my goal is to create my thesis defense powerpoint. using the text enclosed in triple quotes, I want you to create highly accurate very detailed hierarchial bullet point slide contents, using your max output context window token . the output must be formatted as accurate detailed hierarchial slides with bullet points (max 3 main bullets in each slide), summarized sentences, with clinical tone.

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Discussion
This study evaluated the patterns of EGFR status among patients diagnosed with TNBC in Kerman, Iran, and assessed its correlation with various clinicopathological variables. Consistent with results reported by Atik et al., who observed EGFR positivity in 87.2% of TNBC cases versus 8% in non-TNBC groups (26), our study revealed a markedly higher prevalence of EGFR expression in the TNBC subgroup. 
This substantial overexpression suggests that EGFR may serve as a distinguishing biomarker for TNBC, facilitating more accurate diagnosis and informing targeted therapeutic interventions. Similarly, Changavi et al. reported EGFR positivity in 89.47% of triple-negative cases (27), reinforcing the consistent association between EGFR overexpression and TNBC across different populations.
Our investigation also highlighted the association of TNBC with higher tumor grades and younger patient demographics, echoing observations by Kanapathy Pillai et al. (28), who found TNBC predominantly in younger individuals with high-grade tumors in a Malaysian cohort. In our study, a significant proportion of TNBC cases were classified as grade 3, suggesting a more aggressive disease course in younger populations and emphasizing the necessity for tailored therapeutic strategies that address the unique molecular and clinical characteristics of TNBC in this demographic.
Additionally, we observed a high proliferation index in TNBC cases, consistent with previous reports indicating an aggressive tumor phenotype associated with elevated Ki-67 levels (29,30). This heightened proliferative activity underscores the aggressive nature of TNBC and highlights the potential utility of proliferation markers in prognostication and treatment planning.
The correlation between EGFR expression and clinicopathological features was evident in our study, mirroring findings by Sood and Nigam (31), who identified a significant association between EGFR positivity and higher histological grades. Furthermore, Wang et al. demonstrated that EGFR expression post-neoadjuvant chemotherapy was associated with poorer disease-free survival (32), suggesting its potential role as a prognostic marker. These insights elucidate molecular underpinnings contributing to the aggressive behavior of TNBC and highlight EGFR as a viable target for therapeutic intervention.
Despite the promising association between EGFR expression and TNBC aggressiveness, clinical trials targeting EGFR have yielded mixed results. Carey et al. reported limited efficacy of EGFR inhibitors in unselected TNBC populations (17), indicating that EGFR-targeted therapies may be beneficial only in specific patient subsets. This discrepancy underscores the necessity for precise biomarker-driven patient selection to identify individuals most likely to benefit from such therapies. Our study contributes to this evidence by demonstrating a high prevalence of EGFR expression in TNBC, which may assist in stratifying patients for potential EGFR-targeted treatment regimens.
Furthermore, the heterogeneity of TNBC subtypes, as delineated by Lehmann et al. and Burstein et al. (7,10), suggests that EGFR expression may vary among different molecular classifications of TNBC. This variability necessitates a nuanced clinical management approach, where therapies are tailored based on specific molecular subtypes, enhancing treatment efficacy and patient outcomes. Our findings support the integration of EGFR as a critical biomarker within the diagnostic and therapeutic landscape of TNBC, aligning with efforts to refine molecular subtyping for improved clinical management.
The demographic and pathological characteristics observed in our study, notably the younger age at diagnosis and the predominance of high-grade tumors, are particularly concerning given their association with poor prognosis and increased mortality rates. This emphasizes the urgent need for early detection strategies and the development of effective targeted therapies to mitigate the aggressive nature of TNBC in younger populations.
This study has limitations, including its retrospective design and inherent biases. Additionally, the sample size, although adequate, may need to fully capture the diverse molecular landscape of TNBC, potentially limiting the generalizability of our findings. Future studies with larger cohorts and prospective designs are warranted to validate these findings and explore the therapeutic implications of EGFR overexpression in TNBC.

Conclusion
Our study highlights the significant role of EGFR expression in the pathophysiology of TNBC among the Iranian population, consistent with global research trends. The high prevalence of EGFR positivity in TNBC underscores its potential as a therapeutic target and prognostic marker. Future research should focus on stratifying TNBC patients based on EGFR expression and evaluating the efficacy of EGFR-targeted therapies to enhance treatment outcomes and improve survival rates in this aggressive breast cancer subtype.

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Genetics of breast cancer

• Approximately 10% of breast cancer cases are related to heredity and family history.
• Mutations in two genes that protect against cancer, BRCA1 and BRCA2, show an autosomal-dominant inheritance pattern in breast cancer.
• A large number of mutations in the BRCA genes have been described, but few have been found in families with no history of consanguineous marriage.