BC-NED · FGFR1/CCND1 amp · ER− in liver
The science behind the case
Metastatic HR+/HER2 0 breast cancer with neuroendocrine differentiation, outside the standard guidelines. Here: the pathology, the molecular profile, the therapeutic hypothesis and the material that exists. Below, what we are looking for.
For the curious
Explained without jargon
Go to the professional detailWhat does she have?
A breast cancer that spread to the bones and, since July 2026, to the liver. It's mostly luminal, the type that usually depends on hormones, but some of its cells have features of another type, called neuroendocrine.
Why isn't standard treatment enough?
Guidelines treat it as a luminal breast cancer and leave the neuroendocrine part out. Hormone therapies stopped holding it back. And in the liver, the test for the estrogen receptor, the very target of those therapies, came back negative.
Is there a way to target it?
Yes, there are leads. Analysis of the tumor, including cell by cell, has found possible weak points: altered or active genes that some treatments use as targets. They're still hypotheses, and need confirming first.
What's being done now?
Since 7 October 2026 she's been on Dato-DXd, an antibody that carries a drug to the tumor, in the TROPION-Breast06 trial. And at Dana-Farber, her liver and bone biopsies are being read cell by cell. The first results are in.
The tumor, in schematic form
A breast tumor with neuroendocrine features
It is a breast-type (luminal) tumor. Some of its cells also carry neuroendocrine features. In the two biopsies read cell by cell (liver and bone, 2026) those cells are mixed within the tumor, not a separate camp. What changes with the tissue and the technique (staining, DNA, RNA, PET) is how it looks.
Illustrative diagramFirst results
The tumor
- Luminal tumor cell
- With neuroendocrine features
One cell, up close
- Estrogen receptor: present in the breast. In the liver, staining came back 0%, yet its gene is still switched on in the RNA.
- HER2: she does not have it (0 in four readings).
- Extra copies of the FGFR1 and CCND1 genes.
In the blood
- Changes in RB1 and ESR1: only in blood, at a very low fraction (under 2%), and in no tissue.
Neither the cell, nor the number of dots, nor their position is data.
What comes from the cell-by-cell reading (scattered neuroendocrine features, estrogen receptor in the RNA) is first results. The rest comes from reports from 2024 to 2026.
The figures, one by one, with their source
The full tables, report by report:
- Estrogen receptor (ER): present in the breast, absent on liver staining · 95%, 100% and 85% in three readings of the breast tumor (2024-2026) · 0% in the liver (2026)
- …yet the estrogen receptor gene is still switched on in the RNA of the 2026 biopsies read cell by cell, although liver staining came back 0%. (It was also high in the RNA of the 2024 breast tumor, where staining was positive.)
- Progesterone receptor (PR): discordant between laboratories in the breast (5%, 100%, 20%) · 5% in the liver (2026)
- HER2: she does not have it (0) in four readings: three of the breast tumor and one of the liver
- Somatostatin receptors: the DOTATOC PET (May 2026) saw them in several bone lesions, not all, and the liver had no lesions yet · the SSTR2 gene barely shows in the cell-by-cell RNA (2026)
- Extra copies of the FGFR1 gene · 13 copies (breast 2024, TSO500) · amplified in bone 2026 (FoundationOne; 33 copies in its research annex) · 5-7 copies in blood 2026 (diluted signal) · active in liver and bone RNA
- Extra copies of CCND1 and its neighbours FGF3/FGF4/FGF19 · 20 and 18 copies (breast 2024) · 37 in the 2026 bone research annex · 6-7.6 in blood
- A single point change in the estrogen receptor gene (ESR1 D538G), only in blood and at a very low fraction · 0.24% (April) · 0.84-1.38% (May) · not seen in the April Guardant nor in any tissue
- RB1 alterations, a cell-cycle brake, seen only in blood and at a very low fraction · three in April (1.58%, 1.48%, 0.28%) · only one in May (0.19-0.68%) · none in tissue (breast 2024, bone 2026)
- Few mutations overall (3-4 per megabase) · microsatellites stable or with low instability
- PIK3CA not mutated in breast 2024, bone 2026 and blood 2026 (one of the most frequent alterations in this tumor type, and she does not have it)
- Neuroendocrine features (chromogranin, synaptophysin, INSM1) · 80% of tumor cells in one reading of the 2024 breast biopsy; another 2024 reading did not report them · 2026 re-read: focal chromogranin, heterogeneous synaptophysin, mosaic INSM1 · bone 2026: synaptophysin positive (little tumor tissue; chromogranin not reported) · liver 2026: chromogranin A and synaptophysin positive, no percentage · cell by cell: scattered, no separate group; real INSM1 in the liver
- Liver and bone: compatible with the same tumor (same main genes, FGFR1 active in both, RNA copy profile compatible with a single clone; the exome could confirm it)
- Almost no defences inside: a "cold" tumor · T lymphocytes around 1 in 100 cells in the liver, or fewer · TILs <5% in the breast tumor (2026) · PD-L1 CPS 0 in breast (2024) and liver (2026)
- Division rate (Ki67) · 60% breast 2024 · 40% 2026 re-read · ≈15% bone 2026 (small, decalcified sample) · not reported in the liver. Not a trend: different tissues and methods
What this diagram does not say
- Cell-by-cell results (status as of 18 October 2026): figures from the analysis by Polaris, Miriam's system, on the lab's data, not from the lab report; two small pieces of two lesions.
- Bone is decalcified to be cut and that damages RNA: its reading is noisier.
- RNA is not protein: what is "switched on" must be confirmed by tissue staining.
- The exome (WES) and HLA type are missing: without them there are no tumor-specific mutations nor candidates for a personalised therapy.
- Copy figures come from different tests and samples (2024 breast, 2026 bone, blood) and are not comparable; blood figures are fractions under 2%.
- The PET detects somatostatin receptors as a whole, without telling subtypes apart; RNA measures one specific gene (SSTR2).
- The discordance between 0% ER staining in the liver and an active ER program in RNA is open and in front of her medical team. Nothing on this page recommends treatment.
The route
From tissue to a therapy made for her tumour
Goal: a therapy designed on the profile of this tumor (N-of-1), decided by her medical team.
The vaccine trials explored in June were not accessible then (there was not enough tissue to manufacture one); they are not closed for good and are still being reviewed. This is the route to build a therapy from her own tumor: five steps, each depending on the one before. Today the case is at step 2, and treatment to control the disease continues in parallel.
- 01
Keep the tumour
DoneThere is tumour tissue from several biopsies (the latest from this summer), stored so it can be analysed in depth.
- 02
Read the tumour
In progressSequence the tumour’s DNA, see which genes each cell expresses and compare it with her healthy blood, keeping only what belongs to the tumour. Breast, bone and liver tissue is already at the Dana-Farber lab (the last shipment arrived on 23 September). The healthy blood sample is still pending.
- 03
Find the targets
PendingLook for the mutations only the tumour has and that her immune system could recognise. That also requires knowing her HLA: the molecules that show pieces of the tumour to her T cells and decide which ones can be recognised. Her HLA has not been typed yet.
- 04
Design the therapy
PendingThose targets can be used to make a personalised vaccine or to prepare T cells that recognise them (TCR-T, TIL). Another path, CAR-T, targets proteins on the tumour surface and is chosen from other data. More than one can be combined, and the aim is the one with the most evidence for her case. The decision belongs to her medical team.
- 05
Reach it
OpenA clinical trial or a manufacturer able to make it. The search is open to any country.
Explanatory material: it describes the path, it does not promise results. Decisions are made by her medical team.
What we’re looking for
- Laboratories or groups able to predict and validate neoantigens from paraffin (tumor/germline WES + 10x Flex scRNA-seq with first results) and to manufacture personalized therapy (neoantigen vaccine, TIL, TCR-T, CAR-T) for an HR+/HER2 0 breast carcinoma with neuroendocrine differentiation and liver metastasesThe first results are in Cell by cell
- High-resolution HLA class I/II typing and tumor MHC-I/B2M status: comes from blood, uses no tissue, and opens or closes TCR-T and vaccine
- Target IHC on the liver tissue (TROP2, Nectin-4, DLL3, SSTR2, B7-H3, CEA): this is the data point that opens or closes ADC, radioligand and cell therapy options
For professionals
Tools
- Cell by cell
- Explore the cell-by-cell data
- Breast, liver and bone, at a glance
- The case in data
- The slides, under the microscope
Share it with your doctor or tumor board: helpmiriam.com/caso · decision support, not medical advice.
All toolsClinical summary
At a glance
The essentials in ten seconds, before the molecular detail.
- Diagnosis
- Invasive breast carcinoma NST with neuroendocrine differentiation, HR+/HER2 IHC 0, de novo stage IV (multiple bone metastases at presentation, presenting as spinal cord compression at L3)
- Histology
- Invasive carcinoma NST with neuroendocrine differentiation, grade 2 (Nottingham 3+2+2 in 2024; 3+2+1 on the 2026 review); micropapillary and cribriform DCIS; IHC subtype luminal B HER2−. Liver metastasis (2026): carcinoma with neuroendocrine differentiation (chromogranin A and synaptophysin positive), consistent with the known breast carcinoma
- Stage
- De novo IV (bone at diagnosis; liver since Jul 2026)
- Receptors
- ER · 95 / 100 / 85 % (primary) · 0 % (liver 2026)
- PR · 5 / 100 / 20 % (primary) · 5 % 2+ (liver 2026)
- HER2 IHC · 0 / 0 / 0 (primary) · 0 (liver 2026)
- Ki67 · 60 % (breast 2024) / 40 % (breast, 2026 review) / ~15 % (bone 2026) / not reported (liver 2026)
- Targets
- TROP-2: target of the ADC (not measured in tissue) · SSTR+ on Ga-68 PET, bone only (May 2026)
- Material and where it is
- Bone, right ilium · Dana-Farber (shipped 27 Aug 2026, received 2-3 September)
- Liver, segment IVa · Block at Dana-Farber (shipped 21 Sep, received 23 Sep 2026, with its report), per the patient's email to the lab of 24 Sep
The anomaly
Why doesn't this tumor fit the protocols?
On paper this is a luminal breast cancer (HR+/HER2−). In the 2024 diagnostic biopsy, 80% of the neoplastic cells expressed chromogranin and synaptophysin (CD56 negative); on review of the same block in 2026 the expression is focal and heterogeneous, and the markers also appear in bone (synaptophysin) and in the liver (chromogranin A and synaptophysin), with no percentage.
The tumor also carries amplification of FGFR1 and CCND1. Current protocols recommend treating it as standard luminal and ignoring the neuroendocrine component.
The 2019 WHO classification reserves “neuroendocrine neoplasm of the breast” for tumors with more than 90% neuroendocrine cells; this is a carcinoma NST with neuroendocrine differentiation, which falls outside that category and is treated with the luminal breast-cancer guidelines. The evidence on its prognosis is retrospective and inconsistent across series; no published cohort is de novo stage IV in premenopausal patients. On this site we call it BC-NED as a working label, not as a diagnostic category.
The thesis: biology, not the organ of origin, should guide treatment.
Pathology
The same tumour, read at three sites
There is tissue from three sites and time points: the breast, read three times at three centres, the bone and the liver. The differences between reads are themselves information, not an error: the most recent breast column (Vall d’Hebron, 2026) is the most complete, not necessarily the “correct” one. The neuroendocrine component appears at all three sites. The estrogen receptor, high in the primary, is negative in the liver metastasis, the lesion that grew during the last hormonal treatment.
| Murcia · 2024 | MD Anderson · DIPCAN · 2024 | Vall d’Hebron · 2026 (breast) | Bone · right ilium · Jul 2026 | Liver · Aug 2026 | |
|---|---|---|---|---|---|
| ER (estrogen) | 95% | 100% | 85% · high · H 225 | not tested | 0% |
| PR (progesterone) | 5% | 100% | 20% · low · H 25 | not tested | 5% (2+) |
| HER2 | 0 | 0 · incomplete, barely perceptible membrane staining in fewer than 10% of cells | 0 (no membrane staining) | IHC not tested · ERBB2 unaltered | 0 |
| Ki-67 | 60% | no data | 40% | ~15% | not reported |
| Grade (Nottingham) | II (3+2+2) | 2 (2+2+2) | 2 (3+2+1) | no data | no data |
| Subtype (IHC) | no data | no data | Luminal B · HER2− | no data | no data |
| Neuroendocrine differentiation | Chromogranin and synaptophysin in 80% of the neoplastic cells · CD56 − | no NE markers in the report | Heterogeneous synaptophysin · focal+ chromogranin · mosaic INSM1 | Synaptophysin + | Chromogranin A + · Synaptophysin + |
| Other markers | CK19 + · GATA-3 + · in situ carcinoma 20% | PD-L1 CPS 0% | TILs under 5% · E-cadherin + · mosaic CK19 · no vascular invasion | no data | no data |
| Genomics | no data | TSO500: FGFR1 13 copies · CCND1 20 copies · FGF3/4/19 18 copies | no data | FoundationOne CDx: FGFR1 amplified (33 copies in the research file) · CCND1/FGF3/4/19 amplified (37 in the research file) · TMB 4 · MSS · no ESR1, RB1, TP53 or PIK3CA | pending (Dana-Farber) |
Murcia 2024 (local biopsy) · MD Anderson · DIPCAN 2024 (extended profile) · Vall d’Hebron · Pathology · report signed 10/06/2026 (earlier signature 19/05/2026). That report lists synaptophysin twice (“heterogeneous” and “negative”). The slide was reviewed in a meeting on 29 September 2026 and, according to what was said there, confirms the expression; there is no written report of that review and no request for clarification to the hospital. Here “heterogeneous” is used, with that reservation. Bone: right-ilium biopsy in Zurich, 8/07/2026, and FoundationOne CDx on it. Liver: core needle biopsy of 18/08/2026 of a ~2.2 cm lesion in segment IVa; the Vall d’Hebron report, signed 21/09/2026, is an immunohistochemistry review and includes neither Ki-67 nor SSTR2.
What these reads do not say
These reads describe the tissue; they are not a consensus diagnosis. Reconciling the discordances is pending tumour-board review. The RB1 variants and ESR1 D538G were seen in blood and not in bone; the liver has no genomic profile yet. The bone pathologist notes that neuroendocrine grading is not established on small biopsies. That the loss of the estrogen receptor explains the progression is a hypothesis, not a finding.
Molecular profile
The tumor’s genomic map
The profile crosses four sources: the primary tissue (NGS, 2024), the July 2026 bone biopsy (FoundationOne CDx), immunohistochemistry of the liver metastasis (August 2026) and the liquid biopsy (ctDNA, 2026). The same engine recurs across all tissue: amplification of FGFR1 (8p11) and of the 11q13 cluster (CCND1, FGF3/FGF4/FGF19). What changes is the estrogen receptor, which is gone in the liver. Each row notes how it was measured.
Detailed molecular profile
TSO500 2024 + FoundationOne CDx 2026 + VIGex + IHC + ctDNA + Ga-68 PET
Alterations, methods and clinical implication
Cross of every available molecular source, with no added interpretation. Each row shows the method by which the result was obtained.
| Alteration | Result | Method / Source | Category | Clinical implication |
|---|---|---|---|---|
| FGFR1 (8p11) | 13 copies (2024 primary) · amplified (2026 bone; 33 copies in the research file) | TSO500 primary 2024 · FoundationOne CDx bone Jul 2026 | Luminal driver | 8p11 amplicon with NSD3 and ZNF703. Associated with resistance to endocrine therapy and CDK4/6i; a possible target for FGFR inhibitors and everolimus, as a hypothesis. How to read the copy numbers: note below the table. |
| CCND1 · FGF3/4/19 (11q13) | 20 and 18 copies (2024 primary) · amplified (2026 bone; 37 in the research file) | TSO500 primary 2024 · FoundationOne CDx bone 2026 · ctDNA | 11q13 cluster | Co-amplified with FGFR1 across all tissue studied. FGF19 is the FGFR4 ligand. Its value for predicting response to CDK4/6i is not established. |
| Gene expression (RNA) | FGFR1 p99.9 · ESR1 p98.6 · ERBB3 p97.8 · PD-L1 p25 | VIGex (VHIO, Jun 2026) on the 2024 primary block | Transcriptome | The FGFR1 amplification is transcribed: it sits at the 99.9th percentile of the lab’s pan-cancer set (overexpressed from the 95th). ESR1 is also high in the primary. PD-L1 at the 25th percentile. No pathogenic fusions. Cellularity 50%. This is the 2024 primary, not the ER 0% liver metastasis. |
| ER / PR | Primary ER 85–100% · Liver ER 0% / PR 5% | IHC primary (3 reads) · IHC liver biopsy (report 21 Sep 2026) | Hormone receptor | Receptor change: the liver metastasis has lost the estrogen receptor. It coincides with liver progression on fulvestrant + a KAT6 inhibitor; that it is the cause is a hypothesis. With PR 5% it remains HR+ under the TROPION-Breast06 definition (ER or PR ≥1%). |
| HER2 | 0 in every read | IHC primary (×3) · IHC liver 2026 · ERBB2 unaltered (F1CDx) | Receptor | HER2 IHC 0, not HER2-low. One read of the primary (MD Anderson, 2024) describes incomplete, barely perceptible membrane staining in fewer than 10% of cells; the other two and the liver, none. It is the entry requirement for the Dato-DXd trial. |
| TROP-2 | Not measured | — | ADC target | In fourth line since 7 October 2026: datopotamab deruxtecan 6 mg/kg every 3 weeks in TROPION-Breast06 (Vall d'Hebron); the clinical course documents her inclusion and schedules the first cycle that day. Target of datopotamab deruxtecan. The trial does not require it for entry; it studies it as exploratory. |
| NE differentiation | 80% of neoplastic cells (2024) · focal/heterogeneous (2026) | IHC primary · bone (synaptophysin) · liver (CgA and synaptophysin) | BC-NED subtype | The neuroendocrine component appears at all three sites, including the progressing liver lesion. NE-tumour therapies (radioligands, platinum): hypothesis. |
| SSTR (somatostatin) | Positive in bone, heterogeneous | Ga-68 DOTATOC PET (May 2026) | Radioligand target | Uptake in bone metastases, with some lesions without gallium, and focal in the breast. In May the liver had no lesions: its SSTR status is unknown. SSTR2 IHC in tissue: not done. |
| Ki67 | 60% · 40% · ~15% | IHC primary (2024 and 2026 review) · bone (2026) | Grade | In NE tumours, Ki67 ≥20% would be compatible with high grade: a hypothesis, not the assigned grade (confirmed: Nottingham grade II) ⁺⁺. The bone pathologist notes that NE grading is not established on small biopsies. |
| ESR1 p.D538G | In ctDNA · not in bone | VHIO360 (Apr and May 2026) · Guardant360 CDx (May 2026) · not detected on Guardant360 (Apr 2026) or FoundationOne CDx (bone) | Endocrine resistance | Aromatase-inhibitor resistance mutation seen in blood: 0.24% in April and 0.84–1.38% in May, depending on the platform. Absent from the April Guardant360 and from bone tissue: inter-lesion heterogeneity or a clone at another site. With ER 0% in the liver, its weight as a target drops. |
| RB1 | 3 variants in ctDNA · not in tissue | Guardant360 (Apr 2026) · TSO500 2024 · FoundationOne CDx 2026 | Resistance / NE | p.V622Yfs*33 (1.58%), p.R661W (1.48%) and p.F226* (0.28%); in May only p.V622Yfs*33 is reported (0.19% on Guardant360 CDx and 0.68% on VHIO360, same draw). Neither the primary nor the 2026 bone has them. The hypothesis of neuroendocrine transformation through RB1 loss rests on blood, not tissue. |
| TMB / MSI / HRD / PD-L1 | TMB 4 · MSS · HRDsig − · PD-L1 CPS 0 in the primary (2024) and in the liver biopsy (22C3, report of 25-09-2026) | FoundationOne CDx bone 2026 (TSO500 2024: low TMB and MSI) · PD-L1: IHC of the primary (MD Anderson, 2024) and IHC of the liver biopsy (22C3) | Immunogenomics | Few mutations, so few classic neoantigen candidates; this shapes the personalised-vaccine route. FoundationOne TMB also counts synonymous variants. No profile for checkpoint inhibitors. |
| TP53 · PIK3CA · PTEN · AKT1 · BRCA1/2 | No reportable alteration | FoundationOne CDx bone 2026 (PIK3CA also negative on TSO500 2024) | Other pathways | No PI3K/AKT target and no homologous-recombination target in this tissue. |
| ARID1A p.L2238fs | 0.11% (new, May 2026) | VHIO360 (drawn 13 May 2026) | ctDNA · low frequency | ARID1A frameshift, seen only in that draw and at very low frequency. |
| SMO p.V319D | 0.26–0.56% (VUS) | ctDNA May 2026: Guardant360 CDx 0.26% · VHIO360 0.56% | Uncertain significance | Variant of uncertain clinical significance, under watch. |
Sources and methodological notes
The first bone biopsy (right iliac, April 2026) had no evaluable tumour. The second (Zurich, 8 July 2026) did, and FoundationOne CDx was run on it at 61% tumour purity. The liver metastasis (biopsy of 18 August 2026) has been studied by immunohistochemistry and has no genomic profile yet. FoundationOne has no matched normal: the exome with germline DNA at Dana-Farber is what will separate somatic from inherited.
Sources: TSO500 on primary FFPE tissue (DIPCAN, MD Anderson Madrid, 2024) · FoundationOne CDx on the Zurich bone biopsy (July 2026) · IHC of the primary (2024 and 2026 review), bone (2026) and liver (Vall d'Hebron Pathology, report of 21-09-2026) · ctDNA: VHIO360 (April and May 2026), Guardant360 (April 2026) and Guardant360 CDx (May 2026) · VIGex gene expression (VHIO, June 2026) on the primary block · Ga-68 DOTATOC PET-CT (May 2026).
⁺⁺ In neuroendocrine oncology, Ki67 is the primary grading marker: G1 (<3%), G2 (3–20%), G3 (>20%). By that logic, a high Ki67 would be compatible with a high-grade neuroendocrine component (NEC G3): a hypothesis, not the assigned grade. The confirmed histological grade is Nottingham Grade II; reconciling it is pending tumour-board review.
How to read the FGFR1 and CCND1 copy numbers
FGFR1: 13 copies in the 2024 primary (TSO500; the sender estimated 75% tumor and the laboratory warns that the copy number is not reliable below 50%; VIGex measured 50% in the same block). In the 2026 bone, the clinical FoundationOne CDx report says “FGFR1 amplification” with no figure; the 33 copies of FGFR1 and 37 of the 11q13 cluster come from the research file of that analysis (“for research use only”, computational purity 61%). Different platforms, samples and purities: the amplification is firm, the figures are not comparable with each other.
Therapeutic axes
Where to aim
Several candidate targets follow from all of the above. These are the therapeutic axes the molecular profile points to, each with its own treatment rationale.
- See the evidence: TROP-2 → Dato-DXd (under way since 7 Oct 2026)
- See the evidence: Amplified FGFR1 → FGFRi
- See the evidence: SSTR+ in bone → PRRT
- See the evidence: ER 0% in liver → endocrine axis
- See the evidence: CgA/Syn+ in liver → neuroendocrine axis
Tap or hover the highlighted words and markers to see what they mean.
Hypotheses derived from the molecular profile, not prescribed treatments. Only the TROP-2 axis is in use, and within a trial. The Dana-Farber analysis and target immunohistochemistry on the liver (TROP-2, SSTR2, DLL3) could confirm or rule out these axes.
Molecular workup
The molecular analysis, test by test
Which question each test answers.
| Test | What it answers |
|---|---|
| Germline reference (tumour-normal) | Without it there is no telling which variant belongs to the tumour and which is inherited. FoundationOne has none |
| Tissue genomic profile (panel) | Confirms amplified FGFR1 (8p11) and 11q13; finds no ESR1, RB1, TP53 or PIK3CA. TMB 4, MSS |
| Exome (WES) | The basis for neoantigen prediction; reliable only with the germline |
| Single-cell RNA-seq (10x Genomics Flex) | Tells whether the tumour is a mix of populations or one that has changed identity, and which targets each one really expressesThe first results are in Cell by cell |
| Extended IHC | TROP-2 → Dato-DXd · SSTR2 → PRRT · DLL3 → anti-DLL3 · Rb loss → CDK4/6i resistance |
| High-resolution HLA typing | Decides which tumour peptides can be shown to her T cells: opens or closes the personalised vaccine and TCR-T |
| Epigenetics | Helps classify the tumour and understand how it changes identity |
| Liquid biopsy (ctDNA) | Saw ESR1 D538G and RB1, which bone tissue does not confirm. The TROPION-Breast06 trial plans serial liquid biopsies |
| Immunopeptidomics (HLA peptidome) | Would confirm which antigens actually reach the cell surface. There is no fresh tissue |
| Phosphoproteomics | Would measure the real activation of the pathways (FGFR, PI3K, MAPK, cell cycle). There is no frozen tissue |
| Organoids + drug screening | Would test drugs on the tumour outside the body. There is no live tissue |
Decision support
Consultation support material: it describes which analyses exist and what each one answers; it is not a treatment indication. What is analysed and how is decided by the lab doing it, and clinical decisions by the treating medical team.
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