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Radioligand therapy target profile

MAD1L1 as a Radioligand Therapy Target

mitotic arrest deficient 1 like 1 · Ensembl ENSG00000002822 · Data updated 2026-08-01

MAD1L1, mitotic arrest deficient 1 like 1, is a cell-surface protein. In Human Protein Atlas immunohistochemistry, MAD1L1 staining is highest in pancreatic cancer (100% of samples positive), lymphoma (100% of samples positive) and bladder cancer (100% of samples positive). Clinical status: Discovery-stage (no clinical drug program).

LocalizationCell-Surface
Top cancer (IHC)Pancreatic Cancer
InternalizationNot assessed
Clinical stageDiscovery-stage (no clinical drug program)
Active trialsSee ClinicalTrials.gov
Cancer association (Open Targets)0.48

Is MAD1L1 a good radioligand therapy target?

Scored against the six criteria that decide whether a protein can become a radioligand therapy:

MAD1L1 expression in cancer

Protein expression of MAD1L1 across 20 cancer types from Human Protein Atlas immunohistochemistry. The score is a weighted staining intensity from 0 to 1; "% positive" is the share of patient samples with detectable staining.

Cancer typeIHC scoreLevel% positive
Pancreatic Cancer0.89High100%
Lymphoma0.81High100%
Bladder Cancer0.81High100%
Melanoma0.79High100%
Glioma0.78High100%
Head and Neck Cancer0.75High100%
Thyroid Cancer0.75High100%
Gastric Cancer0.75High100%
Colorectal Cancer0.73High100%
Prostate Cancer0.70High100%
Cervical Cancer0.69High100%
Lung Cancer0.69High100%
Testicular Cancer0.69High100%
Ovarian Cancer0.69High92%
Endometrial Cancer0.67High100%
Breast Cancer0.64High100%
Skin Cancer0.61High100%
Neuroendocrine Tumors0.58High75%
Liver Cancer0.56High83%
Kidney Cancer0.52High73%

Is MAD1L1 internalized?

Nuclens has not yet extracted internalization evidence for MAD1L1. Internalization matters for radioligands because an internalizing receptor traps the radionuclide inside the tumor cell. Run a full analysis to pull the latest literature.

MAD1L1 clinical trials

Discovery-stage (no clinical drug program). Nuclens hasn't indexed trials for MAD1L1 yet. Search ClinicalTrials.gov for MAD1L1 trials.

MAD1L1 normal tissue expression

Normal-tissue expression in dose-limiting organs (kidney, liver, bone marrow, salivary glands) drives radioligand dosimetry risk. Nuclens is re-validating its normal-tissue values, so they are not shown here yet. See MAD1L1 in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.

MAD1L1 gene essentiality (DepMap)

CRISPR knockout effect across 1258 cancer cell lines: -0.09 (not essential). Radioligands kill by radiation, not by blocking the target, so essentiality matters less than for inhibitors. A non-essential target can still be an excellent radioligand target.

Related pancreatic cancer radioligand targets

EGFR · HER3 (ERBB3) · c-MET (MET) · Mesothelin (MSLN) · FAP · CEA (CEACAM5) · STEAP2 · SSTR2

See all radioligand therapy targets in pancreatic cancer.

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Data sources

Subcellular localization: UniProt via Open Targets (CC BY 4.0 / CC0). Tumor immunohistochemistry: Human Protein Atlas (CC BY-SA 4.0). Clinical trials: ClinicalTrials.gov (public domain). Gene essentiality: DepMap (CC BY 4.0). Internalization and shedding: AI-extracted from PubMed abstracts, so verify against the cited papers before relying on them. Nuclens is a first-pass triage layer, not a substitute for wet-lab validation or clinical dosimetry. Derived expression data on this page is shared under CC BY-SA 4.0.