How this document came to be
About this sample
A principal investigator at a university medical school came to us with a tight, deadline-bound commission: to produce a pre-manuscript survey of the literature and current thinking on their assigned review topic — Prostaglandins and Leukotrienes in Immuno-Oncology.
Unlike an open-ended discovery question, this was a defined-scope synthesis problem. The field is large, fast-moving, and spread across decades of murine mechanism studies and a more recent — and oftendiscordant — body of human trial data. The client needed it mapped, sourced, and structured quickly, without sacrificing rigour.
This topic is hard to review due to its internal tensions: the same lipid mediator can be immunosuppressive in one cell type and protective in another, and promising preclinical targets have repeatedly underdelivered in the clinic. Capturing those contradictions faithfully, rather than smoothing them over, was central to the brief.
We began by discussing the client’s goals and assessing the available tools and public resources, including our own. We also considered systems developed by other teams. When another tool is better suited to a particular task, we recommend it.
In this case, our research-writing and data-mining system was a good fit. Working with the client, we turned the initial idea into a focused research brief and developed the prompt reproduced below. The system generated a “writing kit,” which our specialists then checked and revised in consultation with the client. We verified the bibliographic references and performed an internal review tracing the quantitative and mechanistic claims to their cited sources.
The brief we developped with the client
“Create a comprehensive and deep academic review on the following topic: ‘Prostaglandins and Leukotrienes in Immuno-Oncology: Mechanisms and Measures in Murine Models and Human Trials.’ Cover the arachidonic acid–COX/LOX network in the tumour microenvironment, including PGE2 amplification and the pro-resolving mediators that oppose it. Detail receptor-level mechanisms — EP2/EP4, DP1/DP2, IP, BLT1/BLT2, and the cysteinyl leukotriene receptors — and how each reshapes myeloid, T cell, and NK cell function. Distinguish clearly between findings established in murine models and those tested in human trials, giving due weight to negative and contradictory results. Address therapeutic strategies (selective receptor antagonists, dual COX-2/5-LO blockade, and checkpoint-inhibitor combinations) and the measurement and biomarker approaches — including LC–MS/MS eicosanoid quantification and spatial immune mapping — used to assess pathway activity. Close with the open questions and translational gaps that should guide future work.”
A note on deliverables
This PDF document itself is a small part of our full research output. The client deliverables include PRISMA-compliant literature search strategies, PubMed retrievals, writing blocks the client may use for reconstruction and revision while catering to different reporting formats, a reference database compatible with major bibliographic software, Python codefor data extraction and analysis, and more.
Our team has verified the bibliographic references and checked the quantitative claims against their cited sources. This document is a literature synthesis intended to support manuscript development; it is not itself a peer-reviewed publication, and nothing in it constitutes medical advice.
Provenance
Prepared and published by Cellformatica with the client’s permission. © 2026 Cellformatica.
