Hypertension is the most prevalent comorbidity in cancer patients. Consequently, many cancer patients are prescribed antihypertensive drugs before cancer diagnosis or during cancer treatment. However, whether antihypertensive drugs affect the incidence, treatment efficacy, or prognosis of cancer remains unanswered. For instance, renin-angiotensin and β-adrenergic signaling may be involved not only in blood pressure elevation but also in cell proliferation, angiogenesis, and tissue invasion. Therefore, the inhibition of these pathways may have beneficial effects on cancer prevention or treatment. In this article, we reviewed several studies regarding antihypertensive drugs and cancer. In particular, we focused on the results of clinical trials to evaluate whether the use of antihypertensive drugs affects future cancer risk and prognosis. Unfortunately, the results are somewhat inconsistent, and evidence demonstrating the effect of antihypertensive drugs remains limited. We indicate that the heterogeneity in the study designs makes it difficult to clarify the causal relationship between antihypertensive drugs and cancer. We also propose that additional experimental studies, including research with induced pluripotent cells derived from cancer patients, single-cell analyses of cancer cell clusters, and clinical studies using artificial intelligence electronic health record systems, might be helpful to reveal the precise association between antihypertensive drugs and cancer risk.

BACKGROUND: Cancer-related incidence and mortality rates are rapidly increasing worldwide. However, no studies have examined the effect of cancer as a single factor on the use of traditional, complementary, and alternative medicine (T&CAM). We aimed to determine the effect of cancer occurrence on T&CAM utilization using Korea Health Panel (KHP) data.
METHODS: We analyzed longitudinal data (49,380 observations) derived from 12,975 Korean adult participants with complete KHP data from 2011 to 2014 and 2016, and divided them into two groups based on cancer diagnosis. A panel multinomial logit model was used to assess whether the participants used T&CAM or conventional medicine or both in outpatient settings. Additionally, a negative binomial regression model was used to examine the effect of cancer on the number of outpatient visits for T&CAM.
RESULTS: In total, 25.54% of the study participants in the cancer group used T&CAM, which was higher than that in the non-cancer group (18.37%, p < 0.0001). A panel multinomial logistic regression analysis using KHP data showed that cancer occurrence was significantly more likely to be associated with \'Using both Korean medicine and conventional medicine\' (Coef. = 0.80, p = 0.017) and \'Not using Korean medicine but using conventional medicine\' (Coef. = 0.85, p = 0.008) than \'Not using Korean medicine and conventional medicine.\' A panel negative binomial regression showed a significant effect of cancer on increasing the number of T&CAM outpatient visits (Coef. = 0.11, p = 0.040).
CONCLUSIONS: Our findings showed that cancer occurrence within an individual led to the simultaneous use of conventional medicine and T&CAM. In addition, the occurrence of cancer significantly increased the number of T&CAM outpatient visits among participants already using T&CAM. It was also found that T&CAM has been utilized more often by the most vulnerable people, such as medical beneficiaries and those with a low level of education.

Studies have reported conflicting results on the association between the use of renin-angiotensin-aldosterone system (RAAS) inhibitors and cancer development. We compared the incidence of cancer between patients using RAAS inhibitors and other antihypertensive drugs. This retrospective observational cohort study used data from seven hospitals in Korea that were converted for use in the Observational Medical Outcomes Partnership Common Data Model. A total of 166,071 patients on antihypertensive therapy across the databases of the seven hospitals were divided into two groups according to the use of RAAS inhibitors. The primary outcome was the occurrence of cancer. A total of 166,071 patients across the databases of the seven hospitals was included in the final analysis; 26,650 (16%) were in the RAAS inhibitors group and 139,421 (84%) in the other antihypertensive drugs group. The meta-analysis of the whole cohort showed a lower incidence of cancer occurrence in the RAAS inhibitor group (9.90 vs. 13.28 per 1000 person years; HR, 0.81; 95% confidence interval [CI], 0.75-0.88). After propensity-score matching, the RAAS inhibitor group consistently showed a lower incidence of cancer (9.90 vs. 13.28 per 1000 person years; HR, 0.86; 95% CI, 0.81-0.91). The patients using RAAS inhibitors showed a lower incidence of cancer compared with those using other antihypertensive drugs. These findings support the association between the use of RAAS inhibitors and cancer occurrence.

BACKGROUND: Treatment for non-small cell lung cancer (NSCLC) has greatly improved in recent years. However, noninvasive early screening for carcinogenesis and progression unclear. The aim of this study was to explore the predictive value of peripheral blood immune cells in untreated NSCLC patients.
METHODS: We retrospectively enrolled 305 untreated NSCLC patients and 132 healthy participants from February 2016 to August 2019 in Peking Union Medical College Hospital. Immune cell levels were determined by flow cytometry and routine blood tests.
RESULTS: NSCLC patients had lower levels of T lymphocytes, NK cells, CD8+ T cells, naïve CD4+/CD4+, naïve CD4+ T cells and higher levels of CD4+ T cells, memory CD4+/CD4+ T cells, memory CD4+ T cells, CD4+CD28+/CD4+ T cells, CD4+CD28+ T cells, CD8+CD28+/CD8+ T cells, CD8+HLA-DR+/CD8+ T cells, CD8+HLA-DR+ T cells T cells, CD8+CD38+/CD8+ T cells, CD8+CD38+ T cells and CD4+/CD8+ T cells than those in controls. The percentages of specific lymphocyte subtypes were significantly different in cancer patients versus healthy individuals. For instance, cancer patients had lower levels of B cells, CD4+ T cells, naïve CD4+/CD4+ T cells, naïve CD4+ T cells, CD4+CD28+ T cells, CD8+CD28+ T cells and higher levels of NK cells, white blood cells (WBC), monocytes, neutrophils, eosinophils, basophils, monocytes to lymphocyte ratio (MLR), neutrophils to lymphocyte ratio (NLR), eosinophil to lymphocyte ratio (ELR), basophil to lymphocyte ratio (BLR), and blood platelet to lymphocyte ratio (PLR).
CONCLUSIONS: Abnormal T cell levels can be used as an independent predictive biomarker for noninvasive early screening in NSCLC occurrence and progression.

Cancer among patients with systemic sclerosis (SSc) would appear to be more prevalent than in the general population. Pathophysiological hypotheses are multiple, involving intertwined factors such as immune system antitumoral response, oxygen species dysregulation, and immunosuppressive treatments. We aimed to identify SSc patients with cancer monitored at our center, describing their clinical and immunological characteristics, such as cancer-specific outcomes. We focused in particular on the temporal relationships between cancer onset and SSc diagnosis. A retrospective study was conducted on SSc patients from Montpellier University Hospital from 2003 to 2018. Clinical characteristics and outcomes of each SSc patient with cancer were recorded. Fifty-five patients with SSc and at least one cancer was included (median age 56 years (47-66)), with a median follow-up time of 11 years (4-15). Sixty-four metachronous malignancies were identified (12 patients had two cancers). Among them, early-onset cancer occurrences (±5 years from SSc diagnosis) included 23 cancers (39% breast cancers, 13% lung cancers, and 13% gastro-intestinal tract cancers). Twenty-two cancers occurred 10 years (±5 years) after SSc diagnosis (14% breast cancers, 23% gastrointestinal (GI) tract cancers, and 18% lung cancers). Patients without any of the two autoantibodies (anti-centromere (ACA) and anti-topoisomerase (ATA-scl70) antibodies) were more prevalent in the early-onset cancer subgroup (14 vs. 6, p = 0.02). This study brought to light two peaks of cancer occurrence in SSc patients. Early-onset cancers were associated with SSc with a specific immunological signature. Late-onset cancers might be the consequence of a subtle interplay between repeated target organ inflammation, immunosuppressant use, mesenchymal cell dysfunction and subsequent genetic alterations.

The risk of cancer is higher in patients with renal diseases and diabetes compared with the general population. The aim of this study was to assess in dialyzed patients, the association between diabetes and the risk to develop a cancer after dialysis start.
All patients who started dialysis in the French region of Poitou-Charentes between 2008 and 2015 were included. Their baseline characteristics were extracted from the French Renal Epidemiology and Information Network and were linked to data relative to cancer occurrence from the Poitou-Charentes General Cancer Registry using a procedure developed by the INSHARE platform. The association between diabetes and the risk of cancer was assessed using the Fine & Gray model that takes into account the competing risk of death.
Among the 1634 patients included, 591 (36.2 %) had diabetes and 91 (5.6 %) patients developed a cancer (n = 24 before or at dialysis start, and n = 67 after dialysis start). The risk to develop a cancer after dialysis initiation was lower in dialyzed patients with diabetes than without diabetes (SHR = 0.54; 95 %CI: 0.32-0.91). Moreover, compared with the general population, the cancer risk was higher in dialyzed patients without diabetes, but not in those with diabetes.
The risk of developing a cancer in the region of Poitou-Charentes is higher in dialyzed patients without diabetes than with diabetes.

In order to identify the signature genes of tumorigenesis, the pattern-recognition method was used to analyze the gene methylation (ME) data which included only normal and cancer samples and was collected from the TCGA (The Cancer Genome Atlas) database. Here, we analyzed the DNA methylation profiles of the six types of cancer and the ME signature genes for each cancer were selected by means of a combination of correlation, student\'s t-test and Elastic Net. Modeling by support vector machine, the accuracy of ME signature genes can be as high as 98 % for training set and as high as 97 % for the independent test set, the recognition accuracy of stage I is more than 97 % for training set and more than 98 % for test set. Then, the common signature genes and common pathways emerging in multiple cancers were obtained. A functional analysis of these signature genes indicates that the identified signatures have direct relationship with tumorigenesis and is very important for understanding the pathogenesis of cancer and the early therapy.

DNA nuclease/helicase 2 (DNA2), a multi-functional protein protecting the high fidelity of genomic transmission, plays critical roles in DNA replication and repair processes. In the maturation of Okazaki fragments, DNA2 acts synergistically with other enzymes to cleave the DNA-RNA primer flaps via different pathways. DNA2 is also involved in the stability of mitochondrial DNA and the maintenance of telomeres. Moreover, DNA2 potentially participates in controlling the cell cycle by repairing the DNA replication faults at main checkpoints. In addition, previous evidences demonstrated that DNA2 also functions in the repair process of DNA damages, such as base excision repair (BER). Currently, large studies revealed the structures and functions of DNA2 in prokaryotes and unicellular eukaryotes, such as bacteria and yeast. However, the studies that highlighted the functions of human DNA2 (hDNA2) and the relationships with other multifunctional proteins are still elusive, and more precise investigations are immensely needed. Therefore, this review mainly encompasses the key functions of DNA2 in human cells with various aspects, especially focusing on the genome integrity, and also generalizes the recent insights to the mechanisms related to the occurrence of cancer and other diseases potentially linked to the mutations in DNA2.