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Objective: Breast cancer (BC) is a significant health concern and one of the most diagnosed cancers in women, both in Turkey and globally. Despite advances in the management of BC, axillary lymph node involvement remains a significant consideration for treatment planning, local recurrence, and prognosis. We aimed to evaluate the contribution of F-18 fluorodeoxyglucose-positron emission tomography/computed tomography (F-18 FDG-PET/CT) in detecting axillary lymph node metastasis compared to ultrasound (US). Materials and Methods: Eighty patients who were diagnosed with stage I and II BC and underwent US and F-18 FDG-PET/CT scans before surgery were enrolled in this study. Those who did not undergo F-18 FDG-PET/CT imaging, patients with distant metastases at the time of diagnosis and patients with micrometastases in the axilla were excluded from the analysis. Imaging results of the status of axillary lymph nodes were verified with the final pathology report of axillary lymph nodes. Results: The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of F-18 FDG-PET/CT for the detection of ipsilateral axillary lymph node metastases were 75%, 77.27%, 72.97%, 79.07%, and 76.25%. The corresponding values for US were 72.22%, 81.82%, 76.47%, 78.26%, and 77.50%, respectively. When US finding is negative or suspicious in axillary lymph node evaluation, the accuracy of F-18 FDG-PET/CT for the detection of ipsilateral axillary lymph node metastases were 65.38%, 83.33%, 70.83%, and 79.55%, respectively. Conclusion: This study found that F-18 FDG-PET/CT does not provide an additional advantage over US in assessing the axilla in early-stage disease. [ABSTRACT FROM AUTHOR]

Macroautophagy/autophagy is an evolutionarily conserved cellular stress response mechanism. Autophagy induction in the tumor microenvironment (stroma) has been shown to support tumor metabolism. However, cancer cell-derived secreted factors that initiate communication with surrounding cells and stimulate autophagy in the tumor microenvironment are not fully documented. We identified CTF1/CT-1 (cardiotrophin 1) as an activator of autophagy in fibroblasts and breast cancer-derived carcinoma-associated fibroblasts (CAFs). We showed that CTF1 stimulated phosphorylation and nuclear translocation of STAT3, initiating transcriptional activation of key autophagy proteins. Additionally, following CTF1 treatment, AMPK and ULK1 activation was observed. We provided evidence that autophagy was important for CTF1-dependent ACTA2/α-SMA accumulation, stress fiber formation and fibroblast activation. Moreover, promotion of breast cancer cell migration and invasion by activated fibroblasts depended on CTF1 and autophagy. Analysis of the expression levels of CTF1 in patient-derived breast cancer samples led us to establish a correlation between CTF1 expression and autophagy in the tumor stroma. In line with our in vitro data on cancer migration and invasion, higher levels of CTF1 expression in breast tumors was significantly associated with lymph node metastasis in patients. Therefore, CTF1 is an important mediator of tumor-stroma interactions, fibroblast activation and cancer metastasis, and autophagy plays a key role in all these cancer-related events. Abbreviations: ACTA2/α-SMA: actin, alpha 2, smooth muscle CAFs: cancer- or carcinoma-associated fibroblasts CNT Ab.: control antibody CNTF: ciliary neurotrophic factor CTF1: cardiotrophin 1 CTF1 Neut. Ab.: CTF1-specific neutralizing antibody GFP-LC3 MEF: GFP-fused to MAP1LC3 protein transgenic MEF LIF: leukemia inhibitory factor IL6: interleukin 6 MEFs: mouse embryonic fibroblasts MEF-WT: wild-type MEFs OSM: oncostatin M TGFB/TGFβ: transforming growth factor beta [ABSTRACT FROM AUTHOR]

The aim of this study was to provide an update on ovarian function and the mechanisms of gonadal damage after exposure to chemotherapy in breast cancer survivors. The alkylating agents are toxic to both primordial and growing follicles. However, anti-metabolite drugs are more likely to destroy preantral and antral follicles. Younger patients are more likely to have a higher ovarian reserve, and therefore, more likely to retain some residual ovarian function after exposure to gonadotoxic regimens. However, there can be significant variability in ovarian reserve among patients of the same age. Furthermore, patients with critically diminished ovarian reserve may continue to menstruate regularly. Therefore age and menstrual status are not reliable indicators of good ovarian reserve and might give a false sense of security and result in an adverse outcome if the patient is consulted without considering more reliable quantitative markers of ovarian reserve (antral follicle count and anti-Müllerian hormone) and fertility preservation is not pursued. In contrast to well-documented ovarian toxicity of older chemotherapy regimens, data for newer taxane-containing protocols have only accumulated in the last decade and data are still very limited regarding the impact of targeted therapies on ovarian function. [ABSTRACT FROM AUTHOR]