC. Notably, DNMT1 has been identified as a critical regulator of PRKCZ methylation. Conclusion Our findings elucidate the tumor-suppressive function of PRKCZ and provide insights into the molecular mechanisms underlying its downregulation in BC.

Purpose: This study aimed to investigate the molecular characteristics associated with better prognosis in breast cancer. Methods: We performed targeted sequencing of 962 genes in 56 samples, categorizing them into long-term and short-term survival groups as well as chemotherapy-sensitive and chemotherapy-resistant groups for further analyses. Results: The results indicated that the tumor mutational burden values were significantly higher in the short-term survival and chemotherapy-resistant groups (p = 0.008 and p = 0.003, respectively). Somatic mutation analysis revealed that the mutation frequencies of BCL9L and WHSC1 were significantly lower in the long-term survival group than those in the short-term survival group (p = 0.029 and p = 0.024, respectively). CREB-regulated transcription coactivator 1 (CRTC1) mutations occurred significantly more frequently in the chemotherapy-resistant group (p = 0.027) and were associated with shorter progression-free survival (p = 0.036).Signature weighting analysis showed a significant increase in Signature.3, which is associated with homologous recombination repair deficiency in the chemotherapy-sensitive group (p = 0.045). Conversely, signatures related to effective DNA repair mechanisms, Signature.1 and Signature.15, were significantly reduced (p = 0.002 and p < 0.001, respectively). Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that gene mutations were significantly enriched in the JAK-STAT signaling pathway. Conclusion This study, through intergroup comparative analysis, found that immunotherapy (using programmed death 1/programmed death-ligand 1 inhibitors) may improve the prognosis of patients with short survival and chemotherapy resistance. Additionally, the study revealed that mutations in BCL9L and WHSC1 could serve as biomarkers for breast cancer prognosis, while CRTC1 mutations and Signature.3 could predict chemotherapy response. The study also found that the JAK-STAT pathway might be a potential therapeutic target for chemotherapy resistance. Therefore, this study identifies molecular characteristics that influence the prognosis of breast cancer patients, providing important theoretical insights for the development of personalized treatment strategies.

Purpose: Patients undergoing breast surgery may experience chronic postoperative pain in the breasts, upper extremities, and axillary regions, and no established methods for preventing this pain are available at present. This study aimed to investigate whether coaptation of the transected intercostal nerve can prevent the development of neuropathic and chronic breast pain after mastectomy in implant-based breast reconstruction. Methods: A prospective, double-blind, randomized controlled trial was conducted by dividing patients who underwent implant-based breast reconstruction after mastectomy into a control group without nerve coaptation and an experimental group with nerve coaptation.Patient clinical information was collected, and a survey using the pain and quality of life scale was conducted at 6 and 12 months after surgery. Results: Fifteen patients completed the study, including seven in the control group and eight in the experimental group. The two groups showed no significant differences in terms of clinical factors. The experimental group exhibited lower Short-Form McGill Pain Questionnaire scores than the control group at 6 and 12 months postoperatively, with a statistically significant difference at 6 months. Numerical Rating Scale and Present Pain Intensity scores for both groups were in the “no to mild” range throughout the study period, with no statistically significant differences between the groups. Although the difference in the BREAST-Q™ results did not reach statistical significance, the experimental group showed an improvement in the quality of life. Conclusion Intercostal nerve coaptation after mastectomy in implant-based breast reconstruction may facilitate initial nerve recovery. Although trial results are needed to fully determine the clinical impact, our findings support the ongoing scientific and clinical efforts to use this technique.

Phyllodes tumors (PTs) represent an uncommon category of fibroepithelial neoplasms found in the breast tissue and are classified as benign, borderline, or malignant based on their histopathological features. Histological assessment remains the cornerstone of a PT diagnosis. However, recent genomic advancements have revealed the biological mechanisms underlying PTs, particularly malignant phyllodes tumors (MPTs). This comprehensive review integrates current genomic and molecular investigations that have elucidated the distinguishing features of PTs. Mutations in the MED12 gene represent early tumorigenic phenomena that are often observed in benign lesions, whereas modifications in the TERT promoter, alterations in TP53, and amplification of EGFR are associated with malignant transformation. Moreover, novel transcriptomic investigations have characterized discrete molecular subtypes exhibiting epithelial and fibrous attributes, thereby enriching our understanding of MPT heterogeneity. Actionable genomic modifications, including dysregulation of the PI3K/Akt/mTOR, MET, and IGF1R signaling cascades, represent promising directions for targeted therapeutic strategies; however, clinical validation is still insufficient. Advances in patient-derived models have created functional platforms conducive to drug screening and preclinical evaluation. Molecular examination has expanded our understanding of PTs, revealing the genomic components linked to malignant progression and identifying prospective therapeutic targets. Nevertheless, obstacles remain in the practical application of these discoveries, primarily owing to the intratumoral heterogeneity and rarity of MPTs. Future investigations should prioritize the integration of diverse omics methodologies, enhancement of preclinical testing frameworks, and establishment of global data-sharing initiatives to promote biomarker-driven treatment strategies.

Purpose: Breast cancer gene (BRCA) mutation is a well-known risk factor for breast cancer, and clinical interest in prophylactic mastectomy has increased in recent years.We investigated patients who were BRCA mutation carriers and underwent contralateral risk-reducing mastectomy (RRM), focusing on the incidence of occult malignancy after contralateral RRM. Methods: Prospectively collected data of patients with breast cancer treated at a single institution were retrospectively reviewed. Patients who underwent RRM with BRCA mutation who underwent RRM between January 2010 and November 2023 were included in this study.Among patients who underwent contralateral RRM, those with a primary cancer diagnosis were included, and those with occult malignancy on the contralateral RRM side were reviewed additionally. The demographics and pathologies of both primary breast cancer and occult malignancies were evaluated. Results: In our institution, 925 patients were identified as BRCA mutation carriers, and 320 patients underwent contralateral RRM along with primary breast cancer surgery. BRCA2 mutation occurred more frequently (54.8%) in the overall BRCA mutation cohort. Furthermore, we reviewed 320 patients diagnosed with breast cancer and detected as BRCA mutation carriers who underwent contralateral RRM; high proportion of them were BRCA1 mutation carriers.Interestingly, we found a low incidence of only seven patients (2.2%) with occult malignancy on contralateral RRM side, which is different from that reported in other nations. Conclusion The incidence of occult malignancy in the contralateral breast of breast cancer patients with breast cancer with BRCA mutation is significantly low, and may be influenced by several factors. Increased utilization of screening and advancements in diagnostic technologies in South Korea have reduced the chance of occult malignancy in RRM, and a variety of pathologic examination methods may affect the rate of incidence.

Young female early breast cancer (≤ 40 years) treatment presents unique challenges due to its aggressive features. Using data from the Taiwan Cancer Registry (2007–2017), this study investigated its clinical characteristics, treatment patterns, and prognostic factors. The proportion of young female breast cancer declined from 12% to 8% during the study period.Triple-negative (TN) breast cancer was more prevalent in younger patients, while hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative subtypes increased with age. Stages II and III were observed more frequently in older patients, whereas extremely young patients (20–29 years) exhibited compromised overall and recurrencefree survival. Subtype analysis revealed worse outcomes for TN and hormone receptornegative/human epidermal growth factor receptor 2-positive (HER2+) cases. Treatment patterns showed that targeted therapy was more commonly administered to younger patients with HER2+, while endocrine therapy was used less frequently for HR+ cases, reflecting tolerability and treatment compliance challenges. Future research should focus on optimizing therapeutic strategies and addressing long-term survivorship to enhance care for young women with breast cancer.

Purpose: Human epidermal growth factor receptor 2 (HER2)-low breast cancer has the potential to emerge as a distinct subtype. Several studies have compared the differences between HER2-low and HER2-0 breast cancers, but no consensus has been reached.Additionally, a biomarker to predict pathological complete response (pCR) rates in patients with HER2-low breast cancer remains to be identified. Methods: We collected data from 777 patients across three centers, stratifying them into HER2-low and HER2-0 groups. We compared differences in survival and pCR rates between the two groups and investigated potential biomarkers that could reliably predict pCR. Results: The study found that patients with HER2-0 breast cancer had higher pCR rates compared to patients with HER2-low tumors (289 patients [30.1%] vs. 475 patients [18.1%], p < 0.0001). Survival analysis showed no significant advantage for HER2-low tumors over HER2-0 breast cancers. Binary logistic analysis revealed that androgen receptor (AR) expression predicts poorer pCR rates in both the overall patient group and the HER2-0 breast cancer group (overall patients: odds ratio [OR], 0.479; 95% confidence interval [CI], 0.250–0.917; p = 0.026 and HER2-0 patients: OR, 0.267; 95% CI, 0.080–0.892; p = 0.032). In contrast, programmed death ligand 1 (PD-L1) expression was associated with more favorable pCR rates in the overall patient group (OR, 3.199; 95% CI, 1.020–10.037; p = 0.046). Conclusion There is currently insufficient evidence to classify HER2-low breast cancer as a distinct subtype. Our study revealed that AR expression, along with negative PD-L1 expression, contributes to lower pCR rates.