ALK1 Gene Rearranged Pulmonary Sarcomatoid Carcinoma Masquerading as Tuberculosis in a Young Male
Ayushi SAHAY1, Rajiv KUMAR1, Amit JANU2, Kumar PRABHASH3
1Department of Pathology, Tata Memorial Center, Homi Bhabha National Institute (HBNI), Parel, MUMBAI, INDIA
2Department of Radiology, Tata Memorial Center, Homi Bhabha National Institute (HBNI), Parel, MUMBAI, INDIA
3Department of Medical Oncology, Tata Memorial Center, Homi Bhabha National Institute (HBNI), Parel, MUMBAI, INDIA
Keywords: Pulmonary sarcomatoid carcinoma, Pulmonary tuberculosis, ALK gene rearrangement, Lung cancer, Crizotinib
Pulmonary sarcomatoid carcinoma is rare, with limited treatment options and poor prognosis. In contrast to other non small cell lung
carcinomas, not much is known about its molecular biology. In an endemic country like India, lung cancer is often masked by tuberculosis
and presents in advanced stages. We report here an unusual case of pulmonary sarcomatoid carcinoma, in a young non-smoker male, who had
co-existent tuberculosis masking and delaying the diagnosis of malignancy. On molecular study, the tumor showed ALK gene rearrangement,
both by immunohistochemistry and fluorescence in-situ hybridization, which has been reported only twice previously. Presence of ALK gene
rearrangements in sarcomatoid carcinoma has significant therapeutic implications and potential for altering the prognosis of this fatal disease.
Hence we recommend performing ALK gene rearrangement analysis in all cases of sarcomatoid lung carcinomas. The report discusses the
diagnostic approach and provides insight into the molecular pathogenesis of this exceedingly rare malignancy.
Pulmonary sarcomatoid carcinoma (PSC) is a rare, clinically
aggressive subtype of non-small-cell lung carcinoma
(NSCLC), that accounts for <1% of all lung cancers (1,2). In
contrast to NSCLC, especially Adenocarcinoma, wherein
discovery of targetable therapy (e.g. for EGFR, ALK1 and
ROS1) has resulted in remarkable impact in the therapeutic
outcomes, the genetic abnormalities in PSC are largely
poorly defined. Hence, very limited targeted therapeutic
options are available, till date (3-5).
We herein report a unique case of ALK1 gene rearranged
PSC in a young male, which was masked by co-existent
tuberculosis. ALK1 gene rearrangements are rarely
described in PSC and till date only a handful of case reports
have been published in the literature.
A 33-year-old, non-smoker male presented with history of
low grade fever and weight loss for the last year. He was
initially evaluated in some other hospital. A large necrotic
left para-tracheal mediastinal lymphadenopathy, near the
arch of the aorta was detected by computerized tomography
(CT) scan. He was empirically started on anti-Kochís
therapy (AKT) and showed partial initial response to the
therapy as his fever subsided with treatment, the nutritional
status improved, and the size of the lymph nodes were reduced on the follow-up CT scans. Seven months later, a
cystic collection developed in the supraclavicular region,
and fine needle aspiration cytology and histopathology
showed necrotising granulomatous inflammation, which
was positive for acid fast bacilli by the ZN stain. A TB
Genexpert analysis confirmed Mycobacterium tuberculosis
and hence, AKT was continued.
In addition, he developed a gradually progressing painful
swelling on the left side of the chest wall over a period of
four months. CT scan reported an infective collection with
osteomyelitis involving the 7th and 8th ribs. He underwent
drainage of the collection, with excision of the underlying 7th,
8th and 9th ribs. Surprisingly, histopathological examination
showed a high grade malignant tumor. The patient was then
referred to our cancer centre for further management. On
histopathology review, a poorly differentiated malignant
tumor composed of large spindled to epithelioid cells
with areas of necrosis was seen. No definitive glandular
or squamoid differentiation was noted. Frequent mitoses
(18-20/10HPF) were noted. The underlying ribs as well
as resection margins were also involved by the tumour.
The differential diagnosis based on histopathology ranged
from malignant mesothelioma, epithelioid sarcoma,
malignant melanoma to poorly differentiated sarcomatoid
carcinoma. Accordingly, immunohistochemistry (IHC)
was performed. The tumour was strongly and diffusely
positive for AE1/AE3, and CK7, while negative for calretinin, WT1, and D2-40 (podoplanin) (mesothelial
markers); S100 protein and Melan A (melanoma markers),
and CD34 (epithelioid sarcoma markers). The tumor cells
were also negative for other epithelial (CK20, TTF1, Hep-
Par1, PAX8) and mesenchymal markers (CD31, Desmin,
SMA, S100). INI1 was retained in the tumor cells. Hence,
possibility of metastatic poorly differentiated carcinoma
with sarcomatoid differentiation and involving the chest
wall was suggested and radiological correlation for the
possible primary site was requested. Serum tumor markers
for CEA (0.76 ng/ml) were determined and were within
Positron emission tomography (PET) scan revealed an
ill-defined hypodense soft tissue lesion with peripheral
enhancement at the post-operative site, measuring
approximately 5 x 3 cm, with a maximum SUV of 15.48
Mev, suggestive of either residual malignancy or Kochís
etiology (in view of the past history of tuberculosis). Few mediastinal pleural nodules were also noted at the D3/
D4, D4/D5 and D6 levels. However, uptake on PET scan
was not significant (Figure 1A-C). Based on the imaging
findings, and as the residual lesion was resectable, the
patient was re-explored and en-bloc excision of the tumor
with a wedge resection of the left lower lobe and 7th-10th
rib was performed. However, complete R0 excision could
not be achieved, because intra-operatively multiple small
mediastinal and diaphragmatic pleural nodules were
identified, and confirmed to be positive for malignancy on
intraoperative frozen section.
Click Here to Zoom
|Figure 1: Fluorine-18 fluorodeoxyglucose Positron emission tomography/ Contrast enhanced computed tomography scan images
showing an A) ill defined lobulated hypodense soft tissue lesion with peripheral enhancement in the left chest wall at the post-operative
site, B) which is metabolically active. The lesion extends along the 7th and 8th intercostal spaces. C) Few metabolically active mediastinal
nodules are also noted.
Histopathological examination revealed a tumor with
a similar morphology to that of the prior excision, albeit
with more spindled and sarcomatous appearing areas and
numerous lymphovascular emboli (Figure 2A-D). The
tumour was also seen to involve the lung parenchyma and
pleura and showed mediastinal lymph node metastasis.
The tumor was additionally strongly positive for vimentin, while negative for estrogen receptor, Napsin A, and p63
(Figure 3A-D). The special stain for mucin (mucicarmine)
Click Here to Zoom
|Figure 2: A) Spindle shaped tumor cells in sheets with vesicular nuclei and prominent nucleoli. Frequent mitosis is seen (arrows) (H&E;
x400). B) Other areas showing dissociated epithelioid to rhabdoid tumor cells with abundant cytoplasm and eccentric, pleomorphic
vesicular nuclei with prominent nucleoli. Multinucleation is noted (H&E; x400). C) Tumor infiltration in the lung (H&E; x100). D)
Tumor invasion in underlying bones (rib) (H&E; x40).
Click Here to Zoom
|Figure 3: A) Strong immunopositivity for CK7 in the majority of the tumor cells (IHC; x100). B) Strong diffuse immunopositivity
for Vimentin (IHC; x100). C) Strong, diffuse, granular immunopositivity for ALK-1 (IHC; x200). D) Break apart Fluorescence In-situ
hybridization (FISH) for ALK showing split signal (white arrow) and loss of green signal (broken arrow). More than 15% of the tumor
cells showing splits and loss of green signals was considered as positive for ALK gene rearrangement.
Based on the imaging finding, spindle cell histomorphology
and IHC results, a diagnosis of PSC of the spindle cell
carcinoma type was made.
Further treatment options, including adjuvant radiotherapy
and/or chemotherapy were discussed in a multidisciplinary
clinic, in view of residual disease (R2 resection), with
metastatic mediastinal lymphadenopathy. The patient
was started on palliative chemotherapy (paclitaxel and
carboplatin) and molecular profiling of the tumor was
initiated. The tumor showed strong diffuse granular
cytoplasmic positivity for ALK-1 Amplification IHC using the ventana D5F3 antibody clone. Subsequently, ALK-
1 gene rearrangement was confirmed, using break apart
fluorescence in situ hybridization (FISH) probes (Figure
3A-D). The tumour was negative for other biomarkers
i.e. EGFR mutations, ROS1 rearrangements and MET
amplification. The tumor cells showed focal positivity of
weak intensity for PDL1 with the Ventana SP263 antibody
Considering ALK1 positivity, the patient was switched
to Crizotinib. However he developed transaminitis and
Crizotinib had to be discontinued after only six days of
therapy. The patient eventually developed lower back
pain, with difficulty in walking. An MRI scan revealed
extradural soft tissue metastatic lesions at the D4-5 and
D8-9 regions, for which the patient received palliative radiotherapy. However, his pain gradually worsened, with
increasing sensorimotor deficit. Hence, he was restarted on
Crizotinib with monitoring of liver function. Nevertheless,
the patientís general condition kept on deteriorating over
the next few days. He developed abdominal distension
and respiratory distress and succumbed to cardiac arrest
despite all efforts.
PSC is a heterogeneous group of rare and aggressive lung
tumors, with unclear histogenesis, that accounts for 0.1%-
0.4% of all lung cancers (1). PSC typically occurs in older,
heavily smoking men and has a predilection for upper
lobe involvement (1,2). The classification of sarcomatoid
carcinomas of the lung has posed significant challenges over the years, due to their rare occurrence and heterogeneous
histology. According to the most recent 2015 World Health
Organization (WHO) classification of lung tumours, PSC
is not a single entity but has five subgroups, which include:
pleomorphic carcinoma, spindle cell carcinoma, giant cell
carcinoma, carcinosarcoma, and pulmonary blastoma (1).
Early surgery with post-operative adjuvant chemotherapy
remains the preferred treatment. However, the prognosis
remains poor, even in early stage disease (6,7).
We have documented here an extremely challenging case of
PSC, unravelling the difficulties faced for establishing the
diagnosis, as well as during treatment. The demographic
profile was unusually different, as the patient was young
(33 years old) and a non-smoker. Further, due to presence
of coexisting tuberculosis in this patient, the possibility of malignancy was not considered initially, both clinically as
A diagnosis of PSC may be suspected on small biopsy or
cytology, but commonly requires surgical resection to
reach a conclusive definition (1). PSCs, and especially
spindle cell carcinoma, are usually entirely composed of
spindle-shaped cells without differentiated carcinomatous
elements. The key role of IHC is to distinguish sarcomatoid
carcinomas from sarcomatoid mesothelioma, primary
or metastatic sarcomas, and metastatic sarcomatoid
carcinoma (e.g., renal), as well as to exclude mimics, such as
metastatic melanoma (1,7,8). Although, cytokeratins have
significant diagnostic value in sarcomatoid carcinomas,
staining is often focal and weak, and in some cases it
can even be completely negative. Hence, it can be useful
to utilize a panel of cytokeratins in suspected PSC. The
markers of glandular and squamous differentiation, i.e.,
TTF1 and p40, respectively, can be negative as observed in
the current case, but these markers should always be used
as focal positivity can be seen in a subset of cases (7,8).
In this case, distinction from sarcomatoid mesothelioma
was difficult, considering the clinical presentation and
histomorphological findings. Further, IHC results for
specific differentiation markers may be negative in both
tumor types. Sarcomatoid mesotheliomas are commonly
negative or only weakly or focally positive for mesothelial
markers. Pathologists should also keep in mind that
mesothelial markers may be aberrantly expressed in PSC.
BAP-1 negativity and GATA binding protein 3 (GATA3)
positivity have been recently described to be very helpful in
ruling out PSC and supporting the diagnosis of sarcomatoid
Finally, distinction of sarcomatoid carcinoma from
primary or metastatic sarcoma can be equally problematic.
Just as sarcomatoid carcinomas may be virtually negative
for keratins, some high-grade sarcomas are known to
express keratins, usually weakly and focally. Thus, focal
labeling for keratins should not be used as the sole criterion
supporting the diagnosis of sarcomatoid carcinoma over
sarcoma, and conversely, the lack of detectable keratins,
particularly in a small sample, does not favor sarcoma over
sarcomatoid carcinoma (8). Hence, a careful evaluation of
clinicopathological, IHC and molecular findings has been
advised to render the correct final diagnosis.
The molecular characterization of lung adenocarcinoma
has revolutionized the treatment of lung cancer with the
discovery of targetable genetic alterations such as EGFR
mutations and ALK gene rearrangements (3,4). Specific
targeted agents like gefitinib, afatinib, osimertinib (for EGFR mutated tumors) and crizotinib/ceritinib (for ALK
rearranged lung adenocarcinomas) have been approved by
the Food and Drug Administration (FDA) for clinical use
Due to the rarity of PSC, the molecular profile has been
barely characterized. The unresolved diagnostic, prognostic
and therapeutic issues underline the urgent need to better
define the molecular profiles of these tumors in order to
identify new potential markers (5,7). Different studies have
reported that a significant percentage of PSC cases may
present gene alterations similar to other NSCLC types and
alteration in tumor protein p53 gene (TP53) can be found
in approximately 70% of PSC cases. In addition, KRAS (30-
40% of patients) and MET genes (13-20%) are the most
common driver oncogene mutations noted in PSC (7).
However, targetable mutations in PSC are less frequent
than in NSCLC with adenocarcinoma histology, with EGFR
mutations reported in 8-22% cases in various studies (7,9-
11). The efficacy of EGFR tyrosine kinase inhibitors (TKI)
in PSC has also varied between studies, and was inferior
when compared to adenocarcinoma (7).
Of note, none of these large studies described ALK gene
rearrangement in PSC. A study of head and neck sarcomatoid
carcinoma demonstrated ALK gene rearrangement in two
out of 10 cases (20%), one of whom was administered
Crizotinib and showed symptom improvement and disease
stabilization for four months (12). The first case of ALKpositive
PSC in an elderly non-smoker female was reported
by Ali et al., in a metachronous second lung primary after
resection of a lung adenocarcinoma, which also showed
ALK-1 gene rearrangement. (13). Since then, only handful
of reports of ALK rearrangements were reported in PSC
and the effects of targeted therapies against this mutation
have been shown to be varied, but mostly with ineffective
or partial responses (13-16).
On molecular analysis of 33 PSC cases, Terra et al. found
ALK gene rearrangement in a single case (3%), similar
to the reported frequency in adenocarcinoma (5). The
patient, in contrast to ours, was a 58-year-old female with
an eight pack-year smoking history. The first report of
ALK-rearranged advanced PSC treated by Crizotinib was
by Murakami et al. in 2015, but the response was transient
(14). Karim et al. demonstrated EML4-ALK translocations
in two patients out of 25 cases of PSC. One of the patients
received Crizotinib and had the longest overall survival
compared to the other patients in the study cohort (15).
Crizotinib was started in view of advanced stage in the
index case, as this PSC revealed ALK1 gene rearrangement.
However, it had to be temporarily stopped due to drug
toxicity, and the patient succumbed to death within a very
short time. Hence, the clinical impact of identifying this
targetable mutation could not be established in our case.
In addition, MET amplification and mutations have also
been described in PSC (17). Considering that Crizotinib
targets both ALK and MET mutations, this agent might
play an important role in treating patients with PSC.
Additional studies are required to clearly determine the
efficacy of molecular targeted therapies against PSC.
Recently, immunotherapy has also demonstrated
encouraging results in the treatment of NSCLC. Although
PDL-1 expression was noted in only 5% of the tumor
cells in the present case, high PDL-1 expression (53% and
69.2%) has been recorded by some researchers (18,19).
This suggests that PSC expresses greater levels of PD-L1
and it may represent a potential therapeutic target for PSC
in the future.
The co-existence of pulmonary tuberculosis has been
reported in 0.7% of lung cancer cases (20). The association
of tuberculosis with PSC has not been reported in any of the
prior published reports in the literature. Significant overlap
in the clinical presentation and radiological features was
reported between tuberculosis and lung cancer (21,22).
Chandra et al. had reported that, out of 123 lung cancer
patients, 23 (17%) had been initially labelled and treated as
tuberculosis, resulting in a significant delay in the diagnosis
of malignancy (mean difference of 65.6 days). India being an
endemic country for tuberculosis, starting of AKT for any
suspicious opacities on chest radiographs without proper
evaluation was the main reason assigned for the delay in
lung cancer diagnosis and treatment. Thus, in patients
with already confirmed active tuberculosis, presence of
lung cancer is rarely suspected, with consequent delay
in diagnosis resulting in advanced stage at presentation
as happened in the index case (23). According to Wu et
al., an occult lung cancer may reactivate the tuberculosis
by lowering the patientís immunity in endemic countries
where a significant proportion of the population is infected
with latent tuberculosis. Conversely, chronic inflammation
due to pulmonary tuberculosis itself may cause multistep
transformation of cells, leading to lung cancer (24).
Although, our patient initially benefitted from AKT, the
malignancy was clinically and radiologically masked,
which had resulted in a delayed diagnosis, with mortal
consequences. Further, he could not tolerate the Crizotinib
well, which may be attributed to a possible drug interaction with AKT. Hence, this case highlights the difficulties
encountered in diagnosing and treating a case of PSC with
To conclude, we report here a rare case of ALK1 gene
rearranged PSC, in a young non-smoker male, which was
camouflaged by co-existent tuberculosis. We recommend
that comprehensive molecular analysis, especially for
ALK1, should be carried out in all PSCs to gather robust
data regarding the molecular biology of this rare tumor.
Hopefully, this will open up new therapeutic options for
patients with this deadly disease in the future.
CONFLICT of INTEREST
The authors declare no conflict of interest
This research received no specific grant from any funding
agency in the public, commercial, or not-for-profit sectors.
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