Search

The COVID‐19 pandemic has had a global impact on the environment and economy and has affected hospital administration and patient behaviour. Since human‐to‐human coronavirus transmission occurs via droplets and physical contact, health care professionals are particularly vulnerable to contracting COVID‐19. Many cytopathology laboratories updated their workflow, established new standard biosafety protocols, and built digital pathology or telescope platforms to mitigate these risks and deal with the shortage of health care personnel. The COVID‐19 pandemic also disrupted medical education—all indoor training events, including conferences, multidisciplinary tumour boards, seminars, and microscope inspections were postponed. As a result, many laboratories now use new web‐based applications and platforms to maintain educational programs and multidisciplinary tumour boards. To comply with government directives, health care facilities postponed non‐emergency surgeries, reduced the number of routine medical examinations, restricted visitor numbers, and scaled back cancer screening activities, resulting in a sharp decline in cytopathology diagnoses, cancer screening specimens, and molecular testing for cancer. Subsequent misses or delays in the diagnosis and treatment of cancer were not uncommon. This review aims to provide comprehensive summaries of the consequences of the COVID‐19 pandemic for cytopathology, particularly in terms of cancer diagnosis, workload, human resources, and molecular testing. [ABSTRACT FROM AUTHOR]

Background Hydroa vacciniforme ( HV) is associated with Epstein-Barr virus ( EBV) infection and a risk of transformation to lymphoma. Methods We retrospectively analyzed six HV cases for EBV association and transformation to HV-like T-cell lymphoma. Clinicopathologic features were reviewed and cases were assessed for EBV-encoded RNA ( EBER) by in situ hybridization, double staining with immunohistochemistry and EBER and for T-cell clonality. Results The male-to-female ratio was 5:1, with a median age at diagnosis of 18.5 years. All patients initially had recurrent vesicles, necrotic ulcers or scars on sun-exposed areas. Symptoms were present before diagnosis between 2 weeks to 10 years. The mean follow-up time was 106.3 months. Four patients (67%) were EBV-positive. All four EBV-positive and one EBV-negative patients had relapsing clinical course. Double staining proved EBV infection in T-cells. Moreover, one EBV-positive patient developed HV-like T-cell lymphoma with hemophagocytosis after 209 months of recurrent papulovesicular eruptions and eventually died. T-cell clonality was successfully performed in four HV patients and all showed polyclonal results; the transformed HV-like T-cell lymphoma was monoclonal. Conclusions In EBV endemic areas, HV is frequently (67%) associated with EBV infection, but transformation to HV-like T-cell lymphoma seems to be uncommon (17%) and bear a dismal outcome. [ABSTRACT FROM AUTHOR]

Tumor‐associated macrophages (TAMs) are a major component of the tumor microenvironment (TME) and are key cells in regulating tumor development, metastasis, immune responses, inflammation, and chemoresistance. In response to TME stimulation, circulating monocytes are recruited and differentiated as TAMs. Most TAMs are defined as alternatively activated (M2) phenotype to create immunosuppressive TME and support tumor progression. In contrast, classically activated (M1) TAMs can produce pro‐inflammatory cytokines and enhance immune responses against tumor development. Autophagy is a conserved catabolic process to control cellular homeostasis and biological function. Emerging evidence reveals crucial contribution of autophagy in modulating TAM plasticity and functional polarization in TME. In this review, we introduce the current understanding of autophagy‐regulated TAM function in development of cancer. We focus on how autophagy modulates antigen presentation, LC3‐associated phagocytosis, cytokine secretion, inflammasome regulation, recruitment, differentiation, and polarization of TAMs and suggest strategies for potential therapeutics by targeting autophagy in TAMs. We expect this review can provide a new notion of future cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Discovering the interactions between the persons mentioned in a set of topic documents can help readers construct the background of the topic and facilitate document comprehension. To discover person interactions, we need a detection method that can identify text segments containing information about the interactions. Information extraction algorithms then analyze the segments to extract interaction tuples and construct a network of person interaction. In this article, we define interaction detection as a classification problem. The proposed interaction detection method, called feature-based interactive segment recognizer (FISER), exploits 19 features covering syntactic, context-dependent, and semantic information in text to detect intra-clausal and inter-clausal interactive segments in topic documents. Empirical evaluations demonstrate that FISER outperformed many well-known relation extraction and protein-protein interaction detection methods on identifying interactive segments in topic documents. In addition, the precision, recall, and F1-score of the best feature combination are 72.9%, 55.8%, and 63.2%, respectively. [ABSTRACT FROM AUTHOR]

Aims: USP6 rearrangement underpins self‐limiting fibroblastic/myofibroblastic neoplasms, including nodular fasciitis (NF), myositis ossificans (MO), aneurysmal bone cyst (ABC), and related variants. The aim of this study was to characterise UPS6 and fusion partners in order to delineate the clinicopathological, genetic and bone‐forming features in such lesions of soft tissue (ST). Methods and results: Break‐apart fluorescence in‐situ hybridisation (FISH) validated USP6 rearrangement in 31 of 35 NF [comprising three of three fasciitis ossificans (FO) cases, seven of eight cellular variant of fibroma of tendon sheath (C‐FTS), four of six MO, three of three ST‐ABC, and two of two fibro‐osseous pseudotumours of digits (FOPD)]. As determined with FISH and reverse transcription polymerase chain reaction, MYH9–USP6 was the commonest fusion in four C‐FTS and 20 NF, including one intravascular case and two infantile (one retroperitoneal) cases. The presence of MYH9–USP6 confirmed the diagnosis of two NFs> 50 mm with prominent ischaemic necrosis. COL1A1–USP6 was predominant in ossifying lesions, including all FO, MO, ST‐ABC and FOPD with identified partner genes, and was also present in non‐ossifying head and neck NF (HN‐NF) and C‐FTS in two cases each. A cervical NF of a 14‐month‐old girl harboured the novel COL1A2–USP6. Ossifying lesions showed considerable genetic and morphological overlaps. Sharing COL1A1–USP6, FO and FOPD showed similar central or haphazard bone matrix deposition. Besides zonation of outward bone maturation, four COL1A1–USP6‐positive MO had incipient to sieve‐like pseudocysts reminiscent of ST‐ABC. Conclusion: MYH9–USP6 is present in some C‐FTS and most NF, including rare variants, but is unrelated to bone formation. All bone‐forming USP6‐rearranged lesions adopt COL1A1 as the 5′ partner, indicating close genetic kinships. However, COL1A1/COL1A2 also contributes to the pathogenesis of minor subsets of non‐ossifying USP6‐rearranged HN‐NF and C‐FTS. [ABSTRACT FROM AUTHOR]

Hutchinson–Gilford progeria syndrome (HGPS) is a rare laminopathy that produces a mutant form of prelamin A, known as Progerin, resulting in premature aging. HGPS cells show morphological abnormalities of the nuclear membrane, reduced cell proliferation rates, accumulation of reactive oxygen species (ROS), and expression of senescence markers. Lysophosphatidic acid (LPA) is a growth factor‐like lipid mediator that regulates various physiological functions via activating multiple LPA G protein‐coupled receptors. Here, we study the roles of LPA and LPA receptors in premature aging. We report that the protein level of LPA3 was highly downregulated through internalization and the lysosomal degradation pathway in Progerin‐transfected HEK293 cells. By treating Progerin HEK293 cells with an LPA3 agonist (OMPT, 1‐Oleoyl‐2‐O‐methyl‐rac‐glycerophosphothionate) and performing shRNA knockdown of the Lpa3r transcript in these cells, we showed that LPA3 activation increased expression levels of antioxidant enzymes, consequently inhibiting ROS accumulation and ameliorating cell senescence. LPA3 was shown to be downregulated in HGPS patient fibroblasts through the lysosomal pathway, and it was shown to be crucial for ameliorating ROS accumulation and cell senescence in fibroblasts. Moreover, in a zebrafish model, LPA3 deficiency was sufficient to cause premature aging phenotypes in multiple organs, as well as a shorter lifespan. Taken together, these findings identify the decline of LPA3 as a key contributor to the premature aging phenotypes of HGPS cells and zebrafish. [ABSTRACT FROM AUTHOR]