Publications by authors named "M A M Nijland"

Background: High dose chemotherapy and autologous stem cell transplantation (HDT/ASCT) remains the preferred first line consolidation strategy for newly diagnosed multiple myeloma (MM). However, The role of HDT/ASCT in first relapse is uncertain in the context of novel therapies. This study evaluates real-world outcomes of MM patients in first relapse, focusing on the role of consolidative HDT/ASCT.

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Next Generation Sequencing-based subtyping and interim- and end of treatment positron emission tomography (i/eot-PET) monitoring have high potential for upfront and on-treatment risk assessment of diffuse large B-cell lymphoma patients. We performed Dana Farber Cancer Institute (DFCI) and LymphGen genetic subtyping for the HOVON84 (n = 208, EudraCT-2006-005174-42) and PETAL (n = 204, EudraCT-2006-001641-33) trials retrospectively combined with DFCI genetic data (n = 304). For all R-CHOP treated patients (n = 592), C5/MCD- and C2/A53-subtypes show significantly worse outcome independent of the international prognostic index.

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Introduction: Enteropathy-associated T-cell lymphoma (EATL) is a peripheral T-cell lymphoma (PTCL) with a poor prognosis. Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with or without etoposide consolidated by autologous stem cell transplantation (ASCT) are recommended for fit PTCL patients. The role of etoposide and ASCT in EATL is unclear.

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Article Synopsis
  • High-dose methotrexate (HD-MTX) is commonly used to treat patients with central nervous system lymphoma, but it carries risks of unpredictable toxicity and pharmacokinetic variability.
  • The study aimed to characterize the population pharmacokinetics of HD-MTX and identify predictors for the risk of kidney and liver damage.
  • Results indicated that factors like estimated glomerular filtration rate (eGFR), treatment regimen, and MTX dose significantly impact PK variability and toxicity risk, with specific concentration thresholds linked to increased chances of nephrotoxicity.
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Previous studies in rodents suggest that mismatch between fetal and postnatal nutrition predisposes individuals to metabolic diseases. We hypothesized that in nonhuman primates (NHP), fetal programming of maternal undernutrition (MUN) persists postnatally with a dietary mismatch altering metabolic molecular systems that precede standard clinical measures. We used unbiased molecular approaches to examine response to a high fat, high-carbohydrate diet plus sugar drink (HFCS) challenge in NHP juvenile offspring of MUN pregnancies compared with controls (CON).

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