Volatile organic compounds for the detection of hepatocellular carcinoma—A scoping review

Hepatocellular carcinoma(HCC)is an increasingly common and the second leading cause of cancer mortality worldwide with a 5-year survival rate about 12%.Less than 20%of HCC patients are eligible to curative treatment owing to the late presentation.Clearly,there is a need for a readily accessible,early screening tool.This scoping review critically appraises and synthesizes the current published knowledge about the use of exhaled volatile organic compounds(VOCs)as a potential noninvasive means for HCC detection aiming to advance this nascent field.A systematic electronic search was conducted.The search strategy included all studies published until the 24th of March 2023 using a combination of relevant keywords.The search yielded 9 publications using the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines.Two of the studies described in vitro experiments,and seven clinical studies were conducted on small groups of patients.Overall,42 headspace gases were analyzed in the in vitro studies.Combined,the clinical studies included 420 HCC patients and 630 controls.The studies reported potential role for a combination of VOCs in the diagnosis of HCC.However,there is lack of consensus.Although there appears to be promise in VOCs research associated with HCC,there is no single volatile biomarker in exhaled breath attributed to HCC and data from extracted studies indicates a lack of standardization.Large multicentre population studies are required to verify the existence of VOCs linked to HCC.

A key role for PTP1B in dendritic cell maturation, migration, and T cell activation

Dendritic cells(DC)are the major antigen-presenting cells bridging innate and adaptive immunity,a function they perform by converting quiescent DC to active,mature DC with the capacity to activate naı¨ve T cells.They do this by migrating from the tissues to the T cell area of the secondary lymphoid tissues.Here,wedemonstrate thatmyeloid cell-specific genetic deletion of PTP1B(LysM PTP1B)leads to defects in lipopolysaccharide-driven bone marrow-derivedDC(BMDC)activation associated with increased levels of phosphorylated Stat3.We showthatmyeloid cell-specific PTP1Bdeletion also causes decreased migratory capacity of epidermal DC,aswell as reduced CCR7 expression and chemotaxis to CCL19 by BMDC.PTP1B deficiency in BMDC also impairs their migration in vivo.Further,immature LysM PTP1B BMDC display fewer podosomes,increased levels of phosphorylated Src at tyrosine 527,and loss of Src localization to podosome puncta.In co-culture with T cells,LysM PTP1B BMDC establish fewer and shorter contacts than control BMDC.Finally,LysMPTP1BBMDCfail to present antigen to T cells as efficiently as controlBMDC.These data provide first evidence for a key regulatory role for PTP1B in mediating a central DC function of initiating adaptive immune responses in response to innate immune cell activation.