ObjectiveTo estimate the direct and indirect costs of active smoking in Vietnam.MethodA prevalence-based disease-specific cost of illness approach was utilised to calculate the costs related to five smoking-related diseases: lung cancer, cancers of the upper aerodigestive tract, chronic obstructive pulmonary disease, ischaemic heart disease and stroke. Data on healthcare came from an original survey, hospital records and official government statistics. Morbidity and mortality due to smoking combined with the average per capita income were used to calculate the indirect costs of smoking by applying the human capital approach. The smoking-attributable fraction was calculated using the adjusted relative risk values from phase II of the American Cancer Society Cancer Prevention Study (CPS-II). Costs were classified as personal, governmental and health insurance costs.ResultsThe total economic cost of smoking in 2011 was estimated at 24 679.9 billion Vietnamese dong (VND), equivalent to US$1173.2 million or approximately 0.97% of the 2011 gross domestic product. The direct costs of inpatient and outpatient care reached 9896.2 billion VND (US$470.4 million) and 2567.2 billion VND (US$122.0 million), respectively. The government’s contribution to these costs was 4534.3 billion VND (US$215.5 million), which was equivalent to 5.76% of its 2011 healthcare budget. The indirect costs (productivity loss) due to morbidity and mortality were 2652.9 billion VND (US$126.1 million) and 9563.5 billion VND (US$454.6 million), respectively. These indirect costs represent about 49.5% of the total costs of smoking.ConclusionsTobacco consumption has large negative consequences on the Vietnamese economy.

Burden of disease has been used to assess population health status. This article presents the first estimations of burden of disease in Vietnam in 2008 using disability-adjusted life years (DALYs). DALYs were calculated using the Global Burden of Disease (GBD) methods. Incidence, prevalence of diseases, and causes of death was extracted from Vietnam data. Disability weights were borrowed from GBD and Dutch research. In 2008, the total burden of disease in Vietnam was 12.3 million DALYs. Noncommunicable diseases dominated the total burden of diseases in Vietnam, accounting for 71% of the total burden, and cardiovascular disease was the leading cause group of premature death. While pneumonia was an important cause of burden in Vietnamese children, stroke and depression were the main causes of disease burden among adults. The study provides a snapshot of Vietnamese health status and offers guidance for health policymaking in Vietnam.

Schizophrenia is a highly disabling mental health disorder that imposes a considerable economic burden on a health care system. This paper aimed to examine the cost and effectiveness of alternative pharmaceutical interventions and the effects of family intervention (FI) for schizophrenia from the government perspective in order to introduce the most cost-effective intervention applicable to Vietnam. A Markov model was developed to estimate costs and health outcome over patients' lifetimes when using typical and atypical antipsychotic drugs, alone or in combination with family intervention. Health outcome was measured in terms of disability-adjusted life years averted. Monte Carlo simulation was used for uncertainty analysis. According to our findings, interventions using typical or atypical drugs combined with FI were found to be the most effective and least costly compared to a 'do-nothing' scenario. Interventions using atypical drugs alone were estimated to be much less favourable due to a considerably higher cost. This is a very first attempt on cost-effectiveness analysis of interventions for schizophrenia in Vietnam, and recommendations are made for future research to determine the most cost-effective intervention.

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Squamous cell carcinomas (SCC) originate from stratified squamous epithelium in diverse anatomical locations that share common histological features and genetic mutations. Non-melanoma skin cancer, head and neck cancer (HNSCC), esophageal cancer (ESCC), and non-small cell lung cancer (sqNSCLC) make up the majority of SCC cases and together represent the largest subtype of cancer. There is a significant unmet need for effective treatment options post-progression of standard-of-care therapies. Alterations in receptor tyrosine kinase signaling pathways are commonly found in SCCs, e.g. EGFR is expressed in 90% of HNSCC, 76% of ESCC and 82% of sqNSCLC. However, the combination of EGFR targeting antibody cetuximab with chemotherapy confers limited clinical benefit and even initially sensitive tumors often develop resistance. Studies in SCC have implicated HER3, a key dimerization partner of HER family members, as one likely cause of treatment failure, through HER3 heterodimer activation of PI3K/AKT and MAPK/ERK pathways. In this study, we investigated the potential of combining HER3 and EGFR inhibitors to improve efficacy and overcome resistance. Previous attempts to target HER3 have shown limited clinical efficacy due to suboptimal HER3 inhibition, especially the lack of efficacy in ligand-independent activation mechanisms. They also lacked biomarker stratification for patients where HER3 inhibition would confer benefit. HMBD-001 is a clinical-stage anti-HER3 antibody which is being evaluated in a first-in-human, open-label, multi-center, dose escalation and expansion Phase I/IIa trial in patients with HER3 expressing advanced solid tumors (NCT05057013). HMBD-001 was rationally developed to uniquely block the HER3 heterodimerization interface to potently inhibit all HER3 dimer formation, including ligand-dependent and independent HER3 dimerization. Here, we show that dual blockade of EGFR and HER3 using cetuximab and HMBD-001 robustly inhibits tumor growth and is superior to either monotherapy. In multiple cell and patient derived SCC xenograft models, including models of HNSCC, ESCC and sqNSCLC, selected based on a novel gene signature that is robustly predictive of response, HMBD-001 in combination with cetuximab demonstrated up to 100% tumor growth inhibition and the abrogation of PI3K signalling. This combination was well tolerated with no relapse observed, even after a prolonged period of over 100 days in selected models. This study lays the foundation for testing HMBD-001 in combination with EGFR inhibitors in clinical settings. Better combination strategies of SoC and targeted therapeutics alongside a potent anti-HER3 mAb, in biomarker-selected patient populations, have the potential to meaningfully improve patient outcomes and prolong clinical benefit. Citation Format: Weiyi Toy, Dipti Thakkar, Khang Luu, Bui Ngoc Linh Chi, Jason Lai, Debleena Ray, Namita Gandhi, Alejandro Mas, Konrad Paszkiewicz, Piers Ingram, Jerome Boyd-Kirkup. Anti-HER3 antibody, HMBD-001, in combination with an EGFR inhibitor effectively inhibits tumor growth in biomarker-selected pre-clinical models of squamous cell carcinomas [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2659.