Breast cancer prevention and treatment have become major issues that urgently need to be addressed in the field of global public health. As a key pathological transitional stage in the progression of breast cancer， preneoplastic breast cancer （PBC） carries a significant risk of clinical transformation. Effective intervention in the progression of PBC is of great clinical significance in preventing the occurrence of breast cancer. Pathological studies have shown that abnormal angiogenesis is a key mechanism driving the transformation of PBC into breast cancer. Vascular endothelial growth factor （VEGF）， as a core regulatory molecule that promotes angiogenesis， plays a pivotal role in this process. The malignant transformation of PBC is closely associated with the abnormal activation of the VEGF-mediated pro-angiogenic network. Although modern medicine has achieved certain therapeutic effects through surgery and endocrine therapy， clinical limitations such as invasiveness， drug resistance， and adverse reactions still exist. Recent studies have demonstrated that the VEGF signaling system mediates the phosphatidylinositol 3-kinase-protein kinase B （PI3K/Akt） signaling pathway and the mitogen-activated protein kinase （MAPK） pathway. In addition， the hypoxia-inducible factor-1α （HIF-1α）/VEGF signaling pathway and the delta-like ligand 4 （DLL4）/Notch receptor 1 （Notch1） signaling pathway， together with other pathways， form a complex regulatory network that plays a central role in angiogenesis during PBC. Traditional Chinese medicine （TCM）， characterized by multi-component synergy， multi-pathway regulation， and high safety， demonstrates significant advantages in inhibiting pathological angiogenesis and blocking PBC progression by targeting the VEGF signaling pathway. From the perspective of VEGF pathway regulation， this paper systematically reviews the latest research progress on TCM in inhibiting angiogenesis and intervening in PBC， and discusses its mechanisms and application value in the early prevention and treatment of PBC， with the aim of providing references for optimizing clinical intervention strategies for PBC.

OBJECTIVETo study the expression of anaplastic lymphoma kinase (ALK) and survivin proteins in anaplastic large cell lymphoma (ALCL) and there clinical significance.

METHODSThe morphologic characteristics were studied by routine light microscopy. Immunohistochemical staining for ALK and survivin proteins was performed using LSAB method.

RESULTSALK protein was positive in 51 cases (63%) and negative in 30 cases (37%) of the 81 cases of ALCL studied. The prognosis of patients with ALK protein expression was better than those without ALK expression (P < 0.05). As for survivin protein, there were various degrees of expression in all the 77 ALCL cases studied. High level of survivin protein expression was observed in 33 cases (42.9%), while low level of expression was seen in 44 cases (57.1%). The expression of survivin protein did not correlate with that of ALK protein (P > 0.05). The survival rate was significantly lower in patients with high survivin protein expression (P < 0.05). In cases with ALK protein expression, the prognosis was less favorable if there was also high co-expression of survivin protein (P < 0.05). In ALK protein negative cases, prognosis did not significantly correlate with the expression of survivin protein (P > 0.05). In addition, multivariate analysis confirmed the prognosis value of ALK protein expression, survivin protein expression and constitutional symptoms.

CONCLUSIONSurvivin protein expression can serve as an independent prognostic predictor of unfavorable clinical outcome in patients with ALCL, especially when ALK protein is positive.

Adolescent ; Adult ; Aged ; Biomarkers, Tumor ; metabolism ; Child ; Child, Preschool ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Inhibitor of Apoptosis Proteins ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Male ; Microtubule-Associated Proteins ; metabolism ; Middle Aged ; Multivariate Analysis ; Neoplasm Proteins ; metabolism ; Prognosis ; Protein-Tyrosine Kinases ; metabolism ; Receptor Protein-Tyrosine Kinases ; Survival Analysis ; Young Adult

OBJECTIVETo investigate the detrimental effects of hemorrhagic shock on the structure and function of mitochondria DNA (mtDNA) encoding cytochrome oxidase genes in intestinal epithelial cells.

METHODSWistar rats were used and divided into two groups: hemorrhagic shock group and control group. Hemorrhagic shock model of rats was utilized in this experiment. The mtDNA was extracted from the intestinal epithelial cells and amplified by polymerase chain reaction (PCR) with different primers of cytochrome oxidase (COX I, COX II and COX III). The products of PCR were directly sequenced.

RESULTSHemorrhagic shock could result in the point mutagenesis in mitochondrial genome encoding cytochrome oxidase (COX I and COX II). There were 4, 4, 22, 16, 35 point mutations in COX I from 5545 to 6838 bp in 5 shocked rats. There were five point mutations in COX II from 7191 to 7542 bp at the site of t7191c, t7212c, a7386g, a7483g, c7542g in 1 shocked rat. There was no mutation found in COX III.

CONCLUSIONSHemorrhagic shock could significantly induce the damage of the gene of cytochrome oxidase encoded by mtDNA.

Animals ; Base Sequence ; DNA, Mitochondrial ; genetics ; Electron Transport Complex IV ; genetics ; Intestinal Mucosa ; enzymology ; Male ; Mutation ; Polymerase Chain Reaction ; Rats ; Rats, Wistar ; Shock, Hemorrhagic ; enzymology ; genetics