Epistamai Bio · Oncology Dashboard
CONFIDENTIAL · MDT · RESEARCH USE ONLY
Prostate adenocarcinoma · cT1c · Gleason 6 · MDT decision-support

TMPRSS2:ERG prostate
adenocarcinoma —
localised & low-risk.

Clinical stage cT1c · Gleason 3+3=6 (Grade Group 1) · NCCN very-low / low risk · Decipher genomic score 0.27 (Low). Needle biopsy 2024-06-07. PSA low and stable — 0.7 ng/mL (2010) → 1.2 ng/mL (Jun 2026; a May 1.7 settled to 1.2 on repeat). Caris whole-exome + RNA profiling identifies a TMPRSS2:ERG fusion and a pathogenic FANCM frameshift; the tumour is MSI-stable, TMB-low, with DDR / HRR genes wild-type.
Patient
Timothy Barrows
M · DOB 1957-03-23 · age 69
Diagnosis
Prostate adenocarcinoma · cT1c
Grade
Gleason 3+3=6 (GG1)
Primary site
Prostate
NCCN risk
Very-low / low
Decipher
0.27 · Low risk
Biopsy
Needle · 2024-06-07
Latest PSA
1.2 ng/mL · Jun 2026
Care
Brigham & Women’s · Epistamai Bio
Pathology · diagnosisCaris TN25-217936 · collected 04 Feb 2025
Prostate adenocarcinoma · TMPRSS2:ERG-fusion · Gleason 3+3=6
needle biopsy · Grade Group 1 · clinical stage cT1c · NCCN very-low / low risk
Clinical profile
Age at dx67 · 2024
Primary siteProstate
Gleason3+3=6 (Grade Group 1)
Clinical stagecT1c
NCCN riskVery-low / low
ManagementActive-surveillance candidate
Monitoring · Jun 2026 LATEST PSA
Latest PSA1.2 ng/mL · Jun 2026
Recent change1.7 (May) → 1.2 (Jun repeat) · blip resolved
PSA density~0.03 · well below 0.15
Prostate MRIPI-RADS 5, stable · 43 ml ← 36 ml
Decipher0.27 · Low · 10-yr met 0.7%
StatusStable low-risk · continue surveillance
Tumour molecular profile · snapshotclick any chip / card → Genomics
TMPRSS2:ERG
fusion (RNA)
Truncal · defining
FANCM
p.G945fs
Pathogenic · VAF 31%
ERG
RNA rank #3
Highest-expressed driver
AR
IHC 2+, 95%
Androgen-driven
Genomic
Fusion + 1 SNV
TMPRSS2:ERG · FANCM p.G945fs
+ VUS: ADGRA2 · GPS2 · IRS2 · STIL
→ Genomics · alterations
Copy number
14 intermediate CN
no high-level amp · no actionable CNA
APOBEC3B · EZH2 · GNAS · KMT2C…
→ Genomics · copy number
Biomarker signature
MSS · TMB-low
TMB 3 Mut/Mb · LOH 2%
DDR / HRR genes wild-type
→ Genomics · biomarkers
Immune & PD-L1
PD-L1 neg
SP142 0% · HER2 / ERBB2 neg
genomically quiet tumour
→ Genomics · biomarkers

Case timeline · 2024 → 2026

The verified document trail to date. Click a tab in the left rail for the underlying data.
Jun 2024
Diagnosis

Needle biopsy (07 Jun 2024). Gleason 3+3=6, cT1c. PSA ~1.2–1.35 ng/mL.

Jul 2024
Decipher classifier

Genomic score 0.27 → Low risk. Framed as an active-surveillance candidate.

Feb–Jul 2025
Caris profiling

Whole-exome + RNA (collected 04 Feb 2025). TMPRSS2:ERG fusion; FANCM p.G945fs.

2026 · current
Monitoring

PSA 1.7 (May) → 1.2 (Jun repeat). Prostate MRI 43 ml, PI-RADS 5 stable. On surveillance.

What this dashboard integrates

  • Genomics & biomarkers — Caris whole-exome (DNA) + RNA fusion/expression, IHC, MSI/TMB/LOH signatures.
  • Transcriptome — tumour RNA-seq, 27,224 expressed genes ranked by TPM (ask Atlas for any gene).
  • PSA & imaging — longitudinal PSA (2010→2026), prostate MRI volume/size, Decipher risk.
  • Still to load — germline (Invitae / EPI exome), Galleri MCED, tumour-informed MRD panel, pathology (Gleason cores), radiology Feb 2026, labs trends.

Genomics & biomarkers

Caris whole-exome (DNA-tumour) + RNA profiling, case TN25-217936 (collected 2025-02-04, reported 2025-07-18). All values transcribed from the final report; unclassified variants are listed separately.

Biomarker signature

Quick-glance biomarker panel for this ERG-fusion prostate adenocarcinoma. Fusion, copy-number, germline and the Decipher classifier each have their own section below.
TMB
3 mut/Mb Low
Not hypermutated — below the 10 mut/Mb checkpoint-inhibitor threshold (EPI research exome concordant: 0.76 mut/Mb).
MSI
Stable MSS
Microsatellite stable on sequencing — no mismatch-repair–driven hypermutation signal.
Genomic LOH
Low 2% of segments Low
2% genome-wide loss-of-heterozygosity — well below the ≥16% HRD threshold.
PD-L1 (SP142)
Negative 0% Neg
No tumour PD-L1 expression — checkpoint monotherapy not supported on this marker.
AR (IHC)
Positive 2+, 95% AR-driven
Strong, near-uniform nuclear androgen-receptor expression — AR-driven disease.
HER2 / ERBB2 (IHC)
Negative score 0 Neg
No HER2 over-expression despite abundant RNA (ERBB2 TPM 1,093).
Decipher
0.27 Low risk
Low genomic-risk group · 10-yr metastasis risk 0.7%. See the Decipher section ↓.
TMPRSS2 :: ERG
Detected Fusion
Defining ERG-subtype fusion; ERG is the 3rd-highest-expressed gene (Z +5.1). See Fusions ↓.
Ki-67 (proliferation)
not assayed
Not reported on the Caris panel; Gleason 3+3=6 implies low proliferative grade.
DDR / HRR status

Core homologous-recombination genes (BRCA1/BRCA2, ATM, CDK12, PALB2, RAD51 family, CHEK2) returned mutation not detected on tumour sequencing, and the germline panel is negative (see Germline ↓) — so PARP / platinum rationale is not supported on current data.

Pathogenic / likely-pathogenic alterations

GeneTestAnalyteAlterationVAFCall
FANCMCaris WESDNA-tumourp.G945fs · c.2832_2839delins52 · exon 1431%Pathogenic
TMPRSS2:ERGCaris WESRNA-tumourTMPRSS2::ERG fusion (multiple breakpoints)—Pathogenic fusion
ARID2EPI exomeDNA-tumourp.V1503VX frameshift · chr12:45,852,631 T>TA6%Likely Pathogenic
Show 25 variants of uncertain significance (Caris + EPI exome)
GeneTestProteinConsequenceVAFCall
ADGRA2Caris WESp.Q832R · exon 16missense49%VUS
GPS2Caris WESp.P175Q · exon 7missense44%VUS
IRS2Caris WESp.P1021Q · exon 1missense44%VUS
STILCaris WESp.A802V · exon 14missense51%VUS
GABREEPI exomep.V477Dmissense58.8%VUS
ZNF629EPI exomep.T822Xframeshift34.5%VUS
C4orf54EPI exomep.R111Wmissense32.5%VUS
USP43EPI exomep.T802Imissense32.0%VUS
GALNT5EPI exomep.T511Pmissense30.3%VUS
KLHDC7BEPI exomep.D84Nmissense29.4%VUS
SPARCL1EPI exomep.E61Dmissense29.4%VUS
WNT6EPI exomep.R274Cmissense27.0%VUS
BLTP1EPI exomep.E1813EXframeshift25.0%VUS
SYCE1EPI exomep.R180Wmissense22.5%VUS
SEZ6L2EPI exomep.V554Mmissense22.1%VUS
RPS4Y1EPI exomep.N50Smissense12.0%VUS
SLC7A6OSEPI exomep.D238Vmissense11.4%VUS
LILRA5EPI exomep.G34Dmissense8.6%VUS
RNF126EPI exomep.V143Imissense8.6%VUS
ALPGEPI exomep.P22Lmissense · splice8.1%VUS
TLK1EPI exomep.G237Rmissense7.7%VUS
AGAP5EPI exomep.T306Amissense6.7%VUS
PNISREPI exomep.S672Rmissense6.5%VUS
MAFFEPI exomep.Q115*stop-gained6.2%VUS
CEP131EPI exomep.L955Vmissense5.8%VUS
4 from Caris WES, 21 from the EPI research exome. None lie in established cancer genes; reported for completeness, not actionable.
TMPRSS2:ERG

The defining lesion of ERG-subtype prostate cancer: the androgen-driven TMPRSS2 promoter fused to the ERG oncogenic transcription factor. Corroborated by RNA-seq, where ERG is the 3rd-highest-expressed gene (TPM 12,694) — see Fusions.

FANCM p.G945fs

Frameshift in a Fanconi-anaemia-pathway gene (VAF 31%). FANCM is not a core HRR gene like BRCA1/2; treat PARP/platinum implications cautiously, with the negative germline result.

IHC / protein

MarkerMethodResultNote
AR (androgen receptor)IHCPositive | 2+, 95%Strong, near-uniform nuclear expression — consistent with AR-driven disease.
ERBB2 (HER2/Neu)IHCNegative | Score 0No HER2 over-expression despite abundant RNA (ERBB2 TPM 1,093).
PD-L1 (SP142)IHCNegative | 0%No tumour PD-L1 expression.

Fusion · TMPRSS2 :: ERG

The defining lesion of this tumour. Click either gene for its card.
CARIS RNA-TUMOUR PATHOGENIC 4 BREAKPOINTS RNA-CORROBORATED ERG Z +5.1
5′ PARTNER TMPRSS2 Androgen-driven promoter exon 1 · 5′UTR BREAK 3′ PARTNER ERG PNT ETS DNA-binding domain CHIMERIC mRNA The androgen-regulated TMPRSS2 promoter is placed upstream of ERG → ERG comes under AR transcriptional control → strong ERG over-expression.
Functional consequence

Fuses the androgen-responsive TMPRSS2 promoter to the oncogenic ETS transcription factor ERG. ERG is driven to high expression, reprogramming the prostate epithelium toward an invasive, de-differentiated, AR-cooperative programme. It is the single most common molecular subtype of prostate cancer (~40–50% of PSA-screened cases).

Pathway
Androgen receptor → TMPRSS2 promoter → ERG → EMT / invasion · prostate-lineage de-differentiation
Expression corroboration · RNA-seq
GeneTPMRankZ
ERG (3′)12,6943 / 27,224+5.10
TMPRSS2 (5′)6,52713 / 27,224+4.65
Both partners are extreme expression outliers — functional confirmation the fusion is transcriptionally active.
Therapeutic context

ERG is a transcription factor and not directly druggable; there is no approved ERG- or fusion-targeted therapy. Its main value here is diagnostic / lineage-defining. Investigational angles (ERG inhibitors, BET inhibitors, and the reported PARP-sensitivity of ETS-fusion tumours) remain research-grade. Management continues to be driven by the low-risk clinical picture, not the fusion.

Other fusion

UMAD1:GLCCI1 — an unclassified intrachromosomal fusion (chr7) of uncertain significance; reported for completeness, not actionable.

Breakpoints detected (GRCh38)
Fusion5′ breakpoint3′ breakpointCall
TMPRSS2::ERGchr21:41,506,445 (−)chr21:38,445,621 (−)Pathogenic
TMPRSS2::ERGchr21:41,507,950 (−)chr21:38,445,621 (−)Pathogenic
TMPRSS2::ERGchr21:41,508,081 (−)chr21:38,423,561 (−)Pathogenic
TMPRSS2::ERGchr21:41,508,081 (−)chr21:38,445,621 (−)Pathogenic
UMAD1:GLCCI1chr7:7,801,743 (+)chr7:8,003,908 (+)Unclassified

Copy number

No high-level amplifications or deletions were called. Fourteen genes showed intermediate copy number (average 4–6 copies, not uniform across exons) — reported for completeness, not currently actionable. Click a gene for its card.
APOBEC3BASXL1CREBBPEZH2FANCAFANCCFANCD2GATA3GNASJAK1KIF5BKMT2CNF2WRN

Decipher genomic classifier (Jul 2024)

Veracyte Decipher Prostate — a 22-gene RNA expression classifier run on the diagnostic biopsy (accession MC-470510; ordered by Dr Quoc-Dien Trinh, Brigham & Women's). The score is determined solely by tumour genomics, independent of PSA / Gleason / stage.
Risk with standard therapy for this clinical risk group
0.7%
10-yr metastasis
5-yr 0.3%
0.5%
15-yr PCa mortality
Very favourable
9.6%
Adverse path. at RP
If treated
10-yr metastasis risk vs peers (n=30,544) 0%2%4%6%8% 0.00.450.601.0 Decipher score (patients ordered low → high) LOW · 69% INT 17% HIGH · 14% This patient · 0.27 → 0.7%
38th percentile — 37% of similar men score lower, 62% higher. Predicted 10-yr metastasis risk 0.7%.
Interpretation (per report)

Low NCCN risk and a Decipher-low score indicate less aggressive tumour biology and a favourable prognosis — ideal candidate for active surveillance, more likely to stay on surveillance and less likely to be upgraded/upstaged. Context at testing: cT1c · Gleason 3+3=6 · PSA 1.35 ng/mL · NCCN very-low / low.

Decipher score 0.27 LOW INT HIGH 0.00.450.601.0
0.27 — LOW genomic-risk group

Germline (Invitae, Jun 2024)

Hereditary-cancer germline testing on blood (Invitae #RQ6600191, reported 22-Jun-2024).
Negative
No pathogenic variant

84-gene sequence + del/dup panel (Invitae Lynch Syndrome / hereditary-cancer panel). No pathogenic or likely-pathogenic germline variants identified. Benign / likely-benign variants are not reported.

Key genes covered — all negative
BRCA1BRCA2ATMCHEK2PALB2BARD1BRIP1HOXB13MLH1MSH2MSH6PMS2EPCAMTP53PTENCDH1

…of 84 genes total, including all major prostate-relevant HRR & Lynch genes.

Implication

No inherited driver and no germline basis for PARP / platinum eligibility or cascade family testing on these genes. A negative result does not fully exclude hereditary risk (genes not tested, family history, etc.).

Provenance

Issued under the pseudonym “Tom Flanagan” (same DOB 1957-03-23) — confirmed the same patient (Timothy Barrows). Included as his germline result.

Research somatic exome (EPI · SiMSen CANVAS, Jun 2026)

An independent paired tumour/normal whole-exome (sample EPI_19570323M; xGen Exome v2; CANVAS v0.2.3; research use only), distinct from the Caris panel.
0.76mut/Mb
TMB
Low (26 nonsyn / 34.15 Mb). Concordant with Caris.
3.35%
MSI
MSS (50/1492 sites). Threshold ≥20%.
22
SNV/indel passing
1 likely-pathogenic · 21 VUS/benign.
4
Signatures
From 1250 SBS (cosine 0.905).
Likely-pathogenic finding

ARID2 p.V1503VX frameshift (chr12:45,852,631 T>TA · VAF 6% · Likely Pathogenic). ARID2 is a SWI/SNF chromatin-remodelling subunit and known cancer gene; the low VAF suggests a subclonal event. Not detected on the Caris panel. No directly approved targeted therapy.

Notable HIGH-impact VUS
ZNF629 p.T822X (fs, 34%) · BLTP1 p.E1813EX (fs, 25%) · MAFF p.Q115* (6%) — none in established cancer genes.
Mutational signatures (COSMIC SBS)
SBS565.9%
SBS1216.5%
SBS428.9%
SBS18.7%

SBS5 & SBS1 are clock-like (ageing); SBS42 is associated with haloalkane exposure; SBS12 aetiology unknown. No mismatch-repair or HRD signature.

RNA / transcriptome

Caris tumour RNA-seq — 27,224 expressed genes. For every gene we show absolute TPM, its within-sample rank/percentile (vs all expressed genes in this tumour), and a Z-score = (log₁₀(TPM+1) − mean) / SD across all expressed genes (Z > +2 ≈ top ~2%, Z > +3 ≈ top ~0.3%). Click any gene for its full card. Search any gene in the left rail; Atlas can also quote any gene's values.
27k
Expressed genes
All ranked & Z-scored; full table embedded.
#3
ERG rank
TPM 12,694 · Z +5.10 — fusion driver.
#157
AR rank
TPM 950 · Z +3.37 — androgen receptor.
Z>+2
Outlier threshold
Top ~2% of the expressed genome.
How a gene is flagged
HIGHZ ≥ +2 (top ~2%) · MEDZ +1 to +2 · NOTE0 to +1 · lowbelow mean expression

Transcriptome explorer

Canonical prostate / pan-cancer functional gene panels. Click a family to expand its per-gene rows (TPM · rank · within-sample %ile · Z); chips mark a DNA/RNA finding. Click any gene name for its full multi-platform card.
Prostate lineage & AR axis15 genes · top TMPRSS2 (z +4.65)
GeneTPMRank /27k%ileZ
TMPRSS2 FUSION6,52713100.0+4.65
KLK33,6572599.9+4.27
KLK23,1943399.9+4.18
AR IHC95015799.4+3.37
AMACR67722599.2+3.14
HOXB1334238998.6+2.69
NKX3-120562997.7+2.35
TRPM816083496.9+2.18
STEAP11281,05596.1+2.03
FOLH11221,11095.9+2.00
KLK41181,15795.8+1.98
STEAP21101,24495.4+1.93
FKBP51061,29495.3+1.91
PCA3672,02892.6+1.60
SLC45A3235,15581.1+0.91
not in expressed set: ACPP
ERG / ETS & fusion9 genes · top ERG (z +5.10)
GeneTPMRank /27k%ileZ
ERG FUSION12,6943100.0+5.10
SPOP1,14012199.6+3.49
UMAD1324,07785.0+1.11
FLI1314,16984.7+1.10
ETV1225,38780.2+0.87
GLCCI1225,40380.2+0.87
ETV5147,31773.1+0.57
ETV4127,75271.5+0.51
SPINK10.522,02619.1-0.93
PI3K – AKT – mTOR / PTEN11 genes · top PTEN (z +4.25)
GeneTPMRank /27k%ileZ
PTEN3,5842799.9+4.25
TSC23,4533099.9+4.23
AKT12,3994899.8+3.98
AKT21,5789099.7+3.70
PIK3CB86417499.4+3.30
MTOR82918499.3+3.28
TSC171821099.2+3.18
PIK3CA31043598.4+2.62
RICTOR1211,11995.9+1.99
PDK1562,40091.2+1.49
INPP4B323,99285.3+1.13
Cell cycle & MYC12 genes · top CCND1 (z +4.19)
GeneTPMRank /27k%ileZ
CCND13,2503299.9+4.19
MYC2,8923999.9+4.11
CDK41,4809699.7+3.66
CDKN1B1,08113099.5+3.45
RB129245998.3+2.58
CDKN2A15088196.8+2.14
MYCN443,07688.7+1.33
CDK6304,27984.3+1.07
CCNE19.48,85367.5+0.35
AURKA4.811,65857.2-0.04
FOXM12.913,91548.9-0.30
E2F11.218,11533.5-0.67
DNA repair / HRR16 genes · top CDK12 (z +3.50)
GeneTPMRank /27k%ileZ
CDK121,15411899.6+3.50
MLH11,12912399.6+3.48
ATM93116299.4+3.35
ATR32540898.5+2.65
MSH225650898.1+2.49
FANCA CN24254198.0+2.46
BRCA117674897.3+2.24
CHEK217475797.2+2.24
PALB217177197.2+2.23
RAD51B16280997.0+2.19
FANCC CN1111,22895.5+1.94
FANCD2 CN1061,30095.2+1.91
FANCM MUT801,68593.8+1.72
CHEK1781,73293.6+1.71
BRCA2284,47683.6+1.03
RAD512.514,69346.0-0.38
Neuroendocrine / lineage plasticity12 genes · top REST (z +0.73)
GeneTPMRank /27k%ileZ
REST176,27177.0+0.73
NCAM1118,08670.3+0.47
FOXA2108,48468.8+0.41
SOX27.79,65664.5+0.23
DLL36.910,08363.0+0.17
ENO23.513,04052.1-0.20
POU2F32.814,10348.2-0.32
INSM12.814,15248.0-0.33
CHGB2.414,93245.2-0.40
CHGA2.215,27043.9-0.44
SYP1.417,66635.1-0.64
ASCL11.218,40732.4-0.69
Surface & theranostic targets12 genes · top KLK2 (z +4.18)
GeneTPMRank /27k%ileZ
KLK23,1943399.9+4.18
ERBB2 IHC1,09312899.5+3.46
STEAP11281,05596.1+2.03
FOLH11221,11095.9+2.00
STEAP21101,24495.4+1.93
TMEFF2632,16192.1+1.56
TACSTD2462,96089.1+1.35
CD276205,72679.0+0.82
DLL36.910,08363.0+0.17
PSCA2.315,05144.7-0.42
CEACAM52.115,44943.3-0.45
MSLN0.621,55820.8-0.90
AR co-regulators & lineage TFs10 genes · top FOXA1 (z +4.31)
GeneTPMRank /27k%ileZ
FOXA13,8932299.9+4.31
NCOR151227999.0+2.95
HOXB1334238998.6+2.69
NCOR217376497.2+2.23
GATA21321,02196.3+2.05
NCOA21171,16895.7+1.97
GRHL21101,25195.4+1.93
NCOA3602,26891.7+1.53
NCOA1314,14484.8+1.10
ONECUT21.716,50339.4-0.55
RTK signalling13 genes · top ERBB3 (z +4.46)
GeneTPMRank /27k%ileZ
ERBB34,9211899.9+4.46
FGFR12,5314399.8+4.02
ERBB2 IHC1,09312899.5+3.46
PDGFRB98815099.5+3.39
IGF1R77719699.3+3.23
EGFR46329698.9+2.89
FGFR237135398.7+2.74
RET32241298.5+2.65
KIT16082697.0+2.18
ERBB41161,17395.7+1.97
NTRK11011,35295.0+1.88
MET682,00892.6+1.61
ALK572,36891.3+1.50
Immune & checkpoint11 genes · top CD68 (z +1.26)
GeneTPMRank /27k%ileZ
CD68403,39587.5+1.26
CD276205,72679.0+0.82
CD274 IHC7.59,78464.1+0.21
PDCD16.210,53161.3+0.11
CD3D4.711,77556.7-0.05
CTLA42.714,31147.4-0.34
CD41.916,09740.9-0.51
GZMB1.616,90437.9-0.58
FOXP31.517,30736.4-0.61
PDCD1LG21.417,56035.5-0.63
CD8A0.919,80427.3-0.79
not in expressed set: IFNG
Apoptosis / survival9 genes · top TP53 (z +4.07)
GeneTPMRank /27k%ileZ
TP532,7154099.9+4.07
AKT12,3994899.8+3.98
MDM438234798.7+2.76
MDM226748898.2+2.52
MCL119068097.5+2.30
BCL2L11181,15395.8+1.98
BCL2532,53890.7+1.45
BAX324,07985.0+1.11
BIRC53.712,89752.6-0.18

Caris WTS expression percentile · 93 genes (prostate cohort)

Each cell is this case’s Caris WTS TPM-rank percentile against Caris’s internal cohort of profiled Prostate Cancer patients (0–100). Sorted high→low; click any gene for its entity card.
≥90 pct 75–89 60–74 40–59 25–39 <25
ERG100
SPOP99
DLL396
ROR196
ERBB395
TP5395
MAGEA493
MTOR92
NTRK189
FGFR288
PTEN88
RET88
SRC86
SSTR385
FOLR184
NRG184
ROR284
RAD51D83
MYC82
PALB282
CDK1280
FANCL80
PDCD179
CLDN1878
ALK76
TSC275
CCND174
FGFR374
PRAME72
IGF1R70
NTRK370
MLH169
PIK3CA68
TSC167
CDKN2A66
EPHA266
SSTR266
TACSTD266
SSTR565
BRAF64
PPP2R2A64
HRAS62
KDR62
ROS161
FANCA60
MUC160
NTRK260
PARP160
RB160
BRD458
RAD51C58
NECTIN456
MUC1655
ADORA2A53
CHEK252
ERBB251
ATM50
MTAP50
CLDN649
EGFR49
KDM1A44
LAG342
BARD140
NRAS40
CTLA439
CCNE138
CD27438
RAD51B38
NF136
AR34
TOP134
ABCB132
MDM232
PDCD1LG232
MET28
XPO128
CEACAM526
BRCA125
KRAS23
MSLN23
ATR22
SLFN1122
CHEK120
PARP218
TP53BP118
CD27617
BRIP115
FOLH113
TGFB113
BRCA210
RAD513
MKI672
VEGFA2
Method note

Values are the Caris “Percentile in Cancer Type” — each gene’s whole-transcriptome (WTS) TPM expressed as a percentile against a distribution of Caris’s internal cohort of profiled prostate-cancer cases (report TN25-217936, Additional Results pp.7–8). High = expressed higher than most prostate cancers — a cross-patient comparison, distinct from the within-sample rank used elsewhere on this tab. Selected genes are those Caris reports for tumour-type relevance / trial matching.

Highest-expressed genes

GeneTPMRank%ileZ
ENSG0000028080024,6371100.0+5.54
MT-RNR214,9572100.0+5.21
ERG12,6943100.0+5.10
NPM112,5344100.0+5.09
RMRP12,1295100.0+5.07
RN7SK10,7776100.0+4.99
PRKAR1A9,1277100.0+4.88
MAX9,0378100.0+4.87
GNAS8,9979100.0+4.87
CTNNA18,69610100.0+4.84
CDH17,65911100.0+4.76
MYH117,24812100.0+4.72
TMPRSS26,52713100.0+4.65
EEF26,00214100.0+4.60
NFIB5,7421599.9+4.57
ARID1A5,2351699.9+4.51
RPL22P15,1391799.9+4.49
ERBB34,9211899.9+4.46
TMSB4XP64,9181999.9+4.46
RNA5S14,3082099.9+4.37
TPT13,9132199.9+4.31
FOXA13,8932299.9+4.31
CREBBP3,6822399.9+4.27
SMARCA43,6762499.9+4.27
Method note

Rank, percentile and Z are computed within this tumour's own transcriptome (no matched-normal cohort available). Z is a within-sample outlier score, not a tumour-vs-normal fold-change. Values from the Caris Ranked-TPM export.

PSA & imaging monitoring

Longitudinal PSA (2010→2026), kinetics, prostate MRI and biopsy pathology for a man on active surveillance for Gleason 3+3=6 (Grade Group 1) prostate adenocarcinoma. PSA reference 0.00–4.00 ng/mL — every value is well below threshold.

PSA trend · hover or click a point

20 measurements, Jun 2010 → Jun 2026 · y-axis 0–2.0 ng/mL (all readings far below the 4.0 normal limit) · ▲ = biopsy · ◆ = prostate MRI. Click a point for its full breakdown.
Selected reading

Click any point on the curve to see its value, change vs the previous draw, vs the last-4 average, position within the all-time range, and any same-visit biopsy/MRI.

Latest PSA
1.2 ng/mL
Jun 2026 · −29% vs May (1.7)
Range (nadir→peak)
+240%
0.5 (2014) → 1.7 (2026)
PSA density
0.03
1.2 ÷ 43 ml · threshold 0.15
Velocity (2 yr)
+0.16
ng/mL/yr · threshold 0.75
Doubling time
5.3 yr
recent · trigger < 3 yr

PSA kinetics & guideline-based evaluation

Each metric is shown against its commonly-cited active-surveillance threshold. The marker (│) on each bar is the threshold; the fill is this patient.
PSA velocityReassuring

Recent 2-yr +0.16, 3-yr +0.08, since-nadir +0.05 ng/mL/yr — all below the historic 0.75 ng/mL/yr concern threshold (bar marker). PSA velocity is a soft signal on surveillance (confounded by BPH and assay noise).

PSA doubling time> trigger

Recent 2-yr ~5.3 yr; 3-yr ~12 yr; long-term ~15 yr. A PSADT < 3 yr (marker) is a common prompt to re-stage/treat — not met. The Jun-2026 repeat (1.2) brought PSA back down, so the Feb→May 2026 uptick did not persist.

PSA densityVery low

~0.03 ng/mL/cc (latest 1.2 ÷ 43 ml; 0.03–0.04 across the recent range) — far below the 0.15 threshold (marker). A growing gland (36→43 ml) means much of any PSA rise is likely benign BPH bulk, not tumour. (The Jun-2024 MRI printed 0.61, inconsistent with its own PSA 1.19 ÷ 36 ml = 0.03 — a report typo.)

% free PSAStable / low utility

20 → 17 → 13 → 18 → 17% (2024→Jun 2026). The single low (13%, May 2025) recovered to 17–18% — no sustained downtrend; all in the intermediate 10–25% band (marker at 25%). Important: the lab states %-free PSA is not validated below a total PSA of 2.6 ng/mL (his is 1.2–1.7), so these values are not diagnostically reliable here.

Clinical interpretation — PSA in the active-surveillance context

Supports continued surveillance
  • Latest PSA 1.2 (Jun 2026) — and the fasting repeat fell from 1.7 → 1.2, so the May 1.7 was a transient blip, not a sustained rise.
  • PSA density ~0.03 — strongly favours indolent disease; gland growth explains most of any rise.
  • Velocity & doubling time below intervention triggers (PSADT > 3 yr).
  • Both biopsies Grade Group 1 (2024 & 2025); MRI lesion stable PI-RADS 5, no EPE, no nodes.
  • Decipher 0.27 (low) genomic risk (below) — concordant low-risk biology.
Worth watching / caveats
  • Persistent PI-RADS 5 lesion that abuts the capsule (Feb 2026) — keep imaging/biopsy surveillance on schedule.
  • %-free PSA 17% sits in the intermediate band; it dipped to 13% (May 2025) but recovered — and is anyway not validated below total PSA 2.6, so don't over-read it. Watch the trend, not single values.
  • Perineural invasion was noted in one 2024 core (below) — not a reclassifier alone in GG1.
  • Slow secular drift over 16 yr (nadir 0.5 → recent 1.2–1.7) — expected with age/BPH; keep the longitudinal view.
Bottom line · evidence framing

By NCCN / AUA criteria this remains low-risk, organ-confined GG1 disease appropriate for active surveillance. None of the recognised intervention triggers — grade progression to ≥GG2, rising volume of GG1 cancer, PSADT < 3 yr, PI-RADS upgrade, or new EPE — are currently met. The June 2026 repeat already down-trended to 1.2, so the sensible plan is to continue the protocol (PSA ~q3–6 months, MRI ± confirmatory biopsy per schedule) rather than react to a single high reading. Research / MDT decision-support — the treating team owns the decision.

Prostate MRI — click a study for full findings

Two multiparametric prostate MRIs. The same right posterior peripheral-zone lesion is seen on both — PI-RADS 5 but stable in size and without extraprostatic extension.
Lesion location (axial schematic) ANTERIOR (transition zone) TZ peripheral zone 1.6 cm POSTERIOR RIGHT LEFT

Right posterior PZ, mid-gland — the target sampled at biopsy.

MRI #1 — 6 Jun 2024  PI-RADS 5
MGB · multiparametric · gadoliniumdetails
Index lesion: 1.5 cm focal lesion, right peripheral zone, mid-posterior / posteromedial. Markedly hypointense on ADC, markedly hyperintense on high-b DWI, >1.5 cm, positive dynamic contrast enhancement; homogeneous T2 hypointense mass confined to the prostate.
EPE: none on T2 · Transition zone: no suspicious lesion · Seminal vesicles: normal · Nodes: no pelvic adenopathy · Bones: normal, no destructive lesion.
Metrics: volume 36 ml · 4.9 × 4.0 × 3.7 cm · PSA 1.19 → density ~0.03 · membranous urethra 1.6 cm.
Impression: PI-RADS 5 right PZ lesion; meets size/signal criteria but may represent sequelae of prostatitis.
MRI #2 — 23 Feb 2026  PI-RADS 5
RAYUS · multiparametric · Dotaremdetails
Index lesion: 1.6 cm, right posterior PZ, mid-gland — similar to 2024. DWI score 5 (markedly ↓ADC / ↑high-b, ≥1.5 cm); T2 score 3; dynamic contrast positive.
EPE: broadly abuts the capsule, no visualized gross EPE · Seminal vesicles: symmetric · Nodes: none · Bones: no suspicious lesion.
Metrics: volume 43 ml · 3.9 × 5.1 × 4.1 cm · PSA 1.4 → density ~0.03.
Impression: PI-RADS v2 category 5 (clinically significant cancer highly likely); no extracapsular extension or pelvic adenopathy; gland 43 ml.

Change 2024→2026: lesion stable (1.5→1.6 cm), no new EPE/nodes; gland grew 36→43 ml (BPH) — consistent with a stable target and a benign contribution to PSA.

Biopsy pathology — two transperineal fusion biopsies

Both biopsies show Gleason 3+3=6 (Grade Group 1) adenocarcinoma, right-sided (matching the MRI target); the left side is benign. No high-grade disease on either.
Biopsy #1 — 7 Jun 2024
BWH · BS-24-N37363 · transperineal fusioncores
Region (R/L · zone) · finding · Gleason / involvement
Right PZ — target3+3=6 · 10%GG1
Right PZ — postero-medial3+3=6GG1
Right PZ — postero-lateral3+3=6 · 10% & 5% (3/3) · PNI+GG1
Right PZ — anterior—Benign
Left PZ — anterior / postero-lat / postero-med—Benign
Summary3 right cores GG1 · ≤10%perineural invasion present (1 core)
Biopsy #2 — 4 Feb 2025
BWH · BS-25-X07989 · transperineal fusioncores
Region (R/L · zone) · finding · Gleason / involvement
Right PZ — postero-lateral3+3=6 · 30% (1/2); ASAP in 2nd · no PNIGG1
Right PZ — postero-medial3+3=6 · 5% (1/2) · no PNIGG1
Right PZ — mid3+3=6 · 15% · no PNIGG1
Right PZ — anterior—Benign
Left PZ — postero-lateralatypical small acinar proliferationASAP
Left PZ — anterior / postero-medial—Benign
Summary3 right cores GG1 · ≤30%no perineural invasion

Across both biopsies: disease is consistently Grade Group 1, right peripheral zone, low-volume; no upgrade to GG2+ between 2024 and 2025. Left-sided ASAP in 2025 is non-diagnostic atypia, not cancer.

Decipher genomic classifier · Jul 2024 — summary

Genomic risk score 0.27 LOW INT HIGH 0.00.450.601.0
0.27 — LOW genomic-risk group · 38th percentile
10-yr metastasis
0.7%
15-yr PCa mortality
0.5%
Adverse path at RP
9.6%

A 22-gene RNA classifier run on the biopsy. At 0.27 the tumour sits in the Low genomic-risk band, with very low predicted 10-yr metastasis and 15-yr mortality — the report frames such patients as ideal active-surveillance candidates, concordant with the PSA, MRI and pathology above.

→ Full Decipher section (Genomics & biomarkers)

Labs · longitudinal

KeyLowIn rangeHigh

Current abnormals

Click any abnormal to jump to its full trend chart. High = red · low = blue. Note: the “Current abnormals” tiles flag against the dashboard’s single harmonised reference range per analyte; an individual lab may flag more against its own ranges — see the latest-draw interpretation below.

Lab categories

Haematology

View

Latest draw · clinical interpretation (1 Jun 2026)

A read of the most recent comprehensive panels — Quest 1 Jun 2026, with the 11 May 2026 lipids and a same-day Boston Heart hormone panel. Research decision-support, not medical advice.
Renal & metabolic

eGFR 76 mL/min/1.73 with creatinine 1.06 — within normal limits for age. BUN 23 with a BUN/creatinine ratio ~22 points to a mild pre-renal / hydration effect rather than intrinsic renal disease. HbA1c 5.9% sits in the pre-diabetic band and has been stable since 2024 — worth lifestyle attention; a FreeStyle Libre CGM is in use.

Lipids (on therapy)

On atorvastatin 20 mg + ezetimibe: LDL 35, total cholesterol 134, HDL 89, triglycerides 36 mg/dL — an aggressively well-controlled profile, consistent with secondary-prevention intent.

Haematology

Counts are normal (Hb 14.8, WBC 5.8, platelets 218). A mild relative monocytosis (11.3%) sits on a normal absolute count; NLR 2.9 and LMR ~2.0 are unremarkable and there are no cytopenias.

Hormones — interpret with care

Total testosterone is high–normal/elevated (Quest 886 ng/dL; Boston Heart 883), and the two labs’ free-testosterone estimates differ by method (Quest MS 73.3 vs Boston Heart 126.6 pg/mL). Estradiol is mildly elevated (52). No exogenous testosterone is recorded. In an androgen-driven prostate cancer on active surveillance this is relevant MDT context alongside the stable low PSA (1.2 ng/mL).

Caveat

These are observations against the dashboard’s harmonised ranges, not directives; assay differences (immunoassay vs mass-spec) are not reconciled here. The treating multidisciplinary team owns interpretation and any management decision.

Sources & caveats

Derived & dual-lab values
  • NLR / PLR / LMR ratios are calculated from the absolute differential counts; reference cut-offs shown are indicative (marked “calc”), not lab-issued.
  • Testosterone (2026-06-01): both labs are shown — Quest is the longitudinal trend; the Boston Heart same-day result is a separate row (the two differ by assay, esp. free testosterone).
  • A Boston Heart row labelled “PSA 7.7” is almost certainly FSH (matches same-day Quest FSH 8.0) — excluded.
  • DOB: Boston Heart & Cologuard print 1957-03-27; Mass General / Quest / RAYUS print 1957-03-23 (as-is).
Non-blood documents read

Cologuard (stool DNA, 2023-05-30): negative. Galleri MCED (2024-06-17): no cancer signal. Heart Test = Boston Heart cardiac genotyping (2023-11-16), normal-risk. Pathology, Decipher, Caris, Invitae and the exome report carry no blood labs.

Medications & supplements

Current medication, supplement & device list as recorded at the Annual Wellness Visit, 26 May 2026 (Campazzi Concierge Medicine, L. Wagner APRN). List as provided by the patient — doses self-reported, not pharmacy-verified. The visit recorded an explicit indication only for tamsulosin and the lipid-lowering pair; other indications below reflect each agent’s established / labelled use and are flagged as such.
7
Prescription meds
Across 6 therapeutic areas; one (propranolol) PRN only.
3
Supplements & devices
Vitamin D-3, a B-complex, and a continuous glucose sensor.
35mg/dL
LDL-C on therapy
Atorvastatin 20 + ezetimibe 10 — well below targets.
None
Androgen-active agents
No exogenous testosterone and no 5-α-reductase inhibitor — serial PSA is not pharmacologically suppressed.

Prescription medications

Seven agents, colour-tagged by therapeutic area. Doses and schedules are as the patient reported them at the wellness visit.
MedicationDose & scheduleClassIndicationArea
TamsulosinFlomax 0.4 mg cap · once daily Selective α1-adrenergic antagonist Benign prostatic hyperplasia (BPH) Urologic
AtorvastatinLipitor 20 mg · once daily HMG-CoA reductase inhibitor (statin) Hyperlipidaemia — LDL 35 on therapy Lipid
EzetimibeZetia 10 mg · once daily Cholesterol-absorption inhibitor Hyperlipidaemia — statin add-on Lipid
LoratadineClaritin 10 mg · once daily 2nd-generation H1 antihistamine Allergic rhinitis / urticaria (per class) Allergy
PropranololInderal 20 mg · q8hPRN Non-selective β-adrenergic blocker As-needed; indication not specified on list Cardiovascular
Minoxidiloral, low-dose 2.5 mg · once daily Peripheral vasodilator Androgenetic alopecia (established off-label use) Dermatologic
ZolpidemAmbien 5 mg · at bedtime Non-benzodiazepine hypnotic (“Z-drug”) Insomnia (per class) Sleep

Supplements & devices

Over-the-counter supplements and a wearable glucose sensor — reported alongside the prescription list.
Supplement

Vitamin D-3

5000 IU (cholecalciferol) once daily. High-maintenance-dose repletion; tracked via serum 25-OH vitamin D — see Labs · vitamins.

Supplement

Vitamin-B complex

Pure Encapsulations, once daily. High-dose B12, folate and B6 are the standout actives. Per-nutrient label amounts not transcribed here. High supplemental B12/folate can elevate measured serum levels.

Device

FreeStyle Libre 3

Continuous glucose monitor (worn sensor). Supports glycaemic surveillance — HbA1c has sat in the prediabetic range — see Labs · diabetes.

Clinical relevance for the MDT

What this list does — and does not — mean for the active-surveillance plan.
Lipids — at target LDL-C (mg/dL) 35 <70 <100

Atorvastatin 20 + ezetimibe 10 hold LDL at 35 mg/dL — below both the <70 high-risk and <100 general goals. → Labs · lipids

PSA interpretation unaffected

No 5-α-reductase inhibitor (finasteride / dutasteride) appears on the list, so serial PSA is not pharmacologically halved and needs no ×2 correction — serial values can be read at face value. → PSA & imaging

No exogenous androgen

No testosterone, anabolic steroid, or DHEA on the list — consistent with the “exogenous excluded” branch of the testosterone-elevation work-up. (Minoxidil is a vasodilator, not an androgen.) → General medicine

Tamsulosin — dual role

Prescribed for BPH, tamsulosin also served as medical expulsive therapy during the Dec 2024 ureteric-stone episode. No anticholinergic burden or QT-prolonging agent of note on the list. → General medicine

Source: Annual Wellness Visit, 26 May 2026 (Campazzi Concierge Medicine, L. Wagner APRN). List as provided by the patient; not pharmacy-verified.

Vitals · home monitoring

Optional home-observation log. The full Vitals panel (NEWS2 early-warning score, vital-sign trend charts, symptom diary, ECOG, weight, cloud-synced) is patient-agnostic and reusable — lift it from the reference build per HANDOVER.md §6, using the storage key tbarrows_vitals and the cloud endpoint /.netlify/functions/patient-vitals.
Not yet built

For a localised, actively-monitored case this panel is lower priority than PSA/imaging. We can add it if home-obs logging is wanted — say the word and I'll lift the component.

General medicine

Whole-patient, non-oncology health: an active endocrine review (testosterone), past medical / surgical / family history, and the Dec 2024 acute kidney-stone episode. Sources — Annual Wellness Visit 26 May 2026 (Campazzi Concierge Medicine, L. Wagner APRN) and Jupiter Medical Center ED / Urology records.

Testosterone — MDT endocrine review

Mildly elevated, progressively rising total testosterone in a man not on androgen supplementation (ICD R79.89). Flagged at the 26 May 2026 wellness visit; confirmed on a repeat draw 1 Jun 2026. The question, reasoning and plan are laid out in sequence below.
1
Clinical question

Why is total testosterone mildly elevated and climbing — 713 → 886 ng/dL across three annual draws, now above the 827 ng/dL upper reference limit — in a 69-year-old on active surveillance for androgen-driven prostate cancer who takes no testosterone therapy? And does it change management?

2
The data — total testosterone over time
900850 800750700 827 ng/dL · upper reference limit 713 767 793 832 886 Apr ’23Apr ’24 May ’25May ’26Jun ’26 Quest total testosterone, ng/dL · reference 250–827 (lower limit off-scale; chart zoomed to 650–920)
Fractions — Quest vs Boston Heart
FractionRef11 May1 Jun
Total (ng/dL)250–827832886
Free (pg/mL)46–22460.373.3
Bioavailable (ng/dL)110–575124138

Same-day Boston Heart (1 Jun, MS assay): total 883 (ref 188–684) · free 126.6 (ref 57–240). Cross-lab concordant for an elevated total.

Key observation

Only total testosterone is at/above the limit. The bioactive fractions — free (73.3) and bioavailable (138) — sit comfortably mid-range. The abnormality is therefore confined to the protein-bound pool, not the hormone the tissues actually see.

3
Reasoning — differential for a raised total testosterone without therapy
Exogenous androgen (TRT)Excluded

Explicitly not taking testosterone or hormone supplements. Brief creatine (~4 weeks, stopped ~2 months prior) — not an androgen and does not raise serum testosterone.

Assay / lab variationAddressed

Repeat fasting morning draw sent to a second laboratory (Boston Heart) — still 886 (Quest) / 883 (BH). Reproducible across labs and collection times, so not a single-assay artefact.

Endogenous source — testis / adrenalBeing excluded

A true androgen-secreting source (Leydig-cell or adrenal) is uncommon at this level but must be excluded. Testicular/scrotal ultrasound and adrenal-protocol MRI ordered.

Binding-protein (SHBG) effectLikely mechanism

Total high while free & bioavailable are normal is the classic signature of a raised SHBG-bound pool (favoured by age and lean, athletic habitus). SHBG was not measured on these panels — worth adding.

4
Mechanism — the HPG axis and what “total” actually measures
Hypothalamus GnRH Pituitary LH / FSH Testes testosterone Target tissue androgen receptor − negative feedback TOTAL TESTOSTERONE = SHBG-bound albumin-bound bioavailable (albumin-bound + free) free · biologically active Only the free (and albumin-bound → “bioavailable”) fractions act at the receptor. An isolated rise in total with normal free/bioavailable points to the SHBG-bound pool. Segment widths illustrative.
5
Why it matters here — the prostate-cancer lens

This is an androgen-driven tumour — AR IHC 2+ in 95% of cells, AR over-expressed at RNA level (Z +3.4), and the defining TMPRSS2:ERG fusion is itself androgen-regulated — so androgen status is biologically relevant context, not an incidental number. However, the bioactive (free / bioavailable) testosterone is normal, and the disease is low-risk: Gleason 3+3=6, Decipher 0.27 (low). This finding alone does not change active surveillance. PSA is tracked separately (1.7, up from 1.4 → urology review).

See Genomics & biomarkers and PSA & imaging.

6
Workup & plan
  • Repeat fasting AM testosterone (Boston Heart) — done: 886 (Quest) / 883 (BH) → confirms a real elevation, excludes lab error.
  • Full metabolic panel drawn concurrently — normal (renal, hepatic, electrolytes, glucose).
  • MRI abdomen without contrast — adrenal protocol — ordered (CT declined: radiation concern) to exclude an adrenal source.
  • Testicular / scrotal ultrasound — ordered to exclude a testicular (Leydig-cell) source.
  • Continue urology / PSA surveillance; consider adding an SHBG level to characterise the bound fraction.

Bottom line: a reproducible, isolated total-testosterone elevation with preserved bioactive fractions. Assay error is excluded by the cross-lab repeat; an adrenal/testicular source is being formally excluded by imaging. No change to active surveillance pending those results.

Past medical, surgical & family history

Consolidated from the 26 May 2026 Annual Wellness Visit. Never-smoker · NKDA · alcohol/recreational-drug use not on file.
Active problem list — by system
Cardiovascular
  • Ascending aorta dilatation — aortic root 4.7 cm, ascending aorta 4.1 cm (CTA 8/2025), unchanged since 9/2023 · cardiology surveillance (Dr Januzzi)
  • Coronary artery disease
  • BP 142/76 at visit
Endocrine / metabolic
  • Prediabetes — HbA1c 5.9% · fasting glucose 103 (intermittent CGM; metformin discussed)
  • Thyroid nodules — U/S 8/2025: #1 TI-RADS 2 mixed cystic/solid; #2 8×6×5 mm cystic · repeat in fall (Dr Bass)
  • Elevated testosterone — see review above
Renal / genitourinary
  • Nephrolithiasis — 3 mm left renal stone (see acute episode below)
  • BPH — on tamsulosin
Gastrointestinal
  • GERD
  • IBS
  • Proctitis
Musculoskeletal
  • Lumbar disc herniation L4–5 (chronic low-back pain); current L gluteal/low-back pain
  • Right knee — remote ACL + meniscus repair, mild–moderate arthritis (MRI pending)
  • Left shoulder impingement · bilateral carpal tunnel · prior R wrist fracture · R 1st-MPJ sprain / sesamoiditis
Other
  • Left occipital hemangioma
  • Toenail fungus (laser + topical)
  • Prostate adenocarcinoma GG1 (Gleason 3+3=6), active surveillance — see oncology tabs
Surgical history
  • 2019 — endoscopic right carpal-tunnel release
  • 2001 — left hemilaminectomy, L4/L5
  • Nasal septum surgery
  • Right wrist surgery (fracture)
  • Right posterior-neck cyst resection
Wellness-visit snapshot · 26 May 2026

L. Wagner APRN. Vitals: BP 142/76, HR 81, BMI 21.5 (149.6 lb, +2.2/yr), SpO₂ 95%, afebrile. Exam: “fit, trim and muscular for age,” NAD; cardiovascular, respiratory, abdominal and neuro exams normal; GU/rectal deferred.

Family history
Father CHF, dementia · d.2018 Mother Ovarian cancer · d.2011 Patient Prostate cancer Brother Prostate cancer · AFib Brother AFib cancer-affected deceased □ male ○ female  ↗ patient
Hereditary-cancer context

First-degree relatives with prostate cancer (brother) and ovarian cancer (mother) — a pattern that warrants germline attention. The Invitae 84-gene germline panel was negative, so no actionable inherited risk allele was found despite the family history.

Extended family: grandfather — myocardial infarction; grandmother — CHF (d. 80s); a second brother with atrial fibrillation.

→ Genomics ▸ Germline (Invitae)

Open follow-ups from this visit

Right-knee MRI → orthopaedics (Dr Connors) · cardiology CT for aortic surveillance late June (Dr Januzzi) · thyroid U/S follow-up in fall (Dr Bass) · urology active-surveillance & rising-PSA review (Dr Rosoff) · pain management at HSS for left low-back/gluteal pain · prediabetes — episodic CGM, metformin if trend worsens · testosterone — adrenal MRI + testicular U/S (above).

Acute episode — left ureteric stone (Dec 2024)

First presentation of nephrolithiasis. Jupiter Medical Center ED (19 Dec 2024) and urology consult (31 Dec 2024, Dr P. Tenbrink).
19 Dec 2024 · ED L flank pain via EMS CT: 3 mm L UVJ stone 31 Dec 2024 · Urology Stone passed · asymptomatic Renal U/S in 6 mo · stone analysis 2026 · Surveillance Renal U/S: 3 mm L renal stone Hydration · urology f/u
Presentation

67-year-old, sudden-onset left flank pain, arrived by EMS (fentanyl + ondansetron pre-hospital). No prior stone history; denied dysuria, haematuria, fever. Pain resolved after voiding post-CT — likely passed the stone in the department. CVA non-tender on re-exam.

CT abdomen / pelvis (with contrast)

3 mm stone at the left ureterovesical junction with mild left hydroureteronephrosis. No other stones; solid organs, bowel and appendix normal; no adrenal nodules; prostate mildly enlarged; incidental lumbar degenerative disc / facet disease.

ED labs · 19 Dec 2024
BUN 24 H BUN/Cr 22.9 H CO₂ 20 LOW Urine ketones 1+ H AST 43 H Hb 13.4 LOW Hct 41 LOW Creatinine 1.05 OK eGFR 78 OK WBC 9.3 OK Lipase 45 OK CK 223 OK Nitrite / bacteria neg No UTI

Picture of acute pain with reduced intake / mild dehydration — raised BUN and BUN/creatinine ratio, low bicarbonate, urinary ketones and concentrated dark urine — rather than intrinsic renal or infective disease. Renal function preserved (creatinine 1.05, eGFR 78). Normal lipase and a normal CK (checked after recent tennis) exclude pancreatitis and rhabdomyolysis; nitrite-negative with no bacteria excludes UTI. The borderline-low haemoglobin/haematocrit and mildly raised AST accompany a lab note of moderate haemolysis (likely in-vitro artefact). ECG: normal sinus rhythm, normal ECG.

Management

ED: IV morphine, ketorolac, ondansetron and 1 L lactated Ringer’s; discharged home on tamsulosin 0.4 mg (medical expulsive therapy) and Norco PRN. Urology: stone sent for analysis, renal ultrasound at 6 months, hydration and dietary stone-prevention counselling. A subsequent 2026 ultrasound again showed a 3 mm left renal stone — continue hydration and urology follow-up.