OBJECTIVE: This study aimed to develop nomograms that combine clinical factors and MRI tumour regression grade to predict the pathological response of mid-low locally advanced rectal cancer to neoadjuvant chemoradiotherapy.
METHODS: The retrospective study included 204 patients who underwent neoadjuvant chemoradiotherapy and surgery between January 2013 and December 2021. Based on pathological tumour regression grade, patients were categorized into four groups: complete pathological response (pCR, n=45), non-complete pathological response (non-pCR; n=159), good pathological response (pGR, n=119), and non-good pathological response (non-pGR, n=85). The patients were divided into a training set and a validation set in a 7:3 ratio. Based on the results of univariate and multivariate analyses in the training set, two nomograms were respectively constructed to predict complete and good pathological responses. Subsequently, these predictive models underwent validation in the independent validation set. The prognostic performances of the models were evaluated using the area under the curve (AUC).
RESULTS: The nomogram predicting complete pathological response incorporates tumour length, post-treatment mesorectal fascia involvement, white blood cell count, and MRI tumour regression grade. It yielded an AUC of 0.787 in the training set and 0.716 in the validation set, surpassing the performance of the model relying solely on MRI tumour regression grade (AUCs of 0.649 and 0.530, respectively). Similarly, the nomogram predicting good pathological response includes the distance of the tumour\'s lower border from the anal verge, post-treatment mesorectal fascia involvement, platelet/lymphocyte ratio, and MRI tumour regression grade. It achieved an AUC of 0.754 in the training set and 0.719 in the validation set, outperforming the model using MRI tumour regression grade alone (AUCs of 0.629 and 0.638, respectively).
CONCLUSIONS: Nomograms combining MRI tumour regression grade with clinical factors may be useful for predicting pathological response of mid-low locally advanced rectal cancer to neoadjuvant chemoradiotherapy. The proposed models could be applied in clinical practice after validation in large samples.

OBJECTIVE: To investigate whether CCL18 is involved in breast cancer, and the relationship between CCL18 and MVD (MVD was recognized by CD34) which is a well-accepted angiogenic maker of multiple cancers including breast cancer.
METHODS: Immunohistochemistry staining for CCL18 and CD34 was performed on 179 cases, including 29 normal cases as control, 47 cases with benign breast diseases, and 103 cases with breast cancer.
RESULTS: We found that CCL18 was significantly up-regulated in breast cancer samples as compared with benign tumors or normal breast tissues. Moreover, the expression level of CCL18 increased with the size of tumors, the number of lymph node metastasis, and advancing tumor stage, suggesting that CCL18 expression correlates with tumor malignancy scales. At the same time, we found that MVD was also significantly over-expressed in cancer tissues as compared with normal control group and benign tumor group, but it was not significantly differentially expressed among tumors with different malignancy scale like CCL18, while the expression of MVD in CCL18 positive breast cancer cases was higher than in the CCL18 negative breast cancer cases (P=0.016, P<0.05).
CONCLUSIONS: CCL18 is involved in the development of breast cancer. CCL18 is a better biomarker than MVD in determining whether the tumor is malignant and the severity of malignancy of breast cancer.

The phosphoinositide-3 kinase (PI3K) - phosphoinositide-dependent protein kinase 1 (PDK1)-Akt/protein kinase B (PKB) cascade plays a critical role in cardiovascular development and tumor genesis. But the role of PDK1 in the microenvironment of heart and tumor remains unknown. To clarify the effects of PDK1 on tissue microenvironment in vivo, here, we created α-SMA-Cre-mediated excision of PDK1 mice. And the mice were injected subcutaneously with Lewis lung carcinoma (LLC) cells. We found PDK1-deficient mice had post-natal praecox dilated cardiomyopathy, decelerated tumor growth and severe tumor metastasis. Histopathological analysis revealed abnormality of vascular microenvironment in heart and primary tumor. In conclusion, PDK1 plays a pivotal role in regulating cardiac function and tumor metastasis by interfering with microenvironment.