Cellular senescence has been perceived as a barrier against carcinogenesis. However, the senescence-associated secretory phenotype (SASP) of senescent cells can promote tumorigenesis. Here, we show senescent tumour cells are frequently present in the front region of collective invasion of papillary thyroid carcinoma (PTC), as well as lymphatic channels and metastatic foci of lymph nodes. In in vitro invasion analysis, senescent tumour cells exhibit high invasion ability as compared with non-senescent tumour cells through SASP expression. Collective invasion in PTC is led by senescent tumour cells characterized by generation of a C-X-C-motif ligand (CXCL)12 chemokine gradient in the front region. Furthermore, senescent cells increase the survival of cancer cells via CXCL12/CXCR4 signalling. An orthotopic xenograft in vivo model also shows higher lymphatic vessels involvement in the group co-transplanted with senescent cells and cancer cells. These findings suggest that senescent cells are actively involved in the collective invasion and metastasis of PTC.

Cutaneous ageing is an important extrinsic process that modifies the pigmentary system. Because cellular senescence is a fundamental ageing mechanism, we examined the role of senescent cells in ageing pigmentation.

Background and Purpose—: Recent advent of endovascular thrombectomy (EVT) enables us to provide a new perspective on the use of tPA (tissue-type plasminogen activator) through histological analysis of retrieved thrombus. We investigated the responsiveness of intravenous thrombolysis (IVT) according to the thrombus composition in EVT-attempted patients with acute ischemic stroke. Methods—: We reviewed 92 consecutive patients with anterior circulation stroke who received combined IVT and EVT for 2 years. IVT responsiveness is defined as any decrease in the clot burden from baseline computed tomographic angiography to digital subtraction angiography during EVT. We histologically analyzed the relative fractions of red blood cells (RBCs), congregated fibrin and platelets, and white blood cells in the retrieved thrombi using semiautomated color-based segmentation method. Clinical characteristics according to the RBC fraction were investigated, and associated factors with IVT responsiveness were explored. Results—: Fifty-two patients with histological analyses were stratified into lowest, middle, and highest tertiles of RBC fraction. Toward higher RBC fraction, there was more common susceptibility vessel signs on magnetic resonance imaging (50.0% versus 66.7% versus 91.7%; P =0.022) and prevalent IVT responsiveness (25.0% versus 41.7% versus 75.0%; P =0.010). IVT-responsive group (n=23) had higher RBC fraction (45.7±15.5% versus 35.9±12.2%; P =0.010), lower fibrin and platelet (50.4±14.0% versus 58.5±11.1%; P =0.027), and lower white blood cells fraction (3.9±2.1% versus 5.5±3.0%; P =0.027) than IVT-unresponsive group (n=29). After adjusting for potential variables, RBC fraction (odds ratio, 1.05; 95% confidence interval, 1.01–1.10) remained only independent determinant of IVT responsiveness. Conclusions—: In EVT-attempted patients with acute ischemic stroke, IVT responsiveness would be closely associated with RBC fraction.

In recent years throughout Korea, the use of ultrasound-guided core needle biopsy (CNB) has become common for the preoperative diagnosis of thyroid nodules. However, there is no consensus on the pathology reporting system for thyroid CNB. The Korean Endocrine Pathology Thyroid Core Needle Biopsy Study Group held a conference on thyroid CNB pathology and developed guidelines through contributions from the participants. This article discusses the outcome of the discussions that led to a consensus on the pathology reporting of thyroid CNB.

Senescent cells in cancer tissue, including senescent fibroblasts and macrophages, have been reported to increase the malignant potency of cancer cells by secreting senescence-associated secretory phenotype (SASP). Otherwise, Senescence of tumor cells has been believed to inhibit tumor growth by halting the massive proliferation and increasing the chances of immune clearance. In particular, senescent tumor cells (STCs) have been thought that they rarely exist in carcinomas because oncogene-induced senescence needs to be overcome for protumorigenic cells to become malignant. However, recent studies have revealed that a considerable number of STCs are present in cancer tissue, even in metastatic sites. In fact, STCs are widely involved in cancer progression by leading to collective invasion and building a cytokine barrier to protect nonsenescent tumor cells from immune attack. Furthermore, therapy-induced STCs can induce tumor progression and recurrence by increasing stemness. However, obscure causative factors and their heterogeneity in various cancers make it difficult to establish the physiological role of STCs. Here, we summarize and review the current knowledge of the pathophysiology and role of STCs. We also outline the current status of therapeutic strategies for directly removing STCs or modulating the SASPs to maximize the positive functions of STCs while suppressing the negative functions.