Background/Aim: Little evidence is currently available on significant determinants of post-recurrence survival for patients with hormone receptor-positive (HR+), HER2-negative (HER2-) breast cancer. The objective of this study was to evaluate factors influencing post-recurrence survival in HR+/HER2-breast cancer. Patients and Methods: A cohort of 236 patients with recurrent HR+/HER2-breast cancer was retrospectively analyzed to identify significant factors correlating with prognosis after recurrence. Results: Multivariate analysis revealed independent prognostic factors of poor survival as follows: short intervals between recurrence and the end of adjuvant endocrine therapy (ET; p=0.046); short disease-free intervals (p=0.019); liver metastasis (p=0.007) or multiple metastases (p<0.001) at recurrence; and a poor response to first-line treatment (p<0.001). A poor first-line treatment response was significantly associated with a shorter response to a subsequent treatment line (p=0.007). Logistic regression analysis indicated that liver metastasis significantly increased the risk of a poor first-line-ET response (p=0.009). Conclusion: The first-line treatment response was the key to post-recurrence survival in patients with HR+/HER2-breast cancer. Particularly poor responses led to subsequent unfavorable prognostic outcomes.
Breast carcinosarcoma is an extremely rare, clinically aggressive tumor, and no standard treatment has been established. We report about a 34-year-old woman presenting with a 2.5-cm-sized carcinosarcoma in her right breast. She presented to our hospital for examination of this mass. Ultrasonography showed a hypoechoic mass with partially irregular margins. Fine-needle aspiration cytology indicated malignancy. No enlarged lymph nodes or distant metastases were detected. We diagnosed right breast cancer and performed partial mastectomy, sentinel lymph node biopsy, and latissimus dorsi muscle flap transfer. Histological findings revealed that the tumor consisted of a mixture of an epithelial component and a mesenchymal component. The final diagnosis was carcinosarcoma. After undergoing adjuvant chemotherapy and radiotherapy, the patient has had no recurrence, and her cosmesis is maintained. Clinical data of carcinosarcoma are insufficient. Breast conservation and reconstruction for carcinosarcoma may be suitable as local treatments; however, the most appropriate treatment method has not been established.
In totally laparoscopic distal gastrectomy (TLDG) for gastric cancer, accurately determining the proximal resection line may be difficult. This is because identifying the lesion intracorporeally is impossible, due to the lack of tactile sense, and, in addition, unlike the intestine, the most proximal site of the lesion is often different from the main site due to the distorted shape of the stomach. The aim of this study was to introduce a novel method of preoperative endoscopic marking with India ink, taking into consideration the morphological characteristics of the stomach. Between July, 2013 and April, 2016, 20 patients who underwent TLDG were enrolled in this study. Within the 3 days preceding the operation, after identifying the most proximal site of the lesion on the overlooking image of an endoscope, India ink was injected into the spot on the oral side of this site. The stomach was transected along the proximal border of the marked area. In all cases, the marked sites were localized and clearly identified during the operation, and the proximal resection margins were found to be negative on postoperative pathological examination. The mean length of the proximal margin was 46.0±14.0 mm. In conclusion, this preoperative endoscopic marking method may be useful in TLDG for gastric cancer.
Oestrogen receptor (ER)-positive, metachronous, contralateral breast cancer (MCBC) sometimes develops during or soon after completion of hormone therapy (HT), but it is uncertain whether it is HT-resistant. We examined the association between ER-positive second cancer and activation of the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) pathways, which are associated with HT resistance. We examined the treatment-free interval (time after completion of HT for initial cancer) in 41 patients with ER-positive MCBC with a history of adjuvant HT for initial cancer (HT group), and initial-to-second period duration (time after operation of initial cancer to onset of second cancer) in 17 patients with ER-positive MCBC in whom adjuvant HT was not applied to the initial tumour (control group or no HT group). Phosphorylated S6 (pS6) and phosphorylated MAPK (pMAPK) were used as indicators of PI3K/Akt/mTOR and MAPK pathway activity, respectively. Tumours were classified as showing negative, positive or strongly positive staining, and the correlation between staining and treatment-free interval or initial-to-second period duration was evaluated using the Spearman's rank correlation coefficient (ρ). Treatment-free interval and pS6 staining showed a negative correlation (ρ=-0.5355; P=0.0003) in the HT group. There was no correlation between initial-to-second period duration and pS6 staining in the no HT group (ρ=-0.0814; P=0.756). There was no correlation between pMAPK signalling and the treatment-free interval in the HT group (ρ=-0.1560; P=0.330) or the initial-to-second period duration in the no HT group (ρ=-0.0116; P=0.965). Development of a second ER-positive cancer during or soon after completion of HT for the initial cancer may be associated with activation of the PI3K/Akt/mTOR pathway. Care should be taken during follow-up and when selecting adjuvant therapy for second cancer.
Oestrogen receptor (ER)-positive, metachronous, contralateral breast cancer (MCBC) sometimes develops during or soon after completion of hormone therapy (HT), but it is uncertain whether it is HT-resistant. We examined the association between ER-positive second cancer and activation of the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK) pathways, which are associated with HT resistance. We examined the treatment-free interval (time after completion of HT for initial cancer) in 41 patients with ER-positive MCBC with a history of adjuvant HT for initial cancer (HT group), and initial-to-second period duration (time after operation of initial cancer to onset of second cancer) in 17 patients with ER-positive MCBC in whom adjuvant HT was not applied to the initial tumour (control group or no HT group). Phosphorylated S6 (pS6) and phosphorylated MAPK (pMAPK) were used as indicators of PI3K/Akt/mTOR and MAPK pathway activity, respectively. Tumours were classified as showing negative, positive or strongly positive staining, and the correlation between staining and treatment-free interval or initial-to-second period duration was evaluated using the Spearman's rank correlation coefficient (ρ). Treatment-free interval and pS6 staining showed a negative correlation (ρ=-0.5355; P=0.0003) in the HT group. There was no correlation between initial-to-second period duration and pS6 staining in the no HT group (ρ=-0.0814; P=0.756). There was no correlation between pMAPK signalling and the treatment-free interval in the HT group (ρ=-0.1560; P=0.330) or the initial-to-second period duration in the no HT group (ρ=-0.0116; P=0.965). Development of a second ER-positive cancer during or soon after completion of HT for the initial cancer may be associated with activation of the PI3K/Akt/mTOR pathway. Care should be taken during follow-up and when selecting adjuvant therapy for second cancer.
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