AI Article Synopsis

  • The MYD88 L265P mutation, linked to increased cancer cell activity, is prevalent in Waldenstrom macroglobulinemia and non-germinal center diffuse large B-cell lymphoma (DLBCL) but its occurrence in the Pakistani population is not well-documented.
  • A study at the Armed Forces Institute of Pathology analyzed 82 DLBCL cases, finding the mutation in 3.6% of germinal center B-cell (GCB) subtype and 22.2% of non-GCB subtype cases.
  • The significant association (P = 0.024) suggests that targeting this mutation could improve treatment outcomes for DLBCL patients, especially those with the non-GCB subtype.

Article Abstract

MYD88 L265P mutation is a gain-of-function driver mutation. It is observed in a significant proportion of Waldenstrom macroglobulinemia and activated B-cell subtype of diffuse large B-cell lymphoma (DLBCL; non-germinal center subtype). The incidence of this mutation in the subtypes of DLBCL has not yet been documented in the Pakistani population. This study aimed to ascertain the frequency and association of MYD88 L265P mutation within 2 subtypes of DLBCL, germinal center B-cell-like (GCB) and non-GCB B-cell lymphoma (non-GCB), in the local population. This cross-sectional study was conducted at the Armed Forces Institute of Pathology, Punjab, Pakistan. All newly diagnosed cases of DLBCL were included in the study. We analyzed 82 biopsy-proven cases of DLBCL (28 cases of GCB subtype and 54 cases of non-GCB subtype). DNA was extracted from formalin-fixed paraffin-embedded tissue blocks, and a conventional polymerase chain reaction was used to detect the MYD88 L265P mutation. The MYD88 L265P mutation was detected in 01 of 28 (3.6%) cases of the GCB subtype (95% CI: 0%-10%) and in 12 of 54 (22.2%) cases of the non-GCB subtype (95% CI: 11%-33%). Pearsos χ2 test revealed a statistically significant association of MYD88 L265P mutation with non-GCB subtype of DLBCL (P = 0.024). This association will assist in identifying a target population that may benefit from MYD88-specific treatment regimens. This may exponentially improve the outcome of patients with DLBCL harboring this mutation.

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Source
http://dx.doi.org/10.1097/PAI.0000000000001239DOI Listing

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