# Band‐Selective IR PRESS for Brain Tumor Spectroscopy Allows Robust Detection of Lactate

**Authors:** Shun Kishimoto, Daniel R. Crooks, Peng Lu, Yuki Shibata, Olga Kim, Jeeva Munasinghe, Otowa Yasunori, Yamashita Kota, Kazutoshi Yamamoto, W. Marston Linehan, Jing Wu, Murali C. Krishna, Jeffrey R. Brender

PMC · DOI: 10.1002/nbm.70220 · Nmr in Biomedicine · 2026-02-02

## TL;DR

A new MRS method called SPIR-PRESS improves lactate detection in brain tumors by reducing lipid interference, allowing better metabolic profiling without losing other metabolite signals.

## Contribution

SPIR-PRESS is a novel MRS technique that selectively suppresses lipid signals while preserving metabolite sensitivity for more accurate lactate quantification.

## Key findings

- Phantom experiments showed a ~60% increase in lactate sensitivity compared to conventional PRESS with a 288-ms TE.
- SPIR-PRESS detected lactate and key tumor metabolites in mouse gliomas that were undetectable with long TE PRESS.
- The method preserves the full metabolite profile while suppressing lipid signals that overlap with lactate.

## Abstract

Lactate plays a critical role in the tumor microenvironment, driving tumor progression, metastasis, and immune evasion. Despite its importance, in vivo quantification of lactate using magnetic resonance spectroscopy (MRS) has faced challenges, primarily due to the overlapping lipid signal at 1.3 ppm. Current clinical practice employs a long echo time to exploit differences in T2 relaxation between lactate and lipids; however, this approach significantly suppresses signals from other metabolites. Lipid has a notably different T1 relaxation time than lactate and other metabolites, which may be exploited by an inversion recovery sequence to better distinguish them. However, this method has not found wide use because of the loss of signal in other metabolites. Here, we introduce a selective inversion pulse with a short echo time MRS method (SPIR‐PRESS), which mitigates this issue. In phantom experiments, SPIR‐PRESS successfully suppressed lipid signals that could be misinterpreted as lactate in short TE PRESS spectra, while maintaining sensitivity to the full metabolite profile. SPIR‐PRESS demonstrated superior performance in quantifying lactate compared to long echo time PRESS, with ~60% increase in sensitivity for lactate detection compared to conventional PRESS with a 288‐ms TE. In a mouse glioma model, SPIR‐PRESS clearly detected lactate and other key tumor metabolites (total choline, creatine, NAA) in the tumor, which were not detectable in conventional long TE PRESS. These findings highlight SPIR‐PRESS as a promising technique for improved lactate quantification and comprehensive metabolite profiling in tumor environments.

Lactate quantification by MRS is hindered by lipid signal overlap at 1.3 ppm, frequently forcing the use of long echo times that suppress other metabolites. We developed SPIR‐PRESS, a selective inversion recovery technique that suppresses lipids while preserving metabolite sensitivity. Phantom studies showed 60% improved lactate sensitivity versus standard 288 ms TE PRESS. In mouse gliomas, SPIR‐PRESS detected lactate alongside metabolites invisible in conventional long TE spectra. SPIR‐PRESS enables simultaneous lactate quantification and comprehensive metabolic profiling critical for tumor assessment.

## Linked entities

- **Diseases:** brain tumor (MONDO:0021211), glioma (MONDO:0021042)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Sp1 (trans-acting transcription factor 1) [NCBI Gene 20683] {aka 1110003E12Rik, Sp1-1}, Idh1 (isocitrate dehydrogenase 1 (NADP+), soluble) [NCBI Gene 15926] {aka E030024J03Rik, Id-1, Idh-1, Idpc}, Sp2 (Sp2 transcription factor) [NCBI Gene 78912] {aka 4930480I16Rik, mKIAA0048}
- **Diseases:** mitochondrial disease (MESH:D028361), glioma (MESH:D005910), stroke (MESH:D020521), traumatic brain injury (MESH:D000070642), glioblastoma (MESH:D005909), Brain Tumor (MESH:D001932), Cancer (MESH:D009369), metastasis (MESH:D009362), oligodendroglioma (MESH:D009837), CNS tumors (MESH:D016543), hypoxia (MESH:D000860), ischemia (MESH:D007511), ccRCC (MESH:D002292), fat (MESH:D004620), necrotic (MESH:D009336), neuronal distress (MESH:D012128), dislocation (MESH:D004204), immunodeficient (MESH:D007153)
- **Chemicals:** lidocaine (MESH:D008012), Glutamate (MESH:D018698), Lipid (MESH:D008055), nitrogen (MESH:D009584), Cho (MESH:D002794), sodium hydroxide (MESH:D012972), glutamine (MESH:D005973), tau (MESH:C000609666), Egg Yolk Phospholipids (-), D2O (MESH:D017666), Lactate (MESH:D019344), 13C (MESH:C000615229), carbon (MESH:D002244), Soybean Oil (MESH:D013024), PUFA (MESH:D005231), N-acetyl aspartate (MESH:C000179), Intralipid (MESH:C545823), oxygen (MESH:D010100), GABA (MESH:D005680), Glycerin (MESH:D005990), copper (MESH:D003300), PBS (MESH:D007854), xylazine (MESH:D014991), triglyceride (MESH:D014280), Cr (MESH:D003401), water (MESH:D014867)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** GBM1 — Homo sapiens (Human), Glioblastoma, Cancer cell line (CVCL_DG57), UOK161 — Homo sapiens (Human), Renal cell carcinoma, Cancer cell line (CVCL_B128)

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12863986/full.md

## References

59 references — full list in the complete paper: https://tomesphere.com/paper/PMC12863986/full.md

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Source: https://tomesphere.com/paper/PMC12863986