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Background and context: The use of radiotherapy in developing countries is slowly gaining momentum but the gains are accompanied by some pitfalls. The breakdown of a teletherapy (cobalt 60) machine in Uganda is an example of the challenges to be considered while expanding access to treatment. It was a major test for the country and the Uganda Cancer Institute the agency of government responsible for provision of cancer services. It attracted a national and international outcry. This unprecedented response was based on the importance a seemingly old equipment in Kampala was playing in the entire region (Kenya, Tanzania, Rwanda, Burundi, Democratic Republic of Congo and southern Sudan). However, the manner in which the crisis was handled demonstrated clearly how to turn a misfortune into an opportunity given the many lessons learnt. Aim: In this paper we aim to highlight how the breakdown of the equipment triggered a major crisis and the response to the crisis resulting in the restoration of services within a reasonable time frame. We also want to show the long-term service modernization and expansion drive this has triggered within Uganda and the entire region. Strategy/Tactics: The restoration process comprised planning, decommissioning, renovation, security and safety systems, procurement of new machine, installation and commissioning. As this was ongoing there was the need for care provision for patient in need. Concurrently undertaken was public reassurance through building confidence and trust in the capacity for speedy restoration of services. Program/Policy process: All these steps were taken collaboratively within country, region and internationally. In the region there was support from the Aga Khan University Hospital Nairobi and internationally, technical support from the IAEA. Outcomes: Service has been fully restored, a new teletherapy cobalt machines installed and commissioned. The machine has modern capabilities compared with the previous. So far more than 200 patients have been treated. The numbers of patients are steadily increasing hence the government has embarked on modernization and expansion of the radiotherapy services in the country. What was learned: The breakdown of Uganda's radiotherapy machines has provided lessons that are important for handling health system operational crisis which may occur as we try to build complex delivery systems. It provided lessons that are important in the drive for expansion of radiotherapy services in developing countries. In particular that benefit of investments in modern equipment transcends national boundaries. Secondly how to limit potential impact of major crisis through regional and international collaboration. Further that the needs of patients is central in crisis management. Finally need to consider pooling infrastructure investments in tackling NCD's such as the East Africa's centre of excellence for skills and tertiary education project of the East African community. [ABSTRACT FROM AUTHOR]

Background: An improved understanding of oral Kaposi sarcoma-associated herpesvirus (KSHV) viral dynamics could provide insights into transmission risk and guide vaccine development., Methods: We evaluated KSHV oral shedding dynamics in Ugandan adults stratified by Kaposi sarcoma (KS) and human immunodeficiency virus (HIV) status. Participants were followed for ≥4 weeks, with daily home oral swab collection to quantify KSHV using polymerase chain reaction. Shedding rates were defined by number of days with KSHV DNA detected divided by total days with swabs and compared by group using hurdle models., Results: Two hundred ninety-five participants were enrolled; median age was 35 years (range, 18-71 years), and 134 (45%) were male. KSHV was detected more frequently among participants with KS (HIV positive [HIV + ]/KS + , 56/76 [74%]; HIV negative [HIV - ]/KS + , 9/18 [50%]) than those without KS (HIV + /KS - , 36/125 [29%]; HIV - /KS - , 16/76 [21%]); odds of shedding did not differ significantly by HIV status. Among participants with KSHV detected, shedding rates did not differ significantly by group. Median per-participant viral loads among positive samples were lowest in HIV + /KS + (3.1 log 10 copies/mL) and HIV - /KS + (3.3 log 10 copies/mL) participants relative to HIV + /KS - (3.8 log 10 copies/mL) and HIV - /KS - (4.0 log 10 copies/mL) participants. All groups had participants with low viral load intermittent shedding and participants with high viral load persistent shedding. Within each group, individual KSHV shedding rate positively correlated with median KSHV log 10 copies/mL, and episode duration positively correlated with peak viral load., Conclusions: Oral KSHV shedding is highly heterogeneous across Ugandan adults with and without KS and HIV. Persistent shedding is associated with higher median viral loads regardless of HIV and KS status., Competing Interests: Potential conflicts of interest. J. T. S. received consulting fees from Pfizer for advising on SARS-CoV-2 therapeutics and GlaxoSmithKline for advising on HSV vaccines. C. C. receives fees for consulting from Recordati Rare Disease, fees for sitting on the scientific advisory board of Viracta Therapeutics, and research funding from ImmunityBio and Janssen. All other authors report no potential conflicts., (© The Author(s) 2024. Published by Oxford University Press on behalf of Infectious Diseases Society of America.)

An estimated 38 million people live with human immunodeficiency virus (HIV) worldwide and are at excess risk for multiple cancer types. Elevated cancer risks in people living with HIV (PLWH) are driven primarily by increased exposure to carcinogens, most notably oncogenic viruses acquired through shared transmission routes, plus acceleration of viral carcinogenesis by HIV-related immunosuppression. In the era of widespread antiretroviral therapy (ART), life expectancy of PLWH has increased, with cancer now a leading cause of co-morbidity and death. Furthermore, the types of cancers occurring among PLWH are shifting over time and vary in their relative burden in different parts of the world. In this context, the International Agency for Research on Cancer (IARC) and the US National Cancer Institute (NCI) convened a meeting in September 2022 of multinational and multidisciplinary experts to focus on cancer in PLWH. This report summarizes the proceedings, including a review of the state of the science of cancer descriptive epidemiology, etiology, molecular tumor characterization, primary and secondary prevention, treatment disparities and survival in PLWH around the world. A consensus of key research priorities and recommendations in these domains is also presented., (© 2023 International Agency for Research on Cancer; licensed by UICC and The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.)

Background: Co-infection with HIV can result in impaired control of cytomegalovirus (CMV) replication, increasing the likelihood of disease and onward transmission. The objective of this analysis was to measure the impact of HIV on CMV replication in an intensively-sampled cohort in Kampala, Uganda., Methods: CMV seropositive men and women aged 18-65, with or without HIV co-infection, were followed for one month. Daily oral swabs and weekly anogenital swabs and plasma were collected. Quantitative CMV PCR was performed on all samples., Results: Eighty-five participants were enrolled and provided ≥1 oral swab; 43 (51%) were HIV-seropositive. People living with HIV (PLWH; median CD4 count 439 cells/mm3; none on antiretrovirals) had 2-4 times greater risk of CMV detection at each anatomical site assessed. At the oral site, 773 of 1272 (61%) of samples from PLWH had CMV detected, compared to 214 of 1349 (16%) among people without HIV. Similarly, the mean CMV quantity was higher among PLWH at all anatomical sites, with the largest difference seen for oral swabs (mean difference 1.63 log/mL; 95% CI 1.13-2.13). Among PLWH, absolute quantity of CD4+ T-cells was not associated with risk of CMV detection. HIV plasma RNA quantity was positively correlated with oral CMV shedding frequency, but not detection at other sites., Conclusions: Mucosal and systemic CMV replication occurs at higher levels in PLWH than people without HIV, particularly oral shedding, which is a major mode of CMV transmission. Increased CMV replication despite relatively preserved CD4+ T-cell counts suggests that additional interventions are required to improve CMV control in PLWH., Competing Interests: AW has received research funding from NIH, Sanofi, and GSK and personal fees from Aicuris, X-vax, Crozet, Auritec, Merck, and VIR outside of the submitted work. LC receives funding from NIAID outside of the submitted work. CC receives research funding from Amyris, Celularity, iBio, ImmunityBio, and Janssen and sits on the scientific advisory board of Viracta Therapeutics; all are outside of the submitted work. IB is funded by a “Fond de Recherche du Québec – Santé” salary award. CJ has served as a consultant for AbbVie, Medpace, GSK, and Gilead outside of the submitted work and received royalties from UpToDate. SG has received consultant fees and research funding from Moderna, Merck, VBI, GSK, and Meridian Biosciences outside of the submitted work. All other authors have no conflicts to disclose., (Copyright: © 2023 McClymont et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS), yet the viral genetic factors that lead to the development of KS in KSHV-infected individuals have not been fully elucidated. Nearly, all previous analyses of KSHV genomic evolution and diversity have excluded the three major internal repeat regions: the two origins of lytic replication, internal repeats 1 and 2 (IR1 and IR2), and the latency-associated nuclear antigen (LANA) repeat domain (LANAr). These regions encode protein domains that are essential to the KSHV infection cycle but have been rarely sequenced due to their extended repetitive nature and high guanine and cytosine (GC) content. The limited data available suggest that their sequences and repeat lengths are more heterogeneous across individuals than in the remainder of the KSHV genome. To assess their diversity, the full-length IR1, IR2, and LANAr sequences, tagged with unique molecular identifiers (UMIs), were obtained by Pacific Biosciences' single-molecule real-time sequencing (SMRT-UMI) from twenty-four tumors and six matching oral swabs from sixteen adults in Uganda with advanced KS. Intra-host single-nucleotide variation involved an average of 0.16 per cent of base positions in the repeat regions compared to a nearly identical average of 0.17 per cent of base positions in the remainder of the genome. Tandem repeat unit (TRU) counts varied by only one from the intra-host consensus in a majority of individuals. Including the TRU indels, the average intra-host pairwise identity was 98.3 per cent for IR1, 99.6 per cent for IR2 and 98.9 per cent for LANAr. More individuals had mismatches and variable TRU counts in IR1 (twelve/sixteen) than in IR2 (two/sixteen). There were no open reading frames in the Kaposin coding sequence inside IR2 in at least fifty-five of ninety-six sequences. In summary, the KSHV major internal repeats, like the rest of the genome in individuals with KS, have low diversity. IR1 was the most variable among the repeats, and no intact Kaposin reading frames were present in IR2 of the majority of genomes sampled., Competing Interests: None declared., (© The Author(s) 2023. Published by Oxford University Press.)

Kaposi sarcoma (KS), a common HIV-associated malignancy, presents a range of clinicopathological features. Kaposi sarcoma-associated herpesvirus (KSHV) is its etiologic agent, but the contribution of viral genomic variation to KS development is poorly understood. To identify potentially influential viral polymorphisms, we characterized KSHV genetic variation in 67 tumors from 1-4 distinct sites from 29 adults with advanced KS in Kampala, Uganda. Whole KSHV genomes were sequenced from 20 tumors with the highest viral load, whereas only polymorphic genes were screened by PCR and sequenced from 47 other tumors. Nine individuals harbored ≥1 tumors with a median 6-fold over-coverage of a region centering on K5 and K6 genes. K8.1 gene was inactivated in 8 individuals, while 5 had mutations in the miR-K10 microRNA coding sequence. Recurring inter-host polymorphisms were detected in K4.2 and K11.2. The K5-K6 region rearrangement breakpoints and K8.1 mutations were all unique, indicating that they arise frequently de novo. Rearrangement breakpoints were associated with potential G-quadruplex and Z-DNA forming sequences. Exploratory evaluations of viral mutations with clinical and tumor traits were conducted by logistic regression without multiple test corrections. K5-K6 over-coverage and K8.1 inactivation were tentatively correlated (p<0.001 and p = 0.005, respectively) with nodular rather than macular tumors, and with individuals that had lesions in ≤4 anatomic areas (both p≤0.01). Additionally, a trend was noted for miR-K10 point mutations and lower survival rates (HR = 4.11, p = 0.053). Two instances were found of distinct tumors within an individual sharing the same viral mutation, suggesting metastases or transmission of the aberrant viruses within the host. To summarize, KSHV genomes in tumors frequently have over-representation of the K5-K6 region, as well as K8.1 and miR-K10 mutations, and each might be associated with clinical phenotypes. Studying their possible effects may be useful for understanding KS tumorigenesis and disease progression., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2022 Santiago et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Introduction: Lung cancer is a major global public health burden constituting 11.6% of all new cancer diagnoses and 18.4% of all cancer-related mortality., Purpose: To describe the clinical profile and initial treatment of non-small cell lung cancer in Uganda., Methods: We reviewed charts of a cohort of patients with a histologically confirmed diagnosis of non-small cell lung cancer, treated between January 2013 and November 2015 at the Uganda Cancer Institute., Results: A total of 74 patients met the inclusion criteria. The median age was 56 years (IQR 47-70), with 16.2% below the age 45 years, and 51% were female. Only 10 percent were active smokers and the most frequent histological subtype was adenocarcinoma (71%). The majority (91.9%) had stage IV disease at diagnosis and frequent metastases to contralateral lung, liver, and bones. Twenty-seven (27) patients received platinum-based chemotherapy, while 27 patients received erlotinib, and only 4 patients received palliative thoracic radiotherapy. The median survival time was 12.4 months, and the overall response rate was 32.7%. There was no survival difference by type of systemic treatment, and on multivariate analysis, poor performance status was predictive of adverse outcomes (p < 0.001)., Conclusions: Patients with non-small cell lung cancer in Uganda frequently presented with late-stage disease at diagnosis. The majority of patients were female, never-smokers, and had predominantly adenocarcinoma subtype., (© 2021 Kibudde S et al.)

Epstein-Barr virus (EBV) is transmitted by saliva and is a major cause of cancer, particularly in people living with HIV/AIDS. Here, we describe the frequency and quantity of EBV detection in the saliva of Ugandan adults with and without HIV-1 infection and use these data to develop a novel mathematical model of EBV infection in the tonsils. Eligible cohort participants were not taking antiviral medications, and those with HIV-1 infection had a CD4 count >200 cells/mm3. Over a 4-week period, participants provided daily oral swabs that we analysed for the presence and quantity of EBV. Compared with HIV-1 uninfected participants, HIV-1 coinfected participants had an increased risk of EBV detection in their saliva (IRR = 1.27, 95% CI = 1.10-1.47) and higher viral loads in positive samples. We used these data to develop a stochastic, mechanistic mathematical model that describes the dynamics of EBV, infected cells, and immune response within the tonsillar epithelium to analyse potential factors that may cause EBV infection to be more severe in HIV-1 coinfected participants. The model, fit using Approximate Bayesian Computation, showed high fidelity to daily oral shedding data and matched key summary statistics. When evaluating how model parameters differed among participants with and without HIV-1 coinfection, results suggest HIV-1 coinfected individuals have higher rates of B cell reactivation, which can seed new infection in the tonsils and lower rates of an EBV-specific immune response. Subsequently, both these traits may explain higher and more frequent EBV detection in the saliva of HIV-1 coinfected individuals., Competing Interests: The authors have declared that no competing interests exist. Author Fred Okuku was unable to confirm his authorship contributions. On his behalf, the corresponding author has reported their contributions to the best of their knowledge.

Intra-host tumor virus variants may influence the pathogenesis and treatment responses of some virally-associated cancers. However, the intra-host variability of Kaposi sarcoma-associated herpesvirus (KSHV), the etiologic agent of Kaposi sarcoma (KS), has to date been explored with sequencing technologies that possibly introduce more errors than that which occurs in the viral population, and these studies have only studied variable regions. Here, full-length KSHV genomes in tumors and/or oral swabs from 9 Ugandan adults with HIV-associated KS were characterized. Furthermore, we used deep, short-read sequencing using duplex unique molecular identifiers (dUMI)-random double-stranded oligonucleotides that barcode individual DNA molecules before library amplification. This allowed suppression of PCR and sequencing errors to ~10-9/base as well as afforded accurate determination of KSHV genome numbers sequenced in each sample. KSHV genomes were assembled de novo, and rearrangements observed were confirmed by PCR and Sanger sequencing. 131-kb KSHV genome sequences, excluding major repeat regions, were successfully obtained from 23 clinical specimens, averaging 2.3x104 reads/base. Strikingly, KSHV genomes were virtually identical within individuals at the point mutational level. The intra-host heterogeneity that was observed was confined to tumor-associated KSHV mutations and genome rearrangements, all impacting protein-coding sequences. Although it is unclear whether these changes were important to tumorigenesis or occurred as a result of genomic instability in tumors, similar changes were observed across individuals. These included inactivation of the K8.1 gene in tumors of 3 individuals and retention of a region around the first major internal repeat (IR1) in all instances of genomic deletions and rearrangements. Notably, the same breakpoint junctions were found in distinct tumors within single individuals, suggesting metastatic spread of rearranged KSHV genomes. These findings define KSHV intra-host heterogeneity in vivo with greater precision than has been possible in the past and suggest the possibility that aberrant KSHV genomes may contribute to aspects of KS tumorigenesis. Furthermore, study of KSHV with use of dUMI provides a proof of concept for utilizing this technique for detailed study of other virus populations in vivo., Competing Interests: I have read the journal's policy and the authors of this manuscript have the following competing interests: MWS is a founder and equity holder at TwinStrand Biosciences, Inc., which is commercializing Duplex Sequencing technology.

Background: In 2018, approximately 60,000 Ugandans were estimated to be suffering from cancer. It was also reported that only 5% of cancer patients access cancer care and 77% present with late-stage cancer coupled with low level of cancer health literacy in the population despite a wide coverage of primary healthcare facilities in Uganda. We aimed to contribute to reducing the unmet needs of cancer prevention and early detection services in Uganda through capacity building., Methods: In 2017, we conducted two national and six regional cancer control stakeholders' consultative meetings. In 2017 and 2018, we trained district primary healthcare teams on cancer prevention and early detection. We also developed cancer information materials for health workers and communities and conducted a follow-up after the training., Results: A total of 488 primary healthcare workers from 118 districts were trained. Forty-six health workers in the pilot East-central subregion were further trained in cervical, breast, and prostate cancer early detection (screening and early diagnosis) techniques. A total of 32,800 cancer information, education and communication materials; breast, cervical, prostate childhood and general cancer information booklets; health education guide, community cancer information flipcharts for village health teams and referral guidelines for suspected cancer were developed and distributed to 122 districts. Also, 16 public and private-not-for-profit regional hospitals, and one training institution received these materials. Audiovisual clips on breast, cervical, and prostate cancer were developed for mass and social media dissemination. A follow-up after six months to one year indicated that 75% of the districts had implemented at least one of the agreed actions proposed during the training., Conclusions: In Uganda, the unmet needs for cancer control services are enormous. However, building the capacity of primary healthcare workers to integrate prevention and early detection of cancer into primary health care based on low-cost options for low-income countries could contribute to reducing the unmet needs of cancer prevention and early detection in Uganda., (© 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

Background: Communities in low-income countries are characterized by limited access to cancer prevention and early detection services, even for the commonest types of cancer. Limited resources for cancer control are one of the contributors to cancer health disparities. We explored the feasibility and benefit of conducting outreaches in partnership with local communities using the "asset-based community development (ABCD)" model., Methods: We analyzed the quarterly Uganda cancer institute (UCI) community outreach cancer health education and screening output reported secondary data without individual identifiers from July 2016 to June 2019 to compare the UCI-hospital-based and community outreach cancer awareness and screening services based on the ABCD model., Results: From July 2016 to June 2019, we worked with 107 local partners and conducted 151 outreaches. Of the total number of people who attended cancer health education sessions, 201 568 (77.9%) were reached through outreaches. Ninety-two (95%) cancer awareness TVs and radio talk-shows conducted were sponsored by local partners. Of the total people screened; 22 795 (63.0%) cervical, 22 014 (64.4%) breast, and 4904 (38.7%) prostate screening were reached through community outreach model. The screen-positive rates were higher in hospital-based screening except for Prostate screening; cervical, 8.8%, breast, 8.4%, prostate, 7.1% than in outreaches; cervical, 3.2%, breast, 2.2%, prostate, 8.2%. Of the screened positive clients who were eligible for precancer treatment like cryotherapy for treatment of precervical cancer lesions, thousands-folds monetary value and productive life saved relative to the market cost of cancer treatment and survival rate in Uganda. When the total number of clients screened for cervical, breast, and prostate cancer are subjected to the incremental cost of specific screening, a greater portion (98.7%) of the outreach cost was absorbed through community partnership., Conclusions: Outreaching and working in collaboration with communities as partners through asset-based community development model are feasible and help in cost-sharing and leverage for scarce resources to promote primary prevention and early detection of cancer. This could contribute to bridging the cancer health disparities in the target populations., (© 2020 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.)

Introduction: Cancer treatment options in sub-Saharan Africa are scarce despite an increasing burden of disease. Identification of those cancer patients who would benefit most from the limited resources available would allow broader and more effective therapy., Methods: We conducted a retrospective analysis of patients over the age of 18 at the time of a pathologic diagnosis of NHL between 2003 and 2010 who were residents of Kyandondo County (Uganda) and presented to the Uganda Cancer Institute for care., Results: A total of 128 patients were included in this analysis. Chemotherapy was recommended to 117 (91.4%) of the patients; the odds of recommending chemotherapy decreased for each additional month of reported symptoms prior to diagnosis. Of the 117 patients to whom chemotherapy was recommended, 111 (86.7%) patients received at least 1 cycle of chemotherapy; HIV infected patients, as well as those with a lower hemoglobin and advanced disease at the time of diagnosis were significantly less likely to complete therapy. Among the patients who initiated chemotherapy, twenty patients died prior to treatment completion (including nine who died within 30 days). Hemoglobin level at the time of presentation was the only variable associated with early mortality in the adjusted model., Conclusion: In resource-poor areas, it is essential to align health care expenditures with interventions likely to provide benefit to affected populations. Targeting cancer therapy to those with a favorable chance of responding will not only save limited resources, but will also prevent harm in those patients unlikely to realize an effect of cancer-directed therapy.

Background: HIV-associated Kaposi sarcoma (KS) is commonly staged using the AIDS Clinical Trials Group criteria, which classify 3 variables- tumor extent (T), immune status (I), and systemic symptoms (S)-into good risk (0) and poor risk (1). Although validated in the United States and Europe, these criteria have not been systematically evaluated in sub-Saharan Africa, where the burden of KS is greatest., Methods: We reviewed medical charts of adult patients with HIV-associated KS seen at the Uganda Cancer Institute from 1992 to 2007. Vital status at 2 years after KS diagnosis was determined from the medical chart, or by contacting the patient or next of kin. Survival estimates used Kaplan-Meier methods. Predictors were evaluated for 2 periods: 0-4 months and 4-24 months after diagnosis., Results: At 2 years after diagnosis, 167 (41%) patients were alive, 156 (39%) had died, and 81 (20%) were lost to follow-up. The Kaplan-Meier estimate of 2-year survival was 57%. S1 was associated with death in months 0-4 [hazard ratio: 6.4, 95% confidence interval: 1.9-21.1], whereas T1 was associated with death in months 4-24 [hazard ratio: 4.0, 95% confidence interval: 1.4 to 11.5]. Immune status was not associated with survival., Conclusions: Systemic symptoms were strongly associated with death in the early period after KS diagnosis, whereas tumor status was most predictive of death in the 4- to 24-month period. These findings suggest that different processes may influence outcomes in early and late periods following KS diagnosis. Further studies are needed to confirm these observations and to identify better predictors of KS survival in sub-Saharan Africa.

Purpose: In Uganda, the incidence of prostate cancer is increasing at a rate of 5.2% annually. Data describing presentation and outcomes for patients with prostate cancer are lacking., Methods: A retrospective review of medical records for men with histologically confirmed prostate cancer at the Uganda Cancer Institute (UCI) from January 1 to December 17, 2012, was performed., Results: Our sample included 182 men whose mean age was 69.5 years (standard deviation, 9.0 years). Patients who presented to the UCI had lower urinary tract symptoms (73%; n = 131), bone pain (18%; n = 32), increased prostate-specific antigen (PSA; 3%; n = 5), and other symptoms (6%; n = 11). Median baseline PSA was 91.3 ng/mL (interquartile range, 19.5-311.3 ng/mL), and 51.1% of the patients (n = 92) had a PSA value above 100 ng/mL. Gleason score was 9 or 10 in 66.7% of the patients (n = 120). Ninety percent (n = 136) had stage IV disease, and metastatic sites included bone (73%; n = 102), viscera (21%; n = 29), and lymph nodes (4%; n = 5). Spinal cord compression occurred in 30.9% (n = 55), and 5.6% (n = 10) experienced a fracture. A total of 14.9% (n = 27) underwent prostatectomy, and 17.7% (n = 32) received radiotherapy. Gonadotropin-releasing hormone agonist was given to 45.3% (n = 82), 29.2% (n = 53) received diethylstilbestrol, and 26% (n = 47) underwent orchiectomy. Chemotherapy was administered to 21.6% (n = 39), and 52.5% (n = 95) received bisphosphonates. During the 12 months of study, 23.8% of the men (n = 43) died, and 54.4% (n = 98) were lost to follow-up., Conclusion: UCI patients commonly present with high PSA, aggressive Gleason scores, and stage IV disease. The primary treatments are hormonal manipulation and chemotherapy. Almost 25% of patients succumb within a year of presentation, and a large number of patients are lost to follow-up., Competing Interests: Authors’ disclosures of potential conflicts of interest and contributions are found at the end of this article.Prostate Cancer Burden at the Uganda Cancer InstituteThe following represents disclosure information provided by authors of this manuscript. All relationships are considered compensated. Relationships are self-held unless noted. I = Immediate Family Member, Inst = My Institution. Relationships may not relate to the subject matter of this manuscript. For more information about ASCO's conflict of interest policy, please refer to www.asco.org/rwc or jco.ascopubs.org/site/ifc.Fred OkukuNo relationship to discloseJackson OremNo relationship to discloseGeorge HoloyaNo relationship to discloseChris De BoerNo relationship to discloseCheryl L. ThompsonNo relationship to discloseMatthew M. CooneyNo relationship to disclose

Objective: HIV infection is associated with cancer risk. This relationship has resulted in a growing cancer burden, especially in resource-limited countries where HIV is highly prevalent. Little is known, however, about how HIV affects cancer survival in these settings. We therefore investigated the role of HIV in cancer survival in Uganda., Design: Retrospective cohort (N = 802)., Methods: Eligible cancer patients were residents of Kyadondo County, at least 18 years of age at cancer diagnosis, and diagnosed between 2003 and 2010 with one of the following: breast cancer, cervical cancer, non-Hodgkin's lymphoma, Hodgkin's lymphoma, or esophageal cancer. Patients were classified as HIV-infected at cancer diagnosis based on a documented positive HIV antibody test, medical history indicating HIV infection, or an HIV clinic referral letter. The primary outcome, vital status at 1 year following cancer diagnosis, was abstracted from the medical record or determined through linkage to the national hospice database. The risk of death during the year after cancer diagnosis was compared between cancer patients with and without evidence of HIV infection using Cox proportional hazards regression., Results: HIV-infected cancer patients in Uganda experienced a more than two-fold increased risk of death during the year following cancer diagnosis compared to HIV-uninfected cancer patients [hazard ratio 2.28; 95% confidence interval (CI) 1.61-3.23]. This association between HIV and 1-year cancer survival was observed for both cancers with (hazard ratio 1.56; 95% CI 1.04-2.34) and without (hazard ratio 2.68; 95% CI 1.20-5.99) an infectious cause., Conclusion: This study demonstrates the role of HIV in cancer survival for both cancers with and without an infectious cause in a resource-limited, HIV-endemic setting.

The incidence and economic burden of cancer in sub-Saharan Africa is increasing, and innovative strategies are needed to improve prevention and care in this population. This article uses a case of cutaneous T-cell lymphoma in Uganda to propose guidelines for the diagnosis and treatment of this disease in resource-limited settings. These guidelines were developed from the consensus opinion of specialists at the Uganda Cancer Institute and Fred Hutchinson Cancer Research Center as part of an established collaboration. Areas for future investigation that can improve the care of patients in this region are identified.

There is much commonality between chronic noncommunicable and communicable diseases which is best exemplified by cancers of infectious origin. It provides the perfect opportunity for harnessing the advances that have been made in the control of communicable diseases to attempt the control of noncommunicable diseases. There are possibilities at various levels of intervention, at primary, secondary and tertiary levels, which fit well within a well-planned national cancer control strategy. Prevention should proceed through steps of disruption of transmission, improvement in disease recognition and diagnosis, as well as through prompt effective treatment. This principle should work for both infection and the resultant cancer. Research is very important in understanding how best to use the available knowledge and how best to sequentially implement strategies. Finally, policies that acknowledge infection-related cancers as a major problem in the region should be in place., (Copyright © 2012 S. Karger AG, Basel.)

Burkitt lymphoma (BL) was first described in Uganda in 1958 as a sarcoma of the jaw but later confirmed to be a distinct form of Non Hodgkin lymphoma (NHL). This discovery was the defining moment of cancer research in Uganda, which eventually led to the establishment of a dedicated cancer research institute, the Uganda Cancer Institute (UCI) in 1967. The centre was dedicated to Denis Burkitt in recognition of his contribution to cancer research in East Africa. BL is still the commonest NHL in childhood in Uganda. Its incidence has significantly increased recently due to yet unknown factors. Although the human immunodeficiency virus (HIV) was considered a possible reason for the increase, there is no evidence that it has substantially impacted on the epidemiology of the disease. However, for those patients with BL who are co infected with HIV there is a clear impact of the disease on clinical presentation and outcome. HIV-infected patients commonly present with extra facial sites and tend to have poor overall survival (median survival of 11·79 months). In summary, BL, as a disease entity in Uganda, has maintained the same clinical characteristics since its discovery, despite the emergence of HIV during the intervening period., (© 2012 Blackwell Publishing Ltd.)

Introduction: Kaposi sarcoma (KS) is the leading cause of cancer in Uganda and occurs in people with and without HIV. Human herpesvirus-8 (HHV-8) replication is important both in transmission of HHV-8 and progression to KS. We characterized the sites and frequency of HHV-8 detection in Ugandans with and without HIV and KS., Methods: Participants were enrolled into one of four groups on the basis of HIV and KS status (HIV negative/KS negative, HIV positive/KS negative, HIV negative/KS positive, and HIV positive/KS positive). Participants collected oral swabs daily and clinicians collected oral swabs, anogenital swabs, and plasma samples weekly over 4 weeks. HHV-8 DNA at each site was quantified by polymerase chain reaction (PCR)., Results: 78 participants collected a total of 2063 orals swabs and 358 plasma samples. Of these, 428 (21%) oral swabs and 96 (27%) plasma samples had detectable HHV-8 DNA. HHV-8 was detected more frequently in both the oropharynx of persons with KS (24 (57%) of 42 persons with KS vs. 8 (22%) of 36 persons without, p = 0.002) and the peripheral blood (30 (71%) of 42 persons with KS vs. 8 (22%) of 36 persons without, p<0.001). In a multivariate model, HHV-8 viremia was more frequent among men (IRR = 3.3, 95% CI = 1.7-6.2, p<0.001), persons with KS (IRR = 3.9, 95% CI = 1.7-9.0, p = 0.001) and persons with HIV infection (IRR = 1.7, 95% CI = 1.0-2.7, p = 0.03). Importantly, oral HHV-8 detection predicted the subsequent HHV-8 viremia. HHV-8 viremia was significantly more common when HHV-8 DNA was detected from the oropharynx during the week prior than when oral HHV-8 was not detected (RR = 3.3, 95% CI = 1.8-5.9 p<0.001). Genital HHV-8 detection was rare (9 (3%) of 272 swabs)., Conclusions: HHV-8 detection is frequent in the oropharynx and peripheral blood of Ugandans with endemic and epidemic KS. Replication at these sites is highly correlated, and viremia is increased in men and those with HIV. The high incidence of HHV-8 replication at multiple anatomic sites may be an important factor leading to and sustaining the high prevalence of KS in Uganda.