Tumour Heterogeneity and the Consequent Practical Challenges in the Management of Gastroenteropancreatic Neuroendocrine Neoplasms

Reccia, Isabella; Pai, Madhava; Jayant, Kumar; Spalding, Duncan; Frilling, Andrea

doi:10.3390/cancers15061861

Cited by 6 publications

(2 citation statements)

References 202 publications

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“…Some studies simplify their design by selecting a single target lesion with the highest uptake per patient when using [ 68 Ga]Ga-DOTA-TOC PET/CT to evaluate the treatment response of [ 177 Lu]Lu-DOTA-TATE [ 35 ]. However, considering the inherent heterogeneity of NETs, the evaluation of multiple lesions per patient would provide a more comprehensive reflection of tumour characteristics [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Prediction of [177Lu]Lu-DOTA-TATE therapy response using the absorbed dose estimated from [177Lu]Lu-DOTA-TATE SPECT/CT in patients with metastatic neuroendocrine tumour

Ha,

Kim,

et al. 2024

EJNMMI Phys

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Background Peptide receptor radionuclide therapy (PRRT) with [177Lu]Lu-DOTA-TATE has shown efficacy in patients with metastatic neuroendocrine tumours (NETs). Personalised dosimetry is crucial to optimise treatment outcomes and minimise adverse events. In this study, we investigated the correlation between the tumour-absorbed dose (TAD) estimated from [177Lu]Lu-DOTA-TATE SPECT/CT and the therapeutic response. Method A retrospective analysis was conducted on patients with advanced well-differentiated NETs grades 1–3 who underwent PRRT and exhibited greater uptake than liver on pre-therapeutic [68Ga]Ga-DOTA-TOC PET/CT. Target lesions were selected based on the RECIST 1.1 and PERCIST 1.0 criteria using [177Lu]Lu-DOTA-TATE SPECT/CT and pre-therapeutic contrast-enhanced CT scans. For anatomical image analysis, the sum of the longest diameter (SLD) of the target lesions was measured using the RECIST 1.1 criteria for patient-based analysis and the longest diameter (LD) of the target lesion using the RECIST-L criteria for lesion-based analysis. Standardised uptake values (SUVs) were measured on SPECT/CT images, and TADs were calculated based on the SUVs. Dosimetry was performed using a single SPECT/CT imaging time point at day 4–5 post-therapy. Statistical analyses were conducted to investigate correlations and determine the target lesion responses. Results Twenty patients with primary tumour sites and hepatic metastases were included. Fifty-five target lesions, predominantly located in the pancreas and liver, were analysed. The cumulative TAD (lesion-based analysis: r = 0.299–0.301, p = 0.025–0.027), but not the cycle 1 SUV (lesion-based analysis: r = 0.198–0.206, p = 0.131–0.147) or cycle 1 TAD (lesion-based analysis: r = 0.209–0.217, p = 0.112–0.126), exhibited a significant correlation with the change in LD of the target lesion. Binary logistic regression analysis identified the significance of the cumulative TAD in predicting disease control according to the RECIST-L criteria (odds ratio = 1.031–1.051, p = 0.024–0.026). Conclusions The cumulative TAD estimated from [177Lu]Lu-DOTA-TATE SPECT/CT revealed a significant correlation with change in LD, which was significantly higher for the cumulative TAD than for the cycle 1 SUV or TAD. A higher cumulative TAD was associated with disease control in the target lesion. However, considering the limitations inherent to a confined sample size, careful interpretation of these findings is required. Estimation of the cumulative TAD of [177Lu]Lu-DOTA-TATE therapy could guide the platform towards personalised therapy.

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Section: Discussionmentioning

confidence: 99%

Prediction of [177Lu]Lu-DOTA-TATE therapy response using the absorbed dose estimated from [177Lu]Lu-DOTA-TATE SPECT/CT in patients with metastatic neuroendocrine tumour

Ha,

Kim,

et al. 2024

EJNMMI Phys

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“…The ever-increasing complexity that exists within a solid tumor poses a major challenge in implementing precision oncology. This complexity has been recently reviewed by us [11,49] and other groups [50][51][52][53] (see also Appendix A).…”

Section: Introductionmentioning

confidence: 95%

When Therapy-Induced Cancer Cell Apoptosis Fuels Tumor Relapse

Mirzayans

2024

Onco

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Most therapeutic strategies for solid tumor malignancies are designed based on the hypothesis that cancer cells evade apoptosis to exhibit therapy resistance. This is somewhat surprising given that clinical studies published since the 1990s have demonstrated that increased apoptosis in solid tumors is associated with cancer aggressiveness and poor clinical outcome. This is consistent with more recent reports demonstrating non-canonical (pro-survival) roles for apoptotic caspases, including caspase 3, as well as the ability of cancer cells to recover from late stages of apoptosis via a process called anastasis. These activities are essential for the normal development and maintenance of a healthy organism, but they also enable malignant cells (including cancer stem cells) to resist anticancer treatment and potentially contribute to clinical dormancy (minimal residual disease). Like apoptosis, therapy-induced cancer cell dormancy (durable proliferation arrest reflecting various manifestations of genome chaos) is also not obligatorily a permanent cell fate. However, as briefly discussed herein, compelling pre-clinical studies suggest that (reversible) dormancy might be the “lesser evil” compared to treacherous apoptosis.

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Advances in Management of Nonfunctional Pancreas Neuroendocrine Tumors

Acher,

Hallet

2024

Surgical Clinics of North America

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Tumour Heterogeneity and the Consequent Practical Challenges in the Management of Gastroenteropancreatic Neuroendocrine Neoplasms

Cited by 6 publications

References 202 publications

Prediction of [177Lu]Lu-DOTA-TATE therapy response using the absorbed dose estimated from [177Lu]Lu-DOTA-TATE SPECT/CT in patients with metastatic neuroendocrine tumour

Prediction of [177Lu]Lu-DOTA-TATE therapy response using the absorbed dose estimated from [177Lu]Lu-DOTA-TATE SPECT/CT in patients with metastatic neuroendocrine tumour

When Therapy-Induced Cancer Cell Apoptosis Fuels Tumor Relapse

Advances in Management of Nonfunctional Pancreas Neuroendocrine Tumors

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