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Browsing by Author "Ajani, M."

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    Brain weights in adult africans
    (The Brazilian Society of Anatomy (SBA), 2017) Salami, A.; Ajani, M.; Orhorho, I.; Ogun, G.; Adeoye, A.; Okolo, C.; Oluwasola, A.; Ogunbiyi, J.
    Introduction: The average brain weight of adult humans, using Caucasian figures, is said to be between 1300g to 1400g. Few studies have however been done to make actual evaluations of brain weights in adult Africans. This study seeks to examine the weight of brains from people of African descent with respect to variations in sex and age in decades using autopsy specimens. Materials and Methods: Analysis of the weight of brains removed from both male and female adult patients during fresh autopsy of their bodies in our center over a ten year period was done. The study criteria required non-involvement of the central nervous system in the cause of death. The brains were grouped based on age in decades and further grouped into early, middle and late age groups. Descriptive statistical analysis was done using SPSS 20 statistics software. Results: A total of one hundred and sixteen brains were included in the study and the mean brain weight was 1280g with a range between 1015g to 1590g. There was no statistically significant difference in the mean brain weight of the different age groups. The average male brain was heavier than those of females and the difference was statistically significant. Conclusion: The brain weight of adult Africans in our study is similar to that seen in Caucasians. There is no statistically significant difference in the brain weight of adults from early adulthood to the elderly adults. Male adults have statistically heavier brains than the females
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    "Characterization of Nigerian breast cancer reveals prevalent homologous recombination deficiency and aggressive molecular features"
    (Nature Research, 2018) Pitt, J. J.; Riester, M.; Zheng, Y.; Yoshimatsu, T. F.; Sanni, A.; Oluwasola, O.; Veloso, A.; Labrot, E.; Wang, S.; Odetunde, A.; Ademola, A.; Okedere, B.; Mahan, S.; Leary, R.; Macomber, M.; Ajani, M.; Johnson, R. S.; Fitzgerald, D.; Grundstad, A. J.; Tuteja, J. H.; Khramtsova, G.; Zhang, J.; Sveen, E.; Hwang, B.; Clayton, W.; Nkwodimmah, C.; Famooto, B.; Obasi, E.; Aderoju, V.; Oludara, M.; Omodele, F.; Akinyele, O.; Adeoye, A.||; Ogundiran, T.; Babalola, C.; MacIsaac, K.; Popoola, A.; Morrissey, M. P.; Chen, L. S.; Wang, J.; Olopade, C. O.; Falusi, A. G.; Winckler, W.; Haase, K.; Van Loo, P.; Obafunwa, J.; Papoutsakis, D.; Ojengbede, O.; Weber, B.; Ibrahim, N.; White, K. P.; Huo, D.; Olopade, O. I.; Barretina, J
    Racial/ethnic disparities in breast cancer mortality continue to widen but genomic studies rarely interrogate breast cancer in diverse populations. Through genome, exome, and RNA sequencing, we examined the molecular features of breast cancers using 194 patients from Nigeria and 1037 patients from The Cancer Genome Atlas (TCGA). Relative to Black and White cohorts in TCGA, Nigerian HR + /HER2 − tumors are characterized by increased homologous recombination deficiency signature, pervasive TP53 mutations, and greater structural variation—indicating aggressive biology. GATA3 mutations are also more frequent in Nigerians regardless of subtype. Higher proportions of APOBEC-mediated substitutions strongly associate with PIK3CA and CDH1 mutations, which are underrepresented in Nigerians and Blacks. PLK2, KDM6A, and B2M are also identified as previously unreported significantly mutated genes in breast cancer. This dataset provides novel insights into potential molecular mechanisms underlying outcome disparities and lay a foundation for deployment of precision therapeutics in underserved populations.
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    Germline variants and somatic mutation signatures of breast cancer across populations of African and European ancestry in the US and Nigeria
    (John Wiley & Sons Ltd, 2019) Wang, S. F.; Pitt, J. J.; Zheng, Y.; Yoshimatsu, T. F.; Gao, G.; Sanni, A.; Oluwasola, O.; Ajani, M.; Fitzgerald, D.; Odetunde, A.; Khramtsova, G.; Hurley, I.; Popoola, A.; Falusi, A.; Ogundiran, T.; Obafunwa, J.; Ojengbede, O.; Ibrahim, N.; Barretina, J.; White, K. P.; Huo, D.; Olopade, O. I.
    Somatic mutation signatures may represent footprints of genetic and environmental exposures that cause different cancer. Few studies have comprehensively examined their association with germline variants, and none in an indigenous African population. SomaticSignatures was employed to extract mutation signatures based on whole-genome or whole-exome sequencing data from female patients with breast cancer (TCGA, training set, n = 1,011; Nigerian samples, validation set, n = 170), and to estimate contributions of signatures in each sample. Association between somatic signatures and common single nucleotide polymorphisms (SNPs) or rare deleterious variants were examined using linear regression. Nine stable signatures were inferred, and four signatures (APOBEC C>T, APOBEC C>G, aging and homologous recombination deficiency) were highly similar to known COSMIC signatures and explained the majority (60–85%) of signature contributions. There were significant heritable components associated with APOBEC C>T signature (h2 = 0.575, p = 0.010) and the combined APOBEC signatures (h2 = 0.432, p = 0.042). In TCGA dataset, seven common SNPs within or near GNB5 were significantly associated with an increased proportion (beta = 0.33, 95% CI = 0.21–0.45) of APOBEC signature contribution at genome-wide significance, while rare germline mutations in MTCL1 was also significantly associated with a higher contribution of this signature (p = 6.1 × 10−6 ). This is the first study to identify associations between germline variants and mutational patterns in breast cancer across diverse populations and geography. The findings provide evidence to substantiate causal links between germline genetic risk variants and carcinogenesis.
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    Metastatic prostate cancer presenting as a rapidly increasing gluteal muscle mass at an intramuscular injection site
    (Remedy Publications LLC., 2022-02) Olapade-Olaopa, O. E.; Adebayo, A. S.; Osobu, E.; Ajani, M.; Ogunlayi, S.; Magbagbeola, O. A.; Farinre, O. M.; Ogunbiyi, O. J.; Ogunlade, S. O.
    Prostate cancer is the second commonest male cancer globally. However, diagnosis may be delayed or missed due to atypical presentations such as metastases to unusual sites. The axial skeleton, lymph nodes, and viscera are the common sites for prostate cancer metastasis with skeletal muscles being uncommonly affected, and until now there has been no report of metastasis to the gluteal muscles from the disease. We present the case of a 78-year-old man with no lower urinary tract symptoms who presented with a 2-year history of a right supra-gluteal mass at the site of an intramuscular injection hematoma/abscess that rapidly increased in size 5 months prior to presentation and an abnormal gait. CT and MRI scans were suggestive of a malignant mass (possibly a rhabdomyosarcoma) and enlarged multinodular prostate with bilateral lymphadenopathy. A biopsy of the gluteal mass confirmed metastatic adenocarcinoma with the colon or the prostate being possible primaries. His serum PSA was markedly elevated (3441 ng/ml) but his other tumor markers were normal. Prostate biopsies confirmed a Gleason 4+3=7 prostate cancer and ADT was commenced. He responded well and remains in good health 15 months into his treatment with a marked reduction in the size of his gluteal mass and a restoration of a normal gait. His serum PSA and Testosterone are presently 2.4 ng/ml and 0.3 mmol/L respectively.
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    Proliferaton index in pituitary adenomas from a black African population
    (Elsevier B.V., 2016) Salami, A.; Ajani, M.; Adeolu, A.; Ogun, O.; Adeleye, A.; Ogun, O.; Okolo, C.; Malomo, A.; Akang, E.
    Background: The WHO has recognized a variant of pituitary adenomas with potential aggressive behavior which have been termed atypical pituitary adenomas. This group of tumours are recognized by their mitotic rate of more than >3%, p53 expression and invasion of surrounding structures. There has however been no study of the occurrence of these tumours in a black African population. This study is a preliminary attempt to examine this group of tumours in blacks. Methods: This study retrospectively reviewed fifty-seven histologically diagnosed and immunohistochemically characterized pituitary adenomas received in our department over a twenty-one year period. Specimens were stained with ki67, a nuclear marker of cell proliferation which has been identified as the single best predictor of atypical pituitary adenoma. Results: Twelve of the tumours showed atypical features with eight (67%) of these tumours being prolactinomas. Two of the tumours were gonadotrophs and two were null cell adenomas. There was no correlation with age or gender. Two of the tumours required neurosurgical re-exploration with one of these showing a higher mitotic index in the second biopsy. Conclusion: The study suggests similarity in the rate of occurrence of pituitary adenomas with atypical features in a black African population with what is seen in Caucasians. Prolactinomas constitute a significant percentage of the tumours with this feature
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    Whole-genome analysis of Nigerian patients with breast cancer reveals ethnic-driven somatic evolution and distinct genomic subtypes
    (Nature Research, 2021) Ansari-Pour, N.; Zheng, Y.; Yoshimatsu, T. F.; Sanni, A.; Ajani, M.; Reynier, J.-B.; Tapinos, A.; Pitt, J. J.; Dentro, S.; Woodard, A.; Rajagopal, P. S.; Fitzgerald, D.; Gruber, A. J.; Odetunde, A.; Popoola, A.; Falusi, A. G.; Babalola, C. P.; Ogundiran, T.; Ibrahim, N.; Barretina, J.; Van Loo, P.; Chen, M.; White, K. P.; Ojengbede, O.; Obafunwa, J.; Huo, D.; Wedge, D. C.; Olopade, O. I.
    Black women across the African diaspora experience more aggressive breast cancer with higher mortality rates than white women of European ancestry. Although inter-ethnic germline variation is known, differential somatic evolution has not been investigated in detail. Analysis of deep whole genomes of 97 breast cancers, with RNA-seq in a subset, from women in Nigeria in comparison with The Cancer Genome Atlas (n = 76) reveal a higher rate of genomic instability and increased intra-tumoral heterogeneity as well as a unique genomic subtype defined by early clonal GATA3 mutations with a 10.5-year younger age at diagnosis. We also find non-coding mutations in bona fide drivers (ZNF217 and SYPL1) and a previously unreported INDEL signature strongly associated with African ancestry proportion, under scoring the need to expand inclusion of diverse populations in biomedical research. Finally, we demonstrate that characterizing tumors for homologous recombination deficiency has significant clinical relevance in stratifying patients for potentially life-saving therapies.

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