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Changes at the Point-of-Sale for Tobacco Following the 1999 Billboard Ban

Reports on Industry Activity from Outside UCSF (2000)

Objective—This study aimed to assess the effect of the Master Settlement Agreement’s (MSA) 24 April 1999 ban on billboard tobacco advertising on the tobacco industry’s point-of-purchase marketing strategies.

Methods—Observations were conducted from 16 February through 23 June 1999 in 3,464 tobacco-selling retail stores in a total of 191 communities across the nation. Communities were determined by the location of schools in a nationally representative sample of students in grades 8, 10, and 12 in the United States. At each store, information was collected on the extent of interior and exterior tobacco advertising, extent of tobacco functional objects, presence of tobacco promotions, and placement of tobacco and low-height advertisements. Logistic regression and cumulative logit analyses were used to assess changes in pre- and post-ban retail environments, after adjusting for store type, store size, presence of state tobacco control program and urbanicity.

Results—After adjustment for covariates, there were significant post-ban increases in the presence of tobacco sales promotions, the presence and extent of functional objects, the presence of exterior and interior store advertising, and the extensiveness of exterior store advertising.

Conclusions—The observed increase in point-of-purchase marketing in the period following the billboard advertising ban suggests that the tobacco industry may be shifting at least some of the expenditures once spent on billboard advertising to the advertising and promotion at the point-ofpurchase. To the extent that this is so, the intended effects of the MSA billboard ban may not be fully realized.

Cover page: Changes at the Point-of-Sale for Tobacco Following the 1999 Billboard Ban

Article
Peer Reviewed

Progress toward curing HIV infection with hematopoietic cell transplantation

HIV-1 infection afflicts more than 35 million people worldwide, according to 2014 estimates from the World Health Organization. For those individuals who have access to antiretroviral therapy, these drugs can effectively suppress, but not cure, HIV-1 infection. Indeed, the only documented case for an HIV/AIDS cure was a patient with HIV-1 and acute myeloid leukemia who received allogeneic hematopoietic cell transplantation (HCT) from a graft that carried the HIV-resistant CCR5-∆32/∆32 mutation. Other attempts to establish a cure for HIV/AIDS using HCT in patients with HIV-1 and malignancy have yielded mixed results, as encouraging evidence for virus eradication in a few cases has been offset by poor clinical outcomes due to the underlying cancer or other complications. Such clinical strategies have relied on HIV-resistant hematopoietic stem and progenitor cells that harbor the natural CCR5-∆32/∆32 mutation or that have been genetically modified for HIV-resistance. Nevertheless, HCT with HIV-resistant cord blood remains a promising option, particularly with inventories of CCR5-∆32/∆32 units or with genetically modified, human leukocyte antigen-matched cord blood.

Article
Peer Reviewed

Collateral Damage: Insulin-Dependent Diabetes Induced With Checkpoint Inhibitors.

UC San Francisco Previously Published Works (2018)

Insulin-dependent diabetes may occur in patients with cancers who are treated with checkpoint inhibitors (CPIs). We reviewed cases occurring over a 6-year period at two academic institutions and identified 27 patients in whom this developed, or an incidence of 0.9%. The patients had a variety of solid-organ cancers, but all had received either anti-PD-1 or anti-PD-L1 antibodies. Diabetes presented with ketoacidosis in 59%, and 42% had evidence of pancreatitis in the peridiagnosis period. Forty percent had at least one positive autoantibody and 21% had two or more. There was a predominance of HLA-DR4, which was present in 76% of patients. Other immune adverse events were seen in 70%, and endocrine adverse events in 44%. We conclude that autoimmune, insulin-dependent diabetes occurs in close to 1% of patients treated with anti-PD-1 or -PD-L1 CPIs. This syndrome has similarities and differences compared with classic type 1 diabetes. The dominance of HLA-DR4 suggests an opportunity to identify those at highest risk of these complications and to discover insights into the mechanisms of this adverse event.

Cover page: Collateral Damage: Insulin-Dependent Diabetes Induced With Checkpoint Inhibitors.

Article
Peer Reviewed

IL2RA Genetic Heterogeneity in Multiple Sclerosis and Type 1 Diabetes Susceptibility and Soluble Interleukin-2 Receptor Production

UC San Francisco Previously Published Works (2009)

Multiple sclerosis (MS) and type 1 diabetes (T1D) are organ-specific autoimmune disorders with significant heritability, part of which is conferred by shared alleles. For decades, the Human Leukocyte Antigen (HLA) complex was the only known susceptibility locus for both T1D and MS, but loci outside the HLA complex harboring risk alleles have been discovered and fully replicated. A genome-wide association scan for MS risk genes and candidate gene association studies have previously described the IL2RA gene region as a shared autoimmune locus. In order to investigate whether autoimmunity risk at IL2RA was due to distinct or shared alleles, we performed a genetic association study of three IL2RA variants in a DNA collection of up to 9,407 healthy controls, 2,420 MS, and 6,425 T1D subjects as well as 1,303 MS parent/child trios. Here, we report "allelic heterogeneity" at the IL2RA region between MS and T1D. We observe an allele associated with susceptibility to one disease and risk to the other, an allele that confers susceptibility to both diseases, and an allele that may only confer susceptibility to T1D. In addition, we tested the levels of soluble interleukin-2 receptor (sIL-2RA) in the serum from up to 69 healthy control subjects, 285 MS, and 1,317 T1D subjects. We demonstrate that multiple variants independently correlate with sIL-2RA levels.

Cover page: IL2RA Genetic Heterogeneity in Multiple Sclerosis and Type 1 Diabetes Susceptibility and Soluble Interleukin-2 Receptor Production