BackgroundBreast cancer is estimated to be the most common cancer worldwide. We sought to assemble publicly available data from Africa to provide estimates of the incidence of breast cancer on the continent.MethodsA systematic search of Medline, EMBASE, Global Health and African Journals Online (AJOL) was conducted. We included population- or hospital-based registry studies on breast cancer conducted in Africa, and providing estimates of the crude incidence of breast cancer among women. A random effects meta-analysis was employed to determine the pooled incidence of breast cancer across studies.ResultsThe literature search returned 4648 records, with 41 studies conducted across 54 study sites in 22 African countries selected. We observed important variations in reported cancer incidence between population- and hospital-based cancer registries. The overall pooled crude incidence of breast cancer from population-based registries was 24.5 per 100 000 person years (95% confidence interval (CI) 20.1-28.9). The incidence in North Africa was higher at 29.3 per 100 000 (95% CI 20.0-38.7) than Sub-Saharan Africa (SSA) at 22.4 per 100 000 (95% CI 17.2-28.0). In hospital-based registries, the overall pooled crude incidence rate was estimated at 23.6 per 100 000 (95% CI 18.5-28.7). SSA and Northern Africa had relatively comparable rates at 24.0 per 100 000 (95% CI 17.5-30.4) and 23.2 per 100 000 (95% CI 6.6-39.7), respectively. Across both registries, incidence rates increased considerably between 2000 and 2015.ConclusionsThe available evidence suggests a growing incidence of breast cancer in Africa. The representativeness of these estimates is uncertain due to the paucity of data in several countries and calendar years, as well as inconsistency in data collation and quality across existing cancer registries.

High-fat diets have been identified as a major cause of obesity and a potential risk factor for breast cancer. Fat tissue, also known as adipose tissue, produces an excess of estrogen, which has been linked to an increased risk of breast cancer. Determining the impact of HFDs in the development and progression of breast cancer is essential, as it will enable us to identify the role of dietary modification in preventing and managing the disease.The impact of a high-fat diet (HFD) on the development of breast cancer in humans has yet to be fully explained, as very few human studies are available to effectively analyze the effect fatty food has on breast cancer development. This meta-analysis, therefore, seeks to determine the strength of association, if any, between HFD and an increased risk of breast cancer development. This research will help inform good eating habits, potentially reducing the disease's incidence and outcome. This meta-analysis examined eight (8) papers from various nations examining the effect of a high-fat diet as a risk factor for breast cancer development between 2010 and 2020. The study employed the multivariableadjusted hazard ratio (H.R.), odds ratio (OR), or relative risk (R.R.) from the studies. Breast cancer cases were histologically and radiologically confirmed in the studies evaluated, and validated food frequency questionnaires were used to assess their dietary patterns. This metanalysis study found a substantial link between a high-fat diet and an increased risk of breast cancer, with statistically significant results (I 2 = 93.38%, p0.05). Changes in dietary fat consumption may thus help mitigate some of the unfavorable consequences of breast cancer and survival. Even if further research is needed to support this assertion, the findings are compelling enough to advocate for low-fat, healthy diets to avoid breast cancer.

Poly(ADP-ribose) (PAR) polymerase inhibitors (PARPi) either have been approved or being tested in the clinic for the treatment of a variety of cancers with homologous recombination deficiency (HRD). However, cancer cells can develop resistance to PARPi drugs through various mechanisms, and new biomarkers and combination therapeutic strategies need to be developed to support personalized treatment. In this study, a genome-wide CRISPR screen was performed in a prostate cancer cell line with 3D culture condition which identified novel signals involved in DNA repair pathways. One of these genes, TBL1XR1, regulates sensitivity to PARPi in prostate cancer cells. Mechanistically, we show that TBL1XR1 interacts with and stabilizes SMC3 on chromatin and promotes γH2AX spreading along the chromatin of the cells under DNA replication stress. TBL1XR1-SMC3 double knockdown (knockout) cells have comparable sensitivity to PARPi compared to SMC3 knockdown or TBL1XR1 knockout cells, and more sensitivity than WT cells. Our findings provide new insights into mechanisms underlying response to PARPi or platin compounds in the treatment of malignancies.

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