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Page 2 of 8 Block et al. Hepatoma Res 2019;5:21 I http://dx.doi.org/10.20517/2394-5079.2019.17

malignancies occurring in those with HCC has also been observed . This is particularly enlightening that
[2]
HCC has typically carried a grim prognosis as the third leading cause of cancer mortality worldwide .
[3]
The present case report describes a patient with chronic hepatitis B, who sequentially developed bladder
cancer, HCC, and lung adenocarcinoma. His complex sequence of diagnostic evaluations and therapeutic
interventions are first discussed, providing context for a review of the literature on MPMs involving HCC.

CASE REPORT
A 40-year-old Asian man initially presented to an outpatient office in 1987 with a chief complaint of chronic
fatigue for several months. There was no family history of malignancy or hepatitis B. He was found to be
positive for the hepatitis B surface antigen [HBsAg (+)]. He initially had an elevated alanine aminotransferase,
but this returned within normal limits on repeat bloodwork. He demonstrated hepatitis B envelope antigen
(HBeAg) seroconversion on follow-up labs in 1991. At the time of his diagnosis, no antiviral therapy existed,
therefore he was not started on any treatment.

Nine years later, in 2000 at age 53, he developed proteinuria and hematuria and was diagnosed with
bladder cancer. He underwent cystectomy with ureterostomy without complication. Three years later, he
underwent cardiac angioplasty and stopped smoking cigarettes shortly thereafter. In September 2004 at
age 57, abdominal imaging identified a liver mass consistent with HCC (3.4 cm, right lobe, segment 8) with
mild medial segment atrophy suggestive of underlying cirrhosis. He was started on lamivudine 150 mg daily
and then underwent transarterial chemoembolization (TACE) [Figure 1] followed by radiofrequency tumor
ablation. Tenofovir 300 mg daily was then added in May 2010. Hepatitis B virus (HBV) serology at that time
demonstrated HBsAg (+), HBeAg (-), anti-HBe (+) with undetectable HBV DNA.

Despite continued antiviral therapy and undetectable HBV DNA, an abdominal MRI ten years after initial
HCC [Figure 2] in 2014 revealed a new 1.0 cm LI-RADS 5 lesion in segment 7 consistent with recurrent HCC.
At that time, liver function tests were normal, alpha-fetoprotein 2.1 and HBV DNA were still undetectable.
He underwent TACE on 4/14/2014 and remained on lamivudine and tenofovir.

However, three years later, abdominal MR imaging in March 2017 revealed a 0.9 cm liver mass located next
to the prior treatment site in segment 7. Follow-up imaging in June 2017 showed that the mass nearly doubled
in size to 1.9 cm [Figure 3]. This prompted an evaluation for orthotopic liver transplantation (OLT). During
the workup, a chest CT in August 2017 at age 70 showed a lung mass (2.8 cm × 2.4 cm) in the right upper
lobe [Figure 4]. A PET scan characterized the lung mass as hypermetabolic and subsequent biopsy showed
mucinous adenocarcinoma of the lung. Of note, the patient had a 60 pack years smoking, stopping in 2016.

Given this new diagnosis of lung cancer, the patient was no longer eligible for OLT and therapy for both
his recurrent HCC and new lung adenocarcinoma was initiated. For his HCC, he underwent TACE on
early October 2017 followed by two sessions of CT-guided microwave tumor ablations. He also received five
fractions of stereotactic body radiation therapy (SBRT) for his lung adenocarcinoma during this same time
period. Unfortunately, surveillance PET scan in April 2018 [Figure 5] revealed a new left-sided paratracheal
lymph node that was biopsy-proven mucinous adenocarcinoma representing a recurrence which was
wild type for activating genetic aberrations and had a PD-L1 (by SP 263) tumor proportion score of 25%.
Concurrent carboplatin and paclitaxel with radiation to the mediastinum was planned. It was delayed for a
month per patient request.

Concurrent chemotherapy radiation was not done as a repeat CT chest in May 2018 to establish a new
baseline, which showed a new right-sided lung nodule (1.2 cm) [Figure 6] when biopsied was HCC. This was