Introduction
Choriocarcinoma is a highly vascularized and
invasive tumor composed of cytotrophoblasts and
syncytiotrophoblasts without the formation of chorionic villi,
which can be classified into gestational choriocarcinoma (GC) and
non-GC (NGC) based on its origin and pathogenesis. GC is a type of
gestational trophoblastic neoplasia that can arise following any
type of gestation and at any interval after conception.
Approximately 60% of gestational trophoblastic neoplasia cases
arise from a molar pregnancy, 30% follow a miscarriage, and the
remaining 10% occur after an ectopic or term pregnancy (1). Compared with GC, which is associated
with the paternal chromosome (2),
NGC is derived exclusively from the patient's own germline.
Clinically, NGC is rarer, more aggressive, less responsive to
treatment and has a poorer prognosis (3). NGC can be further divided into tumors
of germ cell origin and tumors of non-germ cell origin (4). NGC originating from germ cells can
occur in gonadal or extragonadal tissues; the former is mostly
mixed with other germ cell tumors and pure choriocarcinoma is less
common (5–7); the latter is mostly found in midline
structures, such as the pineal gland, mediastinum and
retroperitoneum (8). The
developmental mechanism of germ cell-derived NGC has not yet been
clarified. It may originate from the aberrant migration of
primordial germ cells during embryonic development, or from the
metastasis of spontaneously regressing choriocarcinoma of the gonad
(9). In addition, NGC of non-germ
cell origin is associated with high-grade somatic cell carcinoma
with clinical manifestations typically reflecting the primary tumor
site. This entity is rare in clinical practice, and studies on its
cytogenetic and molecular abnormalities are scarce (3,10,11).
Given that clinical and preclinical studies on these types of
choriocarcinoma are currently insufficient, future research is
required into their molecular mechanisms and clinical diagnosis and
treatment. The present study describes the rare case of a male
patient with rectal adenocarcinoma that pathologically transformed
into choriocarcinoma, providing insight into the pathogenesis and
clinical management of this rare disease.
Case report
In August 2022, due to anal discomfort and frequent
bowel movements, a 62-year-old male patient was subjected to
computed tomography (CT) of the abdomen at Renji Hospital, Shanghai
Jiao Tong University School of Medicine (Shanghai, China), which
revealed focal thickening of the rectal wall. Colonoscopy pathology
showed high-grade intraepithelial neoplasia and carcinoma in some
areas. At that time, the patient opted for traditional Chinese
medicine and declined surgical or other conventional antitumor
therapies. In November 2023, abdominal CT revealed notable
thickening of the focal part of the rectal wall with multiple
metastatic enlarged lymph nodes, which had markedly progressed from
the previous scan. A CT-guided pelvic mass biopsy was performed,
and the pathology revealed a poorly differentiated adenocarcinoma
(paraffin-embedded; 4-µm thick; light microscopy). The tumor cells
exhibited the following immunohistochemical tissue staining
results: Villin(+), carcinoembryonic antigen (CEA)(+), CK7(−),
CK20(+), Ki67(80%), NKX3.1(−), p63(−), GATA-3(−), InSM1(−) and
human chorionic gonadotropin (HCG)(−) (Figs. 1A, 2
and 3). H&E staining was
performed as follows: Samples were fixed in 10% neutral buffered
formalin at room temperature for 12–48 h, and then stained with
hematoxylin for 3–10 min and eosin for 1–3 min at room temperature.
For immunohistochemistry, sections were blocked with 5% BSA
(Shanghai Macklin Biochemical Co., Ltd.) at room temperature for 20
min. The primary antibodies included Villin, CEA, CK7, CK20, Ki67,
NKX3.1, p63, GATA-3, InSM1, HCG (1:100; 4°C overnight/12-16 h or
room temperature for 30 min; Beijing Zhongshan Golden Bridge
Biotechnology Co., Ltd.). Sections were then incubated with
HRP-conjugated goat anti-mouse/rabbit secondary antibody
(ready-to-use; Fuzhou Maixin Biotechnology Development Co., Ltd.)
at room temperature for 30 min. Notably, HCG was added as a
follow-up test. Genetic testing showed the presence of the KRAS
p.G13D mutation (fluorescent PCR method performed according to the
manufacturer's protocol; AmoyDx Human KRAS/NRAS/PIK3CA/BRAF Gene
Mutation Detection Kit; Amoy Diagnostics Co., Ltd.). These findings
suggested rectal cancer with extensive abdominopelvic lymph node
metastasis. The patient underwent further tumor progression despite
receiving two standard treatment protocols for colorectal cancer.
Of these, first-line treatment was initiated in November 2023 for a
total of five cycles: Bevacizumab, 7.5 mg/kg [intravenous guttate
(ivgtt)] on day 1; oxaliplatin, 130 mg/m2 (ivgtt) on day
1; and capecitabine, 1,000 mg/m2 [oral administration
(po)] twice a day on days 1–14 (once every 3 weeks). Second-line
treatment was initiated in March 2024 for a total of three cycles:
Bevacizumab 7.5 mg/kg (ivgtt) on day 1; irinotecan, 200
mg/m2 (ivgtt) on day 1; and raltitrexed 3
mg/m2 (ivgtt) on day 1 (once every 3 weeks). Following
disease progression on second-line therapy, the patient had
metastases in the liver, right lung and multiple lymph nodes
throughout the body; therefore, they received treatment with oral
trifluridine and tipiracil (TAS-102) chemotherapy [35
mg/m2 (po) twice a day on days 1–5 (once every 2 weeks)]
from June 2024.
A total of 6 days after starting treatment with
TAS-102, the patient presented with dizziness and abdominal
distension. Abdominal CT revealed that the metastasis in the liver
was markedly larger than before and had broken through the hepatic
envelope, with rupture and hemorrhage visible (Fig. 4). Emergency surgery was performed 1
day later. The postoperative pathology (paraffin-embedded tissues;
4-µm thick; light microscopy) was as follows: Liver tumor cells:
CK19(+), AFP(−), SALL4(+), Ki67 (80%), CK8(+), VIM(−), p40(−),
CK20(−), HCG(+), CD30(−), PLAP(+), OCT3/4(−), SATB2(−), GS(−),
Inhibin(+), GATA3(+), CD10(+), p63(some cells +) and programmed
death-ligand 1 (PD-L1) CPS 50 (Figs.
1B, 5 and 6). No mutation was detected in the KRAS
gene test (PD-L1 and KRAS gene tests were not performed during the
initial diagnosis and treatment and were added as a follow-up
test). The immunohistochemistry results were consistent with
choriocarcinoma, with no adenocarcinoma component. Postoperative
measurement of serum β-hCG using a chemiluminescent assay,
performed according to the manufacturer's protocol, was >15,000
mIU/ml (reference range, <5 mIU/ml; Beckman Coulter, Inc.).
Thus, given the history of rectal cancer, transformation of rectal
adenocarcinoma into choriocarcinoma was determined clinically.
Rather than the standard EMA/CO (etoposide, methotrexate,
actinomycin D/cyclophosphamide and vincristine) regimen, cisplatin
therapy replaced actinomycin D due to accessibility. Two cycles of
EMP/CO regimen chemotherapy were administered in August and
September 2024, as follows: Etoposide, 100 mg/m2 (ivgtt)
on days 1–2; methotrexate, 100 mg/m2 [intravenous (iv)]
on day 1 + 200 mg/m2 (continuous intravenous infusion
over 12 h); cisplatin, 25 mg/m2 (ivgtt) on days
1–2/cyclophosphamide 600 mg/m2 (ivgtt) on day 8;
vincristine, 2 mg (iv) on day 8; and leucovorin rescue therapy
following methotrexate chemotherapy (once every 2 weeks). During
this period, the second treatment was delayed due to a perianal
abscess and recurrent fever. Serum β-hCG was monitored during
chemotherapy and showed two decreases, namely 4,109 mIU/ml and
11,900 mIU/ml, after which it increased again to >15,000 mIU/ml
(Fig. 7).
 | Figure 7.β-hCG trend during treatment. The
actual values presented as A, B, D and F are >15,000 mIU/ml, but
they are all shown as 15,000 mIU/ml in the figure. β-hCG levels
were detected at the following timepoints: A, EMP/CO treatment
cycle 1, days 1–2; B, EMP/CO treatment cycle 1 day 8; C, symptoms
of perianal abscess and fever, chemotherapy was halted; D, EMP/CO
cycle 2, days 1–2; E, EMP/CO cycle 2, day 8; F, disease progression
and death. β-hCG, β-human chorionic gonadotrophin. |
In November 2024, the patient checked into the
Emergency Department at Renji Hospital, Shanghai Jiao Tong
University School of Medicine, with a fever, and a CT scan
suggested that the tumor had widely metastasized, involving
multiple organs with obvious progression (Fig. 8). Furthermore, cranial CT showed
multiple space-occupying lesions across the midline of the
bilateral frontal lobes, which were considered metastasis with
hemorrhagic changes (Fig. 8). Due
to the poor general condition of the patient, the family decided
against further aggressive antitumor therapy, and the patient died
after being given optimal symptomatic supportive therapy (including
anti-infective therapy, pain management and nutritional support).
The timeline of the present case is illustrated in Fig. 9.
Discussion
Choriocarcinoma associated with high-grade somatic
cell carcinoma is mainly found in the gastrointestinal tract, where
it tends to exhibit biphasic tumor growth (12,13),
such as in colorectal adenocarcinoma with choriocarcinoma
differentiation (14) (Table I). Although the molecular mechanisms
underlying the development of choriocarcinoma have not been fully
elucidated, studies support the notion of the abnormal
differentiation of somatic cell carcinoma (15,16).
In view of this, the present case report illustrates the
pathological transformation from rectal adenocarcinoma to
choriocarcinoma in a male patient, providing evidence for the
abnormal differentiation of somatic cell carcinoma into
choriocarcinoma from a clinical perspective (17). In addition, some cases have shown
only pure choriocarcinoma without a somatic cell carcinoma
component, which may be due to the more aggressive nature of the
fast-growing choriocarcinoma component (18). For example, in the current case
report, the pathological specimen obtained after surgery for
ruptured liver metastasis did not exhibit any adenocarcinoma
component; only choriocarcinoma was observed.
 | Table I.Case reports of primary
choriocarcinoma of the gastrointestinal tract. |
Table I.
Case reports of primary
choriocarcinoma of the gastrointestinal tract.
| First author,
year | Primary site | Sex | Age, years | Treatment | β-hCG response | Overall
survival | (Refs.) |
|---|
| Liu et al,
2001 | Stomach | Male | 66 | Surgery | Not available | 7 days | (23) |
| Mardi et al,
2014 | Rectum | Female | 54 | Surgery; 5-FU | Postoperative:
4,568 mIU/ml | 50 days | (12) |
| Mitselou, 2020 | Sigmoid colon | Female | 61 | Surgery;
chemotherapy | Postoperative:
112,000 mIU/ml | 2 months | (15) |
| Verbeek et
al, 2004 | Rectum | Female | 54 | Surgery; EPC | Maximum value:
102,000 mIU/ml; post-treatment minimum value: Negative | 8 months | (13) |
| Zhong and Yang,
2024 | Rectum | Female | 60 | FAEV and
bevacizumab; EMA/CO; PD-1 inhibitor and bevacizumab | Maximum value:
38,643 mIU/ml; post-treatment minimum value: >500 mIU/ml | 8 months | (17) |
| Hirotsu et
al, 2019 | Stomach | Male | 78 | Surgery;
EMA/CO | Maximum value: 120
ng/ml; post-treatment: Not available | 10 months | (31) |
| Liu et al,
2001 | Stomach | Male | 55 | Not available | Not available | 12 months | (23) |
| Harada et
al, 2012 | Sigmoid colon | Female | 58 | Surgery; EMA; 5-FU
and CDDP | Maximum value:
2,420 mIU/ml; post-treatment minimum value: Negative | 5 years | (16) |
| Takahashi et
al, 2013 | Stomach | Female | 65 | Surgery; EMA/CO;
RFA | Maximum value:
12,000 mIU/ml; post-treatment minimum value: Negative | 9 years | (18) |
| Jiang et al,
2013 | Ascending
colon | Male | 36 | Surgery; BEP | Minimum value: 3.38
mIU/ml; post-treatment maximum value: 10,000 mIU/ml | Not available | (32) |
NGC is not associated with any form of gestation and
is therefore genetically related only to the patient. In 2017,
Mello et al (10) performed
genomic profiling of NGC and identified the only significant
chromosome copy number change to be 21p11, potentially implicating
this locus in disease development. As for NGC associated with
poorly differentiated somatic cell carcinoma, its rarity makes it
difficult to obtain clear breakthroughs in both clinical and
preclinical studies. Based on the current findings, it is believed
that this type of choriocarcinoma originates from the abnormal
differentiation of somatic cell carcinoma. Krulewski and Cohen
(19) revealed that, at the
epidemiologic level, primary gastric choriocarcinoma had a similar
mean age at onset, male-to-female ratio and geographic distribution
to primary gastric adenocarcinoma. Secondly, Skinner and Whitehead
(20) and Campo et al
(21) reported varying levels of
β-hCG expression in colorectal adenocarcinoma cells as early as
1981 and 1987, respectively, and β-hCG expression may be associated
with poor prognostic factors, such as tumor aggressiveness and
lymph node metastasis. Similarly, in 1986, Lind and Haghighi
(22) observed positive staining
for CEA in colonic choriocarcinoma cells. Moreover, in 2001, Liu
et al (23) detected copy
number gains in chromosomes 1p34-36, 12, 17, 18p and 20, as well as
losses in chromosome 18q, in a case of primary gastric
choriocarcinoma, in which, with the exception of chromosome 12, the
other chromosomal alterations were highly consistent with those of
primary gastric adenocarcinoma. Moreover, the investigators
microscopically identified minute adenocarcinoma components and
transitional cells exhibiting features of both adenocarcinoma and
choriocarcinoma (23), findings
consistent with the microscopic observations reported by Gorczyca
and Woyke (24), suggesting
abnormal differentiation in the neoplastic cells. The
aforementioned studies provide evidence of homology between somatic
cell carcinoma and choriocarcinoma; however, further studies are
needed to prove the cause of such abnormal differentiation and its
rarity.
Newlands (25)
revealed that only 9% of patients with gestational trophoblastic
neoplasia died from the disease, compared with a mortality rate of
84% in patients with non-gestational origins. In particular, NGC
associated with somatic cell carcinoma, while being rare, is often
predicted to be characterized by low clinical target response rates
and short remission periods, with more aggressive clinical
progression and poorer prognosis. The majority of patients tend to
die within 12–18 months of surgery due to advanced disease stage
and the lack of effective treatment (26). As reported in the present case, most
patients with NGC ultimately derive limited clinical benefit from
chemotherapy. However, due to the absence of standardized treatment
protocols, surgery and chemotherapy remain primary therapeutic
approaches for NGC, with chemotherapy regimens typically referenced
to those for other germ cell tumors, such as EMA/CO (8) and BEP (bleomycin, etoposide and
cisplatin regimen) (27), or other
chemotherapy regimens that use this class of drugs as a
cornerstone. Cisplatin, a foundational chemotherapeutic agent for
such diseases, is classified alongside actinomycin D as a
cell-cycle-nonspecific drug. Cisplatin forms DNA cross-links that
disrupt DNA structure, halting replication and transcription,
whereas actinomycin D intercalates into DNA and inhibits RNA
polymerase, thereby blocking RNA transcription. Both agents can
activate pathways such as p53 to initiate the intrinsic apoptotic
pathway (28–30). In the present case, because
actinomycin D was unavailable, cisplatin was substituted, which
slightly reduced the risk of myelosuppression, but increased the
incidence of gastrointestinal adverse reactions and nephrotoxicity.
In terms of efficacy, after pathological confirmation of
choriocarcinoma transformation in the present case, the patient
exhibited a marked decline in β-hCG levels following the first
chemotherapy cycle. However, treatment was delayed due to a
perianal abscess and fever, resulting in a subsequent β-hCG
resurgence. Due to the highly aggressive nature of the disease, the
poor general condition of the patient, the suboptimal response to
chemotherapy and potential chemoresistance, disease progression and
mortality ultimately occurred. β-hCG is secreted by trophoblast
cells, is largely unaffected by inflammation or fever, and can be
used as a straightforward indicator to monitor the efficacy of
cancer treatment (31,32). In this case, changes in β-hCG
indicate that the treatment is not completely ineffective. However,
despite the efficacy of the regimen, maximizing therapeutic
benefits in patients with poor physical fitness is a focus of
future diagnosis and treatment of this disease.
With the current treatment dilemma, effective
treatment options need to be further explored in addition to
conventional chemotherapy. Given the highly vascularized nature of
choriocarcinoma, antiangiogenic therapy may be of benefit. Notably,
while anti-vascular endothelial growth factor (VEGF) upregulates
endoglin expression, endoglin blockade conversely enhances VEGF
expression; this reciprocal relationship suggests that dual
blockade of endoglin and VEGF may yield unexpected therapeutic
efficacy (33,34). This treatment modality has been
attempted in a patient with GC after multiple lines of multidrug
resistance and achieved durable remission for >28 months
(35), implying that this type of
targeted therapy regimen may be considered a novel treatment option
for patients with NGC in the future, potentially overcoming
chemotherapy resistance to improve clinical outcomes. In 2019, Lu
et al (36) revealed that
PD-L1 was strongly expressed in most trophoblastic tumors,
including NGC associated with somatic cell carcinoma. As in the
present case, the subsequent PD-L1 test on the liver metastasis was
positive, suggesting that immune checkpoint blockade may be an
effective therapeutic option for NGC, warranting further
exploration in clinical and preclinical studies. On the one hand,
given that anti-VEGF therapy and immune checkpoint inhibitor
therapy are not conventional first-line options, they were not
selected as the initial treatment regimen in the current case.
Subsequently, due to the rapid disease progression, the patient
became ineligible for further antitumor therapy, thereby precluding
the opportunity to attempt alternative medications. On the other
hand, the patient in the present case had received long-term
bevacizumab (anti-VEGF therapy) during prior treatment for rectal
adenocarcinoma. However, the exact timing of pathological
transformation to choriocarcinoma could not be determined and the
possibility of pre-existing bevacizumab resistance could not be
ruled out. With regard to immune checkpoint inhibitors, a PD-L1
test was not performed prior to treatment; however, had positive
PD-L1 expression been detected before therapy, a different
treatment regimen might have been chosen, potentially leading to
better outcomes. This, to some extent, emphasizes the importance of
prospectively evaluating PD-L1 in this type of disease in the
future. To date, only a minority of patients with somatic
carcinoma-associated NGC have demonstrated favorable clinical
outcomes in reported cases. Most of them underwent complete
resection at an early stage and the patients were generally in good
condition, making them eligible for a variety of treatment options
and regimens (16,18). Consequently, future efforts should
focus on actively exploring novel therapeutic modalities for this
type of NGC.
The present case report illustrates the
transformation from rectal adenocarcinoma to choriocarcinoma,
encompassing subsequent treatment, monitoring and prognosis.
However, it has certain limitations: Firstly, two
immunohistochemical staining figures were unavailable for this
case, therefore, all presented results are derived from the
original pathology reports; secondly, as a single case, it lacks
generalizability, and the non-standard chemotherapy regimen used
may have impacted treatment efficacy; thirdly, genomic confirmation
of the clonal relationship is lacking, resulting in an incomplete
case presentation. Therefore, future research is warranted to
further elucidate the mechanisms underlying this disease
transformation and optimize treatment selection, ultimately aiming
for notable breakthroughs and improved clinical outcomes.
Acknowledgements
Not applicable.
Funding
Funding: No funding was received.
Availability of data and materials
The data generated in the present study may be
requested from the corresponding author.
Authors' contributions
YL, KW and HL completed conception and design. ZP,
XZha and SR obtained medical images and pathology figures. XZho, XM
and QW analyzed and interpreted the data. YL and HL confirm the
authenticity of all the raw data. All authors read and approved the
final manuscript.
Ethics approval and consent to
participate
Not applicable.
Patient consent for publication
Written informed consent was obtained from the
patient before their death for publication of the present case
report.
Competing interests
The authors declare that they have no competing
interests.
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