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At least 19 recordsLinked to original sources
PubMed2026

Association of cancer antigen 15-3 with distant recurrence in immunohistochemically defined breast cancer subtypes in Canadian Cancer Trials Group MA.32.

BACKGROUND: Circulating levels of cancer antigen (CA) 15-3 have been associated with distant breast cancer recurrence; data on breast cancer subtypes are sparse. We examined associations of CA 15-3 with outcomes across immunohistochemically defined breast cancer subtypes in MA.32. METHODS: A total of 3649 participants with T1-3, N0-1, M0 breast cancer were randomly assigned; 2740 (75.1%) provided blood at entry (mean = 278&#x2009;days postdiagnosis) and 6&#x2009;months later. Prognostic associations of baseline and 6-month change in CA 15-3 with distant recurrence-free survival (RFS) were examined in luminal (estrogen receptor-positive and/or progesterone receptor-positive, HER2-negative), triple-negative (estrogen receptor, progesterone receptor, HER2 negative) and HER2-positive (any estrogen receptor, progesterone receptor) breast cancer using Cox proportional hazards models. RESULTS: Mean age was 52&#x2009;years. Breast cancer was luminal in 1589 (58.7%), triple negative in 655 (24.2%), and HER2 positive in 464 (17.1%) participants. Median follow-up was 96&#x2009;months. CA 15-3 at study entry was not associated with outcome in any subtype. Rising CA 15-3 at 6&#x2009;months was associated with poor distant RFS in luminal and triple-negative breast cancer (hazard ratio [HR] per 25% increase&#x2009;=&#x2009;1.41, P&#x2009;<&#x2009;.0001, and HR = 1.35, P&#x2009;<&#x2009;.0001, respectively). New elevations in CA 15-3 at 6&#x2009;months were adversely associated with distant RFS in those with luminal or triple-negative breast cancer (HR = 4.14, 95% CI = 2.69 to 6.38; P&#x2009;<&#x2009;.001; and HR = 3.57, 95% CI = 1.59 to 7.99; P&#x2009;=&#x2009;.002, respectively). In HER2-positive breast cancer, CA15-3 was not associated with distant RFS. CONCLUSION: Rising CA 15-3 was associated with reduced distant RFS in luminal and triple-negative breast cancer but not in HER2-positive breast cancer. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov NCT01101438.

Humans↗
PubMed1978

[Surgical treatment of pulmonary coin lesions found in cancer patients and 6 breast cancers. Solitary metastasis? 2d primary bronchopulmonary cancer? Coin lesions of benign nature?].

Pulmonary diffusion of breast cancer is frequent in those patients who have died of the disease and in those survivors who have not been cured after removal of the breast and X-ray treatment in the advanced states of the disease. When the metastases are identified, they are almost always multiple and bilateral. The appearance of a solitary, late, pulmonary coin lesion (metachrone), in someone with breast cancer certainly suggests a pulmonary metastase, but in fact, it is more likely to be a second cancer than a metastase, that is, a primary bronchopulmonary cancer. The presence of a solitary pulmonary coin lesion in someone who has or who has had breast cancer, presents therefore certain particular problems. After having controlled by xerotomography that there is no pulmonary diffusion in either lung, that there is no invasion of other tissues or organs, and after having controlled locally around the breast cancer, then it is imperative to remove the lesion without delay since it is certainly malignant and most probably a second cancer, that is, a primary bronchopulmonary cancer, an adenocarcinome, detected at an asymptomatic stage. The prognosis of a broncho-pulmonary adenocarcinome depends on the precocity of its removal.

Adenocarcinoma↗
PubMed1979

Tumor-associated antigens in cervical cancer tissues and in sera from patients with cervical cancer or with head and neck cancer.

Hyperimmune New Zealand White rabbit sera prepared against partially purified tumor-associated antigens (TAA) of invasive cervical cancer tissues (CaCx's) were used to demonstrate TAA in CaCx's and circulating TAA (C-TAA) in sera from patients with cervical cancer or with head and neck cancer. Anti-CaCx serum adsorbed with pooled normal cervical tissue (NCx) antigen preparations and with lyophilized pooled normal human plasma gave precipitin in gel reactions with CaCx but not with NCx, which indicated the presence of TAA in CaCx. The adsorbed antisera reacted with sera from patients with cervical and head and neck cancers, which indicated the presence of C-TAA in such sera. False-positive reactions with control sera from normal humans or from patients with benign gynecologic diseases were much less frequently observed. Statistical analysis of data obtained by the testing of 96 coded serum samples from the National Cancer Institute-Mayo Clinic Serum Bank (Rochester, Minn.) revealed that the results were significant and that specificity was high but sensitivity of the assay was relatively low.

Adult↗
PubMed2025

Established Cancer Predisposition Genes in Single and Multiple Cancer Diagnoses.

IMPORTANCE: Much of the understanding of cancer risk associated with rare pathogenic variants (RPVs) is derived from family-based studies or clinically ascertained samples, which may be limited by ascertainment and selection bias. OBJECTIVE: To quantify associations between RPVs in previously implicated cancer predisposition genes and single and multiple cancer diagnoses in a large population-based study. DESIGN, SETTING, AND PARTICIPANTS: In this genetic association study, whole-exome sequencing data were used from the UK Biobank, a UK population-based cohort that enrolled participants aged 40 to 69 years between 2006 and 2010. Participants who were involved in the whole-exome sequencing release of 200&#x202f;000 genomes in 2020 were included in this study. This analysis included White participants only, as findings in other racial and ethnic groups had small sample sizes. Participants were diagnosed before or after biobank enrollment until March 2024. EXPOSURES: The sequencing data of a set of 96 previously implicated cancer predisposition genes were analyzed and compared using 2 methods. To determine the statistical significance of an association, a robust optimal sequence kernel association test was used, while odds ratios (ORs) and 95% CIs were obtained through Firth logistic regression. MAIN OUTCOMES AND MEASURES: The primary study outcome was the diagnosis of 1 of 11 cancers (bladder, breast, central nervous system, colorectal, lung, melanoma, ovary, pancreatic, prostate, renal, thyroid) defined by relevant diagnosis codes in inpatient hospital diagnosis, cancer registry, and/or death registry data. RESULTS: Data from 183&#x202f;627 participants (101&#x202f;414 [55.2%] female) were analyzed, including 25&#x202f;824 participants with at least 1 cancer diagnosis, of whom 23&#x202f;704 (91.8%) had a single cancer diagnosis and 2130 (8.2%) had 2 or more cancer diagnoses. A total of 157&#x202f;793 controls had no cancer diagnosis. The median (IQR) age was 62 (56-65) years in participants with at least 1 cancer diagnosis, compared to 57 (50-63) years in those without a cancer diagnosis. Genetic variation in 16 genes was significantly associated with at least 1 cancer of interest (ATM, BARD1, BRCA1, BRCA2, BRIP1, CDKN2A, CHEK2, HOXB13, MITF, MLH1, MSH2, MSH6, NF1, PALB2, RAD51C, and RAD51D). The presence of an RPV in 1 of these 16 genes was associated with increased odds of at least 1 cancer (OR, 1.87; 95% CI, 1.76-1.98) and multiple primary cancers (OR, 2.56; 95% CI, 2.18-2.99). Carrier frequency was 6.28% and 8.36%, respectively. CONCLUSIONS AND RELEVANCE: This genetic association study demonstrates several established associations between cancer predisposition genes and cancer diagnoses in an unselected population-based study. These results also demonstrate that RPVs in cancer predisposition genes are associated with multiple primary cancer diagnoses, suggesting that multigene panel testing may be warranted in these individuals.

Humans↗
PubMed2026

Cancer stemness-modulating (CSM) proteins in pan-cancer chemoresistance: regulatory roles and mechanisms.

Cancer stemness is a property of cancer cells that plays critical roles in tumorigenesis and therapeutic resistance. We previously identified and categorized, based on literature evidence, a group of fourteen cancer stemness-modulating (CSM) circular RNAs (circRNAs) in colorectal cancer (CRC), which we termed CSM-circRNAs. In the present work, we show that the proteins regulated by these CRC CSM-circRNAs, with one exception for which information is currently unavailable, are bona fide modulators of cancer stemness across a wide range of cancer types. We, therefore, designate these proteins as CSM-proteins. As chemoresistance is a major trait of cancer stemness, we further investigated the molecular mechanisms through which CSM-proteins contribute to chemoresistance. Our analysis reveals that twelve CRC CSM-proteins are implicated in chemoresistance across fourteen cancer types and resistance to ten therapeutic agents. Nine distinct chemoresistance mechanisms are identified and organized into five broader functional axes: survival, drug processing, genome maintenance, plasticity and adaptation, leading us to propose an integrated mechanistic framework for CSM-protein-mediated chemoresistance. Most CSM-proteins operate across multiple functional axes in different cancer contexts, with survival-associated mechanisms, particularly apoptosis evasion, and epithelial-mesenchymal transition-associated plasticity emerging as the predominant modes of chemoresistance. Furthermore, transcriptional regulatory CSM-proteins exhibit broader mechanistic profiles than other molecular categories, although the strength and extent of evidence vary across proteins and cancer types. Taken together, the proposed CSM-protein pan-cancer chemoresistance framework offers a biologically and therapeutically relevant regulatory network for understanding the mechanisms underlying cancer chemoresistance based predominantly on preclinical evidence. Our findings may provide a preclinical conceptual foundation for the development of combinatorial therapeutic strategies targeting cancer stemness and chemoresistance through the CSM-circRNA-CSM-protein regulatory axis.

Cancer stemness↗
PubMed2025

Evaluating Patient Experience With Genomic Medicine: A Content Analysis of National Cancer Institute-Designated Cancer Centers' Websites.

BACKGROUND: National Cancer Institute-designated cancer centers (NCI-CCs) throughout the United States are mandated to translate state-of-the-art cancer research to communities and enhance clinical care for patients within their catchment areas. NCI-CCs play a vital role in national cancer initiatives focused on optimizing cancer care via personalized medicine in which improved risk assessment, screening, and genetic testing are foundational. In this era of targeted personalized care, although genetics has been incorporated into cancer centers, it is unknown how these innovations are being communicated to the public and communities served on cancer center websites. There is particularly limited knowledge surrounding how NCI-CCs publicly communicate their efforts to integrate patient-reported experiences with genomics to fulfill their overall mission and reduce the cancer burden in their catchment areas. OBJECTIVE: The objective of this study was to evaluate how NCI-CCs publicly share information on their websites related to cancer center programming and activities to measure and incorporate patients' experiences with the use of genetics to guide cancer care. METHODS: For all NCI-CCs providing clinical care (N=65), we conducted a review of publicly available and published information and assessed five domains relevant to patients' experiences with genomic medicine: whether NCI-CCs (1) provided genetic testing, (2) directly expressed a goal of delivering personalized care, (3) provided pharmacogenomic testing, (4) assessed patient-reported experience measures with genomic medicine (including patient-reported outcomes [PROs] and other patient experience measures [OPEMs]), and (5) indicated an established infrastructure or set of resources to evaluate patient experience. We conducted a content analysis of the publicly available websites of NCI-CCs using the validated directed approach to content analysis. We quantified the results of our content analysis using count measures based on a binary (yes or no) coding scheme. RESULTS: While almost all the NCI-CCs (64/65, 98%) discussed providing personalized care and performing genetic testing on their websites, we found that 58% (38/65) indicated online that they assessed PROs or other patient experience measures with genomic medicine. Fewer centers (25/65, 38%) discussed on their websites having a mechanism for evaluating patients' experiences with genomic medicine that captured broader types of information beyond PROs, such as measures of patient education or care team communication. Finally, approximately 1 in 3 NCI-CCs (23/65, 35%) indicated having an established infrastructure with departmental resources dedicated to monitoring patients' experiences. These centers reflecting a built-in infrastructure were 8% to 12% more likely to publicly communicate targeted activities to assess patients' experiences with genomic medicine. CONCLUSIONS: With the burgeoning use of genomics in research and clinical care, comprehensive evaluation and incorporation of measures of patients' experiences with genomic medicine present a key opportunity to enhance cancer care at NCI-CCs.

Humans↗
PubMed2025

Predicting breast cancer risk and its association to biopsychosocial factors among Taiwanese women with a family history of breast cancer: an investigation based on the Gail model.

BACKGROUND: First-degree relatives with breast cancer have a two-fold higher risk than women without a family history. The Gail model approach has been employed in numerous studies to investigate the risk of breast cancer among women in a variety of countries. Nevertheless, the studies investigating the correlation between the level of breast cancer risk and biopsychosocial factors among Taiwanese women with a family history of breast cancer (FHBC) are limited. By using the Gail model, we explored the breast cancer risk score and its relationship to biopsychosocial factors among Taiwanese women with FHBC. METHODS: The present study was a cross-sectional study from secondary data of the Taiwan Biobank from 2008 to 2018. Self-reports were conducted to determine biopsychosocial factors. A total of 3,060 women aged 35-70 years with and without FHBC were considered eligible for enrollment. The Gail model, which utilizes six questions, was used to estimate individual five-year absolute breast cancer risk. Women with scores at least 1.66% and above were categorized as high risk. In addition, we performed bivariate and multivariate logistic regression analysis using SPSS version 27 to predict the associations between biopsychosocial factors and the risk of breast cancer based on the Gail model. All analyses were stratified by age. RESULTS: Among the 3,060 Taiwanese women, there was a statistically significant difference in breast cancer risk score between the groups with and without FHBC (p&#x2009;=&#x2009;<&#x2009;0.001), stratified by age, of which 574 in FHBC group (34.2%) were identified as having a high breast cancer risk based on the Gail model. Furthermore, six out of 15 biopsychosocial factors were significantly associated with breast cancer risk in women under 50 years of age, while seven factors showed significant associations in women aged 50 years and older. Logistic regression analysis identified five biopsychosocial factors as consistent and significant predictors of breast cancer risk in women aged 50 years and older, highlighting this group as particularly vulnerable. CONCLUSIONS: This study concludes that the Gail model identifies Taiwanese women who have a higher estimated risk of breast cancer based on cross-sectional data. Various biopsychosocial factors are associated with higher risk estimates in this population particularly in older women. Professionals can assist women in recognizing risk factors beyond the inevitable risk by encouraging regular screenings, positive behavior, and health promotion.

Humans↗
PubMed1979

Aryl hydrocarbon hydroxylase activity in pulmonary alveolar macrophages and lymphocytes from lung cancer and noncancer patients: a correlation with family histories of cancer.

Aryl hydrocarbon hydroxylase (AHH) activity was measured in pulmonary alveolar macrophages (PAMs) and peripheral blood lymphocytes from cigarette smokers with and without primary lung cancer. Frequency distribution analysis of AHH induction ratios for the two groups revealed an increased number of individuals in the lung cancer patient group with high lymphocyte induction values (P less than 0.05). A similar increase was not shown for high-PAM AHH values in lung cancer patients (P greater than 0.2). When individual PAM and lymphocyte AHH values were compared between noncancer and lung cancer patients, a positive correlation was observed for noncancer patients (r=0.195, P less than 0.001), but no correlation of these values was noted for lung cancer patients. The lung cancer patients were divided into three subgroups of patients showing (I) high PAM and low lymphocyte AHH levels, (II) low PAM and low lymphocyte AHH levels, and (III) low PAM and high lymphocyte AHH levels. When the incidence of family history of cancer was compared for these subgroups, no family cancer history was recorded for persons in subgroup II; however, individuals in subgroups I and III presented family cancer history incidence of 9.5% and 39.3%, respectively. Patients in group III averaged 6 years younger than those in group I. These data suggest that familial factors may be identified among lung cancer patients and that these factors appear to associate as either a cause of an effect with the capacity of pulmonary alveolar macrophages and lymphocytes to be induced for AHH. The data support the hypothesis that high AHH values may be characteristic of lung cancer patients but show that enzyme values determined from a single tissue, either PAMs or lymphocytes, may not be appropriate for showing whether high AHH inducibility is correlated with lung cancer.

Aryl Hydrocarbon Hydroxylases↗
PubMed2026

Comprehensive Genomic Analysis of Normal and Cancer Cells Elucidates the Elevated Mutation Burden in Cancer.

Self-renewing normal tissues generate several somatic mutations at each division. Previous studies have reported that cancer cells have more mutations than their normal counterparts. It is not obvious why dramatic differences in mutation burdens between normal tissues and cancers should exist. To fully understand human tumorigenesis, the increase of mutation burden in cancers will have to be understood. Here, we provided a systematic comparison of mutational burdens in normal and cancer cells from five different organs, revealing a four-fold increase of mutation burdens in cancerous vs. non-cancerous cells. Three proposed hypotheses that could account for the increased mutation burdens in cancer are: the classical hypothesis, where driver gene mutations explain the higher mutational burden; the catastrophic hypothesis, where extreme mutational events lead to large-scale genomic alterations; and the tail hypothesis, where differences in baseline mutation rates among individuals account for the differences. Testing through orthogonal observations showed that the observed medians and distributions of mutation burdens in cancers could be explained by the hypotheses to various degrees of significance, and only the tail hypothesis could easily explain the increase in median mutation burdens in the normal tissues of cancer patients compared to the normal tissues of non-cancer patients. Overall, this study characterizes an increased mutation burden across multiple types of cancer compared to normal tissue and provides insights into the contributing factors. A tenable hypothesis proposed in this study involving fundamental differences in baseline mutation rates among individuals could have implications for cancer prevention strategies.

Journal Article↗
PubMed2025

Recessive FANCM cancer syndrome with high cancer risks, chemotherapy toxicity, chromosome fragility, and gonadal failure.

PURPOSE: Heterozygous FANCM variants have been associated with breast cancer. Only a few studies have examined other cancer types. Biallelic truncating variants have been linked to a Fanconi anemia (FA)-like cancer prone syndrome in case reports; however, the range of cancers and the risk estimates are lacking. METHODS: We studied the association of Finnish-enriched variants c.5101C>T p.(Gln1701Ter) and c.5791C>T p.(Arg1931Ter) with risk of any cancer and FA-related conditions in the FinnGen data with 500,348 individuals. RESULTS: Heterozygous c.5101C>T (N = 10,940) was associated not only with an increased risk of breast cancer (odds ratio = 1.24, P = 2.7 &#xd7; 10-6) but also with risks of other cancer types, including hypopharyngeal (odds ratio = 3.98, P = 3.6 &#xd7; 10-7), suggesting a risk effect wider than previously described. Homozygous c.5101C>T (N = 76) was associated with a high risk of breast, head and neck, gastrointestinal, gynecological, hematologic, skin, and lung cancer, whereas c.5791C>T was rare. Additionally, high recessive risks of ovarian dysfunction and hematologic side effects after cancer treatment were detected, but no risks of bone marrow failure or physical features of FA. CONCLUSION: Based on the pattern of risks associated with biallelic variants, we suggest a novel FANCM cancer syndrome that is separate from FA and other characterized cancer susceptibility syndromes.

Humans↗
PubMed2025

Circulating microRNA panels for multi-cancer detection and gastric cancer screening: leveraging a network biology approach.

BACKGROUND: Screening tests, particularly liquid biopsy with circulating miRNAs, hold significant potential for non-invasive cancer detection before symptoms manifest. METHODS: This study aimed to identify biomarkers with high sensitivity and specificity for multiple and specific cancer screening. 972 Serum miRNA profiles were compared across thirteen cancer types and healthy individuals using weighted miRNA co-expression network analysis. To prioritize miRNAs, module membership measure and miRNA trait significance were employed. Subsequently, for specific cancer screening, gastric cancer was focused on, using a similar strategy and a further step of preservation analysis. Machine learning techniques were then applied to evaluate two distinct miRNA panels: one for multi-cancer screening and another for gastric cancer classification. RESULTS: The first panel (hsa-miR-8073, hsa-miR-614, hsa-miR-548ah-5p, hsa-miR-1258) achieved 96.1% accuracy, 96% specificity, and 98.6% sensitivity in multi-cancer screening. The second panel (hsa-miR-1228-5p, hsa-miR-1343-3p, hsa-miR-6765-5p, hsa-miR-6787-5p) showed promise in detecting gastric cancer with 87% accuracy, 90% specificity, and 89% sensitivity. CONCLUSIONS: Both panels exhibit potential for patient classification in diagnostic and prognostic applications, highlighting the significance of liquid biopsy in advancing cancer screening methodologies.

Neoplasms↗
PubMed2024

Epigenetic dynamics of aging and cancer development: current concepts from studies mapping aging and cancer epigenomes.

PURPOSE OF REVIEW: This review emphasizes the role of epigenetic processes as incidental changes occurring during aging, which, in turn, promote the development of cancer. RECENT FINDINGS: Aging is a complex biological process associated with the progressive deterioration of normal physiological functions, making age a significant risk factor for various disorders, including cancer. The increasing longevity of the population has made cancer a global burden, as the risk of developing most cancers increases with age due to the cumulative effect of exposure to environmental carcinogens and DNA replication errors. The classical 'somatic mutation theory' of cancer cause is being challenged by the observation that multiple normal cells harbor cancer driver mutations without resulting in cancer. In this review, we discuss the role of age-associated epigenetic alterations, including DNA methylation, which occur across all cell types and tissues with advancing age. There is an increasing body of evidence linking these changes with cancer risk and prognosis. SUMMARY: A better understanding about the epigenetic changes acquired during aging is critical for comprehending the mechanisms leading to the age-associated increase in cancer and for developing novel therapeutic strategies for cancer treatment and prevention.

Humans↗
PubMed2026

Non-Cancer Causes of Death in Patients With Metastatic Hormone-Sensitive Prostate Cancer: A Real-World Analysis.

BACKGROUND: As overall survival improves in metastatic hormone-sensitive prostate cancer (mHSPC), non-cancer causes of death are increasingly relevant. METHODS: We conducted a real-world multicenter study of patients diagnosed with mHSPC treated with ADT alone or in combination. Causes of death before progression to castration-resistant prostate cancer (CRPC) were classified as cancer- or non-cancer-related. Deaths were classified as non-cancer-related if they occurred in the absence of cancer progression. RESULTS: Among 565 patients, 35 (6.2%) died from non-cancer-related causes without disease progression, mainly infections (34%) and cardiovascular events (20%). CONCLUSIONS: Non-cancer mortality represents a meaningful proportion of deaths in mHSPC, supporting systematic cardiovascular risk evaluation and infection-prevention strategies.

Humans↗