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BACKGROUND: The objective of this review was to assess the quality and strength of the evidence provided by human observational studies for a causal association between exposure to radiofrequency electromagnetic fields (RF-EMF) and risk of the most investigated neoplastic diseases. METHODS: Eligibility criteria: We included cohort and case-control studies of neoplasia risks in relation to three types of exposure to RF-EMF: near-field, head-localized, exposure from wireless phone use (SR-A); far-field, whole body, environmental exposure from fixed-site transmitters (SR-B); near/far-field occupational exposures from use of hand-held transceivers or RF-emitting equipment in the workplace (SR-C). While no restrictions on tumour type were applied, in the current paper we focus on incidence-based studies of selected "critical" neoplasms of the central nervous system (brain, meninges, pituitary gland, acoustic nerve) and salivary gland tumours (SR-A); brain tumours and leukaemias (SR-B, SR-C). We focussed on investigations of specific neoplasms in relation to specific exposure sources (i.e. E-O pairs), noting that a single article may address multiple E-O pairs. INFORMATION SOURCES: Eligible studies were identified by literature searches through Medline, Embase, and EMF-Portal. Risk-of-bias (RoB) assessment: We used a tailored version of the Office of Health Assessment and Translation (OHAT) RoB tool to evaluate each study's internal validity. At the summary RoB step, studies were classified into three tiers according to their overall potential for bias (low, moderate and high). DATA SYNTHESIS: We synthesized the study results using random effects restricted maximum likelihood (REML) models (overall and subgroup meta-analyses of dichotomous and categorical exposure variables), and weighted mixed effects models (dose-response meta-analyses of lifetime exposure intensity). Evidence assessment: Confidence in evidence was assessed using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. RESULTS: We included 63 aetiological articles, published between 1994 and 2022, with participants from 22 countries, reporting on 119 different E-O pairs. RF-EMF exposure from mobile phones (ever or regular use vs no or non-regular use) was not associated with an increased risk of glioma [meta-estimate of the relative risk (mRR) = 1.01, 95 % CI = 0.89-1.13), meningioma (mRR = 0.92, 95 % CI = 0.82-1.02), acoustic neuroma (mRR = 1.03, 95 % CI = 0.85-1.24), pituitary tumours (mRR = 0.81, 95 % CI = 0.61-1.06), salivary gland tumours (mRR = 0.91, 95 % CI = 0.78-1.06), or paediatric (children, adolescents and young adults) brain tumours (mRR = 1.06, 95 % CI = 0.74-1.51), with variable degree of across-study heterogeneity (I2 = 0 %-62 %). There was no observable increase in mRRs for the most investigated neoplasms (glioma, meningioma, and acoustic neuroma) with increasing time since start (TSS) use of mobile phones, cumulative call time (CCT), or cumulative number of calls (CNC). Cordless phone use was not significantly associated with risks of glioma [mRR = 1.04, 95 % CI = 0.74-1.46; I2 = 74 %) meningioma, (mRR = 0.91, 95 % CI = 0.70-1.18; I2 = 59 %), or acoustic neuroma (mRR = 1.16; 95 % CI = 0.83-1.61; I2 = 63 %). Exposure from fixed-site transmitters (broadcasting antennas or base stations) was not associated with childhood leukaemia or paediatric brain tumour risks, independently of the level of the modelled RF exposure. Glioma risk was not significantly increased following occupational RF exposure (ever vs never), and no differences were detected between increasing categories of modelled cumulative exposure levels. DISCUSSION: In the sensitivity analyses of glioma, meningioma, and acoustic neuroma risks in relation to mobile phone use (ever use, TSS, CCT, and CNC) the presented results were robust and not affected by changes in study aggregation. In a leave-one-out meta-analyses of glioma risk in relation to mobile phone use we identified one influential study. In subsequent meta-analyses performed after excluding this study, we observed a substantial reduction in the mRR and the heterogeneity between studies, for both the contrast Ever vs Never (regular) use (mRR = 0.96, 95 % CI = 0.87-1.07, I2 = 47 %), and in the analysis by increasing categories of TSS ("<5 years": mRR = 0.97, 95 % CI = 0.83-1.14, I2 = 41 %; "5-9 years ": mRR = 0.96, 95 % CI = 0.83-1.11, I2 = 34 %; "10+ years": mRR = 0.97, 95 % CI = 0.87-1.08, I2 = 10 %). There was limited variation across studies in RoB for the priority domains (selection/attrition, exposure and outcome information), with the number of studies evenly classified as at low and moderate risk of bias (49 % tier-1 and 51 % tier-2), and no studies classified as at high risk of bias (tier-3). The impact of the biases on the study results (amount and direction) proved difficult to predict, and the RoB tool was inherently unable to account for the effect of competing biases. However, the sensitivity meta-analyses stratified on bias-tier, showed that the heterogeneity observed in our main meta-analyses across studies of glioma and acoustic neuroma in the upper TSS stratum (I2 = 77 % and 76 %), was explained by the summary RoB-tier. In the tier-1 study subgroup, the mRRs (95 % CI; I2) in long-term (10+ years) users were 0.95 (0.85-1.05; 5.5 %) for glioma, and 1.00 (0.78-1.29; 35 %) for acoustic neuroma. The time-trend simulation studies, evaluated as complementary evidence in line with a triangulation approach for external validity, were consistent in showing that the increased risks observed in some case-control studies were incompatible with the actual incidence rates of glioma/brain cancer observed in several countries and over long periods. Three of these simulation studies consistently reported that RR estimates > 1.5 with a 10+ years induction period were definitely implausible, and could be used to set a "credibility benchmark". In the sensitivity meta-analyses of glioma risk in the upper category of TSS excluding five studies reporting implausible effect sizes, we observed strong reductions in both the mRR [mRR of 0.95 (95 % CI = 0.86-1.05)], and the degree of heterogeneity across studies (I2 = 3.6 %). CONCLUSIONS: Consistently with the published protocol, our final conclusions were formulated separately for each exposure-outcome combination, and primarily based on the line of evidence with the highest confidence, taking into account the ranking of RF sources by exposure level as inferred from dosimetric studies, and the external coherence with findings from time-trend simulation studies (limited to glioma in relation to mobile phone use). For near field RF-EMF exposure to the head from mobile phone use, there was moderate certainty evidence that it likely does not increase the risk of glioma, meningioma, acoustic neuroma, pituitary tumours, and salivary gland tumours in adults, or of paediatric brain tumours. For near field RF-EMF exposure to the head from cordless phone use, there was low certainty evidence that it may not increase the risk of glioma, meningioma or acoustic neuroma. For whole-body far-field RF-EMF exposure from fixed-site transmitters (broadcasting antennas or base stations), there was moderate certainty evidence that it likely does not increase childhood leukaemia risk and low certainty evidence that it may not increase the risk of paediatric brain tumours. There were no studies eligible for inclusion investigating RF-EMF exposure from fixed-site transmitters and critical tumours in adults. For occupational RF-EMF exposure, there was low certainty evidence that it may not increase the risk of brain cancer/glioma, but there were no included studies of leukemias (the second critical outcome in SR-C). The evidence rating regarding paediatric brain tumours in relation to environmental RF exposure from fixed-site transmitters should be interpreted with caution, due to the small number of studies. Similar interpretative cautions apply to the evidence rating of the relation between glioma/brain cancer and occupational RF exposure, due to differences in exposure sources and metrics across the few included studies. OTHER: This project was commissioned and partially funded by the World Health Organization (WHO). Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; and ARPANSA as a WHO Collaborating Centre for Radiation Protection. REGISTRATION: PROSPERO CRD42021236798. Published protocol: [(Lagorio et al., 2021) DOI https://doi.org/10.1016/j.envint.2021.106828].

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Rationale: Pleomorphic adenoma (PA) is the most prevalent salivary gland tumour, accounting for 60%-80% of all benign salivary gland tumours, and frequently affects the parotid gland. Their epithelial and connective tissue origins can explain the 'pleomorphic' nature of tumours. This tumour is most common in women between 30 and 50 years. Patient Concerns: A 45-year-old female came with the chief complaint of a slow-growing, painless swelling on the left side of her face that had been present for 25 years. Diagnosis: PA of the parotid gland was diagnosed using computed tomography and fine-needle aspiration cytology. PA is a slowly progressing, asymptomatic swelling that rarely exceeds 6 cm in its greatest dimension; in our case, it was 13 cm × 10 cm and weighed 5 kg. Treatment: The ideal management is the surgical removal of the tumour mass, which was done under general anaesthesia. Early diagnosis and treatment planning was critical. Complete removal of the tumour without remnants is crucial to prevent a recurrence. Total parotidectomy was done in this case. Outcomes: There was no evidence of recurrence after comprehensive local surgical resection of the tumour during the follow-up period. Take-away Lessons: This case report is significant as it sheds light on the successful treatment approach for a large pleomorphic adenoma. It can provide valuable insights into the management of similar cases, potentially leading to improved patient outcomes and guiding future treatment strategies.

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Microsecretory adenocarcinoma (MSA) is a new type of salivary gland neoplasm identified in the 2022 World Health Organization Classification of Head and Neck Tumour (Skalova et al., Head Neck Pathol 16:40-53, 2022) and is characterized by a unique set of histomorphologic and immunohistochemical features and a recurrent MEF2C::SS18 fusion. MSA was initially misdiagnosed as another salivary gland tumour due to its similar morphology; until recently, only fewer than 50 cases were reported. We present a case of MSA of the hard palate with diverse architectural growth patterns, bland cytological features, abundant basophilic intraluminal secretions and fibromyxoid stroma. The tumour cells were positive for the SOX10, S100, and p63 protein and negative for the p40 protein according to immunohistochemistry. SS18 gene rearrangement was demonstrated via break-apart fluorescence in situ hybridization. We also provided a comprehensive literature review and integrated the clinicopathological features, immunophenotype, and molecular alterations of the disease. A comprehensive understanding of MSA enables us to accurately distinguish and categorize MSA from other salivary gland tumours with analogous morphologies.

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Rationale: Low-grade intraductal carcinoma (LG-IC), is a rare malignant tumour of the salivary glands which has a very good prognosis and must be differentiated from the other types of salivary gland malignant tumours, which have a totally different behaviour and a worse prognosis. Patient Concerns: A case is presented of a 52-year-old woman who was first diagnosed and treated in another clinic in 2019 for an LG-IC in the left submandibular gland space. Two years later, she was admitted to our department with a new lesion, this time in the upper jaw lip on the left side, which also turned out to be LG-IC. Diagnosis: Magnetic resonance imaging and positron emission tomography-computed tomography were performed in order to diagnose and adequately stage the disease prior to the therapeutic intervention. Outcomes: A 6-month follow-up reveals no sign of recurrence. Takeaway Lessons: Literature on this rare histopathological entity, as well as the differential diagnosis with the other malignant lesions of the salivary glands and the frequency of metastasis, were reviewed.

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c-KIT is an important diagnostic marker in salivary gland tumours and is expressed in most adenoid cystic carcinomas. Histologically similar salivary gland tumours with variable immunohistochemical expression for c-KIT pose a challenge and make diagnostic reliability ambivalent. An electronic search was performed in MEDLINE by PubMed, Google Scholar, Scopus, Trip, Cochrane Library, and EMBASE up to 31 December 2023, without period restriction. The articles that investigated CD117 or c-KIT in salivary gland tumours were included for review. Sensitivity, specificity, and positive and negative predictive values of c-KIT immunohistochemical expressions were derived and subjected to meta-analysis using Open Meta analyst for Sierra software. The risk of bias in selected studies was analysed using the QUADAS-2 tool, and RevMan 5.4 was used to output the result. Forty-three articles were reviewed, and 2285 salivary gland cases were analysed. Adenoid cystic carcinoma had an overall expression of 84.9%. A similar expression was found in epimyoepithelial carcinoma (79.1%), lymphoepithelial carcinoma (75%), myoepithelial carcinoma (60.8%), monomorphic adenoma (94.1%), and pleomorphic adenoma (74.7%). The sensitivity, specificity, and positive and negative predictive values of c-KIT/CD117 for adenoid cystic carcinoma with other salivary gland tumours were 84.99%, 69.09%, 84.79%, and 69.41%, respectively. Current evidence shows that c-KIT, despite its sensitivity, is not specific and therefore cannot be a useful diagnostic marker for distinguishing adenoid cystic carcinoma from other salivary gland tumours. Further research on other salivary gland tumours that exhibit comparable expression is necessary to validate the diagnostic accuracy of c-KIT.

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PURPOSE: The correct classification of salivary gland pathologies is crucial for choosing a treatment method and determining the prognosis. Better outcomes are now achievable thanks to the introduction of new therapy approaches, such as targeted therapies for malignant salivary gland tumors. To apply these in clinical routine, a clear classification of the lesions is required. METHODS: The following review examines all changes from the first World Health Organization (WHO) Classification of salivary gland pathologies from 1972 to fifth edition from 2022. Possible developments in the diagnosis and classification of salivary gland pathology are also presented. RESULTS: The current WHO classification is the fifth edition. With the development of new diagnostic methods, based on genetic alterations, it provides insight into the molecular basis of lesions. This has resulted in the evolution of classification, introduction of new entities and reclassification of existing ones. CONCLUSIONS: Genetic alterations will become increasingly more significant in the identification of salivary gland pathologies in the future. These alterations will be helpful as prognostic and predictive biomarkers, and may also serve as targets for anti-cancer therapies.

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Adenoid cystic carcinoma is a malignant neoplasm primarily of the salivary gland, which can also involve lacrimal glands and other exocrine glands. Adenoid cystic carcinoma rarely presents in the buccal mucosa and young children, and among the major salivary glands, it rarely occurs in the sublingual gland. We are presenting two cases of Grade 1- adenoid cystic carcinoma. One in the buccal mucosa of an eight-year-old boy and another in the sublingual gland of a 50-year-old female patient. The site and age of occurrence can make a huge difference in diagnosis and treatment planning due to the unpredictability of the lesion. Proper diagnosis, treatment planning, and appropriate treatment help improve the lesion's prognosis. Even though such lesions rarely occur, awareness among the Oral and maxillofacial fraternity is very important in providing proper patient care.

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AIMS: The discovery of tumour type-specific gene fusion oncogenes in benign and malignant salivary gland and sinonasal (SGSN) tumours has significantly increased our knowledge about their molecular pathology and classification. METHODS AND RESULTS: We developed a new targeted multiplexed next-generation sequencing (NGS)-based method that utilizes ligation dependent reverse-transcriptase polymerase chain reaction (LD-RT-PCR) to detect oncogenic fusion transcripts involving 116 genes, leading to 96 gene fusions known to be recurrently rearranged in these tumours. In all, 180 SGSN tumours (formalin-fixed, paraffin-embedded samples, 141 specimens and 39 core needle biopsies) from the REFCORpath (French network for rare head and neck cancers) with previously identified fusion genes by fluorescent in situ hybridisation (FISH), RT-PCR, or molecular immunohistochemistry were selected to test its specificity and sensitivity and validate its diagnostic use. Tested tumours encompassed 14 major tumours types, including secretory carcinoma, mucoepidermoid carcinoma, adenoid cystic carcinoma, salivary gland intraductal carcinoma, clear cell carcinoma, pleomorphic adenoma, adamantinoma-like Ewing Sarcoma, EWSR1::COLCA2 sinonasal sarcoma, DEK::AFF2 sinonasal carcinoma, and biphenotypic sinonasal sarcoma. In-frame fusion transcripts were detected in 97.8% of cases (176/180). Gene fusion assay results correlated with conventional techniques (immunohistochemistry [IHC], FISH, and RT-PCR) in 176/180 tumours (97.8%). CONCLUSION: This targeted multiplexed NGS-based LD-RT-PCR method is a robust, highly sensitive method for the detection of recurrent gene fusions from routine clinical SGSN tumours. It can be easily customized to cover new fusions. These results are promising for implementing an integrated NGS system to rapidly detect genetic aberrations, facilitating accurate, genomics-based diagnoses, and accelerate time to precision therapies in SGSN tumours.

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Purpose: To determine the role of functional magnetic resonance imaging techniques (diffusion-weighted magnetic resonance imaging [DW-MRI] and dynamic contrast-enhanced magnetic resonance imaging [DCE-MRI]) in the differentiation of various salivary gland tumours. Material and methods: In this prospective study, we evaluated 32 patients with salivary gland tumours using functional MRI. Diffusion parameters (mean apparent diffusion coefficient [ADC], normalized ADC and homogeneity index [HI]),semiquantitative DCE parameters (time signal intensity curves [TICs]) and quantitative DCE parameters (Kep, Ktrans and Ve) were analysed. Diagnostic efficiencies of all these parameters were determined to differentiate benign and malignant tumours as well as to characterize 3 major subgroups of salivary gland tumours, namely pleomorphic adenoma, Warthin tumour, and malignant tumours. Results: Mean ADC, normalized ADC and HI were insignificant in differentiating benign and malignant tumours but were significant in differentiating pleomorphic adenomas, Warthin tumours, and malignant tumours. Mean ADC was the best parameter in predicting both pleomorphic adenomas and Warthin tumours (AUC: 0.95 and 0.89, respectively). Amongst DCE parameters, only TIC pattern could differentiate between benign and malignant tumours, with an accuracy of 93.75% (AUC: 0.94). The quantitative perfusion parameters aided greatly in characterizing pleomorphic adenomas, Warthin tumours and malignant tumours. For predicting pleomorphic adenomas, the accuracy of Kep and Ktrans was 96.77% (AUC: 0.98) and 93.55% (AUC: 0.95), respectively and for predicting Warthin tumours, the accuracy of both Kep and Ktrans was 96.77% (AUC: 0.97). Conclusions: DCE parameters (particularly TIC, Kep and Ktrans) had higher accuracy in characterizing various tumour subgroups (pleomorphic adenomas, Warthin tumours, and malignant tumours) than DWI parameters. Hence, dynamic contrast-enhanced imaging adds immense value with only a minimum time penalty to the examination.

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Tumors of the salivary gland are a group of complex, heterogeneous lesions that are located either in the parotid gland, submandibular gland, sublingual gland, or minor salivary glands. These tumors have a wide range of etiology, pathophysiology, treatment, and prognosis. Multiple salivary gland tumors are extremely rare and usually occur more commonly in major salivary glands than in minor glands. A 61-year-old man with a chief complaint of swelling in the upper jaw for the past eight years reported to the department of oral and maxillofacial surgery. Incisional biopsy revealed a canalicular adenoma (CA) of the minor salivary gland of the palate. Wide local excision was done with closure using a buccal pad of fat and a collagen sheet. Surprisingly, the excisional biopsy was suggestive of synchronous low-grade polymorphous adenocarcinoma (PAC) with CA of the minor salivary gland of the palate. This appears to be the first reported case of PAC with CA found in the palate.

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Salivary gland tumours (SGT) demonstrate geographical variation. The primary objective of this study was to determine the types, frequency, distribution, and demographics of non-neoplastic and neoplastic salivary gland pathology at Waikato Hospital, New Zealand (NZ) over a 10-year period. Following this we conducted a 10-year retrospective review of SGT epidemiology from international literature. In total 825 patients were identified, 31% (256/825) with non-neoplastic salivary gland pathology, 34% (284/825) with benign neoplastic pathology, 14% (118/825) with primary malignant lesions, 18% (146/825) with metastatic SGTs, and 3% (21/825) with lymphoma. Patients had a mean (range) age of 58 (3-102) years, were predominantly male (58%, 476/825), and NZ European (65%, 536/825). Tumours were most prevalent in the parotid gland (85%, 484/569), of which 44% (211/484) were malignant. Pleomorphic adenoma was the most common benign (71%, 203/284) and overall (36%, 203/569) tumour, while mucoepidermoid carcinoma (25%, 29/118) and squamous cell carcinoma (SCC) (73%, 106/146) were the most common primary malignant and metastatic SGTs, respectively. Our literature review identified 18 studies consisting of 33,933 patients, of whom 71% (24,013/33,933) had benign SGTs. Pleomorphic adenoma (68%, 16404/24013) and mucoepidermoid carcinoma (29%, 2826/9621) were the most common benign and malignant SGTs, respectively. Low numbers of non-neoplastic and metastatic SGTs were reported in the literature. This research provides a greater understanding of differences in their global distribution. Consistent with previous literature, pleomorphic adenoma and mucoepidermoid carcinoma were the most common benign and malignant SGTs. In NZ, we found high rates of malignant SCC to the parotid gland, consistent with the epidemiology of non-melanoma skin cancer in the country.

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BACKGROUND: Salivary gland tumours (SGT) are a relatively rare group of neoplasms with a wide range of histopathological appearance and clinical features. To date, most of the epidemiological studies on salivary gland tumours are limited for a variety of reason including being out of date, extrapolated from either a single centre or country studies, or investigating either major or minor glands only. METHODS: This study aimed to mitigate these shortcomings by analysing epidemiological data including demographic, anatomical location and histological diagnoses of SGT from multiple centres across the world. The analysed data included age, gender, location and histological diagnosis from fifteen centres covering the majority of the world health organisation (WHO) geographical regions between 2006 and 2019. RESULTS: A total of 5739 cases were analysed including 65% benign and 35% malignant tumours. A slight female predilection (54%) and peak incidence between the fourth and seventh decade for both benign and malignant tumours was observed. The majority (68%) of the SGT presented in major and 32% in the minor glands. The parotid gland was the most common location (70%) for benign and minor glands (47%) for malignant tumours. Pleomorphic adenoma (70%), and Warthin's tumour (17%), were the most common benign tumours whereas mucoepidermoid carcinoma (26%) and adenoid cystic carcinoma (17%) were the most frequent malignant tumours. CONCLUSIONS: This multicentre investigation presents the largest cohort study to date analysing salivary gland tumour data from tertiary centres scattered across the globe. These findings should serve as a baseline for future studies evaluating the epidemiological landscape of these tumours.

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Salivary gland tumors are diagnostically challenging owing to the morphological diversity within any tumor type and overlapping histomorphology and immunohistochemistry amongst different tumours. In past two decades, rapid progress has been made in the field of understanding the pathogenesis of these tumours with the discovery of many tumour specific translocations and rearrangements. This includes CRTC1-MAML2 and CRTC-MAML2 in mucoepidermoid carcinoma, MYBNFIB and MYBL1-NFIB fusions in adenoid cystic carcinoma, PLAG1 and HMGA2 in pleomorphic adenoma, ETV6-NTRK3 in secretory carcinoma, NR4A3 rearrangements in acinic cell carcinoma, PRKD1 mutations in polymorphous adenocarcinoma and EWSR1-ATF1 in clear cell carcinoma. This review is a lens for progress made till date in the molecular pathology of salivary gland tumours with a special focus on their role as diagnostic tools and implications on clinical management of the patient as prognostic and predictive markers.

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The aim of the present systematic review was to critically analyse the relationship between tumour suppressor genes (TSGs) promoter methylation, a potent mechanism of gene silencing, and the development of salivary gland tumours, as well as the possible effect on clinical/histological characteristics. Review protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO) database (registration ID CRD42020218511). A comprehensive search of Web of Science, Scopus, PubMed, and Cochrane Central Register of Controlled Trials was performed utilizing relevant key terms, supplemented by a search of grey literature. Newcastle-Ottawa Quality Assessment Scale (NOQAS) was used for the quality assessment of included studies. Sixteen cross-sectional and 12 case-control studies were included in the review, predominantly dealing with methylation in TSGs related to DNA repair, cell cycle, and cell growth regulation and differentiation. Quantitative synthesis could be performed on P16 (inhibitor of cyclin-dependent kinase 4a), RASSF1A (Ras association domain family 1 isoform A) and MGMT (O6-methylguanine DNA methyltransferase) genes only. It showed that P16 and RASSF1A genes were more frequently methylated in salivary gland tumours compared to controls (P = .0002 and P < .0001, respectively), while no significant difference was observed for MGMT. Additionally, P16 did not appear to be related to malignant transformation of pleomorphic adenomas (P = .330). In conclusion, TSG methylation is involved in salivary gland tumour pathogenesis and several genes might play a considerable role. Further studies are needed for a better understanding of complex epigenetic deregulation during salivary gland tumour development and progression.

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Salivary gland lesions comprise for about 2-6.5% of all head and neck neoplasms in adults. They are accessible for FNAC (Fine Needle Aspiration Cytology). The risk of fistula formation and/or tumour implantation are low compared to surgical biopsy. FNAC can also provide a distinction between asalivary and non-salivary lesion, benign and malignant lesions. 67 patients were studied prospectively over 5 years. FNAC was performed pre-operatively and histopathological examination post-operatively in patients who underwent surgery and were willing to participate in the study. 59.7% of the lesions were non-neoplastic and 58.2% were neoplastic (37.3% benign and 20.8% malignant). Pleomorphic adenoma was the most common benign neoplasm while mucoepidermoidand adenoid cystic carcinoma both were the most frequent malignant lesion. Among the non-neoplastic lesions, the most number of cases were of chronic sialadentis. In our study, FNAC has a sensitivity of 94.54% specificity of 80.95% for neoplastic lesions. It was seen that FNAC was a useful diagnostic tool in the evaluation of salivary gland lesions because of its simplicity, excellent patient compliance and rapid diagnosis. This cost effective tool is invaluable in planning the surgical management of the patient.

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Background: Salivary gland tumours are relatively uncommon, and there exists considerable diagnostic difficulty. This is due to individual lesions having diverse histopathological features, presence of number of types and variants, and overlapping histological features in different tumour entities. Aim: The current study aimed at assessing the expression of centromere protein F (CENPF) in benign and malignant salivary gland tumours and to evaluate the efficacy of CENPF as a proliferative marker to aid in the diagnosis of malignancy so that it will help in surgical pathology practice. Materials and Methods: The study group involved 20 cases of benign salivary gland tumours, 20 cases of malignant salivary gland tumours, and 10 normal salivary gland tissues. All the cases were subjected to immunohistochemical analysis for CENPF expression and were assessed by two independent observers and further taken up for evaluation. Statistical Analysis: The results were analysed statistically among different groups using analysis of variance (ANOVA) or Kruskal-Wallis test with Chi-squared test using IBM's Statistical Package for the Social Sciences (SPSS) version 17.0. Results: CENPF expression in normal salivary gland was negative with gradual increase in expression from benign salivary gland tumours to malignant salivary gland tumours. CENPF expression was high in malignant salivary gland tumours. Conclusion: Findings of the study suggest that CENPF can be regarded as a new cell proliferation marker for malignant salivary gland tumours.

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Little attention has been paid to immunohistochemically assessed, lysosomal activities in salivary neoplasia. In an attempt to remedy this, the present investigation applied immunohistochemistry for CD63 antigen (a lysosomal membranous protein) and HSP27 (a molecular chaperone with roles in intracellular homeostasis) to archival paraffin-embedded surgical specimens of 101 benign and malignant, epithelial salivary tumours. Diffuse cytoplasmic CD63 immunoreactivity was seen in serous cells in acinic cell carcinoma, and mucous cells in mucoepidermoid carcinoma, pleomorphic adenoma (PA) and Warthin tumour. Apical rims or bands of CD63 immunoreactivity were also seen in simple cells lining tubular structures in PA, acinic cell carcinoma, mucoepidermoid carcinoma and polymorphous (low-grade) adenocarcinoma; and, occasionally, oncocytic luminal cells in Warthin tumour. HSP27 immunoreactivity was usually seen in non-luminal cells of PA, basal cells of oncocytic tumours, epidermoid cells of mucoepidermoid carcinoma and PA, and cells outlining aggregates or pseudolumina of adenoid cystic carcinoma. Expression of CD63 is preferentially associated with differentiated or simple luminal cell phenotypes in epithelial salivary tumours and possibly reflects autophagy of secretory granules or absorption of luminal material. Expression of HSP27 is preferentially associated with non-luminal cells and possibly reflects remodelling of the cytoskeleton.

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BACKGROUND: The World Health Organization (WHO) has an ongoing project to assess potential health effects of exposure to radiofrequency electromagnetic fields (RF-EMF) in the general and working population. Here we present the protocol for a systematic review of the scientific literature on cancer hazards from exposure to RF-EMF in humans, commissioned by the WHO as part of that project. OBJECTIVE: To assess the quality and strength of the evidence provided by human observational studies for a causal association between exposure to RF-EMF and risk of neoplastic diseases. ELIGIBILITY CRITERIA: We will include cohort and case-control studies investigating neoplasia risks in relation to three types of exposure to RF-EMF: near-field, head-localized, exposure from wireless phone use (SR-A); far-field, whole body, environmental exposure from fixed-site transmitters (SR-B); near/far-field occupational exposures from use of handheld transceivers or RF-emitting equipment in the workplace (SR-C). While no restriction on tumour type will be applied, we will focus on selected neoplasms of the central nervous system (brain, meninges, pituitary gland, acoustic nerve) and salivary gland tumours (SR-A); brain tumours and leukaemias (SR-B, SR-C). INFORMATION SOURCES: Eligible studies will be identified through Medline, Embase, and EMF-Portal. RISK-OF-BIAS ASSESSMENT: We will use a tailored version of the OHAT's tool to evaluate the study's internal validity. DATA SYNTHESIS: We will consider separately studies on different tumours, neoplasm-specific risks from different exposure sources, and a given exposure-outcome pair in adults and children. When a quantitative synthesis of findings can be envisaged, the main aims of the meta-analysis will be to assess the strength of association and the shape of the exposure-response relationship; to quantify the degree of heterogeneity across studies; and explore the sources of inconsistency (if any). When a meta-analysis is judged inappropriate, we will perform a narrative synthesis, complemented by a structured tabulation of results and appropriate visual displays. EVIDENCE ASSESSMENT: Confidence in evidence will be assessed in line with the GRADE approach. FUNDING: This project is supported by the World Health Organization. Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; ARPANSA as a WHO Collaborating Centre for Radiation Protection. REGISTRATION: PROSPERO CRD42021236798.

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RESUMEN

Adenoid cystic carcinoma (ACC) is a relatively rare tumour of the minor and major salivary glands. It is uncommon in the parotid gland while it is much more frequent in the submandibular gland and in minor salivary and mucinous glands (oral cavity, oropharynx, and paranasal sinuses). ACC may also arise in secretory glands located in other tissues, such as in the tracheobronchial tree, oesophagus, breast, lungs, prostate, uterine cervix, lachrymal and Bartholin's glands, and skin. The natural history of ACC is characterised by an indolent growth rate, a relatively low probability of regional lymph node metastases and a high likelihood of haematogenous dissemination. ACC has been traditionally subdivided into three histological groups (cribriform, tubular, and solid) based on solid components of the tumour. Some studies have shown that tumours with a solid growth component have a rapid fatal course, compared to tumours without a solid growth component, but other studies have failed to correlate growth patterns with clinical course. The purpose of this review is to analyse the very large number of studies (sometimes contradictory) on ACC. In this first part, the aetiology, epidemiology, histopathology, clinical behaviour and diagnostic workup are examined.^ieng

Il carcinoma adenoide cistico (ACC) è un tumore relativamente raro ad origine dalle ghiandole salivari minori e maggiori. È poco frequente nella parotide mentre lo è molto di più nella ghiandola sottomandibolare, nelle ghiandole salivari minori e in quelle mucinose del cavo orale, orofaringe e seni paranasali. Esso può anche insorgere nelle ghiandole secretrici localizzate in altri tessuti come l'albero tracheo-bronchiale, l'esofago, la mammella, il polmone, la prostata, la cervice uterina, la cute, le ghiandole lacrimali e quelle del Bartolini. La sua storia naturale è caratterizzata da una lenta crescita, da rare metastasi linfonodali e da frequenti metastasi a distanza. Dal punto di vista istologico esso è stato tradizionalmente suddiviso in tre forme (cribriforme, tubulare e solido). Alcuni studi hanno dimostrato che i tumori con una prevalente componente solida hanno una prognosi peggiore rispetto a quelli con prevalente componente cribriforme o tubulare ma altri studi hanno contestato questa affermazione. Il proposito di questa review è quello di analizzare il grande numero di pubblicazioni (talvolta contraddittorie) sul carcinoma adenoide cistico. In questa prima parte saranno discusse l'eziologia, l'epidemiologia, l'istopatologia, la presentazione clinica e l'iter diagnostico.

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