Supplemental-data- GPhoCS-output

Supplemental-data- GPhoCS-outpu

Supplementary Methods

Supplementary Method

Long-term reconstitution with Lgl1^−/− bone marrow does not induce leukaemia.

<p>Unfractionated bone marrow was isolated from chimeric mice one-year post initial foetal liver reconstitution, and transplanted into Ly5.1/Ly5.2 heterozygote recipients. (<b>A–C</b>) Peripheral blood was analysed for the proportion of primary Ly5.2⁺ donor cells in peripheral blood at 5 weeks, 14 weeks, and 16 weeks post transplantation. (<b>D–F</b>) At 16 weeks, the lineage potential and existence of leukemic clones of transplanted bone marrow was assessed by measuring the proportion of primary donor Ly5.2+ B cells (B220⁺, CD19+), CD4 T cells (CD3⁺, CD4⁺) and CD8 T cells (CD3⁺, CD8⁺). Data shown are pooled results from 3 individual donors per genotype.</p

Analysis of peripheral blood in primary reconstituted Lg1^−/− mice.

<p>Lethally irradiated Ly5.1 mice were reconstituted with 1×10⁶ foetal liver cells isolated from E14.5 embryos from Lg1^+/+, Lg1^+/− and Lgl1^−/− mice. (<b>A</b>) >6weeks post reconstitution, composition of the hematopoietic compartment was determined by ADVIA analysis of peripheral blood. (<b>B</b>) Donor derived Ly5.2⁺ lymphocyte populations in the blood of Lg1^+/+ and Lgl1^−/− chimeric mice were identified by flow cytometry and frequencies quantified in (<b>C</b>). Statistics represent mean ± SEM from one reconstitution. Lgl<i>^+/+ n = 4–11</i>, Lgl<i>^+/− n = 7–9</i> Lgl^{−<i>/</i>−}<i>n = 7–9</i>. One representative reconstitution is shown from 4 independent experiments</p

Lgl1 does not function as a tumour suppressor in conjunction with common oncogenes.

<p>Lg1^+/+ and Lgl1^−/− foetal liver cells were infected with either empty vector MigR1-GFP or ICN1-ΔRamΔP-GFP constructs and transplanted into lethally irradiated Ly5.1 recipient mice. (<b>A</b>) Kaplan-Meier analysis of survival of mice following reconstitution with infected foetal liver cells. Kaplan-Meir analysis of survival in lethally irradiated Ly5.1 mice reconstituted Ly5.2+ Lgl1^+/+,Lgl^+/− and Lgl^−/− foetal liver cells in the presence of either the TEL-JAK2 (<b>B</b>) or Eµ-Myc (<b>C</b>) transgenes. Splenocytes (<b>D</b>) or Eµ-Myc B cell lymphomas (<b>E</b>) were isolated from primary chimeric wildtype and Lgl deficient mice and assayed by Q-PCR for expression of both Lgl1 and Lgl2 in triplicate samples. Statistical differences between the means of two data groups was determined by using two-tailed unpaired Student's <i>t</i> test, and <i>p</i> values <0.05 were considered significant. For survival analysis, Kaplan-Meier survival curves were analyzed using Log-rank (Mantel-Cox) test. P<0.05 were considered significant.</p

Data_Sheet_1_Dietary intake of animal-based products and likelihood of follicular lymphoma and survival: A population-based family case-control study.docx

BackgroundThe association between dietary intake of foods of animal origin and follicular lymphoma (FL) risk and survival is uncertain. In this study, we examined the relationship between dietary intake of dairy foods and fats, meat, fish and seafoods, and the likelihood of FL and survival.MethodsWe conducted a population-based family case-control study in Australia between 2011 and 2016 and included 710 cases, 303 siblings and 186 spouse/partner controls. We assessed dietary intake of animal products prior to diagnosis (the year before last) using a structured food frequency questionnaire and followed-up cases over a median of 6.9 years using record linkage to national death data. We examined associations with the likelihood of FL using logistic regression and used Cox regression to assess association with all-cause and FL-specific mortality among cases.ResultsWe observed an increased likelihood of FL with increasing daily quantity of oily fish consumption in the year before last (highest category OR = 1.96, CI = 1.02–3.77; p-trend 0.06) among cases and sibling controls, but no associations with spouse/partner controls. We found no association between the likelihood of FL and the consumption of other types of fish or seafood, meats or dairy foods and fats. In FL cases, we found no association between meat or oily fish intake and all-cause or FL-specific mortality.ConclusionOur study showed suggestive evidence of a positive association between oily fish intake and the likelihood of FL, but findings varied by control type. Further investigation of the potential role of environmental contaminants in oily fish on FL etiology is warranted.</p