BackgroundThere is limited information about the challenges of cancer management and attempts at improving outcomes in Africa. Even though South and North Africa are better resourceds to tackle the burden of breast cancer, similar poor prognostic factors are common to all countries. The five-year overall Survival rate for breast cancer patients does not exceed 60% for any low and middle-income country (LMIC) in Africa. In spite of the gains achieved over the past decade, certain characteristics remain the same such as limited availability of breast conservation therapies, inadequate access to drugs, few oncology specialists and adherence to harmful socio-cultural practices. This review on managing breast cancer in Africa is authored by African oncologists who practice or collaborate in Africa and with hands-on experience with the realities.MethodsA search was performed via electronic databases from 1999 to 2016. (PubMed/Medline, African Journals Online) for all literature in English or translated into English, covering the terms “breast cancer in Africa and developing countries”. One hundred ninety were deemed appropriate.ResultsBreast tumors are diagnosed at earlier ages and later stages than in highincome countries. There is a higher prevalence of triple-negative cancers. The limitations of poor nursing care and surgery, inadequate access to radiotherapy, poor availability of basic and modern systemic therapies translate into lower survival rate. Positive strides in breast cancer management in Africa include increased adaptation of treatment guidelines, improved pathology services including immuno-histochemistry, expansion and upgrading of radiotherapy equipment across the continent in addition to more research opportunities.ConclusionThis review is an update of the management of breast cancer in Africa, taking a look at the epidemiology, pathology, management resources, outcomes, research and limitations in Africa from the perspective of oncologists with local experience.

BackgroundThe motor and cognitive deficits observed in hydrocephalus are thought to be due to axonal damage within the periventricular white matter. This study was carried out to investigate the relationship between ventricular size, cellular changes in brain, and neurobehavioural deficits in rats with experimental hydrocephalus.MethodsHydrocephalus was induced in three-week old rats by intracisternal injection of kaolin. Behavioural and motor function were tested four weeks after hydrocephalus induction and correlated to ventricular enlargement which was classified into mild, moderate or severe. Gross brain morphology, routine histology and immunohistochemistry for oligodendrocytes (CNPase), microglia (Iba-1) and astrocytes (GFAP) were performed to assess the cellular changes.ResultsDecreases in open field activity and forelimb grip strength in hydrocephalus correlated with the degree of ventriculomegaly. Learning in Morris water maze was significantly impaired in hydrocephalic rats. Gradual stretching of the ependymal layer, thinning of the corpus callosum, extracellular oedema and reduced cortical thickness were observed as the degree of ventriculomegaly increased. A gradual loss of oligodendrocytes in the corpus callosum and cerebral cortex was most marked in the severely-hydrocephalic brains, whereas the widespread astrogliosis especially in the subependymal layer was most marked in the brains with mild hydrocephalus. Retraction of microglial processes and increase in Iba-1 immunoreactivity in the white matter was associated ventriculomegaly.ConclusionsIn hydrocephalic rats, oligodendrocyte loss, microglia activation, astrogliosis in cortical areas and thinning of the corpus callosum were associated with ventriculomegaly. The degree of ventriculomegaly correlated with motor and cognitive deficits.

Now that the human genome has been sequenced, along with those of major animal models, there is an urgent need to define those environments that interact with genes. The traditional view focuses on ways that gene products interact with the nuclear environment to regulate cell function, causing the physiologic changes, behaviors, and diseases manifest throughout development and aging. Although this view is essential, it is equally essential to understand the converse relationship, namely, to identify those environments at higher levels of organization that regulate the expression of specific genes. Given the vastness of this problem, one effective strategy is to start with a trait for which some of the genes have already been identified, such as malignant disease. In rats, social isolation and hypervigilance increase the incidence of mammary tumors, accelerate aging, and shorten the life span. We propose that similar environmental regulation of gene expression may underlie the disproportionately high mortality from premenopausal breast cancer of Blacks, a minority group that can experience high levels of loneliness and hypervigilance. Our goal is to identify which environments-social, psychological, hormonal, and cellular-regulate genetic mechanisms of mammary cancer risk as well as the specific times in the life span when they do so.

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Environmental exposure to vanadium occurs in areas of persistent burning of fossil fuels; this metal is known to induce oxidative stress and oligodendrocyte damage. Here, we determined whether vanadium exposure (3 mg/kg) in mice during the first 3 postnatal months leads to a sustained neuroinflammatory response. Body weight monitoring, and muscle strength and open field tests showed reduction of body weight gain and locomotor impairment in vanadium-exposed mice. Myelin histochemistry and immunohistochemistry for astrocytes, microglia, and nonphosphorylated neurofilaments revealed striking regional heterogeneity. Myelin damage involved the midline corpus callosum and fibers in cortical gray matter, hippocampus, and diencephalon that were associated with axonal damage. Astrocyte and microglial activation was identified in the same regions and in the internal capsule; however, no overt myelin and axon damage was observed in the latter. Double immunofluorescence revealed induction of high tumor necrosis factor (TNF) immunoreactivity in reactive astrocytes. Western blotting analysis showed significant induction of TNF and interleukin-1β expression. Together these findings show that chronic postnatal vanadium exposure leads to functional deficit and region-dependent myelin damage that does not spare axons. This injury is associated with glial cell activation and proinflammatory cytokine induction, which may reflect both neurotoxic and neuroprotective responses.

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The pterion which marks the union of 4 bones of the cranium is located superior to the zygomatic arch and posterior to the frontozygomatic suture. It is an important neurosurgical landmark for the lateral/pterional approach and has racial differences in both its location and pattern of union of the bones. This study aims to analyze the location and types of pterion in adult Nigerian skulls. Bilateral sides of 37 adult dry skulls were studied. The pterion types were classified; linear distances from the centre of the pterion to the midpoint of the zygomatic arch and to the frontozygomatic suture were measured; these were analyzed for side and gender differences. Sphenoparietal was the most common pterion type (86.1%) followed by frontotemporal (8.3%), stellate (5.6%), and epipteric types (0%). The mean distances from the pterion to the midpoint of zygomatic arch were 39.74 ± 0.505 mm and 37.95 ± 0.657 mm in males and females, respectively, while the distances to the frontozygomatic suture were 31.87 ± 0.642 mm and 30.35 ± 0.836 mm. The vertical position of the pterion was significantly higher in males than females. Bilateral occurrence is statistically insignificant. This information will be of neurosurgical and anthropological importance.

Vanadium is a transitional metal with an ability to generate reactive oxygen species in the biological system. This work was designed to assess memory deficits in mice chronically exposed to vanadium. A total of 132 male BALB/c mice (4 weeks old) were used for the experiment and were divided into three major groups of vanadium treated, matched controls, and animals exposed to vanadium for three months and thereafter vanadium was withdrawn. Animals were tested using Morris water maze and forelimb grip test at 3, 6, 9, and 12 months of age. The results showed that animals across the groups showed no difference in learning but had significant loss in memory abilities after 3 months of vanadium exposure and this trend continued in all vanadium-exposed groups relative to the controls. Animals exposed to vanadium for three months recovered significantly only 9 months after vanadium withdrawal. There was no significant difference in latency to fall in the forelimb grip test between vanadium-exposed groups and the controls in all age groups. In conclusion, we have shown that chronic administration of vanadium in mice leads to memory deficit which is reversible but only after a long period of vanadium withdrawal.