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Purpose: The aim of this study was to investigate the demographic and molecular characteristics, overall survival (OS), cancer-specific survival (CSS), and prognostic factors affecting the survival of patients with single primary breast cancer (SPBC) and patients with multiple primary cancers in their life time in which one of them is breast cancer (MPC). Methods: Using data from SEER 17 Research Plus, patients with breast cancer diagnosed between 2010 and 2019 were included in this study. Race, marital status, laterality, tumor size, molecular subtype, grade, stage, radiotherapy-chemotherapy treatment, and surgery data were analyzed in the data obtained after excluding patients with missing values. Kaplan-Meier survival analysis was used for survival analysis, and Cox regression analysis was used to evaluate the prognostic factors. Results: 573175 patients were included in the study. The mean age of MPC patients was significantly higher than SPBC patients (65.99 ± 12.68, 60.33 ± 13.47, P < .001, respectively). Patients with SPBC had significantly more hormone receptor (HR)-positive/Her2 positive, HR-negative/Her2-negative, and HR-negative/Her2-positive molecular subtypes; patients with MPC had more HR-positive/Her2-negative subtypes (P < .001). Grade 3 tumor status, locoregional spread, and distant metastasis were significantly higher in SPBC patients (P < .001). Overall survival and CSS rates were significantly higher in SPBC patients (P < .001). In MPC patients, overall hazard ratio was 1.631 times higher than SPBC, and the cancer-specific hazard ratio was 1.096 times higher (95% CI [1.606-1.656], 95% CI [1.071-1.121], respectively). Conclusion: Although patients with SPBC have worse prognostic tumor characteristics, OS and CSS rates are better than patients with MPC. [ABSTRACT FROM AUTHOR]

Abstract Lung cancer complicated by follicular lymphoma has rarely been reported in the literature. A 69‐year‐old male with an abnormal shadow on a chest radiograph was referred to our hospital. A mass in the right lung was seen on chest computed tomography (CT). Positron emission tomography‐CT showed fluorodeoxyglucose accumulation in the esophagus and multiple intra‐abdominal lymph nodes, in addition to the right lung lesion. The lung lesion was diagnosed as a pulmonary adenocarcinoma after biopsy. Upper and lower gastrointestinal endoscopies did not reveal the presence of a tumor. Open lymph node biopsy was performed to determine the course of treatment, leading to a diagnosis of follicular lymphoma. The patient finally underwent radical resection for lung cancer; the follicular lymphoma was judged to be low‐grade and was followed up. When complications involving other organs are detected during systemic examination of a patient with lung cancer, it is necessary to distinguish between metastasis to other organs and complications of other malignant diseases, as this will greatly influence the treatment strategy.

Lung cancer complicated by follicular lymphoma has rarely been reported in the literature. A 69‐year‐old male with an abnormal shadow on a chest radiograph was referred to our hospital. A mass in the right lung was seen on chest computed tomography (CT). Positron emission tomography‐CT showed fluorodeoxyglucose accumulation in the esophagus and multiple intra‐abdominal lymph nodes, in addition to the right lung lesion. The lung lesion was diagnosed as a pulmonary adenocarcinoma after biopsy. Upper and lower gastrointestinal endoscopies did not reveal the presence of a tumor. Open lymph node biopsy was performed to determine the course of treatment, leading to a diagnosis of follicular lymphoma. The patient finally underwent radical resection for lung cancer; the follicular lymphoma was judged to be low‐grade and was followed up. When complications involving other organs are detected during systemic examination of a patient with lung cancer, it is necessary to distinguish between metastasis to other organs and complications of other malignant diseases, as this will greatly influence the treatment strategy. [ABSTRACT FROM AUTHOR]

Abstract Background As a key enzyme in ceramide synthesis, longevity assurance homologue 2 (LASS2) has been indicated to act as a tumour suppressor in a variety of cancers. Ferroptosis is involved in a variety of tumour processes; however, the role of LASS2 in regulating ferroptosis has yet to be explored. This article explores the potential underlying mechanisms involved. Methods Bioinformatics tools and immunohistochemical staining were used to evaluate LASS2 expression, and the results were analysed in relation to overall survival and clinical association in multiple cancers. Coimmunoprecipitation-coupled liquid chromatography-mass spectrometry (co-IP LC-MS) was performed to identify potential LASS2-interacting proteins in thyroid, breast, and liver cancer cell lines. Transcriptomics, proteomics and metabolomics analyses of multiple cancer cell types were performed using MS or LC–MS to further explore the underlying mechanisms involved. Among these tumour cells, the common LASS2 interaction partner transferrin receptor (TFRC) was analysed by protein–protein docking and validated by coimmunoprecipitation western blot, immunofluorescence, and proximity ligation assays. Then, we performed experiments in which tumour cells were treated with Fer-1 or erastin or left untreated, with or without inducing LASS2 overexpression, and assessed the molecular biological and cellular functions by corresponding analyses. Results Low LASS2 expression is correlated with adverse clinical characteristic and poor prognosis in patients with thyroid cancer, breast cancer or HCC. Multiomics analyses revealed significant changes in the ferroptosis signalling pathway, iron ion transport and iron homeostasis. Our in vitro experiments revealed that LASS2 overexpression regulated ferroptosis status in these tumour cells by affecting iron homeostasis, which in turn inhibited tumour migration, invasion and EMT. In addition, LASS2 overexpression reversed the changes in tumour cell metastasis induced by either Fer-1 or erastin. Mechanistically, LASS2 interacts directly with TFRC to regulate iron homeostasis in these tumour cells. Conclusions In summary, our study reveals for the first time that LASS2 can inhibit tumour cell metastasis by interacting with TFRC to regulate iron metabolism and influence ferroptosis status in thyroid, breast, and liver cancer cells, these results suggest potential universal therapeutic targets for the treatment of these cancers.

Background: As a key enzyme in ceramide synthesis, longevity assurance homologue 2 (LASS2) has been indicated to act as a tumour suppressor in a variety of cancers. Ferroptosis is involved in a variety of tumour processes; however, the role of LASS2 in regulating ferroptosis has yet to be explored. This article explores the potential underlying mechanisms involved. Methods: Bioinformatics tools and immunohistochemical staining were used to evaluate LASS2 expression, and the results were analysed in relation to overall survival and clinical association in multiple cancers. Coimmunoprecipitation-coupled liquid chromatography-mass spectrometry (co-IP LC-MS) was performed to identify potential LASS2-interacting proteins in thyroid, breast, and liver cancer cell lines. Transcriptomics, proteomics and metabolomics analyses of multiple cancer cell types were performed using MS or LC–MS to further explore the underlying mechanisms involved. Among these tumour cells, the common LASS2 interaction partner transferrin receptor (TFRC) was analysed by protein–protein docking and validated by coimmunoprecipitation western blot, immunofluorescence, and proximity ligation assays. Then, we performed experiments in which tumour cells were treated with Fer-1 or erastin or left untreated, with or without inducing LASS2 overexpression, and assessed the molecular biological and cellular functions by corresponding analyses. Results: Low LASS2 expression is correlated with adverse clinical characteristic and poor prognosis in patients with thyroid cancer, breast cancer or HCC. Multiomics analyses revealed significant changes in the ferroptosis signalling pathway, iron ion transport and iron homeostasis. Our in vitro experiments revealed that LASS2 overexpression regulated ferroptosis status in these tumour cells by affecting iron homeostasis, which in turn inhibited tumour migration, invasion and EMT. In addition, LASS2 overexpression reversed the changes in tumour cell metastasis induced by either Fer-1 or erastin. Mechanistically, LASS2 interacts directly with TFRC to regulate iron homeostasis in these tumour cells. Conclusions: In summary, our study reveals for the first time that LASS2 can inhibit tumour cell metastasis by interacting with TFRC to regulate iron metabolism and influence ferroptosis status in thyroid, breast, and liver cancer cells, these results suggest potential universal therapeutic targets for the treatment of these cancers. [ABSTRACT FROM AUTHOR]

BackgroundLong-term survivors of cutaneous malignant melanoma (CMM) risk subsequent malignancies due to both host-related and environmental risk factors. This retrospective population-based study differentially assesses the risk of synchronous and metachronous cancers in a cohort of CMM survivors stratified by sex.MethodsThe cohort study (1999–2018) included 9,726 CMM survivors (M = 4,873, F = 4,853) recorded by the cancer registry of all 5,000,000 residents in the Italian Veneto Region. By excluding subsequent CMM and non-CMM skin cancers, the incidence of synchronous and metachronous malignancies was calculated according to sex and tumor site, standardizing for age and calendar year. The Standardized Incidence Ratio (SIR) was calculated as the ratio between the number of subsequent cancers among CMM survivors and the expected number of malignancies among the regional population.ResultsIrrespective of the site, the SIR for synchronous cancers increased in both sexes (SIR = 1.90 in males and 1.73 in females). Both sexes also demonstrated an excess risk for synchronous kidney/urinary tract malignancies (SIR = 6.99 in males and 12.11 in females), and women had an increased risk of synchronous breast cancer (SIR = 1.69). CMM male survivors featured a higher risk of metachronous thyroid (SIR = 3.51, 95% CI [1.87, 6.01]), and prostate (SIR = 1.35, 95% CI [1.12, 1.61]) malignancies. Among females, metachronous cancers featured higher SIR values than expected: kidney/urinary tract (SIR = 2.27, 95% CI [1.29, 3.68]), non-Hodgkin’s lymphoma (SIR = 2.06, 95% CI [1.24, 3.21]), and breast (SIR = 1.46, 95% CI [1.22, 1.74]). Females had an overall increased risk of metachronous cancers in the first 5 years after CMM diagnosis (SIR = 1.54 at 6–11 months and 1.37 at 1–5 years).ConclusionAmong CMM survivors, the risk of metachronous non-skin cancers is higher than in the general population and differs significantly by sex. These results encourage sex-tailored interventions for metachronous secondary cancer prevention.

Abstract Background Breast cancer is an umbrella term referring to a group of biologically and molecularly heterogeneous diseases originating from the breast. Globally, incidences of breast cancer has been increasing dramatically over the past decades. Analyses of multiple clinical “big data” can aid us in clarifying the means of preventing the disease. In addition, predisposing risk factors will be the most important issues if we can confirm their relevance. This study aims to provide an overview of the predisposing factors that contribute to a higher possibility of developing breast cancer and emphasize the signs that we ought to pay more attention to. Methods This is a matched nested case-control study. The cohort focused on identifying the eligible risk factors in breast cancer development by data screening (2000-2013) from the Taiwan National Health Insurance Research Database (NHIRD) under approved protocol. A total of 486,069 females were enrolled from a nationwide sampled database, and 3281 females was elligible as breast cancer cohort, 478,574 females who had never diagnosed with breast cancer from 2000 to 2013 were eligible as non-breast cancer controls, and matched to breast cancer cases according to age using a 1:6 ratio. Results We analyzed 3281 breast cancer cases and 19,686 non-breast cancer controls after an age-matched procedure. The significant predisposing factors associated with breast cancer development including obesity, hyperlipidemia, thyroid cancer and liver cancer. As for patients under the age of 55, gastric cancer does seem to have an impact on the development of breast cancer; compared with their counterparts over the age of 55, endometrial cancer appears to exhibit an evocative effect. Conclusions In this nationwide matched nested case-control study, we identified obesity, hyperlipidemia, previous cancers of the thyroid, stomach and liver as risk factors associated with breast cancer. However, the retrospective nature and limited case numbers of certain cancers still difficult to provide robust evidence. Further prospective studies are necessitated to corroborate this finding in order to nip the disease in the bud. Trial registration The studies involving human participants were reviewed and approved by the China Medical University Hospital [CMUH104-REC2-115(AR-4)].

Simple Summary: This study addressed the under-investigated issue of second primary cancer occurring in colorectal cancer survivors. Our aim was to explore whether patients recovered from a first colorectal cancer were at higher risk of developing a subsequent primary cancer. The hypothesis was that exposure to cancer treatment, enhanced health surveillance and shared risk factors may lead to an excess risk of second primary cancer in this population. The number of cases of second primary cancer exceeded the expected in this population, mainly driven by female genital cancers, and especially observed in the first years after colorectal cancer diagnosis. Our findings are overall consistent with previous studies, providing valuable information to better characterize and predict mortality from second primary cancer in subjects who suffered from first colorectal cancer. Background: Cancer survivors are at risk of developing second primary cancers (SPC). We investigated the risk of SPC in colorectal cancer (CRC) survivors in Sicily, Southern Italy. Methods: We analyzed data from the Eastern Sicily cancer registry covering 2.5 million people diagnosed and followed up between 2003 and 2017. We calculated the standardized incidence ratio (SIR) and 95% confidence interval (CI) of SPC overall and by cancer type, using the general Sicily population rates as reference. Results: A total of 19,040 cases of CRC and 1453 cases of SPC were included in the analysis. Mean age of occurrence of SPC was 68.1. The SIR for any SPC was 1.11 (95% CI 1.05–1.17); it was higher in women (1.18; 95% CI 1.08–1.29) than in men (1.07; 95% CI 0.97–1.14, p-value of difference 0.07). The SIR was increased for SPC from the ovary (SIR 2.01; 95% CI 1.33–2.95), kidney (SIR 2.00; 95% CI 1.54–2.56), endometrium (SIR 1.94; 95% CI 1.45–2.54), bladder (SIR 1.22, 95% CI 1.04–1.43) and stomach (1.29; 95% CI 0.98–1.66). The SIR for CRC as SPC was 0.84 (95% CI 0.70–1.01). No increased incidence was found for lung, prostate, breast, thyroid and liver cancer. The SIR for SPC overall and several cancers decreased with time of follow-up. Conclusions: In this population, CRC survivors have an 11% higher risk of developing a SPC than the general population, particularly cancers of the ovary, kidney, endometrium, bladder and stomach. Follow-up for SPC is required, especially during the first 5 years from CRC diagnosis. [ABSTRACT FROM AUTHOR]

Hypohidrotic ectodermal dysplasia (HED) is a rare hereditary disease characterized by hypoplasia of tissues derived from the ectoderm, such as hair, teeth, and sweat glands. There have been no reports of oral cancer in HED patients. Here, we report a case of multiple oral cancers in a patient with HED. A 24-year-old woman with HED visited our hospital for oligodontia-associated dental treatment. During follow-up, metachronous squamous cell carcinoma occurred in the left maxillary gingiva and right mandibular gingiva. Although surgery and chemoradiation were performed, the cancer progressed to unresectable cervical lymph node metastasis. Cetuximab-based therapy was selected as the subsequent anticancer therapy, and administered for 11 months. Because the patient developed sick sinus syndrome, which is an unlikely side effect of cetuximab, anticancer therapy could not be continued. The patient eventually died at 36 years old. We concluded that careful follow-up focusing on possibility of early onset of oral cancer is required, and cetuximab can be a treatment option for cancers in patients with HED. [ABSTRACT FROM AUTHOR]

We report the case of a 60-year-old male with a fever for two months and a skin rash for approximately one month prior to visiting his local doctor and subsequent admission to the hospital. Clinical findings included fever, weight loss, and night sweats. Computed tomography (CT) revealed an irregularly shaped mass bordering the upper lobe of the left lung and mediastinum, as well as hepatosplenomegaly. Suspecting lung cancer or malignant lymphoma, the patient was referred to our hospital for further evaluation. Positron emission tomography-computed tomography (PET/CT) revealed hepatosplenomegaly with accumulation of contrast agents in the liver, spleen, and bone marrow, as well as in a mass in the left upper lobe. A liver biopsy revealed atypical cells in the sinusoids, and immunohistochemical staining confirmed B-cell lymphoma. Chemotherapy was initiated immediately. PET/CT at the follow-up evaluation showed that the hepatosplenomegaly and bone marrow-related accumulation of contrast agents had resolved, but the accumulation of contrast agents in the mediastinal lymph nodes and the left upper lobe mass persisted, despite shrinkage. A bronchoscopy and mediastinal lymph node biopsy were performed. Histopathological examination revealed that the lung mass was most likely a small-cell carcinoma of the lung. Clinically, the malignant lymphoma was considered intravascular large B-cell lymphoma. As a result of appropriate treatment for both cancers, the patient's survival period improved., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Fukui et al.)

Background: Breast cancer is an umbrella term referring to a group of biologically and molecularly heterogeneous diseases originating from the breast. Globally, incidences of breast cancer has been increasing dramatically over the past decades. Analyses of multiple clinical "big data" can aid us in clarifying the means of preventing the disease. In addition, predisposing risk factors will be the most important issues if we can confirm their relevance. This study aims to provide an overview of the predisposing factors that contribute to a higher possibility of developing breast cancer and emphasize the signs that we ought to pay more attention to.Methods: This is a matched nested case-control study. The cohort focused on identifying the eligible risk factors in breast cancer development by data screening (2000-2013) from the Taiwan National Health Insurance Research Database (NHIRD) under approved protocol. A total of 486,069 females were enrolled from a nationwide sampled database, and 3281 females was elligible as breast cancer cohort, 478,574 females who had never diagnosed with breast cancer from 2000 to 2013 were eligible as non-breast cancer controls, and matched to breast cancer cases according to age using a 1:6 ratio.Results: We analyzed 3281 breast cancer cases and 19,686 non-breast cancer controls after an age-matched procedure. The significant predisposing factors associated with breast cancer development including obesity, hyperlipidemia, thyroid cancer and liver cancer. As for patients under the age of 55, gastric cancer does seem to have an impact on the development of breast cancer; compared with their counterparts over the age of 55, endometrial cancer appears to exhibit an evocative effect.Conclusions: In this nationwide matched nested case-control study, we identified obesity, hyperlipidemia, previous cancers of the thyroid, stomach and liver as risk factors associated with breast cancer. However, the retrospective nature and limited case numbers of certain cancers still difficult to provide robust evidence. Further prospective studies are necessitated to corroborate this finding in order to nip the disease in the bud.Trial Registration: The studies involving human participants were reviewed and approved by the China Medical University Hospital [CMUH104-REC2-115(AR-4)]. [ABSTRACT FROM AUTHOR]

Background: Prophylactic granulocyte-colony stimulating factor (G-CSF) has been shown to effectively prevent febrile neutropenia (FN) and grade 3/4 neutropenia during myelosuppressive treatment. The present study reports the clinical efficacy and safety of the prophylactic use of G-CSF with a half dose for cancer patients with an intermediate risk of FN combined with ≥1 patient-specific risk during multiple chemotherapy. Methods: This multicenter, one-arm, and open-label clinical study involved 151 patients [median age, 54 years old (range, 46.0–62.5); 38.4% female] with malignant tumors, including >20 different cancers. These patients underwent a total of 604 cycles of chemotherapy and received a half dose of PEG-rhG-CSF administration prior to each cycle. Results: The incidence rate of FN was 3.3% for this cohort during chemotherapy. Chemotherapy delay occurred in 6 (4.0%) patients for 12 (2.0%) cycles. Early termination of cancer treatment occurred in 14 (9.3%) patients. In this cohort, 23 (15.2%) patients required antibiotic use during courses of chemotherapy. A total of 28 (18.5%) patients experienced clear adverse effects during cancer treatment. Conclusion: The prophylactic PEG-rhG-CSF with a half dose can both efficaciously and safely prevent neutropenia for patients of diverse cancers with an intermediate risk of FN combined with ≥1 patient-specific risk during chemotherapy. [ABSTRACT FROM AUTHOR]

Background: Tryptophan and its metabolites have been found related to various cancers, but the direction of this relationship is still unclear. The purpose of this study is to explore the causal associations of tryptophan and kynurenine with multiple cancers based on the bidirectional Mendelian randomization analysis. Methods: The data of a genome-wide association study meta-analysis on 7,824 individuals was used to explore the genetic variants strongly associated with tryptophan and kynurenine. Genetic instruments of four specific cancers were obtained from available summary-level data of 323,590 European participants. Bidirectional Mendelian randomization analysis was conducted to examine possible causality. Sensitivity analysis was performed to test heterogeneity and horizontal pleiotropy. COX regression analysis was conducted to explore associations between dietary tryptophan and cancer mortality in NHANES 1988-1994. Results: No evidence of any causal association of tryptophan and kynurenine with the risk of four specific cancers was shown, except for weak correlations were suggested between lung or prostate cancer and kynurenine. Multiple sensitivity analyses generated similar results. Our findings from COX regression analysis were consistent with the above results. Conclusions: Our study did not find any causal relationship between tryptophan and kynurenine and multiple cancers. The associations still need further research. [ABSTRACT FROM AUTHOR]

Abstract Background Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is often caused by Helicobacter pylori and has a good prognosis. Rarely, patients with MALT lymphoma may have gastric cancer and have a poor prognosis. Case presentation We herein report a case in which surgical treatment was achieved for a 72-year-old male patient with gastric and duodenal MALT lymphoma coexisting multiple gastric cancers. He underwent upper endoscopy for epigastric discomfort, which revealed mucosal erosion on the posterior wall of the middle body of the stomach, an elevated lesion on the duodenal bulb, and a raised tumor on the antrum of the stomach. He was diagnosed with gastric and duodenal MALT lymphoma with early gastric cancer. One month after H. pylori eradication, a second upper endoscopy revealed no improvement in the gastric or duodenal mucosa, and areas of strong redness with a shallow recess just below the cardia of the stomach. As a result, a diagnosis of gastric and duodenal MALT lymphoma with two gastric cancers was made. Total gastrectomy with proximal duodenum resection using intraoperative upper endoscopy and regional lymph node dissection was performed. Pathologically, gastric and duodenal MALT lymphoma and three gastric cancers were detected. Since one of them was an advanced cancer, he started taking S-1 after his general condition improved. Conclusion For early detection of gastric and duodenal MALT lymphoma or gastric cancer, appropriate upper endoscopy and a biopsy are important. It is necessary to select a suitable treatment, such as H. pylori eradication, endoscopic treatment, surgery, chemotherapy, and irradiation, according to the disease state.

BackgroundTryptophan and its metabolites have been found related to various cancers, but the direction of this relationship is still unclear. The purpose of this study is to explore the causal associations of tryptophan and kynurenine with multiple cancers based on the bidirectional Mendelian randomization analysis.MethodsThe data of a genome-wide association study meta-analysis on 7,824 individuals was used to explore the genetic variants strongly associated with tryptophan and kynurenine. Genetic instruments of four specific cancers were obtained from available summary-level data of 323,590 European participants. Bidirectional Mendelian randomization analysis was conducted to examine possible causality. Sensitivity analysis was performed to test heterogeneity and horizontal pleiotropy. COX regression analysis was conducted to explore associations between dietary tryptophan and cancer mortality in NHANES 1988-1994.ResultsNo evidence of any causal association of tryptophan and kynurenine with the risk of four specific cancers was shown, except for weak correlations were suggested between lung or prostate cancer and kynurenine. Multiple sensitivity analyses generated similar results. Our findings from COX regression analysis were consistent with the above results.ConclusionsOur study did not find any causal relationship between tryptophan and kynurenine and multiple cancers. The associations still need further research.

BackgroundProphylactic granulocyte-colony stimulating factor (G-CSF) has been shown to effectively prevent febrile neutropenia (FN) and grade 3/4 neutropenia during myelosuppressive treatment. The present study reports the clinical efficacy and safety of the prophylactic use of G-CSF with a half dose for cancer patients with an intermediate risk of FN combined with ≥1 patient-specific risk during multiple chemotherapy.MethodsThis multicenter, one-arm, and open-label clinical study involved 151 patients [median age, 54 years old (range, 46.0–62.5); 38.4% female] with malignant tumors, including >20 different cancers. These patients underwent a total of 604 cycles of chemotherapy and received a half dose of PEG-rhG-CSF administration prior to each cycle.ResultsThe incidence rate of FN was 3.3% for this cohort during chemotherapy. Chemotherapy delay occurred in 6 (4.0%) patients for 12 (2.0%) cycles. Early termination of cancer treatment occurred in 14 (9.3%) patients. In this cohort, 23 (15.2%) patients required antibiotic use during courses of chemotherapy. A total of 28 (18.5%) patients experienced clear adverse effects during cancer treatment.ConclusionThe prophylactic PEG-rhG-CSF with a half dose can both efficaciously and safely prevent neutropenia for patients of diverse cancers with an intermediate risk of FN combined with ≥1 patient-specific risk during chemotherapy.

Secondary bladder tumors are relatively rare among all bladder tumors, while bladder metastases from breast cancer have been rarely reported. Furthermore, signet-ring differentiation may appear in the metastases from a breast invasive lobular carcinoma regardless of whether the primary breast tumor had signet-ring cells, which may cause diagnostic uncertainty. We report a case of a 55-year-old female patient with diffuse bladder thickening as the chief complaint and no specific clinical manifestations. While the cystoscopy showed multiple scattered red protuberances, the biopsy suggested signet-ring-cell carcinoma. The gastroscopy results suggested poorly differentiated adenocarcinoma with signet-ring cells. Considering the patient's history of invasive lobular carcinoma of the breast, chronic myeloid leukemia, and metastatic endometrial carcinoma from the breast, we performed an immunohistochemical analysis and the results indicated that signet-ring-cell carcinomas of the stomach and bladder originated from the invasive lobular carcinoma of the breast. We performed positron emission tomography/computed tomography and the results showed that there were multiple bone metastases already present. This was the first English case report of invasive lobular carcinoma of the breast metastasizing to the uterus, stomach, bladder, and bones with multiple signet-ring-cell variations. This study shares our reasons for misdiagnosing and opinions on diagnosing and treating for this kind of cases. [ABSTRACT FROM AUTHOR]

T-cell exhaustion is one of the main reasons of tumor immune escape. Using single-cell transcriptome data of CD8+ T cells in multiple cancers, we identified different cell types, in which Pre_exhaust and exhausted T cells participated in negative regulation of immune system process. By analyzing the coexpression network patterns and differentially expressed genes of Pre_exhaust, exhausted, and effector T cells, we identified 35 genes related to T-cell exhaustion, whose high GSVA scores were associated with significantly poor prognosis in various cancers. In the differentially expressed genes, RGS1 showed the greatest fold change in Pre_exhaust and exhausted cells of three cancers compared with effector T cells, and high expression of RGS1 was also associated with poor prognosis in various cancers. Additionally, RGS1 protein was upregulated significantly in tumor tissues in the immunohistochemistry verification. Furthermore, RGS1 displayed positive correlation with the 35 genes, especially highly correlated with PDCD1 , CTLA4 , HAVCR2 , and TNFRSF9 in CD8+ T cells and cancer tissues, indicating the important roles of RGS1 in CD8+ T-cell exhaustion. Considering the GTP-hydrolysis activity of RGS1 and significantly high mRNA and protein expression in cancer tissues, we speculated that RGS1 potentially mediate the T-cell retention to lead to the persistent antigen stimulation, resulting in T-cell exhaustion. In conclusion, our findings suggest that RGS1 is a new marker and promoting factor for CD8+ T-cell exhaustion and provide theoretical basis for research and immunotherapy of exhausted cells. [ABSTRACT FROM AUTHOR]

Abstract Background Many cancers are increased in immunosuppressed patients and evidence is accumulating that immune dysfunction may be a contributing risk factor for second primary cancers (SPCs). The aim of this study was to explore the potential influence of immune mechanisms in SPC. Methods We used the Swedish Cancer Registry (1990‐2015) to select 13 male and 14 female first primary cancers (FPCs) that are known to be related to immune suppression. We assessed relative risks (RRs) for any of these as concordant (same first and second cancer) and discordant FPC‐SPC pairs. Hierarchical clustering of significant RRs was performed for cancers as FPC and SPC. Results Concordant risks for SPCs were excessive in men and women for nasal (RRs 59.3 for men and 150.6 for women), tongue/mouth (51.7 and 100.8), and lip (32.4 and 61.2) cancers. Heatmaps showed that some cancers, such as skin cancer, tongue/mouth cancers, and non‐Hodgkin lymphoma had multiple bidirectional associations as FPC and SPC. Nasal cancer and chronic lymphocytic leukemia had associations mainly as FPC while liver and kidney cancers showed most associations as SPC. Conclusions Immune dysfunction may be a plausible contributing factor for most of the associations, which calls for experimental verification.

T-cell exhaustion is one of the main reasons of tumor immune escape. Using single-cell transcriptome data of CD8+ T cells in multiple cancers, we identified different cell types, in which Pre_exhaust and exhausted T cells participated in negative regulation of immune system process. By analyzing the coexpression network patterns and differentially expressed genes of Pre_exhaust, exhausted, and effector T cells, we identified 35 genes related to T-cell exhaustion, whose high GSVA scores were associated with significantly poor prognosis in various cancers. In the differentially expressed genes, RGS1 showed the greatest fold change in Pre_exhaust and exhausted cells of three cancers compared with effector T cells, and high expression of RGS1 was also associated with poor prognosis in various cancers. Additionally, RGS1 protein was upregulated significantly in tumor tissues in the immunohistochemistry verification. Furthermore, RGS1 displayed positive correlation with the 35 genes, especially highly correlated with PDCD1, CTLA4, HAVCR2, and TNFRSF9 in CD8+ T cells and cancer tissues, indicating the important roles of RGS1 in CD8+ T-cell exhaustion. Considering the GTP-hydrolysis activity of RGS1 and significantly high mRNA and protein expression in cancer tissues, we speculated that RGS1 potentially mediate the T-cell retention to lead to the persistent antigen stimulation, resulting in T-cell exhaustion. In conclusion, our findings suggest that RGS1 is a new marker and promoting factor for CD8+ T-cell exhaustion and provide theoretical basis for research and immunotherapy of exhausted cells.

Introduction: Multiple primary malignancies (MPMs) are likely to develop in patients with colorectal cancer (CRC); however, their prognoses are unclear. This study aims to investigate the prognostic impacts and clinicopathological features of multiple CRCs and extracolorectal malignancies (EMs) with CRC. Methods: We retrospectively evaluated a total of 22,628 patients with stage I–III CRC who underwent curative resection at 24 referral institutes in Japan between January 2004 and December 2012. MPMs were classified as synchronous CRCs (SCRCs), metachronous CRCs, synchronous EMs (SEMs), and metachronous EMs. Results: The presence of SCRCs (odds ratio 1.54, p < 0.001) was independently associated with SEMs in the multivariate analyses. SEMs were the strongest poor prognostic factor for OS (hazard ratio [HR] 2.21, p < 0.001) and RFS (HR 1.69, p < 0.001) compared with age, sex, and primary T and N factors. The incidence of stomach cancer was the highest in EMs, followed by lung, breast, and prostate cancers. Multiple CRCs were evenly distributed throughout the right-side colon to the rectum. Discussion/Conclusion: SEMs were a strong poor prognostic factor for patients with stage I–III CRC. Patients with CRC, particularly those with SCRCs, should be surveyed for SEMs, especially for stomach and lung cancers. [ABSTRACT FROM AUTHOR]

Purpose: Little is known about difference between synchronous colorectal cancer (SCRC) and metachronous colorectal cancer (MCRC) despite the relevance for this selected patient group. The aim of this retrospective review was to analyze patients with SCRC and MCRC. Methods: All patients who underwent surgery for SCRC and MCRC between 1982 and 2019 were included in this retrospective analysis of our tertiary referral center. Clinical, histological, and molecular genetic characteristics were analyzed. The primary endpoint was cause-specific survival, evaluated by the Kaplan-Meier method. Secondary endpoints were recurrence-free survival and the identification of prognostic factors. Results: Overall, 3714 patients were included in this analysis. Of those, 3506 (94.4%) had a primary unifocal colorectal cancer (PCRC), 103 (2.7%) had SCRC, and 105 (2.8%) had MCRC. SCRC occurred more frequently in elderly (p=0.009) and in male patients (p=0.027). There were no differences concerning tumor stages or grading. Patients with SCRC did not show altered recurrence or survival rates, as compared to unifocal tumors. However, MCRC had a lower rate of recurrence, compared to PCRC (24% vs. 41%, p=0.002) and a lower rate of cause-specific death (13% vs. 37%, p<0.001). Five-year cause-specific survival rates were 63±1% for PCRC, 62±6% for SCRC (p=0.588), and 88±4% for MCRC (p<0.001). Multivariable analysis revealed that MCRC were an independent favorable prognostic parameter regarding case-specific survival. Conclusion: Patients with SCRC seem to not have a worse prognosis compared to patients with PCRC. Noteworthy, patients with MCRC showed better survival rates in this retrospective analysis. [ABSTRACT FROM AUTHOR]

Abstract Background Although rare cancers account for 27% of cancer diagnoses in the US, there is insufficient research on survivorship issues in these patients. An important issue cancer survivors face is an elevated risk of being diagnosed with new primary cancers. The primary aim of this analysis was to assess whether a history of rare cancer increases the risk of subsequent cancer compared to survivors of common cancers. Methods This was a prospective cohort study of 16,630 adults with personal and/or family history of cancer who were recruited from cancer clinics at 14 geographically dispersed US academic centers of the NIH-sponsored Cancer Genetics Network (CGN). Participants’ self-reported cancer histories were collected at registration to the CGN and updated annually during follow-up. At enrollment, 14% of participants reported a prior rare cancer. Elevated risk was assessed via the cause-specific hazard ratio on the time to a subsequent cancer diagnosis. Results After a median follow-up of 7.9 years, relative to the participants who were unaffected at enrollment, those with a prior rare cancer had a 23% higher risk of subsequent cancer (95% CI: -1 to 52%), while those with a prior common cancer had no excess risk. Patients having two or more prior cancers were at a 53% elevated risk over those with fewer than two (95% CI: 21 to 94%) and if the multiple prior cancers were rare cancers, risk was further elevated by 47% (95% CI: 1 to 114%). Conclusion There is evidence suggesting that survivors of rare cancers, especially those with multiple cancer diagnoses, are at an increased risk of a subsequent cancer. There is a need to study this population more closely to better understand cancer pathogenesis.

Background: Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is often caused by Helicobacter pylori and has a good prognosis. Rarely, patients with MALT lymphoma may have gastric cancer and have a poor prognosis. Case presentation: We herein report a case in which surgical treatment was achieved for a 72-year-old male patient with gastric and duodenal MALT lymphoma coexisting multiple gastric cancers. He underwent upper endoscopy for epigastric discomfort, which revealed mucosal erosion on the posterior wall of the middle body of the stomach, an elevated lesion on the duodenal bulb, and a raised tumor on the antrum of the stomach. He was diagnosed with gastric and duodenal MALT lymphoma with early gastric cancer. One month after H. pylori eradication, a second upper endoscopy revealed no improvement in the gastric or duodenal mucosa, and areas of strong redness with a shallow recess just below the cardia of the stomach. As a result, a diagnosis of gastric and duodenal MALT lymphoma with two gastric cancers was made. Total gastrectomy with proximal duodenum resection using intraoperative upper endoscopy and regional lymph node dissection was performed. Pathologically, gastric and duodenal MALT lymphoma and three gastric cancers were detected. Since one of them was an advanced cancer, he started taking S-1 after his general condition improved. Conclusion: For early detection of gastric and duodenal MALT lymphoma or gastric cancer, appropriate upper endoscopy and a biopsy are important. It is necessary to select a suitable treatment, such as H. pylori eradication, endoscopic treatment, surgery, chemotherapy, and irradiation, according to the disease state. [ABSTRACT FROM AUTHOR]

Multiple primary malignancies are defined as two or more primary malignant tumors diagnosed in one individual; they are further classified to synchronous or metachronous based on the period between each cancer diagnosis and the other. The diagnosis of four synchronous cancers is exceedingly rare. We report a case of a 72-year-old man, diagnosed with synchronous quadruple cancers, Hurthle cell carcinoma and papillary carcinoma of the thyroid, as well as squamous cell carcinoma and carcinoid tumor of the lung. [ABSTRACT FROM AUTHOR]

Background: Many cancers are increased in immunosuppressed patients and evidence is accumulating that immune dysfunction may be a contributing risk factor for second primary cancers (SPCs). The aim of this study was to explore the potential influence of immune mechanisms in SPC. Methods: We used the Swedish Cancer Registry (1990‐2015) to select 13 male and 14 female first primary cancers (FPCs) that are known to be related to immune suppression. We assessed relative risks (RRs) for any of these as concordant (same first and second cancer) and discordant FPC‐SPC pairs. Hierarchical clustering of significant RRs was performed for cancers as FPC and SPC. Results: Concordant risks for SPCs were excessive in men and women for nasal (RRs 59.3 for men and 150.6 for women), tongue/mouth (51.7 and 100.8), and lip (32.4 and 61.2) cancers. Heatmaps showed that some cancers, such as skin cancer, tongue/mouth cancers, and non‐Hodgkin lymphoma had multiple bidirectional associations as FPC and SPC. Nasal cancer and chronic lymphocytic leukemia had associations mainly as FPC while liver and kidney cancers showed most associations as SPC. Conclusions: Immune dysfunction may be a plausible contributing factor for most of the associations, which calls for experimental verification. [ABSTRACT FROM AUTHOR]

Background: Although rare cancers account for 27% of cancer diagnoses in the US, there is insufficient research on survivorship issues in these patients. An important issue cancer survivors face is an elevated risk of being diagnosed with new primary cancers. The primary aim of this analysis was to assess whether a history of rare cancer increases the risk of subsequent cancer compared to survivors of common cancers.Methods: This was a prospective cohort study of 16,630 adults with personal and/or family history of cancer who were recruited from cancer clinics at 14 geographically dispersed US academic centers of the NIH-sponsored Cancer Genetics Network (CGN). Participants' self-reported cancer histories were collected at registration to the CGN and updated annually during follow-up. At enrollment, 14% of participants reported a prior rare cancer. Elevated risk was assessed via the cause-specific hazard ratio on the time to a subsequent cancer diagnosis.Results: After a median follow-up of 7.9 years, relative to the participants who were unaffected at enrollment, those with a prior rare cancer had a 23% higher risk of subsequent cancer (95% CI: -1 to 52%), while those with a prior common cancer had no excess risk. Patients having two or more prior cancers were at a 53% elevated risk over those with fewer than two (95% CI: 21 to 94%) and if the multiple prior cancers were rare cancers, risk was further elevated by 47% (95% CI: 1 to 114%).Conclusion: There is evidence suggesting that survivors of rare cancers, especially those with multiple cancer diagnoses, are at an increased risk of a subsequent cancer. There is a need to study this population more closely to better understand cancer pathogenesis. [ABSTRACT FROM AUTHOR]

Highlights • 17 SNPs were significantly associated with the expression of 18 cis-genes. • MYL2 and PTGFR in HNSC, 4 genes (F8, SATB2, G6PD and UGT1A6) in KIRP, 3 genes (CHMP4C, MAP3K1 and MECP2) in LUAD were all strongly associated with cancer stage levels. • SATB2 was correlated with HNSC survival, and MPP1was strongly associated with the survival of SARC. Abstract Genetic variants can predict other "linked" diseases because alterations in one or more genes in vivo may affect relevant phenotype properties. Our study systematically explored the pan-cancer common gene and cancer type-specific genes based on GWAS loci and TCGA data of multiple cancers. It was found that there were 17 SNPs were significantly associated with the expression of 18 genes. Associations between the 18 cis-regulatory genes and the pathologic stage of each cancer showed that MYL2 and PTGFR in HNSC, 4 genes (F8, SATB2, G6PD and UGT1A6) in KIRP, 3 genes (CHMP4C, MAP3K1 and MECP2) in LUAD were all strongly associated with cancer stage levels. Additionally, the survival association analysis showed that SATB2 was correlated with HNSC survival, and MPP1 was strongly associated with the survival of SARC. This study will shed light on the biological pathways involved in cancer-genetic associations, and has the potential to be applied to the predictions of the risk of cancers developing in healthy individuals. [ABSTRACT FROM AUTHOR]

Background and Objectives: Cancer recurrence represents treatment failure; the development of new primary tumors is suggestive of persistent exposure to etiological risk factors or genetic predisposition due to mutations in multiple cell lines. Case presentation/Design/Methods: The first case is a 65-years-old Caucasian male who presented with esophageal and lung cancer diagnosed synchronously. Smoking was the common risk factor for both cancers, underscoring field cancerization. The diagnosis and management was a challenge and different from either cancer presenting alone. Multidisciplinary approach was used and led to good outcomes. The second case is a 72-years-old Caucasian male presenting a rare dilemma of genetic mutation leading to multiple primary gastrointestinal cancers in a single individual. The gene explaining this group of cancers has not been diagnosed yet and the field needs to be explored further. Conclusion: Multiple primary cancers can be secondary to a common environmental risk factor or genetic mutations.

Cancer belongs to a class of highly aggressive diseases and a leading cause of death in the world. With more than 100 types of cancers, breast, lung and prostate cancer remain to be the most common types. To identify essential network markers (NMs) and therapeutic targets in these cancers, the authors present a novel approach which uses gene expression data from microarray and RNA‐seq platforms and utilises the results from this data to evaluate protein–protein interaction (PPI) network. Differentially expressed genes (DEGs) are extracted from microarray data using three different statistical methods in R, to produce a consistent set of genes. Also, DEGs are extracted from RNA‐seq data for the same three cancer types. DEG sets found to be common in both platforms are obtained at three fold change (FC) cut‐off levels to accurately identify the level of change in expression of these genes in all three cancers. A cancer network is built using PPI data characterising gene sets at log‐FC (LFC)>1, LFC>1.5 and LFC>2, and interconnection between principal hub nodes of these networks is observed. Resulting network of hubs at three FC levels highlights prime NMs with high confidence in multiple cancers as validated by Gene Ontology functional enrichment and maximal complete subgraphs from CFinder. [ABSTRACT FROM AUTHOR]

The treatment of multiple cancers requires multidisciplinary expertise. In this case, we experienced a multiple cancers case, sigmoid colon cancer and intrahepatic cholangiocarcinoma that required preoperative portal vein embolization (PVE). PVE is often approached by trans-hepatic percutaneous approach or via ileocecal vein (ICV) or veins of the small intestine. In this case, the patient was scheduled to undergo robot-assist surgery for sigmoid colon cancer, and it was planned that the inferior mesenteric vein (IMV) would be cut. PVE from the IMV was performed with hope to reduce complications. This patient had intrahepatic cholangiocarcinoma and sigmoid colon cancer. A radical cure for intrahepatic cholangiocarcinoma was expected by left liver lobectomy. Because of concerns about postoperative liver failure, it was decided to perform PVE. PVE via IMV approach was performed simultaneously with robot-assisted surgery for sigmoid colon cancer. The patient was discharged without complications 12 days after surgery. PVE is a very important technique for massive hepatic resection. Percutaneous trans-hepatic approach has the potential to damage vessels, bile duct, normal liver. Venous approaches, including via ICV, have the potential to damage vessels. In this case, we performed PVE from the IMV because we thought this approach would reduce the risk of complications. The patient successfully underwent PVE without complications. PVE via IMV was successfully performed without complications. In multiple cancers case, this approach would be better approach than any other PVE approach like this case. • This case is portal vein embolization (PVE) via inferior mesenteric vein (IMV) approach. • We did this approach simultaneously with a robot-surgery for colon cancer. • This approach may reduce complications in a case of simultaneous liver and left sided colon cancer. [ABSTRACT FROM AUTHOR]

Background: Long-term survivors of cutaneous malignant melanoma (CMM) risk subsequent malignancies due to both host-related and environmental risk factors. This retrospective population-based study differentially assesses the risk of synchronous and metachronous cancers in a cohort of CMM survivors stratified by sex., Methods: The cohort study (1999-2018) included 9,726 CMM survivors (M = 4,873, F = 4,853) recorded by the cancer registry of all 5,000,000 residents in the Italian Veneto Region. By excluding subsequent CMM and non-CMM skin cancers, the incidence of synchronous and metachronous malignancies was calculated according to sex and tumor site, standardizing for age and calendar year. The Standardized Incidence Ratio (SIR) was calculated as the ratio between the number of subsequent cancers among CMM survivors and the expected number of malignancies among the regional population., Results: Irrespective of the site, the SIR for synchronous cancers increased in both sexes (SIR = 1.90 in males and 1.73 in females). Both sexes also demonstrated an excess risk for synchronous kidney/urinary tract malignancies (SIR = 6.99 in males and 12.11 in females), and women had an increased risk of synchronous breast cancer (SIR = 1.69). CMM male survivors featured a higher risk of metachronous thyroid (SIR = 3.51, 95% CI [1.87, 6.01]), and prostate (SIR = 1.35, 95% CI [1.12, 1.61]) malignancies. Among females, metachronous cancers featured higher SIR values than expected: kidney/urinary tract (SIR = 2.27, 95% CI [1.29, 3.68]), non-Hodgkin's lymphoma (SIR = 2.06, 95% CI [1.24, 3.21]), and breast (SIR = 1.46, 95% CI [1.22, 1.74]). Females had an overall increased risk of metachronous cancers in the first 5 years after CMM diagnosis (SIR = 1.54 at 6-11 months and 1.37 at 1-5 years)., Conclusion: Among CMM survivors, the risk of metachronous non-skin cancers is higher than in the general population and differs significantly by sex. These results encourage sex-tailored interventions for metachronous secondary cancer prevention., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Guzzinati, Buja, Grotto, Zorzi, Manfredi, Bovo, Del Fiore, Tropea, Dall’Olmo, Rossi, Mocellin and Rugge.)

O cancro do pulmão é a causa mais comum de morte por doença oncológica. Os doentes com diagnóstico de neoplasia - qualquer que seja a localização - têm risco acrescido de desenvolver um segundo tumor. Pretendeu-se caracterizar uma população com neoplasia do pulmão e o diagnóstico síncrono ou metácrono de tumor primário com outra localização. Foi feito um estudo retrospectivo, referente ao período de 2000-2007, analisando-se os processos clínicos de doentes seguidos na Unidade de Pneumologia Oncológica do nosso hospital em que estavam referenciadas duas neoplasias. Dos doentes seguidos na Unidade (n=1046) no período referido, 4,2% (n=44) tinham evidência de duas neoplasias. A maioria (88,6%) dos doentes eram homens, com idade média elevada (70,1±10 anos). Oitenta e seis por cento (n=38) tinham hábitos tabágicos e 65,4% dos doentes com registo de história familiar de neoplasia (n=26) tinham história familiar relevante (n=17). A doença oncológica manifestou-se em primeiro lugar na próstata, cólon, cabeça e pescoço ou bexiga. O cancro do pulmão foi em geral a segunda neoplasia. O intervalo de tempo médio entre a primeira e a segunda neoplasia foi de 62,9±64,9 meses (max: 240, min: 0), sendo que geralmente a segunda neoplasia foi detectada em estádio avançado. A sobrevivência média foi de 8,6±8,24 meses (max: 32; min: 1), permanecendo vivos quatro doentes. Os presentes dados levam-nos a sugerir vigilância clínica prolongada em doentes com diagnóstico prévio de cancro. Sugerimos um algoritmo que possibilite vigiar melhor estes doentes e estudo prospectivo para verificar se existem marcadores moleculares nesta população.Lung cancer is the leading form of cancer death worldwide. Cancer patients are at a high risk of developing a second cancer. The present study attempts to determine the characteristics of a population with lung cancer diagnosed with another cancer. We analysed records of patients from the Department of Lung Oncology of our hospital from 2000 to 2007 who were identified as having two or more tumours. We found 4.2% (n=44) multiple cancers among the registered cases (n=1046), 88.6% males, (high) mean age 70.1±10 years old. About 86% (n=38) of the patients were smokers or ex -smokers. From the patients with record of family history, 65.4% (n=17) had relevant family history of cancer. The majority of the first malignancy diagnosed was prostate, colon, head and neck and bladder. Lung cancer was essentially the second malignancy. The mean time lag between the two diagnoses was 62.9±64.9 months (max. 240, min. 0), with the second cancer usually detected at an advanced stage. The mean survival of patients who had a second primary lung cancer was 8.6±8.24 months (max. 32, min. 1), with four patients still surviving. Lung cancer was essentially the second malignancy. The mean time lag between the two diagnoses was 62.9±64.9 months (max. 240, min. 0), with the second cancer usually detected at an advanced stage. The mean survival of patients who had a second primary lung cancer was 8.6±8.24 months (max. 32, min. 1), with four patients still surviving.

Background and Objectives: Cancer recurrence represents treatment failure; the development of new primary tumors is suggestive of persistent exposure to etiological risk factors or genetic predisposition due to mutations in multiple cell lines. Case presentation/Design/Methods: The first case is a 65-years-old Caucasian male who presented with esophageal and lung cancer diagnosed synchronously. Smoking was the common risk factor for both cancers, underscoring field cancerization. The diagnosis and management was a challenge and different from either cancer presenting alone. Multidisciplinary approach was used and led to good outcomes. The second case is a 72-years-old Caucasian male presenting a rare dilemma of genetic mutation leading to multiple primary gastrointestinal cancers in a single individual. The gene explaining this group of cancers has not been diagnosed yet and the field needs to be explored further. Conclusion: Multiple primary cancers can be secondary to a common environmental risk factor or genetic mutations. [ABSTRACT FROM AUTHOR]

The connection between microRNA expression and cancers has been identified, and microRNAs may be considered as important prognostic biomarkers. However, it is still inconsistent whether expression of let-7 can predict prognosis in patients with multiple cancers. A meta-analysis was performed by searching PubMed, EMBASE, and ISI Web of Science databases. All data were extracted from articles comparing prognosis in patients with multiple cancers having low expression of let-7 with those having high expression. Pooled hazard ratios (HRs) and corresponding 95 % confidence intervals (CIs) were calculated. Subgroup analyses were conducted for cancer type and ethnicity. A total of 1,757 cases of multiple cancers were involved for this meta-analysis. The HR of low let-7 expression in multiple cancers was 1.80 (95 % CI 1.18-2.76), and that in lung cancer was 1.99 (95 % CI 1.17-3.40). A subgroup analysis was performed on ethnicity; combined HR was 1.61 (95 % CI 0.84-3.11) for Asians and 1.94 (95 % CI 1.11-3.39) for non-Asians. Low expression of let-7 might predict poor prognosis in patients with multiple cancers, especially in lung cancer. Furthermore, let-7 might be a biomarker in non-Asian patients with favorable prognosis. [ABSTRACT FROM AUTHOR]

Multiple head and neck cancers are not rare entities and according to studies in the literature, their incidence is increasing. The emergence of multiple cancers is explained by the phenomenon of "field cancerization". Patients with cancer of the upper digestive and respiratory tract develop most often a second malignancy, usually in the upper aero-digestive tract and among them, those with larynx cancer ranks first among patients with multiple cancers. In the literature and in practice, we met rare combination of multiple cancers, associations that appear to be "random", cannot be explained by any of the hypotheses developed: exposure to carcinogens, genetic susceptibility, and immunodeficiency or cancer treatments after index tumor. Follow-up of patients who have had a head and neck cancer and periodic control are important for early detection of multiple cancers. [ABSTRACT FROM AUTHOR]

Objectives: Lung cancer is increasingly diagnosed as a second cancer. Our goal was to analyse the characteristics and outcomes of early-stage resected lung adenocarcinomas in patients with previous cancers (PC) and correlations with adenocarcinoma subtypes., Methods: We retrospectively reviewed data of patients radically operated on for stage I-II lung adenocarcinoma in 9 thoracic surgery departments between 2014 and 2017. Overall survival (OS) and time to disease relapse were evaluated between subgroups., Results: We included 700 consecutive patients. PC were present in 260 (37.1%). Breast adenocarcinoma, lung cancer and prostate cancer were the most frequent (21.5%, 11.5% and 11.2%, respectively). No significant differences in OS were observed between the PC and non-PC groups (P = 0.378), with 31 and 75 deaths, respectively. Patients with PC had smaller tumours and were more likely to receive sublobar resection and to be operated on with a minimally invasive approach. Previous gastric cancer (P = 0.042) and synchronous PC (when diagnosed up to 6 months before lung adenocarcinoma; P = 0.044) were related, with a worse OS. Colon and breast adenocarcinomas and melanomas were significantly related to a lower incidence of high grade (solid or micropapillary, P = 0.0039, P = 0.005 and P = 0.028 respectively), whereas patients affected by a previous lymphoma had a higher incidence of a micropapillary pattern (P = 0.008)., Conclusions: In patients with PC, we found smaller tumours more frequently treated with minimally invasive techniques and sublobar resection, probably due to a more careful follow-up. The impact on survival is not uniform and predictable; however, breast and colon cancers and melanoma showed a lower incidence of solid or micropapillary patterns whereas patients with lymphomas had a higher incidence of a micropapillary pattern., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery.)

Background: Testicular cancer treatment has become standardized in the 1980s involving radiotherapy preferentially for seminoma and chemotherapy for nonseminoma. The late effects of these therapeutic practices have not been properly evaluated because of the relatively short time since their application. [ABSTRACT FROM PUBLISHER]

Background: To examine the incidence, characteristics, and outcomes for second malignancies following the diagnosis of a primary solid tumor in pediatric patients. Methods: The Surveillance, Epidemiology, and End Results (SEER) database was queried from 1973 to 2005, excluding recurrences, in patients <20 y. Results: A total of 31,685 cases of pediatric solid malignancies were identified. Overall, 177 patients were diagnosed with a unique second malignancy before the age 20 (0.56%) The mean follow-up was for 8.5 y (2 mo–30.8 y). Mean age at diagnosis of the primary tumor was 7.7 y. The most common primary malignancies were CNS tumors (22.5%), followed by soft tissue sarcoma (15.8%), retinoblastoma (14.1%), and bone tumors (13%). Hematologic malignancies (35.5%) were the most common second malignancies noted in the cohort, followed by bone tumors (18%) and soft tissue sarcomas (15%). Hematologic malignancies had a shorter latency (3.1 y) compared with solid second tumors (11.6 y). The overall 10-y survival for the entire cohort was 41.5%. For most tumor categories, development of a secondary malignancy was associated with lower 5- and 10-y survival than expected. Conclusions: CNS tumors, retinoblastoma, and soft tissue sarcomas in children are the most common solid primary tumors, with an increased risk of a second malignancy. Leukemia is the most common second malignancy seen in pediatric solid tumors. Second malignancies are associated with significantly reduced survival rates compared with the general childhood cancer population. [Copyright &y& Elsevier]

Both cigarette smoking and alcohol drinking are well-established risk factors for esophageal squamous cell carcinoma (ESCC), and the relationship of dose to cancer risk has already been described. Furthermore, the synergistic effect of these two factors has been reported. Our case–control study revealed the odds ratio of ESCC to be 50.1 for those who were both heavy smokers and heavy drinkers in comparison to people who neither drank nor smoked. In patients with ESCC, head and neck cancers as well as dysplastic lesions are frequently observed. Heavy smoking and heavy drinking are closely related to such multicentric carcinogenesis events in the upper aerodigestive tract (UADT), including the esophagus and head andneck region. Polymorphisms in acetaldehyde dehydrogenase 2 (ALDH2) are reported to be a key event in deciding individual susceptibility to UADT cancer. Patients with inactive ALDH2, in whom facial flushing is usually observed after the drinking of alcohol, are at high risk for ESCC as well as multiple UADT cancers. For the early detection of the disease, effective follow up using endoscopy with Lugol staining or narrow band imaging endoscopy is strongly recommended for high-risk populations, such as smokers, heavy drinkers, people with experience of flushing after the drinking of alcohol, and patients with UADT cancer. [ABSTRACT FROM AUTHOR]