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Wang, Yuan‐Yuan; Wang, Wen‐Da; Sun, Zhi‐Jun
doi: 10.1002/ijc.34421pmid: 36602290
Immunotherapy has pioneered a new era of tumor treatment, in which the immune checkpoint blockade (ICB) exerts significant superiority in overcoming tumor immune escape. However, the formation of an immune‐suppressive tumor microenvironment (TME) and the lack of effective activation of the immune response have become major obstacles limiting its development. Emerging reports indicate that cancer stem cells (CSCs) potentially play important roles in treatment resistance and progressive relapse, while current research is usually focused on CSCs themselves. In this review, we mainly emphasize the collusions between CSCs and tumor‐infiltrating immune cells. We focus on the summary of CSC‐immune cell crosstalk signaling pathways in ICB resistance and highlight the application of targeted drugs to improve the ICB response.
Wang, Qianyu; Shen, Xiaofei; Chen, Gang; Du, Junfeng
doi: 10.1002/ijc.34464pmid: 36752642
Immunotherapy, especially with immune checkpoint inhibitors (ICIs), has shown advantages in cancer treatment and is a new hope for patients who have failed multiline therapy. However, in colorectal cancer (CRC), the benefit is limited to a small subset of patients with microsatellite instability‐high (MSI‐H) or mismatch repair‐deficient (dMMR) metastatic CRC (mCRC). In addition, 45% to 60% of dMMR/MSI‐H mCRC patients showed primary or acquired resistance to ICIs. This means that these patients may have potential unknown pathways mediating immune escape. Almost all mismatch repair‐proficient (pMMR) or microsatellite‐stable (MSS) mCRC patients do not benefit from ICIs. In this review, we discuss the mechanisms of action of ICIs and their current status in CRC. We then discuss the mechanisms of primary and acquired resistance to ICIs in CRC. Finally, we discuss promising therapeutic strategies to overcome resistance to ICIs in the clinic.
Entrop, Joshua P.; Weibull, Caroline E.; Smedby, Karin E.; Jakobsen, Lasse H.; Øvlisen, Andreas K.; Molin, Daniel; Glimelius, Ingrid; Marklund, Anna; Holte, Harald; Fosså, Alexander; Smeland, Knut B.; El‐Galaly, Tarec C.; Eloranta, Sandra
doi: 10.1002/ijc.34552pmid: 37119033
Kurasawa, Shimon; Imaizumi, Takahiro; Maruyama, Shoichi; Tanaka, Keitaro; Kubo, Yoko; Nagayoshi, Mako; Ikezaki, Hiroaki; Suzuki, Sadao; Koyama, Teruhide; Koriyama, Chihaya; Kadota, Aya; Katsuura‐Kamano, Sakurako; Kuriki, Kiyonori; Wakai, Kenji; Matsuo, Keitaro
Wellbrock, Maike; Spix, Claudia; Ronckers, Cécile M; Grabow, Desiree; Filbert, Anna‐Liesa; Borkhardt, Arndt; Wollschläger, Daniel; Erdmann, Friederike
doi: 10.1002/ijc.34556pmid: 37158619
Childhood cancer is the leading disease‐related cause of death among under 15 year olds in Europe. Since primary preventive measures are lacking, improving survival probabilities and long‐term well‐being remain primary goals. With this report, we provide the first long‐term assessment and interpretation of patterns in childhood cancer survival in Germany, covering a period of 30 years. Using data from the German Childhood Cancer Registry, we assessed temporal patterns of cancer survival among children (0‐14 years) diagnosed in Germany from 1991 to 2016, by cancer type, age at diagnosis and sex. We calculated overall survival (OS) and average annual percentage changes of the respective 5‐year OS estimates. OS improved across all cancer types, age groups as well as for boys and girls over time. Five‐year OS for all childhood cancers combined increased from 77.8% in 1991‐1995 to 86.5% in 2011‐2016, with stronger improvements during the early 1990s. The most pronounced survival improvement was seen for acute myeloid leukaemia, at 2% annually and 5‐year OS recently reaching 81.5%. Survival improvements for some diagnoses such as neuroblastoma, renal tumours and bone tumours have flattened out. Tremendous enhancements in diagnostics, treatment and supportive care have affected average survival improvements for most cancer types. Recently, survival improvements have decelerated overall and for some cancer types, it plateaued at an unsatisfactory level. As not all children benefited equally from the survival improvements, personal factors (eg, socioeconomic circumstances, health literacy, access to care) likely affect individual prognosis and warrant further investigation.
Chan, Jeffrey Shi Kai; Lee, Yan Hiu Athena; Hui, Jeremy Man Ho; Liu, Kang; Dee, Edward Christopher; Ng, Kenrick; Liu, Tong; Tse, Gary; Ng, Chi Fai
doi: 10.1002/ijc.34557pmid: 37183319
Our study investigated how adverse cardiovascular outcomes are impacted by cardiovascular comorbidities in patients with prostate cancer treated by androgen deprivation therapy (ADT). Using prospective, population‐based data, all Hong Kong patients with prostate cancer who received ADT during 1 January 1993 to 3 March 2021 were identified and followed up for the endpoint of cardiovascular hospitalization/mortality until 31 September 2021, whichever earlier. Multivariable competing risk regression was used to compare the endpoint's cumulative incidence between different combinations of major cardiovascular comorbidities (heart failure [HF], myocardial infarction [MI], stroke and/or arrhythmia), with noncardiovascular death as competing event. Altogether, 13 537 patients were included (median age 75.9 [interquartile range 70.0‐81.5] years old; median follow‐up 3.3 [1.5‐6.7] years). Compared to those with none of prior HF/MI/stroke/arrhythmia, the incidence of the endpoint was not different in those with only stroke (subhazard ratio [SHR] 1.06 [95% confidence interval (CI): 0.92‐1.23], P = .391), but was higher in those with only HF (SHR 1.67 [1.37‐2.02], P < .001), arrhythmia (SHR 1.63 [1.35‐1.98], P < .001) or MI (SHR 1.43 [1.14‐1.79], P = .002). Those with ≥2 of HF/MI/stroke/arrhythmia had the highest incidence of the endpoint (SHR 1.94 [1.62‐2.33], P < .001), among whom different major cardiovascular comorbidities had similar prognostic impacts, with the number of comorbidities present being significantly prognostic instead. In conclusion, in patients with prostate cancer receiving ADT, the sole presence of HF, MI or arrhythmia, but not stroke, may be associated with elevated cardiovascular risks. In those with ≥2 of HF/MI/stroke/arrhythmia, the number of major cardiovascular comorbidities may be prognostically more important than the type of comorbidities.
Chang, Vicky C.; Rhee, Jongeun; Berndt, Sonja I.; Moore, Steven C.; Freedman, Neal D.; Jones, Rena R.; Silverman, Debra T.; Gierach, Gretchen L.; Hofmann, Jonathan N.; Purdue, Mark P.
doi: 10.1002/ijc.34487
Voss, Féline O.; Thuijs, Nikki B.; Duin, Sylvia; Özer, Müjde; Beurden, Marc; Berkhof, Johannes; Steenbergen, Renske D. M.; Bleeker, Maaike C. G.
doi: 10.1002/ijc.34537pmid: 37074263
The precursor lesions of vulvar squamous cell carcinoma (VSCC) include human papillomavirus (HPV)‐associated and HPV‐independent squamous neoplasia with a varying cancer risk. Our study aimed to validate the accuracy of previously identified DNA methylation markers for detection of such high‐grade vulvar intraepithelial neoplasia (VIN). A large clinical series of 751 vulvar lesions, originally diagnosed as high‐grade VIN, were reassessed and categorized into HPV‐associated or HPV‐independent vulvar disease categories. Together with 113 healthy vulvar controls, all samples were tested for 12 methylation markers with quantitative multiplex methylation‐specific PCR (qMSP). Performance of individual markers and selection of an optimal marker panel for detection of high‐grade VIN was determined by logistic regression analysis. SST was the best‐performing individual marker (AUC 0.90), detecting 80% of high‐grade VIN cases, with excellent detection of HPV‐independent VIN (95%), known to have the highest cancer risk. Merely 2% of controls tested methylation positive for SST. Selection of a marker panel, including ZNF582, SST and miR124‐2, resulted in a comparably high accuracy for detection of high‐grade VIN (AUC 0.89). In conclusion, we clinically validated the accuracy of 12 DNA methylation markers for detection of high‐grade VIN. SST, as a sole marker or in a panel, provides an optimal diagnostic tool to distinguish high‐grade VIN in need of treatment, particularly HPV‐independent VIN, from low‐grade or reactive vulvar lesions. These findings warrant further prognostic validation of methylation biomarkers for cancer risk stratification of patients with VIN.
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Childbirth rates in classical Hodgkin lymphoma (cHL) survivors have historically been reduced compared to the general population. Understanding if contemporary treatment protocols are associated with reduced fertility is crucial as treatment guidelines shift toward more liberal use of intensive chemotherapy. We identified 2834 individuals aged 18‐40 years with cHL in Swedish and Danish lymphoma registers, and in the clinical database at Oslo University Hospital diagnosed 1995‐2018, who were linked to national medical birth registers. Cox regression adjusted for stage, performance status, year, and age at diagnosis was used to estimate hazard ratios (HRs) and 95% confidence intervals (CI) contrasting time to first childbirth by treatment groups (ABVD, 2‐4 BEACOPP, 6‐8 BEACOPP) up to 10 years after diagnosis. Overall, 74.8% of patients were treated with ABVD, 3.1% with 2‐4 BEACOPP and 11.2% with 6‐8 BEACOPP. Adjusted HRs comparing childbirth rates in individuals treated with 6‐8 BEACOPP, and 2‐4 BEACOPP to ABVD were 0.53 (CI: 0.36‐0.77) and 0.33 (CI: 0.12‐0.91) for males, and 0.91 (CI: 0.61‐1.34) and 0.38 (CI: 0.12‐1.21) for females. Cumulative incidence of childbirths after 10 years was 19.8% (CI: 14.5%‐27.0%) for males and 34.3% (CI: 25.8%‐45.6%) for females treated with 6‐8 BEACOPP. Proportions of children born after assisted reproductive technique (ART) treatments were 77.4% (CI: 60.2‐88.6%) for males following 6‐8 BEACOPP, and <11% for females. Among ABVD treated patients the corresponding proportions were 12.2% (CI: 8.5%‐17.3%) and 10.6% (CI: 7.4%‐14.9%). BEACOPP treatment is associated with decreased childbirth rates compared to ABVD in male, but not female, cHL patients, despite widespread access to ART in the Nordics.
doi: 10.1002/ijc.34554pmid: 37158671
The association between kidney function and cancer incidence is inconsistent among previous reports, and data on the Japanese population are lacking. It is unknown whether kidney function modifies the cancer risk of other factors. We aimed to evaluate the association of estimated glomerular filtration rate (eGFR) with cancer incidence and mortality in 55 242 participants (median age, 57 years; 55% women) from the Japan Multi‐Institutional Collaborative Cohort Study. We also investigated differences in cancer risk factors between individuals with and without kidney dysfunction. During a median 9.3‐year follow‐up period, 4278 (7.7%) subjects developed cancer. Moderately low and high eGFRs were associated with higher cancer incidence; compared with eGFR of 60‐74 ml/min/1.73 m2, the adjusted hazard ratios (HRs) (95% confidence intervals [CIs]) for eGFRs of ≥90, 75‐89, 45‐59, 30‐44 and 10‐29 ml/min/1.73 m2 were 1.18 (1.07‐1.29), 1.09 (1.01‐1.17), 0.93 (0.83‐1.04), 1.36 (1.00‐1.84) and 1.12 (0.55‐2.26), respectively. High eGFR was associated with higher cancer mortality, while low eGFR was not; the adjusted subdistribution HRs (95% CIs) for eGFRs of ≥90 and 75‐89 ml/min/1.73 m2 were 1.58 (1.29‐1.94) and 1.27 (1.08‐1.50), respectively. Subgroup analyses of participants with eGFRs ≥60 and <60 ml/min/1.73 m2 revealed elevated cancer risks of smoking and family history of cancer in those with eGFR <60 ml/min/1.73 m2, with significant interactions. Our findings suggest that the relationship between eGFR and cancer incidence was U‐shaped. Only high eGFR was associated with cancer mortality. Kidney dysfunction enhanced cancer risk from smoking.
Globally, bladder cancer has been identified as one of the most frequent occupational cancers, but our understanding of occupational bladder cancer risk in Iran is less advanced. This study aimed to assess the risk of bladder cancer in relation to occupation in Iran. We used the IROPICAN case‐control study data including 717 incident cases and 3477 controls. We assessed the risk of bladder cancer in relation to ever working in major groups of the International Standard Classification of Occupations (ISCO‐68) while controlling for cigarette smoking, opium consumption. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CI). In men, decreased ORs for bladder cancer were observed in administrative and managerial workers (OR 0.4; CI: 0.2, 0.9), and clerks (OR 0.6; CI: 0.4, 0.9). Elevated ORs were observed in metal processors (OR 5.4; CI: 1.3, 23.4), and workers in occupations with likely exposure to aromatic amines (OR 2.2; CI: 1.2, 4.0). There was no evidence of interactions between working in aromatic amines‐exposed occupations and tobacco smoking or opium use. Elevated risk of bladder cancer in men in metal processors and workers likely exposed to aromatic amines aligns with associations observed outside Iran. Other previously confirmed associations between high‐risk occupations and bladder cancer were not observed, possibly due to small numbers or lack of details on exposure. Future epidemiological studies in Iran would benefit from the development of exposure assessment tools such as job exposure matrices, generally applicable for retrospective exposure assessment in epidemiological studies.
Per‐ and polyfluoroalkyl substances (PFAS) are highly persistent endocrine‐disrupting chemicals that may contribute to breast cancer development; however, epidemiologic evidence is limited. We investigated associations between prediagnostic serum levels of perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) and postmenopausal breast cancer risk, overall and by hormone receptor status, in a nested case‐control study of 621 cases and 621 matched controls in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. PFOS and PFOA levels were determined based on serum metabolomic profiling performed using ultraperformance liquid chromatography‐tandem mass spectrometry. We used multivariable conditional logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between each PFAS and breast cancer risk, overall, by estrogen receptor (ER) or progesterone receptor (PR) status, and by joint ER/PR status. We found little evidence of association between PFOS or PFOA and breast cancer risk overall. However, in subtype‐specific analyses, we observed statistically significant increased risks of ER+, PR+, and ER+/PR+ tumors for the third vs lowest quartile of serum PFOS (ORs [95% CIs] = 1.59 [1.01‐2.50], 2.34 [1.29‐4.23], and 2.19 [1.21‐3.98], respectively) and elevated but nonstatistically significant ORs for the fourth quartile. Conversely, for PFOA, modest positive associations with ER−, PR−, ER+/PR−, and ER−/PR− tumors were generally seen in the upper quartiles. Our findings contribute evidence supporting positive associations between serum PFOS and hormone receptor‐positive tumors, and possibly between PFOA and receptor‐negative tumors. Future prospective studies incorporating tumor hormone receptor status are needed to better understand the role of PFAS in breast cancer etiology.