Role of PET/CT in Carcinoma of the Colon

Introduction

Colorectal Malignancies

Colorectal cancer is the third most commonly diagnosed malignancy worldwide and the second leading cause of cancer-related death. Approximately two-thirds of tumours arise in the colon and one-third in the rectum.

Over 90% of colonic malignancies are adenocarcinomas arising through a well-characterised adenoma-carcinoma sequence. The remainder comprises neuroendocrine neoplasms, lymphoma, gastrointestinal stromal tumours and rare mesenchymal tumours, each with distinct metabolic behaviour.

Colonic Adenocarcinoma

Colonic adenocarcinoma develops over years to decades through progressive accumulation of genetic and epigenetic alterations in colonic epithelium, usually through an identifiable precursor adenoma. This long preclinical phase is what makes screening effective, and is also why an incidentally detected FDG-avid colonic lesion carries such clinical weight.

Risk Factors

Molecular Pathogenesis

Three overlapping molecular pathways account for the great majority of colonic adenocarcinomas, carrying different prognostic and therapeutic implications.

• Chromosomal instability (CIN) — approximately 85% of cases, following the classical adenoma-carcinoma sequence of APC loss, KRAS activation, SMAD4 and DCC loss, and TP53 inactivation.
• Microsatellite instability (MSI-high) — approximately 15%, arising from deficient mismatch repair. Sporadic cases usually result from MLH1 promoter hypermethylation, germline cases from Lynch syndrome. These tumours are characteristically right-sided, poorly differentiated, mucinous and lymphocyte-rich, and they predict response to immune checkpoint inhibition.
• CpG island methylator phenotype (CIMP) — epigenetic silencing closely associated with BRAF V600E mutation and the serrated pathway.

Anatomy and Pathology

Anatomy

• The colon extends from the ileocaecal valve to the rectosigmoid junction and comprises the caecum, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon and sigmoid colon.
• The ascending colon and proximal two-thirds of the transverse colon are midgut derivatives supplied by the superior mesenteric artery through ileocolic, right colic and middle colic branches.
• The distal transverse, descending and sigmoid colon are hindgut derivatives supplied by the inferior mesenteric artery through left colic and sigmoid branches.
• The ascending and descending colon are retroperitoneal, while the transverse and sigmoid colon are intraperitoneal on a mesentery — which governs patterns of peritoneal dissemination and accounts for the positional variability of these segments between studies.
• Lymphatic drainage proceeds sequentially through epicolic, paracolic, intermediate and principal (apical) stations along the named vessels, the basis of the surgical requirement to retrieve at least twelve nodes.

Histopathology

Conventional Adenocarcinoma

Most colonic carcinomas are gland-forming adenocarcinomas, graded as low grade (well or moderately differentiated, at least 50% gland formation) or high grade (poorly differentiated, less than 50% gland formation). Additional prognostic features reported on the resection specimen include lymphovascular invasion, perineural invasion, tumour budding, tumour deposits and the quality of the mesocolic excision plane.

Variants of Metabolic Importance

Clinical Presentation and Tumour Markers

Clinical Presentation

Presentation differs by site. Right-sided tumours grow in a capacious lumen containing liquid stool and typically present late with iron-deficiency anaemia, fatigue, weight loss or a palpable mass. Left-sided tumours, in a narrower lumen with formed stool, present earlier with altered bowel habit, obstructive symptoms or bleeding. Emergency presentation with obstruction or perforation occurs in up to a fifth of patients and carries a worse prognosis stage for stage.

Tumour Markers

CEA and CA 19-9 figures refer to diagnostic performance against healthy controls; ctDNA figures refer to prediction of recurrence after curative-intent surgery. Results vary with disease stage, assay, threshold and sampling time.

CEA is the principal serum marker in colorectal cancer. It is neither sensitive nor specific enough for screening — elevations occur in smokers and in inflammatory bowel, hepatic and pulmonary disease — but it has three established roles: prognostication at baseline, monitoring of treatment response, and surveillance for recurrence after curative resection. It is in this third role that CEA and PET/CT become directly linked, since an otherwise unexplained rise in CEA is the commonest and best-validated indication for FDG PET/CT in this disease.

A normal CEA does not exclude recurrence; a proportion of recurrent tumours do not secrete it. Rising CEA with negative or equivocal conventional imaging is the classic and strongest indication for FDG PET/CT in colon cancer.

Screening and Diagnosis

Screening

Colon cancer is one of the few malignancies in which screening reduces both incidence and mortality, because removal of the precursor adenoma prevents the cancer. Average-risk screening generally begins at age 45–50 and options include colonoscopy at ten-yearly intervals, annual faecal immunochemical testing, multitarget stool DNA testing, flexible sigmoidoscopy and CT colonography. Higher-risk groups — hereditary syndromes, inflammatory bowel disease, a strong family history — enter earlier and more intensive programmes.

PET/CT has no role in screening. It is neither sensitive enough for small adenomas nor justifiable in terms of cost or radiation exposure. Its relationship to screening is entirely incidental: focal colonic uptake found on a scan performed for another indication is a recognised and clinically significant finding, discussed later in this monograph.

Diagnosis

Diagnosis rests on colonoscopy with biopsy, which provides direct visualisation, histological confirmation, accurate localisation and the opportunity to detect synchronous lesions — present in up to 5% of patients. CT colonography is the principal alternative when colonoscopy is incomplete or contraindicated, and is particularly useful in obstructing tumours that cannot be traversed.

Staging of Colon Cancer

Staging determines whether the patient receives surgery alone, surgery with adjuvant chemotherapy, or systemic therapy for metastatic disease. The AJCC TNM system is used, and it is worth noting that nodal status is ultimately a pathological determination; imaging serves to identify distant disease and to detect nodal involvement outside the standard resection field.

Primary Tumour (T)

Regional Lymph Nodes (N)

Distant Metastasis (M)

The separation of M1c as a distinct category reflects the particularly poor prognosis of peritoneal disease and is directly relevant to imaging, because peritoneal metastasis is the pattern of spread that both CT and PET detect least reliably.

Stage Grouping

Patterns of Tumour Spread

Local Extension

Tumour spreads through the bowel wall into pericolic fat and adjacent organs.

T4 disease occurs in approximately 10–15% of patients.

Local T staging is determined by contrast-enhanced CT and histopathology; PET has little additional value.

Nodal Dissemination

• Spread follows the vascular pedicles in an orderly fashion from epicolic and paracolic nodes to intermediate and apical nodes.

Regional nodal involvement is present in approximately 40% of surgically treated patients.

FDG PET/CT has limited sensitivity because metastatic nodes are often small and close to the intensely avid primary tumour.

Haematogenous Metastasis

Liver: present in 14–18% at diagnosis and develops in up to 50% during the disease course.

Lung: develops in approximately 10–15%.

Bone: occurs in 3–7%; brain metastases occur in approximately 0.6–3.2%.

Ovary: develops in approximately 3–5% of women, particularly with mucinous or signet-ring tumours.

Peritoneal Dissemination

Present in approximately 4–8% at diagnosis and may occur in up to 20–25% of patients with advanced disease.

Small or sheet-like deposits are frequently underestimated by CT and FDG PET/CT; therefore, a negative scan does not exclude limited peritoneal disease.

Imaging of Colon Cancer

Imaging Work-up

After endoscopic diagnosis, standard staging comprises contrast-enhanced CT of the chest, abdomen and pelvis. This defines local extent, nodal disease, hepatic and pulmonary metastases and peritoneal involvement, and is sufficient for the majority of patients. MRI of the liver is added when hepatic metastases are being considered for resection. PET/CT enters the pathway selectively, and predominantly in the metastatic and recurrent settings.

Computed Tomography

Contrast-enhanced CT with adequate bowel distension remains the reference standard for initial staging. It is widely available, reproducible, fast, and provides the anatomical roadmap for surgery. Its weaknesses are the characterisation of small hepatic lesions, the detection of small-volume peritoneal disease and the assessment of nodal status, where size criteria perform poorly.

Magnetic Resonance Imaging

Liver MRI with hepatobiliary contrast agents and diffusion-weighted imaging is the most sensitive modality for hepatic metastases, particularly for lesions below 1 cm and in the chemotherapy-treated liver where steatosis and sinusoidal injury degrade CT sensitivity. Any patient being considered for hepatic metastasectomy should have dedicated liver MRI; PET/CT is not a substitute for it.

Comparative Summary of Imaging Modalities

Treatment of Colon Cancer

Understanding the treatment pathway is essential to reporting PET usefully, because the value of a finding depends entirely on the decision it alters.

Localised Disease

• Segmental colectomy with en-bloc lymphadenectomy is the standard operation, with at least twelve nodes retrieved for adequate staging. Complete mesocolic excision with central vascular ligation is increasingly practised.
• Stage I disease is treated by surgery alone.
• Stage II disease is treated by surgery, with adjuvant chemotherapy considered in the presence of high-risk features such as T4 disease, perforation, obstruction, lymphovascular or perineural invasion, poor differentiation or fewer than twelve nodes examined. Mismatch repair-deficient stage II tumours have a favourable prognosis and generally do not benefit from fluoropyrimidine monotherapy.
• Stage III disease receives adjuvant oxaliplatin-based chemotherapy, with duration guided by risk stratification.

Metastatic and Recurrent Disease

• Resectable liver or lung metastases — metastasectomy, with or without perioperative chemotherapy, offers genuine long-term survival and is the reason accurate exclusion of additional disease matters so much.
• Ablation and liver-directed therapy — thermal ablation, hepatic arterial infusion and transarterial radioembolisation with ⁹⁰Y microspheres for liver-dominant disease.
• Systemic therapy — fluoropyrimidine backbones with oxaliplatin or irinotecan, combined with bevacizumab or, in RAS and BRAF wild-type left-sided tumours, with anti-EGFR antibodies. Mismatch repair-deficient disease is treated with immune checkpoint inhibition, and BRAF V600E disease with targeted combinations.
• Cytoreductive surgery with HIPEC — for carefully selected patients with limited peritoneal disease, in whom accurate pre-operative assessment of peritoneal burden is critical and imaging consistently underestimates it.

Biological Basis of FDG Uptake in Colon Cancer

Colonic adenocarcinoma is among the most dependable FDG-avid tumours in oncological practice. Malignant colonocytes overexpress GLUT1 and, to a lesser extent, GLUT3, and show increased hexokinase II activity with reduced glucose-6-phosphatase, so that FDG-6-phosphate is efficiently trapped. GLUT1 expression rises progressively along the adenoma-carcinoma sequence. This is why even premalignant adenomas may be FDG-avid, and why incidental focal colonic uptake is so often significant. Chemotherapy also reduces avidity substantially, which is why a scan performed after neoadjuvant treatment performs worse than one performed before it.

Two important exceptions exist. Mucinous adenocarcinoma contains large pools of extracellular mucin with proportionally few viable tumour cells, so measured uptake per unit volume is low; signet-ring cell carcinoma is similarly sparse in metabolically active tissue. Both may appear falsely reassuring on PET despite bulky or aggressive disease.

Against this must be set the physiological activity of the bowel itself. The normal colon shows variable uptake attributable to smooth muscle activity, mucosal lymphoid tissue, luminal contents and colonic microbiota. This activity is typically diffuse or segmental, in contrast to the focal uptake that characterises neoplasia, and it is markedly accentuated by metformin.

Technique

Patient Preparation

Preparation deserves particular attention in colon cancer because the target organ is also the principal source of physiological artefact.

• Fasting for at least six hours, with water permitted.
• Blood glucose checked before injection and ideally below 150–200 mg/dL.
• Metformin withheld for 24–48 hours where clinically safe. Metformin produces intense diffuse uptake throughout the small and large bowel that can obscure a primary tumour, mask nodal disease and generate false positives. This is the single most important preparation issue specific to colonic imaging, and diabetes is common in this population.
• Avoidance of strenuous exercise for 24 hours.
• Administered activity of approximately 3–4 MBq/kg intravenously, with a 60-minute uptake interval.
• Consideration of oral contrast and adequate bowel distension where a diagnostic CT component is planned.
• Documentation of recent chemotherapy, surgery, stoma formation, biopsy or radiotherapy, and of any colony-stimulating factor use.

Acquisition and Interpretation

• Whole-body acquisition from skull base to upper thighs, extended when clinically indicated.
• A diagnostic contrast-enhanced CT component, or co-registration with a recent one, materially improves characterisation of hepatic and peritoneal findings.
• Delayed imaging at two to three hours may help distinguish persistent focal lesions from transient physiological bowel activity, and improves conspicuity of peritoneal deposits.
• Uptake patterns should be classified explicitly as focal, segmental or diffuse, since the differential differs completely between them.
• Quantification with SUVmax, and where available MTV and TLG, which carry independent prognostic weight in metastatic disease.

Role of PET/CT in Diagnosis

PET/CT is not a diagnostic test for colon cancer. Diagnosis is endoscopic and histological, and no guideline recommends metabolic imaging for the detection or characterisation of a primary colonic lesion. There is, however, one diagnostic situation of genuine and frequently encountered importance: the incidental finding of focal colonic FDG uptake on a scan performed for an unrelated indication.

Incidental Focal Colonic Uptake

Incidental focal colorectal FDG uptake occurs in approximately 3.6% of PET/CT examinations.

Nearly 68% of investigated foci represent a premalignant polyp or colorectal malignancy; therefore, every focal uptake warrants colonoscopic evaluation

• SUV does not reliably separate benign from malignant or premalignant lesions.

A complete colonoscopy is recommended (not directed only at the PET-positive segment) because additional lesions may be present elsewhere in the colon and may not demonstrate FDG uptake.

Differential Diagnosis of Colonic cancer

False Negatives

• Mucinous and signet-ring cell carcinoma — the dominant histological cause.
• Small-volume peritoneal deposits below the resolution of the system.
• Small pericolic nodes adjacent to an intensely avid primary tumour.
• Sub-centimetre hepatic and pulmonary metastases.
• Recent chemotherapy, which substantially blunts avidity.
• Hyperglycaemia at the time of injection.

False Positives

• Physiological bowel activity, accentuated by metformin.
• Diverticulitis, colitis and inflammatory bowel disease.
• Adenomatous polyps — not false positives biologically, but not carcinoma.
• Post-operative inflammation, anastomotic granulation tissue and stoma sites.
• Post-radiotherapy inflammatory change.
• Reactive nodes, and marrow and splenic activation after colony-stimulating factors.
• Second primary malignancies, common in this population.

Role of PET/CT in Staging

PET/CT is not recommended for routine initial staging of colon cancer. Contrast-enhanced CT of the chest, abdomen and pelvis answers the staging question in the great majority of patients, and the incremental yield of PET at first presentation is small while the false-positive rate — driven by physiological bowel activity, diverticular disease and adenomatous polyps — is not negligible. Its contribution is stage-dependent and asymmetric.

T Stage

PET/CT contributes nothing useful to T staging. It cannot resolve the layers of the bowel wall, cannot distinguish T1 from T2 disease, and cannot reliably determine peritoneal surface involvement or adherence to adjacent organs. T stage is a CT and pathological determination.

N Stage

Regional nodal staging is the weakest application of PET/CT in colon cancer, for structural rather than biological reasons. Involved pericolic nodes are frequently small, are often multiple, and lie immediately adjacent to an intensely FDG-avid primary tumour, so that partial volume effects and spillover both reduce sensitivity and impair localisation. Reactive nodes are simultaneously a source of false positives. A recent meta-analysis of FDG PET/CT and PET/MRI for nodal metastases in colorectal cancer confirms that diagnostic performance remains insufficient to replace pathological assessment.

The practical consequence is important: a negative PET does not permit omission of lymphadenectomy, and a positive pericolic node rarely changes the operation. Where PET does add value nodally is in the detection of disease outside the standard resection field — retroperitoneal, para-aortic or distant nodal stations — which converts a locoregional problem into a systemic one.

M Stage

This is where PET/CT earns its place. Distant metastases are FDG-avid, lie in tissues of low background activity, and their detection frequently changes management from curative-intent surgery to systemic therapy, or identifies oligometastatic disease amenable to metastasectomy.

Colorectal liver metastasis

• Routine PET/CT is not supported for patients with liver metastases already judged resectable on good-quality contemporary imaging.
• It retains a role where the risk of occult disease is high — multiple or bilobar metastases, high CEA, short disease-free interval, or equivocal conventional findings.
• Liver MRI, not PET, is the correct test for detecting additional intrahepatic lesions.
• Recent chemotherapy blunts avidity and reduces sensitivity for hepatic metastases; interpret a post-chemotherapy study with caution.

Most published evidence combines colon and rectal cancers. A meta-analysis of 2,283 patients reported that 18F-FDG PET/CT had approximately 73% sensitivity and 99% specificity for primary tumour detection, 62% sensitivity and 70% specificity for nodal staging, and 91% sensitivity and 95% specificity for distant metastases.

PET/CT in Restaging and Recurrence

Detection of recurrence is the best-validated indication for FDG PET/CT in colon cancer. Approximately a third of patients treated with curative intent recur, most within the first three years, and a meaningful proportion have oligometastatic disease that remains amenable to curative-intent treatment — which is precisely why accurate whole-body restaging matters.

The Rising CEA Scenario

• Rising CEA with negative or equivocal conventional imaging is the indication for FDG PET/CT in colon cancer. It remains diagnostically valuable even when contrast-enhanced CT is negative or equivocal, so CT need not serve as a gatekeeper.
• Sensitivity is consistently in the range of 94–95%; specificity is lower, around 77–85%, so positive findings in unusual sites warrant confirmation.
• A negative PET in a patient with convincingly rising CEA should prompt short-interval repeat imaging rather than reassurance.
• PET/CT substantially outperforms conventional imaging for recurrence, whereas CEA alone is sensitive but highly non-specific.

Other Restaging Applications

• Distinguishing post-surgical fibrosis and anastomotic scar from viable recurrent tumour when CT is indeterminate.
• Characterising an indeterminate hepatic, pulmonary or nodal lesion before committing to further treatment.
• Evaluation of unexplained symptoms in a treated patient with normal conventional imaging.

PET/CT in Response Assessment

Response assessment in colon cancer is conventionally performed with RECIST on contrast-enhanced CT, and PET has not displaced it. Metabolic imaging nevertheless has defined roles, principally where anatomical change is unreliable.

Systemic chemotherapy

Reductions in SUV, MTV and TLG may predict subsequent radiological response and survival.

Chemotherapy suppresses FDG uptake; PET/CT should preferably be performed before treatment or 4–6 weeks afterward when assessing resectability.

Radioembolization

FDG PET/CT is useful for treatment selection, response assessment and prognosis because treated metastases may show little size reduction on CT.

Post-treatment ⁹⁰Y PET/CT confirms microsphere distribution and enables dosimetry.

Thermal ablation

A thin, uniform peripheral rim of uptake usually reflects inflammation.

Nodular, eccentric or progressively increasing marginal uptake suggests residual or recurrent tumour.

Assessment should preferably be delayed for approximately 4–6 weeks.

Prognostic Role of PET/CT

• High baseline SUVmax is associated with poorer progression-free and overall survival.
• Metabolic tumour volume (MTV) and total lesion glycolysis (TLG) generally outperform SUVmax by integrating tumour burden with metabolic activity.
• MTV and TLG may provide prognostic information independent of established clinical variables.
• PET radiomics may help predict response to systemic therapy but remains investigational and is not ready for routine practice.

A Practical Decision Framework

Guideline Recommendations

Guideline positions are consistent across societies: contrast-enhanced CT of the chest, abdomen and pelvis is the standard staging investigation, PET/CT is not recommended for routine initial staging, and its use is reserved for defined problem-solving situations.

NCCN

• Contrast-enhanced CT of chest, abdomen and pelvis for initial staging.
• PET/CT is not indicated routinely at baseline.
• PET/CT is appropriate for evaluating an equivocal finding on contrast-enhanced CT that would alter management, and in the setting of a rising CEA with negative conventional imaging.
• PET/CT may be considered before planned metastasectomy in selected patients at higher risk of occult disease.
• PET/CT should not be used to monitor response to systemic therapy in place of CT.

ESMO

• CT is the standard staging modality for both localised and metastatic disease.
• PET/CT is not recommended for routine staging.
• It may be used to clarify equivocal lesions, and in the assessment of potentially resectable metastatic disease where the detection of additional sites would change the treatment plan.
• Liver MRI is preferred for characterising hepatic metastases before metastasectomy.

NICE

• Contrast-enhanced CT of chest, abdomen and pelvis for staging.
• Liver MRI for patients being considered for hepatic resection.
• PET/CT reserved for selected patients in whom conventional imaging is inconclusive and the result would change management.

Guideline Comparison

Emerging Tracers

FAPI PET/CT

FAPI targets cancer-associated fibroblasts. Colorectal cancer is a particularly rational target because it is characteristically stroma-rich — the mesenchymal CMS4 subtype especially so — and because normal bowel and liver express little fibroblast activation protein, giving a favourable tumour-to-background ratio with low background noise.

In a preliminary study of 39 patients with primary or recurrent colorectal cancer, 68Ga-FAPI-04 PET/CT demonstrated 100% sensitivity and specificity for primary tumours, 90% sensitivity and 100% specificity for surgically validated nodal metastases, and 100% sensitivity and specificity for peritoneal deposits. These promising results suggest superior performance over FDG PET/CT, particularly for nodal and peritoneal disease; however, they require confirmation in larger prospective multicentre studies.Where FAPI May Matter Most

• Peritoneal disease — the pattern that FDG detects least reliably, and where the low background of FAPI is most advantageous.
• Mucinous and signet-ring tumours — FDG-poor but stroma-rich, a natural complementary indication.
• Hepatic metastases — minimal hepatic background compared with the moderate physiological uptake seen with FDG.
• Post-chemotherapy assessment, where FDG avidity is blunted.

Limitations

• Inflammation-induced fibrosis produces FAPI uptake. Crohn disease, other inflammatory enteritis and tuberculosis all elevate fibroblast activation protein expression, so uptake must be interpreted against clinical symptoms and history.
• Post-surgical and post-radiotherapy fibrosis is similarly FAPI-avid.
• Evidence remains predominantly single-centre and retrospective, with little outcome data.
• No guideline endorsement; limited availability and generator constraints for ⁶⁸Ga.

Investigational Agents

Frequently Asked Questions

Q Is PET/CT recommended for routine staging of newly diagnosed colon cancer?

No. Contrast-enhanced CT of the chest, abdomen and pelvis is the standard staging investigation. PET/CT is reserved for equivocal findings, for a rising CEA with negative conventional imaging, and for selected patients being considered for metastasectomy.

Q What is the strongest indication for PET/CT in colon cancer?

Suspected recurrence with a rising CEA and negative or equivocal conventional imaging. Pooled sensitivity in this setting is consistently in the range of 90–95%, with specificity around 77–85%.

Q Why might a large colonic tumour show low FDG uptake?

Most often because it is a mucinous or signet-ring cell carcinoma. These tumours contain abundant acellular extracellular mucin and relatively few metabolically active cells, so uptake per unit volume is low despite bulky disease. Recent chemotherapy is the other common explanation.

Q What should be done about incidental focal colonic FDG uptake?

Refer for colonoscopy. Pooled data indicate that focal colorectal incidental uptake occurs in about 3.6% of scans and that roughly 68% of such foci prove malignant or premalignant. SUV does not reliably separate benign from malignant lesions, and the colonoscopy should examine the whole colon rather than only the PET-positive segment.

Q Can PET/CT replace lymphadenectomy for nodal staging?

No. Regional nodal staging is the weakest application of PET in colon cancer. Involved pericolic nodes are small and lie adjacent to an intensely avid primary, so sensitivity is inadequate. Nodal status remains a pathological determination requiring at least twelve nodes.

Q Should PET/CT be performed routinely before liver metastasectomy?

Not routinely. The PETCAM randomised trial found surgical management changed in only 8% of patients, and a subsequent meta-analysis found no improvement in overall or disease-free survival. PET remains reasonable where the risk of occult disease is higher — multiple or bilobar metastases, high CEA, synchronous presentation, or equivocal conventional findings.

Q Does metformin affect the study?

Substantially. Metformin causes intense diffuse uptake throughout the small and large bowel that can obscure a primary tumour and generate false positives. It should be withheld for 24–48 hours before the scan where clinically safe.

Q How reliable is PET/CT for peritoneal disease?

Only moderately. Deposits are often thin, sub-centimetre and mobile, and lie against physiological bowel activity. Both CT and PET underestimate the peritoneal cancer index, so a negative study does not permit confident exclusion before cytoreductive surgery.

Q Is FAPI PET going to replace FDG in colorectal cancer?

Not currently. FAPI offers better tumour-to-background contrast and appears more sensitive for primary and metastatic lesions, and it is theoretically well suited to peritoneal and mucinous disease. However, inflammation and fibrosis are also FAPI-avid, the evidence is largely retrospective and single-centre, and there is no guideline endorsement. FDG remains the reference tracer.

High-Yield Clinical Pearls

Selected References

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