Maori and Pacific Peoples With Multiple Myeloma in New Zealand are Younger and Have Inferior Survival Compared to Other Ethnicities: A Study From the Australian and New Zealand Myeloma and Related Diseases Registry (MRDR).

BACKGROUND: Maori and Pacific peoples (MPP) in New Zealand (NZ) have poorer health outcomes than other ethnicities. However, this has not been clinically investigated in multiple myeloma (MM). Using data from the Australian and NZ Myeloma and Related Diseases Registry for all participating centers in NZ, we compared MPP demographics, clinical characteristics, diagnostics, treatment, and outcomes to non-MPP. PATIENTS AND METHODS: MPP were defined as having ≥1 grandparent of this heritage. We tested ethnicity as a predictor of overall survival (OS) with multivariable Cox regression. RESULTS: Of 568 NZ patients with MM (September 2012 to April 2021) and ethnicity data, 138 were MPP. They were diagnosed younger than non-MPP (median age 63 [IQR: 57-72] vs. 70y [62-77], P < .001). Obesity (53 vs. 27%, P < .001), diabetes (24 vs. 8%, P < .001), renal insufficiency (28 vs. 17%, P = .005), pulmonary disease (10 vs. 5%, P = .02) and FISH abnormalities (54 vs. 42%, P = .04) were more common in MPP, and a lower proportion received first-line drug therapy (88 vs. 94%, P = .03) and autologous stem cell transplant (ASCT) (age <70y: 56 vs. 70%, P = .03). OS for MPP was shorter than non-MPP even after adjusting for age, comorbidities, disease stage, performance status, FISH abnormalities and treatment (HR 1.58 [1.04-2.39], P = .03). CONCLUSION: MPP with MM in NZ were younger, a greater proportion had comorbidities and FISH abnormalities at diagnosis, fewer received first-line treatment and/or ASCT, and they had poorer OS than non-MPP. Investigation of modifiable factors to improve outcomes and discern why MM occurs at a younger age in MPP is needed.

Consensus statement on the treatment of transplant-eligible patients with newly diagnosed multiple myeloma in New Zealand.

Multiple myeloma is the second most common blood cancer in New Zealand with higher incidence in Maori and Pacific Island populations. It remains an incurable disease but the rapidly changing treatment landscape has led to improved outcome. In response to recent changes in funding of anti-myeloma therapy in New Zealand, the New Zealand Myeloma Interest Group has reviewed the latest literature and updated the treatment pathway of transplant-eligible patients with newly diagnosed multiple myeloma.

Upfront lower dose lenalidomide is less toxic and does not compromise efficacy for vulnerable patients with relapsed refractory multiple myeloma: final analysis of the phase II RevLite study.

The combination of lenalidomide and dexamethasone is an established treatment for patients with multiple myeloma (MM). Increasingly, treatment attenuation is advocated for frail/elderly patients to minimize toxicity even though there have been no prospective studies to demonstrate whether lenalidomide dose attenuation impacts on response and survival outcome. This prospective multicentre phase II study assessed the efficacy and tolerability of lower dose lenalidomide (15 mg) and dexamethasone (20 mg) in 149 eligible patients with relapsed/refractory MM aged over 59 years and/or with renal impairment. The overall response rate was 71% (complete response 15%). Median (range) progression-free survival (PFS) and overall survival (OS) were 8·9 (6·9-11·5) and 30·5 (20·0-36·2) months, respectively. Upon formal statistical comparison of these endpoints to that of a matched cohort of patients from the pivotal phase III MM009/MM010 studies who received standard-dose lenalidomide (25 mg) and high-dose dexamethasone (40 mg) no difference was seen in PFS (P = 0·34) and OS (P = 0·21). Importantly, grade 3-4 toxicities were reduced with low-dose lenalidomide, mainly lower neutropenia (29% vs. 41%), infections (23% vs. 31%) and venous thromboembolism (3% vs. 13%). This study supports a strategy of lenalidomide dose reduction at the outset for at-risk patients, and prospectively confirms that such an approach reduces adverse events while not compromising patient response or survival outcomes.

Identification of JAK2V617F in patients with polycythemia is highly correlated with conventional criteria for diagnosis of polycythemia vera.

One hundred and forty four patients with a clinical indication of suspected polycythemia vera (PV), essential thrombocythemia, or idiopathic myelofibrosis were screened for JAK2(V617F) and the mutation frequency was 47, 51, and 50%, respectively. Previous investigations enabled 42 of 66 patients with suspected PV to be definitively diagnosed either as PV according to WHO criteria or to have this diagnosis excluded. Ninety-six percent of those with PV were JAK2(V617F), whereas all patients without PV did not have the mutation. Early screening of suspected PV patients for JAK2(V617F) rapidly identifies nearly all those with PV without invasive or less specific conventional investigations.