Development Of Cancer In Patients Research Articles

Estimating cancer risk in immune-mediated inflammatory diseases exposed to varying doses of tumour necrosis factor inhibitors.

The safety profile of high doses of tumour necrosis factor inhibitors (TNFi) therapy for cancer risk in immune-mediated inflammatory diseases (IMIDs) remains uncertain. We evaluated the risk of cancer development in patients with IMIDs exposed to standard and high doses of TNFi compared with those never exposed to TNFi. A cohort study was conducted using the Japanese claims database encompassing over 4.6 million individuals from 2013 to 2021. The study included patients aged 16years or older with new-onset IMIDs, such as inflammatory bowel disease, rheumatoid arthritis, or psoriasis, who had no cancer history. The subdistribution hazard ratios (SHR) for cancer risk in TNFi standard and high dose groups comparing with TNFi unexposed group were estimated using a Fine and Gray model that accounted for the competing risk of death unrelated to cancer. The high dose of TNFi was defined as either a dose escalation or shortening of the intervals during administrations from the standard dose treatment. We identified a total of 42,006 patients with new-onset IMIDs (40,573 in TNFi unexposed, 876 in TNFi standard dose, and 557 in TNFi high dose) and 1211 (2.8%) patients developed cancer, yielding an incidence rate of 787.8 (739.9-828.1) per 100,000 person-years. Neither the standard nor high doses of TNFi significantly increased the cancer risk (TNFi standard dose vs. TNFi unexposed, adjusted SHR, 0.65 [0.40-1.08]; TNF high dose vs. TNFi unexposed, adjusted SHR, 1.12 [0.67-1.87]). There is no association between varying doses of TNFi therapy and cancer risk in IMIDs.

The risk of malignancy in patients with psoriasis treated with long-term tumor necrosis factor-α inhibitor: a systematic review and meta-analysis.

The relationship between tumor necrosis factor-α inhibitors (TNFi) and cancer risk is complex, given their pivotal role in managing chronic inflammatory conditions. Persistent concerns about TNFi therapy potentially increasing cancer risk necessitate a thorough understanding of its long-term effects on cancer development in patients with psoriasis to guide therapeutic decision-making. This systematic review and meta-analysis aimed to evaluate the association between long-term TNFi therapy and cancer risk in patients with psoriasis. Data were collected from PubMed, Embase, and the Cochrane Library, from their inception to January 1, 2024. The studies included adults with psoriasis or psoriatic arthritis receiving TNFi, presenting standardized incidence ratio (SIR) data for cancer. Data extraction followed PRISMA guidelines, with independent extraction by two authors, and pooled data synthesis was conducted using a random-effects model. The primary outcomes were SIRs for all cancers excluding non-melanoma skin carcinoma (NMSC) and for NMSC itself. The secondary outcome was the SIR of specific cancer types. The meta-analysis included eight studies with a total of 32,765 psoriasis patients. The pooled results showed no increased risk of cancers, including all cancers excluding NMSC, melanoma, lymphoma, prostate cancer, and breast cancer, among individuals receiving long-term TNFi therapy for psoriasis compared to the general population. However, subgroup analysis found an elevated risk of NMSC in patients with psoriatic arthritis and a significant increase in the risk of squamous cell carcinoma (SCC) among psoriasis patients treated with TNFi compared to the general population (SIR, 1.84; 95% CI, 1.16 - 2.92 and SIR, 2.84; 95% CI, 1.64 - 4.91, respectively). Our systematic review and meta-analysis indicate that most cancers examined did not demonstrate an increased risk following long-term TNFi therapy in psoriasis patients. However, for patients with psoriatic arthritis or those at high risk of SCC, these findings underscore the importance of personalized treatment strategies that weigh individual risks and benefits.

Pirfenidone and risk of lung cancer development in IPF: a nationwide population-based study.

Idiopathic pulmonary fibrosis (IPF) carries a high risk of lung cancer, but the effect of pirfenidone on lung cancer development remains uncertain. We investigated the association between pirfenidone use and lung cancer development in patients with IPF. We included 10 084 patients with IPF from the national claims database. Propensity score analysis with inverse probability of treatment weighting (IPTW) and landmark analyses were employed to evaluate lung cancer occurrence according to pirfenidone use. The association was evaluated using Cox regression models adjusted for clinical and socioeconomic variables. A single-center IPF clinical cohort (n=941) was used for validating the findings. The mean patient age was 69.4 years, 73.8% were men, and 31.6% received pirfenidone. Lung cancer developed in 766 patients with IPF (7.6%; 21.9 cases per 1000 person-years) during a median follow-up of 3.0 years. After IPTW, the pirfenidone group showed lower incidence (10.4 versus 27.9 cases per 1000 person-years) than the no-pirfenidone group. Landmark analysis at 6 months after IPF diagnosis also showed lower incidence of lung cancer in the pirfenidone group than in the no-pirfenidone group. Pirfenidone use was independently associated with a reduced lung cancer risk (weighted adjusted hazard ratio [HR]: 0.347; 95% confidence interval [CI]: 0.258-0.466). A clinical cohort showed similar association (weighted adjusted HR: 0.716; 95% CI: 0.517-0.991). The association persisted across subgroups defined by age or sex. Pirfenidone use may be associated with a reduced lung cancer risk in patients with IPF.

Analysis of the correlation between gut microbiome imbalance and the development of endometrial cancer based on metagenomics.

Endometrial cancer (EC) is the most prevalent gynecologic malignancy, with a higher risk in obese women, suggesting the potential involvement of gut microbiota in the progression of EC. However, there is no direct evidence of a connection between EC and the human gut microbiota. Using metagenomic sequencing, we investigated the relationship between gut microbiome imbalance and cancer development in patients with EC. In this prospective case-control study, we included 15 patients with EC based on endometrial biopsy in the case group and 15 women admitted to the hospital for female pelvic floor issues during the same time who did not have endometrial lesions from January 2023 to June 2023 in control group. The microbiota structure of EC cases and controls without benign or malignant endometrial lesions during the same time period was analyzed using metagenomic sequencing technology. We employed Alpha diversity analysis to reflect the richness and diversity of microbial communities. Statistical algorithm Bray-Curtis was utilized to calculate pairwise distances between samples, obtaining a beta diversity distance matrix. Subsequently, hierarchical clustering analysis was conducted based on the distance matrix. The results showed that the composition of bacterial colonies in both groups was dominated by Firmicutes, which had a higher proportion in the control group, followed by Bacteroidetes in the control group and Proteobacteria and Bacteroidetes in the case group. The abundance of Klebsiella (P = .02) was significantly higher, and the abundance of Alistipes (P = .04), Anearobutyricum (P = .01), and bacteria in Firmicutes such as Oscillospira and Catenibacterium was markedly lower in the case group than in the control group. These results demonstrated conclusively that a gut microbiome imbalance was associated with the development of EC.

Long term follow up of monoclonal gammopathy of undetermined significance (MGUS) in US Veterans: Racial differences and associations with other malignancies.

7573 Background: Monoclonal gammopathy of undetermined significance (MGUS) is associated with lymphoid malignancies such as lymphoma and myeloma, but the association with other malignancies has not been described in the US veteran population. Methods: Veterans diagnosed with MGUS from 1991-2023 were identified from the US Veteran Affairs Central Cancer Registry (VACCR). Age at the diagnosis of MGUS was divided into four categories of <60, 60-69, 70-79, 80+. Variables collected included demographic factors and the diagnosis of other cancers. Differences were analyzed using the Chi Square test. Results: There were 3975 veterans who met the criteria. Most patients were male (96.7%) with a median age at diagnosis of MGUS of 70.5 (IQR 65.4-76.0). Almost 1/3 of patients were Black and were diagnosed with MGUS at a younger age compared to White veterans (Table, p<0.0001). Over the 32-year period included in this study, 2/3 of patients remained with a diagnosis of MGUS (62.3%) alone whereas 29.4% had 1 additional malignancy diagnosed and 8.3% had 2 or more additional malignancies. Black veterans with MGUS were more likely to have additional malignancies than white patients (41.4% vs 35.9%, p=0.016). MGUS was diagnosed prior to other cancers in 52% of patients and afterward in 48%. The most common cancers diagnosed in patients with MGUS were prostate (31%), lymphomas (13%), GI (12.5%), lung (12.0%), and skin (6.8%). CLL (3.4%), LPL (3.0%). Among lymphomas, CLL (3.4%) and LPL (3.0%) were most common. Of note, multiple myeloma or plasmacytoma was diagnosed in 6.5% of patients. The proportion of patients with MGUS and additional malignancies was comparable in the 4 age cohorts (p=0.072), indicating that younger patients with MGUS were as likely to be diagnosed with additional malignancies as older patients. Conclusions: In US veterans, nearly 1/3 of those diagnosed with MGUS were Black. These patients were younger when diagnosed with MGUS and were more likely to develop additional malignancies compared to White veterans. Over the 32 years of this study, a considerable proportion of veterans with MGUS developed various solid tumors. Further investigation is warranted to understand the racial, genetic, and other factors that may be contributing to the development of cancers in patients with MGUS. [Table: see text]

Association of adipose tissue mediators with the development of cancer in patients with metabolic syndrome

The aim of the study was to summarize the available data on the relationship between adipose tissue mediators and cancer in patients with metabolic syndrome. Material and methods. A literature search was conducted using the PubMed and eliBRARY databases. Of the 400 articles published over the past 20 years, 58 studies were included in the review. Results. There is evidence of an unfavorable course of cancer in patients with metabolic syndrome that is explained by the presence of common pathogenetic pathways. In this review, special attention is paid to adipose tissue mediators that regulate the course of inflammation. The involvement of adipose tissue mediators in the pathogenesis of cancer is discussed. The relationship between adipokines of adipose tissue and the effects of specialized pro-resolving mediators (SpRM), which are metabolites of polyunsaturated fatty acids (resolvins, protectins and maresins), are considered. the associations of mediators that regulate the intensity of inflammation with the metabolic syndrome and cancer are discussed. Conclusion. Further studies will contribute to a better understanding of the relationship between metabolic syndrome and cancer and the search for adequate predictive markers to select the most effective drug strategy for correcting metabolic syndrome.

Cancer-Causing Effects of Orthopaedic Metal Implants in Total Hip Arthroplasty.

Metal implants have been preferentially used in THA due to its biocompatibility, mechanical stability and durability. Yet concerns have emerged regarding their potential to release metallic ions, leading to long-term adverse effects, including carcinogenicity. This study aimed to investigate the risk of cancer development in patients with orthopaedic metal implants in total hip arthroplasty (THA). Patients with THA conducted at a local tertiary implant centre from 2001-2008 were linked to the local cancer registry and followed up to the end of 2023. Standardized incidence ratios (SIRs) for cancer incidence and its confidence interval by Poisson distribution were calculated. Survival analysis was depicted using the Kaplan-Meier method, and the log-rank test was used to assess the differences across groups. The study cohort included 388 patients and 53 cancers diagnosed during follow-up, at least 5 years post THA. All-site cancer risks were increased in patients with THA (SIR: 1.97; 95% CI: 1.48-2.46), validated with chi-square analysis (chi-square = 15.2551, N = 100,388, p < 0.01). A statistically significant increase in multiple site-specific cancers including haematological cancers were identified. Patients with THA were found to have an increased risk for cancer compared to the general population during a mean follow-up of 16 years.

Analysis of the Expression of LSF Transcription Factor in the Regulation of Transcription and TSG101 during the Neoplastic Transformation of Endometrial Cells.

Previous research indicates that carcinogenesis involves disrupting the functions of numerous genes, including factors involved in the regulation of transcription and cell proliferation. For these reasons, in endometrial carcinogenesis, we decided to investigate the expression of TSG101 (a suppressor of tumor transformation) and LSF (a transcription factor involved in numerous cellular processes, such as cell cycle regulation, cell growth, development, and apoptosis). LSF may be involved in the regulation of TSG101 expression. The research material consisted of endometrial cancer samples from 60 patients. The control group consisted of normal endometrium samples donated by 60 women undergoing surgery for benign diseases of the female reproductive organs. The samples were subjected to immunohistochemical staining with antibodies specific to TSG101 and LSF. Specific antibodies were used to identify TSG101 and LSF in the examined histopathological preparations. An approximately 14-fold lower risk of endometrial cancer development was observed in patients with TSG expression in more than 75% of the assessed cells (4% vs. 36%; OR = 0.07; p = 0.0182). There was a four-fold lower risk of endometrial cancer development in patients with LSF expression in more than 50% of the assessed cells (32% vs. 64%; OR = 0.26; p = 0.0262). A more than three-fold lower risk of endometrial cancer development was observed in patients with LSF expression in more than 75% of the assessed cells (24% vs. 52%; OR = 0.29; p = 0.0454). Endometrial cancer was diagnosed in those with a lower level of TSG101 expression than in those with a cancer-free endometrium. Decreased expression of TSG101 may be a marker of endometrial cancer, and increased expression of LSF when diagnosed with endometrial cancer may indicate greater advancement of the disease. These markers might be used as diagnostic and prognostic markers-however, there is a lack of a correlation between them.

Impact of smoking reduction on lung cancer risk in patients with COPD who smoked fewer than 30 pack-years: a nationwide population-based cohort study

BackgroundThe effects of smoking reduction on the incidence of lung cancer in patients with chronic obstructive pulmonary disease (COPD) are not well known. This study aimed to investigate the effects of changes in smoking habits after COPD diagnosis on lung cancer development in patients who smoked less than 30 pack-years.MethodsThis nationwide retrospective cohort study included 16,832 patients with COPD who smoked less than 30 pack-years at the time of COPD diagnosis. Based on changes in smoking habits in the health screening examination data, smokers were categorized into three groups: quitters, reducers, and sustainers. The primary outcome was the risk of lung cancer development, which was estimated using the Cox proportional hazards model. We also modelled the amount of smoking reduction as a continuous variable.ResultsDuring a median follow-up of 4 years, the cumulative incidence of lung cancer was the highest among sustainers, followed by reducers and quitters. Compared with sustainers, reducers (adjusted HR 0.74, 95% CI:0.56–0.98) and quitters (adjusted HR 0.78, 95% CI:0.64–0.96) had a significantly lower risk of lung cancer. Incidence of lung cancer showed a decreasing trend with a decreasing amount of smoking (P for linearity < 0.01).ConclusionsIn patients with COPD who smoked less than 30 pack-years, smoking reduction and cessation lowered the risk of lung cancer.

Esophageal cancer in an adult with congenital esophageal stenosis: a case report

BackgroundCongenital esophageal stenosis (CES) is a rare condition. We encountered a case of esophageal cancer that developed in an adult with persistent CES. Although many studies have investigated the therapeutic outcomes and performed surveillance for symptoms after treatment for CES, few have performed long-term surveillance or reported on the development of esophageal cancer. We report this case because it is extremely rare and has important implications.Case presentationA 45-year-old woman with worsening dysphagia was transferred to our hospital. The patient was diagnosed with CES at 5 years of age and underwent surgery at another hospital. The patient underwent esophageal dilatation for stenosis at 36 years of age. Esophagoscopy performed at our hospital revealed a circumferential ulcerated lesion and stenosis 15–29 cm from the incisors. Histological examination of the biopsy specimen revealed squamous cell carcinoma. Computed tomography (CT) revealed abnormal circumferential wall thickening in parts of the cervical and almost the entire thoracic esophagus. 18F-fluorodeoxyglucose-positron emission tomography-CT revealed increased uptake in the cervical and upper esophagus. No uptake was observed in the muscular layers of the middle or lower esophagus. Based on these findings, the patient was diagnosed with clinical stage IVB cervical and upper esophageal cancer (T3N1M1 [supraclavicular lymph nodes]). The patient underwent a total esophagectomy after neoadjuvant chemotherapy. The esophagus was markedly thickened and tightly adhered to the adjacent organs. Severe fibrosis was observed around the trachea. Marked thickening of the muscular layer was observed throughout the esophagus; histopathological examination revealed that this thickening was due to increased smooth muscle mass. No cartilage, bronchial epithelium, or glands were observed. The carcinoma extended from the cervical to the middle esophagus, oral to the stenotic region. Finally, we diagnosed the patient with esophageal cancer developing on CES of the fibromuscular thickening type.ConclusionsChronic mechanical and chemical irritations are believed to cause cancer of the upper esophagus oral to a persistent CES, suggesting the need for long-term surveillance that focuses on residual stenosis and cancer development in patients with CES.

Association between high levels of nitrogen dioxide and increased cumulative incidence of lung cancer in patients with idiopathic pulmonary fibrosis.

Lung cancer is a fatal complication of idiopathic pulmonary fibrosis (IPF) with a poor prognosis. However, the association between individual exposure to air pollutants and lung cancer development in patients with IPF is unknown. This study aimed to assess the effect of individual exposure to nitrogen dioxide (NO2) on lung cancer development in patients with IPF. We enrolled 1085 patients from an IPF cohort in the Republic of Korea (mean age 65.6 years, males 80.6%). We estimated individual-level long-term exposures to NO2 at the patients' residential addresses using a national-scale exposure prediction model based on data from air quality regulatory monitoring stations. To evaluate the association between NO2 levels and lung cancer development in IPF, we used an individual- and area-level covariates adjusted model as our primary model. The estimated average annual NO2 concentration was 23.1 ppb. During a median follow-up of 4.3 years, 86 patients (7.9%) developed lung cancer. NO2 concentration was associated with lung cancer development in an unadjusted model (HR 1.219; p=0.042), while a marginal association was found in the primary model (HR 1.280; p=0.084). When NO2 concentration was stratified by the median value (21.0 ppb), exposure to high NO2 levels (≥21.0 ppb) was associated with a 2.0-fold increase in the risk of lung cancer development (HR 2.023; p=0.047) in the primary model. Individual exposure to high NO2 levels may increase the risk of lung cancer development in patients with IPF.

Meta-analysis: Risk of pancreatic cancer in patients with inflammatory bowel disease.

Studies exploring the association between inflammatory bowel disease (IBD) and pancreatic cancer have reported inconsistent results. To provide a comprehensive overview of the risk of pancreatic cancer development in patients with IBD. We searched Embase, PubMed, Scopus and ProQuest from inception to 31 October 2023. We included population-based cohort studies examining the risk of incident pancreatic cancer in adult patients with IBD compared to the non-IBD population. We also retrieved Mendelian randomisation (MR) studies investigating the relationship of IBD with pancreatic cancer risk. We conducted random-effects meta-analyses and provided pooled relative risks (RRs) with 95% confidence intervals (CIs). We included 13 studies. Among 11 cohort studies, the risk of developing pancreatic cancer increased by 79% in patients with IBD (RR = 1.79 [95% CI: 1.16-2.75]; I2 = 95.7%). Patients either with Crohn's disease (RR = 1.42 [95% CI: 1.24-1.63]) or ulcerative colitis (RR = 1.50 [95% CI: 1.17-1.92]) had increased risk (p for interaction = 0.72). The annual incidence of pancreatic cancer potentially attributable to IBD increased by 55 cases (95% CI: 17-103) per million. Two MR studies demonstrated that genetic liability to IBD was associated with an increased risk of pancreatic cancer. Our results suggest a moderate increase in the risk of pancreatic cancer in patients with IBD, which may be further heightened by genetic predisposition to IBD. The increased risk of pancreatic cancer is probably similar in Crohn's disease and ulcerative colitis.

The preventative effects of statin on lung cancer development in patients with idiopathic pulmonary fibrosis using the National Health Insurance Service Database in Korea.

Little is known about the effect of statin use in lung cancer development in idiopathic pulmonary fibrosis (IPF). We analyzed the database of the National Health Insurance Service to further investigate the clinical impacts of statin on lung cancer development and overall survival (OS) in IPF patients. The analysis included 9,182 individuals diagnosed with IPF, of which 3,372 (36.7%) were statin users. Compared to statin non-users, the time from diagnosis of IPF to lung cancer development and OS were longer in statin users in IPF patients. In Cox proportional hazard regression models, higher statin compliance, statin use, and being female had an inverse association with lung cancer risk, while older age at diagnosis of IPF and smoking history were associated with higher risk of lung cancer in IPF patients. For OS, statin use, female sex, higher physical activity frequency, and diabetes were associated with longer survival. In contrast, older age at diagnosis of IPF and smoking history were associated with shorter OS in IPF patients. These data from a large population indicate that statin had an independent protective association with lung cancer development and mortality in IPF patients.

Estimation of the Added Cancer Risk Derived From EVAR and CTA Follow-Up.

The aim of this study was to assess the risk of radiation-induced cancer development in patients that have undergone an infrarenal EVAR, stratifying the relative contributions of the procedure and the preoperative and postoperative CTAs. The organ-specific absorbed radiation doses from CTA and the EVAR procedure were estimated from the radiation exposures of 95 and 45 male patients, respectively. Lifetime attributable risk (LAR) cancer predictions were calculated for 14 different organs. Life expectancy was assumed from a previous cohort of patients undergoing infra-renal EVAR. The calculated total excess cancer risk was 0.0046, ie, 1 out of 220 patients will develop a neoplasm after being exposed to the ionizing radiation from the preoperative CTA, the EVAR and annual CTA examinations for 15 years. The procedure and the preoperative CTA contributed with 38% of the total excess risk, while the rest was derived from the follow-up. If the entire CTA based follow-up would have been eliminated, an excess risk of 0.0018 (1/560) would remain. 1 out of 219 patients who have undergone EVAR of an infra-renal AAA have a lifetime risk of developing cancer secondary to the radiation exposures related to the procedure and the CTAs used preoperatively and during follow-up. This risk derives mostly from the yearly postoperative CTAs, underlining the potential benefits of reducing or replacing their use. A simulation-based estimation reinforced the potential deleterious effects of the radiation exposure for patients undergoing Endovascular Aneurysm Repair (EVAR) of Abdominal Aortic Aneurysms (AAA) and subsequently followed by yearly Computer Tomography Angiographies (CTAs). The risk could be as high as 1 out 219 patients developing a neoplasm after 15 years. The largest exposure derives from the follow-up CTAs and efforts to minimize their use as well as the intraoperative radiation are greatly needed. The simulation-based estimations done in this study reinforce potential deleterious effects of the radiation exposure for patients undergoing EVAR of AAA. Efforts should be done to minimize the intraoperative radiation and the number of CTAs used during follow-up.

Pathogenesis of selected multiple primary neoplasms

Introduction and aim. Multiple primary tumors are defined as having more than one primary tumor in a different organ location in the same person. Therefore, it is important to know pathogenesis of multiple primary neoplasms to discover new forms of primary prevention and secondary prevention, especially connected with genetic tests which are important for the future of medicine as a part of personalized medicine. The aim of the study is to present selected aspects of the pathogenesis of multiple primary neoplasms. Material and methods. PubMed databases and Google Scholar were searched. Analysis of the literature. The rising risk of developing multiple primary cancers is a consequence of the progressive growth and ageing of the population and development of cancer in patients previously treated for cancer. The formation of secondary neoplasms may be multifactorial – to a large extent it is associated with genetic factors that may facilitate neoplastic transformation, for example as a result of radiation therapy, chemotherapy, inherited syndromes, environmental factors such as tobacco or alcohol, sometimes random somatic mutations. Conclusion. Knowledge of the pathogenesis of multiple primary tumors can contribute to a better understanding of the problem, as well as help in the prevention or early diagnosis of multiple primary tumors (primary and secondary prevention).

Cancer development in patients hospitalized with systemic lupus erythematosus: A population-level data linkage study.

To explore the association between systemic lupus erythematosus (SLE) with the risk of cancer development and subsequent 5-year mortality in Western Australia (WA). Population-level, data linkage study of SLE patients (n = 2111) and general population comparators (n = 21 110) hospitalized between 1980 and 2014. SLE patients (identified by ICD-9-CM: 695.4, 710.0, and ICD-10-AM: L93.0, M32.0) were nearest matched (10:1) for age, sex, Aboriginality, and temporality. Follow up was from time zero (index SLE hospitalization) to cancer development, death or 31 December 2014. We assessed the risk of cancer development and subsequent 5-year mortality between SLE patients and comparators with univariate and multivariate-adjusted Cox proportional hazards regression models. SLE patients had similar multivariate-adjusted risk (adjusted hazard ratio [aHR] 1.03, 95% confidence interval [CI] 0.93-1.15; p = .583) of cancer development. Cancer development risk was higher in SLE patients <40 years old (aHR 1.58, 95% CI 1.29-1.94; p < .001), and from 1980 to 1999 (aHR 1.16, 95% CI 1.02-1.31; p < .001). SLE patients had higher risk of developing cancer of the oropharynx (aHR 2.13, 95% CI 1.30-3.50), vulvo-vagina (aHR 3.22, 95% CI 1.34-7.75), skin (aHR 1.20, 95% CI 1.01-1.43), musculoskeletal tissues (aHR 2.26, 95% CI 1.16-4.40), and hematological tissues (aHR 1.78 95% CI 1.25-2.53), all p < .05. After cancer development, SLE patients had increased risk of 5-year mortality (aHR 1.31, 95% CI 1.06-1.61); highest in patients <50 years old (aHR 2.03, 95% CI 1.03-4.00), and in those with reproductive system and skin cancers. Hospitalized SLE patients had increased risk of multiple cancer sub-types. Following cancer development, SLE patients had increased risk of 5-year mortality. There is scope to improve cancer prevention and surveillance in SLE patients. Not applicable. This low-risk risk study used de-identified administrative linked health data.

The onset and progression of oral potentially malignant disorders in Fanconi anemia patients: Highlighting early detection of oral cancer

In 2020, Fanconi anemia (FA) was classified as a syndrome with insufficient epidemiological evidence in the oral potentially malignant disorder (OPMD) group by the WHO Collaborating Centre. The paucity of case reports on FA-associated OPMD limits evidence-based management, and such cases have not been analyzed collectively in detail. Hence, the objective of this short communication is to summarize the evidence on the onset and progression of OPMD in FA patients, so as to better understand the natural history of oral cancer development in patients affected by FA. A total of 11 eligible papers containing 1332 FA patients are involved in onset and progression of OPMD in FA patients. Of these, 186 (14.0%) were diagnosed with OPMD. With available data from 4 follow-up studies, 30 (41.1%) of 73 FA patients compatible with OPMD further developed into OSCC at young age (10–30 years old). The evidence on FA with malignant potential comprise clinical epidemiology, oral cytology abnormalities, DNA aneuploidy, loss of autofluorescence, loss of heterozygosity, high-risk human papillomavirus infection, DNA mutations in saliva and plasma samples. Collectively, these can consummate the evidence on FA as a syndrome that may potentiate cancer development in oral cavity mentioned by the WHO. Importantly, it highlights close surveillance is instrumental for FA patients with OPMD to early detect oral cancer.

Multiple Germline Events Contribute to CancerDevelopment in Patients with Li-Fraumeni Syndrome.

Our study clarifies the genomic basis for the phenotypic variability in LFS and highlights the immense benefits of expanding genetic and epigenetic testing of patients with LFS beyond TP53. More broadly, it necessitates the dissociation of hereditary cancer syndromes as single gene disorders and emphasizes the importance of understanding these diseases in a holistic manner as opposed to through the lens of a single gene.

Psoriasis Patients Treated With Methotrexate Have an Increased Risk of Nonmelanoma Skin Cancer: A Systematic Review and Meta-Analysis.

Both psoriasis and methotrexate are associated with an increased risk of nonmelanoma skin cancer. The effect of methotrexate on the development of nonmelanoma skin cancer in patients with psoriasis is currently unknown. To evaluate this relationship, a systematic review of the literature was conducted using databases including Ovid Medline (from 1946), Scopus (from 1970), and Embase (from 1974) through June 2019. Observational comparative and case-control studies comparing psoriasis patients treated with methotrexate to those not treated with methotrexate with data on the subsequent development of nonmelanoma skin cancer in both cohorts were included based on prespecified criteria. Two reviewers analyzed all studies for relevant data, which were analyzed using OpenMeta-Analyst statistical software. Quality was assessed with the Newcastle-Ottawa method. Nine cohort and case-control comparative studies of 1,486 screened abstracts met the inclusion criteria. Of 11,875 reported patients with psoriasis, 2,192 were taking methotrexate. A meta-analysis demonstrated an odds ratio of 2.8 (95% confidence interval = 1.47-5.39; p = 0.002) for nonmelanoma skin cancer development in patients with psoriasis taking methotrexate compared with those not taking methotrexate. Based on these findings, psoriasis patients treated with methotrexate are at a significantly increased (2.8 times higher) risk of developing nonmelanoma skin cancer. Risk counseling can improve healthcare outcomes in patients with psoriasis.

Liver injury indicators and subsequent cancer development among non-fatty liver population.

Little is known about the association between liver indicators (The FIB-4 index, nonalcoholic fatty liver disease fibrosis score (NFS), and fatty liver index (FLI)) and cancer development in patients without preexisting liver disease. We conducted a retrospective cohort study with participants who underwent voluntary health checkups and without fatty liver between 2005 and 2018. Our primary outcome was the development of any type of cancer, and its association with each liver indicator was evaluated. A total of 69,592 participants (mean age: 43.9 years, 29,984 (43.1%) were men) were included. During a median follow-up of 5.1 years, 3779 (5.4%) patients developed cancer. Compared to participants with a low NFS, those with a medium NFS had a higher risk of developing any type of cancer (adjusted hazard ratio [HR]: 1.18, 95% confidence interval [CI]: 1.07-1.31), whereas those with a medium FIB-4 index had a decreased risk of developing any type of cancer compared to those with a low FIB-4 index (adjusted HR: 0.91, 95% CI: 0.83-0.99). Patients with higher scores tended to have a higher risk of digestive organ cancer, regardless of the indicator. A high FLI was also associated with an increased risk of breast cancer (adjusted HR: 2.42, 95% CI: 1.24-4.71); however, those with a medium FIB-4 index (adjusted HR: 0.65, 95% CI: 0.52-0.81) and NFS (adjusted HR: 0.50, 95% CI: 0.35-0.72) had decreased risks of developing breast cancer compared to those with a high FIB-4 index and NFS, respectively. Among patients without fatty liver, a higher liver indicator score was associated with an increased risk of cancer in the digestive organs, regardless of the indicator. Notably, those with a medium FIB-4 index or NFS had a lower risk of developing breast cancer, whereas those with a medium FLI had an increased risk.