DOI:10.2214/AJR.08.1279
AJR 2009; 192:288-294
© American Roentgen Ray Society
Spectrum of 18F-FDG PET/CT Findings in Oncology-Related Recurrent Laryngeal Nerve Palsy
Maria Komissarova1,
Ka Kit Wong1,
Morand Piert1,
Suresh K. Mukherji1 and
Lorraine M. Fig1,2
1 Department of Radiology/Nuclear Medicine, University of Michigan Medical
Center, B1G 505G University Hospital, 1500 E Medical Center Dr., Ann Arbor, MI
48109-0028.
2 Department of Nuclear Medicine, Department of Veterans Affairs Ann Arbor
Health Care System, Ann Arbor, MI.
Received May 22, 2008;
accepted after revision June 24, 2008.
Address correspondence to K. K. Wong
(kakitw{at}hotmail.com).
Abstract
OBJECTIVE. The objective of our study was to review recurrent
laryngeal nerve (RLN) anatomy and describe the typical 18F-FDG
(FDG) PET/CT appearance of vocal cord paresis due to oncology-related RLN
injury including a spectrum of presentations, causes, and sites of nerve
injury.
CONCLUSION. Oncology-related RLN palsy may be caused by direct tumor
invasion or its therapy. FDG PET/CT findings should be recognized to avoid
misdiagnosis. Laryngoscopy confirms the suspected diagnosis and excludes
primary vocal cord neoplasm.
Keywords: laryngeal nerves • oncologic imaging • PET/CT • recurrent laryngeal nerve palsy • vagus nerve • vocal cord paresis
Introduction
The recurrent laryngeal nerves (RLNs) innervate laryngeal
musculature and are involved in phonation, swallowing, coughing, and
breathing. Injury to the RLNs or to the vagus nerves, from which they arise,
usually results in vocal cord paresis and impaired vocal function. The causes
of RLN palsy can be broadly divided into neoplastic; traumatic, particularly
during surgery due to inadvertent crush, traction, transection, ligation, or
thermal injury; and idiopathic
[1]. In a retrospective study
of 291 cases, investigators reported the cause of RLN palsy to be neoplastic
in 29.9%; surgical in 40.2%; traumatic in 8%; idiopathic in 10.7%; central in
3.8%; radiation-induced in 3.4%; inflammatory in 2.0%; cardiovascular in 1.7%;
and other rare causes in 0.3% of the cases, including vascular insults, viral
and bacterial infections, endotracheal intubation, and neurotoxic drugs
[2].
The exact incidence of RLN palsy is difficult to determine because of
underdiagnosis [1]; however,
the increasing number of surgical procedures performed in the neck and
mediastinal regions combined with more frequent detection by imaging
techniques may be expected to cause an increase in the number of cases
identified. Oncology patients who undergo 18F-FDG (FDG) PET/CT for
tumor staging may have concomitant RLN palsy, and the typical metabolic
findings should be recognized and reported to clinicians. In this article, we
review the gross and cross-sectional anatomy of the RLNs and describe a
spectrum of imaging findings, highlighting various locations of injury.
Anatomy
The RLN fibers originate in the nucleus ambiguus in the brainstem medulla
and exit the medulla oblongata, with RLN axons grouped in the vagus nerve. The
vagus nerve exits the cranial vault through the jugular foramen, travels down
the neck, anterior to the jugular vein initially, and then becomes more
posteromedial to the jugular vein as it progresses down the neck. On the left
side, the vagus nerve follows the common carotid artery into the mediastinum
and crosses anterior to the aortic arch, with the left RLN passing inferior
and posterior to the aortic arch and then reversing its course and ascending
along the tracheoesophageal groove, continuing into the visceral compartment
of the neck. The right vagus nerve descends with the right common carotid
artery, and at the bifurcation of the brachiocephalic trunk, the right RLN
loops behind the right subclavian artery and ascends superomedially along the
superior lobe pleura toward the tracheoesophageal groove and into the visceral
neck compartment [1,
3,
4]
(Fig. 1).
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Fig. 1 —Drawing shows gross anatomy of vagus nerves and recurrent laryngeal
nerves (RLN). Vagus nerve exits cranial vault through jugular foramen on
either side, and travels down neck in carotid bundle, giving rise to RLN in
upper mediastinum. Right RLN branches from vagus nerve and loops around
brachiocephalic trunk, while left RLN loops under aortic arch, with longer
course. Both RLNs travel superiorly along tracheoesophageal grooves to
innervate laryngeal musculature. Descent of aortic arch and brachiocephalic
trunk during embryologic development can be visualized to "pull
down" RLNs to their current positions in mediastinum.
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Approximately 0.005% of people have a nonrecurrent laryngeal nerve that
occurs only on the right side
[1,
3,
4]. The non-recurrent laryngeal
nerve diverges from the vagus nerve at the level of the cricoid cartilage and
enters the larynx directly; this unexpected location places it at higher risk
of injury during thyroid surgery
[1]. Because RLNs cannot be
visualized directly with the typical spatial resolution of the CT portion of
an FDG PET/CT study, intimate knowledge of the course of the vagus nerves and
RLNs on cross-sectional images is vital for interpretation (Figs.
2A,
2B,
2C,
2D,
2E,
2F,
2G,
2H, and
2I).
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Fig. 2A —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2B —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2C —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2D —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2E —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2F —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2G —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2H —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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Fig. 2I —Cross-sectional anatomy of vagus nerve and recurrent laryngeal nerve
(RLN) is shown on contrast-enhanced axial CT slices obtained from PET/CT study
in 64-year-old man who presented with non-small cell lung cancer. Images show
courses of vagus nerves (asterisk) and RLNs (triangle) in
neck and upper mediastinum, which were determined by close reference to
cross-sectional anatomy text with cadaveric and imaging correlations.
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FDG PET/CT Findings of RLN Palsy
Oncology patients with vocal cord paresis may present with dysphonia,
hoarseness, throat pain, breathlessness, loss of the upper register of the
voice, or even choking episodes, although a significant number may be
asymptomatic at the time they undergo FDG PET/CT imaging for tumor staging
[3]. This typically occurs in
patients with RLN palsy from a neoplastic cause because tumor infiltrates,
surrounds, or stretches the nerve progressively over a period of time, which
allows the contralateral vocal cord to compensate by adducting farther thereby
improving vocal quality and providing protection from aspiration
[5]. Several diagnostic CT
findings have been described in vocal cord paralysis, including paramedian
position of the vocal cord, tilting of the thyroid cartilage, displaced
arytenoid cartilage, ipsilateral dilatation of the pyriform sinus, prominent
laryngeal ventricle, and atrophy of the posterior cricoarytenoid and
thyroarytenoid muscles [6,
7] (Figs.
3A, and
3B).
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Fig. 3A —Iatrogenic left recurrent laryngeal nerve (RLN) palsy in 74-year-old
man with progressive hoarseness for 2 years. Contrast-enhanced axial CT image
shows laxity of left vocal cord, anteromedial deviation of arytenoid
cartilage, and mild atrophy of thyroarytenoid musculature.
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Fig. 3B —Iatrogenic left recurrent laryngeal nerve (RLN) palsy in 74-year-old
man with progressive hoarseness for 2 years. Thoracic axial CT image shows
surgical clips in aortopulmonary window along expected course of left RLN.
Patient had remote history of bronchogenic carcinoma resection more than 1
decade earlier.
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On FDG PET/CT, unilateral vocal cord paresis appears as asymmetric
increased FDG uptake in the normal vocal cord contralateral to the side of
nerve injury (Figs. 4A,
4B,
4C,
4D,
4E,
5A,
5B,
5C,
5D, and
5E). In the acute and subacute
settings, this finding has been described as being strongly suggestive of
unilateral RLN palsy [8], with
the mechanism attributed to decreased glucose utilization in the paralyzed
cord and compensatory increased workload of the contralateral normal vocal
cord. It is important that this pattern not be misdiagnosed as a primary
glottic neoplasm (Figs. 6A,
6B, and
6C) or as metastatic disease,
both of which may present with unilateral increased FDG uptake on the involved
side because of increased glucose uptake by malignant cells.
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Fig. 4B —Left recurrent laryngeal nerve (RLN) palsy in 60-year-old man with
primary esophageal carcinoma. Axial CT (B) and fused PET/CT (C)
images show medial positioning and laxity of left vocal cord (arrow,
B) associated with asymmetrically reduced FDG uptake. Peak standardized
uptake value of normal and paralyzed vocal cords was 6.2 and 2.6,
respectively.
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Fig. 4C —Left recurrent laryngeal nerve (RLN) palsy in 60-year-old man with
primary esophageal carcinoma. Axial CT (B) and fused PET/CT (C)
images show medial positioning and laxity of left vocal cord (arrow,
B) associated with asymmetrically reduced FDG uptake. Peak standardized
uptake value of normal and paralyzed vocal cords was 6.2 and 2.6,
respectively.
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Fig. 4D —Left recurrent laryngeal nerve (RLN) palsy in 60-year-old man with
primary esophageal carcinoma. Axial CT (D) and fused PET/CT (E)
images show focal FDG uptake in posterior mediastinum localizing to
circumferential esophageal mass (arrow, D). Findings suggest
injury to left RLN as it ascends along tracheoesophageal groove; left vocal
cord paresis was confirmed by laryngoscopy.
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Fig. 4E —Left recurrent laryngeal nerve (RLN) palsy in 60-year-old man with
primary esophageal carcinoma. Axial CT (D) and fused PET/CT (E)
images show focal FDG uptake in posterior mediastinum localizing to
circumferential esophageal mass (arrow, D). Findings suggest
injury to left RLN as it ascends along tracheoesophageal groove; left vocal
cord paresis was confirmed by laryngoscopy.
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Fig. 5A —Left recurrent laryngeal nerve (RLN) palsy in 61-year-old man with
metastatic small cell lung carcinoma who presented with 3-month history of
hoarseness and dysphonia. FDG PET maximum-intensity-projection image shows
numerous scattered foci of abnormal FDG activity in the mediastinum and upper
body.
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Fig. 5B —Left recurrent laryngeal nerve (RLN) palsy in 61-year-old man with
metastatic small cell lung carcinoma who presented with 3-month history of
hoarseness and dysphonia. Axial CT (B) and fused PET/CT (C)
images show asymmetrically reduced FDG uptake and corresponding laxity of left
vocal fold (arrow, B). Peak standardized uptake value of
normal and paralyzed vocal cords was 8.9 and 2.6, respectively.
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Fig. 5C —Left recurrent laryngeal nerve (RLN) palsy in 61-year-old man with
metastatic small cell lung carcinoma who presented with 3-month history of
hoarseness and dysphonia. Axial CT (B) and fused PET/CT (C)
images show asymmetrically reduced FDG uptake and corresponding laxity of left
vocal fold (arrow, B). Peak standardized uptake value of
normal and paralyzed vocal cords was 8.9 and 2.6, respectively.
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Fig. 5D —Left recurrent laryngeal nerve (RLN) palsy in 61-year-old man with
metastatic small cell lung carcinoma who presented with 3-month history of
hoarseness and dysphonia. Axial CT (D) and fused PET/CT (E)
images show focal FDG uptake localizing to mass in aortopulmonary window
(arrow, D) and central photopenia consistent with necrosis.
Injury to left RLN is due to direct infiltration by nodal metastatic disease;
vocal cord paresis was confirmed on laryngoscopy.
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Fig. 5E —Left recurrent laryngeal nerve (RLN) palsy in 61-year-old man with
metastatic small cell lung carcinoma who presented with 3-month history of
hoarseness and dysphonia. Axial CT (D) and fused PET/CT (E)
images show focal FDG uptake localizing to mass in aortopulmonary window
(arrow, D) and central photopenia consistent with necrosis.
Injury to left RLN is due to direct infiltration by nodal metastatic disease;
vocal cord paresis was confirmed on laryngoscopy.
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Fig. 6B —60-year-old man with laryngeal cancer. Axial CT (B) and fused
PET/CT (C) images show asymmetric increased FDG uptake in soft-tissue
mass involving left vocal cord (arrow, B). This appearance of
primary glottic squamous cell carcinoma (peak standardized uptake value =
12.3) should not be confused with that of recurrent laryngeal nerve palsy on
FDG PET or PET/CT.
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Fig. 6C —60-year-old man with laryngeal cancer. Axial CT (B) and fused
PET/CT (C) images show asymmetric increased FDG uptake in soft-tissue
mass involving left vocal cord (arrow, B). This appearance of
primary glottic squamous cell carcinoma (peak standardized uptake value =
12.3) should not be confused with that of recurrent laryngeal nerve palsy on
FDG PET or PET/CT.
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Normal laryngeal FDG activity is symmetric and low grade, with the mean
standardized uptake value (SUV) in normal resting vocal cords reported as 1.77
[9]. Physiologic, symmetric,
increased FDG uptake in the vocal cords occurs if the patient vocalizes at or
soon after the FDG injection
[10] because muscle
contraction related to phonation will show increased metabolic activity
[11]. Asymmetry of vocal cord
FDG uptake may be more striking in the acute and subacute settings and less so
with increasing duration of RLN injury. The ratio of normal-paralyzed vocal
cord peak SUV was 3.4 and 2.4 in our acute cases compared with a ratio of 1.5
in a postsurgical chronic case (Figs.
7A,
7B, and
7C). Detecting cases of
bilateral RLN palsy, which has a greater risk of aspiration, is difficult on
FDG PET alone owing to the reliance on the finding of asymmetric FDG uptake
for diagnosis.
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Fig. 7A —Iatrogenic right recurrent laryngeal nerve (RLN) palsy in
71-year-old woman with papillary thyroid carcinoma. FDG PET
maximum-intensity-projection image shows asymmetric FDG activity in vocal
cords.
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Fig. 7B —Iatrogenic right recurrent laryngeal nerve (RLN) palsy in
71-year-old woman with papillary thyroid carcinoma. Axial CT (B) and
fused PET/CT (C) images show asymmetrically reduced FDG uptake and
corresponding medial position of right vocal fold (arrow, B).
Degree of asymmetry in vocal cord metabolic activity is less striking compared
with acute or subacute RLN palsy. Peak standardized uptake value (SUV) of
normal and paralyzed vocal cords was 3.2 and 2.1, respectively. SUVs of normal
and paralyzed vocal cords may be closer than expected because of either
chronicity or iatrogenic nature of nerve injury. In addition, patients who
have received injections of tetrafluoroethylene fluorocarbon polymer (Teflon)
to medialize paralyzed vocal fold may not have typical metabolic findings.
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Fig. 7C —Iatrogenic right recurrent laryngeal nerve (RLN) palsy in
71-year-old woman with papillary thyroid carcinoma. Axial CT (B) and
fused PET/CT (C) images show asymmetrically reduced FDG uptake and
corresponding medial position of right vocal fold (arrow, B).
Degree of asymmetry in vocal cord metabolic activity is less striking compared
with acute or subacute RLN palsy. Peak standardized uptake value (SUV) of
normal and paralyzed vocal cords was 3.2 and 2.1, respectively. SUVs of normal
and paralyzed vocal cords may be closer than expected because of either
chronicity or iatrogenic nature of nerve injury. In addition, patients who
have received injections of tetrafluoroethylene fluorocarbon polymer (Teflon)
to medialize paralyzed vocal fold may not have typical metabolic findings.
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When RLN palsy is suspected clinically, the combination of FDG PET and CT
findings can make a strong case for the diagnosis of vocal cord paresis,
especially if there is additional evidence for neoplasm along the path of the
RLN providing a plausible mechanism for injury. RLN palsy in the mediastinum
has been described to occur with a number of neoplasms, including esophageal
carcinoma (Figs. 4A,
4B,
4C,
4D, and
4E), head and neck squamous
cell carcinoma (Figs. 8A,
8B,
8C), lung carcinoma (Figs.
5A,
5B,
5C,
5D,
5E,
9A,
9B, and
9C), mediastinal nodal
metastases from any tumor type, and lymphoma, as well as with nonneoplastic
processes, such as sarcoidosis, silicosis, tuberculosis, or even a thoracic
aortic aneurysm owing to mass effect.
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Fig. 8B —Left vagus nerve injury in 65-year-old man with recurrent head and
neck squamous cell carcinoma. Axial CT (B) and fused PET/CT (C)
images show focal FDG uptake localizing to mass in left carotid space
(arrow, B), which is injuring vagus nerve along with axons of
the eventual recurrent laryngeal nerve, causing left vocal cord paresis.
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Fig. 8C —Left vagus nerve injury in 65-year-old man with recurrent head and
neck squamous cell carcinoma. Axial CT (B) and fused PET/CT (C)
images show focal FDG uptake localizing to mass in left carotid space
(arrow, B), which is injuring vagus nerve along with axons of
the eventual recurrent laryngeal nerve, causing left vocal cord paresis.
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Fig. 9A —Left recurrent laryngeal nerve (RLN) palsy in 62-year-old woman with
non-small cell lung carcinoma. FDG PET maximum-intensity-projection image
shows abnormal focal FDG uptake in left neck and mediastinum.
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Fig. 9B —Left recurrent laryngeal nerve (RLN) palsy in 62-year-old woman with
non-small cell lung carcinoma. Axial CT (B) and fused PET/CT (C)
images show focal FDG uptake localizing to left upper lobe mass and extending
into aortopulmonary window (arrow, B). Injury to RLN was due
to infiltration by lung carcinoma, presumed primary in nature.
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Fig. 9C —Left recurrent laryngeal nerve (RLN) palsy in 62-year-old woman with
non-small cell lung carcinoma. Axial CT (B) and fused PET/CT (C)
images show focal FDG uptake localizing to left upper lobe mass and extending
into aortopulmonary window (arrow, B). Injury to RLN was due
to infiltration by lung carcinoma, presumed primary in nature.
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Considering the oncology patient's surgical history is important because
iatrogenic traumatic injury is a leading cause of RLN palsy. Thyroid surgery,
carotid endarterectomy, anterior approach for surgery to the cervical spine,
and skull base operations are the most common procedures associated with this
complication [1] (Figs.
7A,
7B, and
7C). Prior radiation,
chemotherapy, or both should also be considered as potential causes of RLN
palsy. External beam radiation at high doses can result in fibrosis and loss
of vascularity of the nerves in the radiation field, with radiation therapy to
the head and neck increasing the patient's risk for developing vagus nerve
paralysis up to 10 years later
[12,
13].
Chemotherapy agents, particularly those in the vinca alkaloid family (i.e.,
vincristine and vinblastine), are notorious for causing transient laryngeal
nerve neuropathy with most patients recovering function 4-6 weeks after
therapy cessation [14,
15]. Cisplatin-induced
bilateral vocal fold paresis, which resolved on discontinuation of the drug,
has been reported in a patient
[16].
The incidence for right-versus left-sided RLN damage is partially dependent
on anatomy. In the lower neck, the course of the right RLN is more lateral and
oblique than the left, making it prone to injury particularly secondary to
trauma and surgery [17], most
commonly thyroid dissection. However, the length of the left RLN (aorta to
cricothyroid joint)—being at times more than double that of the right
RLN (subclavian artery to cricothyroid joint), 12 cm and 5-6 cm, respectively
[18]—predisposes the
left RLN to a higher rate of injury from nontraumatic causes, such as
neoplastic infiltration.
Our approach to interpreting vocal cord FDG uptake is to decide whether
activity is symmetric. Symmetric vocal cord uptake is likely physiologic,
either in patients with normal resting cords or in patients vocalizing at or
soon after FDG injection. Asymmetry of vocal cord activity in an oncology
patient is suspicious for RLN palsy. A search for abnormal FDG uptake along
the course of the RLN is made and the patient's history should be reviewed for
other causes to explain nerve injury. Although a synchronous primary glottic
tumor as the cause of asymmetric vocal cord FDG activity is uncommon,
association between malignancies is well described: for example, a high
incidence of chest malignancy in patients with head and neck squamous cell
carcinomas was reported by Perlow and colleagues
[19].
For making the distinction between vocal cord paresis and a vocal cord
neoplasm, PET may not be discriminatory. The peak SUV in normal vocal cords in
our two acute cases of RLN palsy was elevated (8.9 and 6.2, respectively);
therefore, the SUV measurements of tumor versus vocal cord paresis likely
overlap. Laryngoscopy is more appropriate to use to confirm the diagnosis of
vocal cord paresis and exclude a synchronous glottic tumor or metastasis.
Further Evaluation
In patients with hoarseness and dysphonia as their presenting complaints,
vocal cord paresis may be found on laryngoscopy. In this setting, radiologic
assessment of the cause of a unilateral paralyzed cord should include imaging
of the entire course of the vagus nerve and RLNs from the skull base to the
pulmonary hila. Diagnostic CT can be used to evaluate the neck and upper
thorax for possible sites of nerve injury, and MRI may be superior to CT for
assessing the skull base [20].
Conversely, although imaging findings are helpful in diagnosing suspected RLN
palsy, the diagnosis of abnormal vocal cord motion is usually confirmed by
laryngoscopy, which shows asymmetric vocal fold movement and bowing and
possibly rotation of the larynx.
Conclusion
The RLNs arise from the vagus nerves to innervate laryngeal musculature and
are primarily involved with phonation. Interruption of the RLN at any point
along its path will result in paralysis of the ipsilateral vocal cord;
therefore, sound knowledge of cross-sectional anatomy is imperative for
correct diagnosis. Oncology patients may have RLN palsy either related to
direct tumor invasion and compression or secondary to therapy. The typical
metabolic appearance of vocal cord paresis on FDG PET/CT should be recognized
to avoid misdiagnosis and reported to clinicians owing to its potential
serious consequences, including morbidity and even mortality from aspiration.
Laryngoscopy should be performed to confirm the diagnosis and rule out a
primary glottic tumor.
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Abstract
Introduction
