Histopathological examination of retrieved slides from a previously performed transrectal ultrasound-guided biopsy (TRUS) confirmed the diagnosis of sarcomatoid carcinoma. (Gleason score 4+4=8, Grade Group 4). Microscopic evaluation with haematoxylin and eosin staining (Figure 1,2) revealed a biphasic neoplasm with high-grade carcinomatous areas interspersed with sarcomatoid spindle cell proliferation, exhibiting marked nuclear atypia and pleomorphism. The absence of glandular differentiation within the sarcomatoid component further supported the diagnosis.
Immunohistochemical (IHC) stains, also retrieved from archival records, were helpful in differentiating the tumor components. The sarcomatoid areas showed strong positivity for vimentin and smooth muscle actin (SMA) (Figure 3), along with special AT-rich sequence-binding protein 2 (SATB2), a marker indicative of mesenchymal differentiation. The carcinomatous component demonstrated retained epithelial markers, with positivity for pan-cytokeratin (Pan-CK), cytokeratin 7 (CK7) (Figure 3), and cytokeratin 20 (CK20). Notably, PSA expression was absent in both tumor components (Table I), indicating dedifferentiation, a characteristic often associated with aggressive behavior in sarcomatoid prostate carcinoma.
Table I: Immunohistochemical expression in sarcomatoid and carcinomatous components
A crucial role of histopathological and immunohistochemical findings:
Immunohistochemical Evaluation:
• The sarcomatoid component demonstrated diffuse positivity for vimentin and smooth muscle actin (SMA), indicating mesenchymal differentiation. Notably, SATB2, although traditionally used as a marker in colorectal and osteoblastic tumors, has been observed in sarcomatoid elements, reflecting aberrant differentiation.
• The carcinomatous component retained epithelial characteristics, showing strong immunoreactivity for Pan-CK, CK7, and CK20.
• PSA was negative in both components, which is a known feature in dedifferentiated or high-grade variants and often correlates with more aggressive tumor biology.
These findings support the diagnosis of sarcomatoid carcinoma rather than a pure sarcoma or carcinosarcoma. The presence of epithelial markers in the carcinomatous portion and the biphasic morphology were key to reaching the final diagnosis. The integration of H&E features and IHC profiles was essential in ruling out:
• Primary prostatic sarcoma, which typically lacks epithelial markers like CKs or Pan-CK.
• STUMP, which is characterized by bland stromal proliferation and lacks significant mitotic activity or nuclear atypia.
• Carcinosarcoma, which may show divergent differentiation but usually has a known prior history of prostate cancer or therapy-related changes.
Hence, histopathology and IHC not only confirmed the biphasic nature of the tumor but also excluded other mimics, reinforcing their indispensable role in diagnosing such rare and aggressive neoplasms.
The differential diagnosis on histopathology includes:
• Primary prostatic sarcoma
• Metastatic sarcomatoid carcinoma
• Carcinosarcoma
In this case, the diagnosis of sarcomatoid carcinoma of the prostate was strongly supported by both histopathological and immunohistochemical findings, while key differentials were systematically excluded. Primary prostatic sarcoma was ruled out due to the clear presence of a biphasic pattern - malignant spindle cells alongside distinct epithelial area, along with diffuse positivity for epithelial markers such as Pan-CK, CK7, and CK20, which are characteristically absent in pure sarcomas. Metastatic sarcomatoid carcinoma was considered; however, there was no clinical or radiological evidence of a primary malignancy elsewhere, and although site-specific markers like TTF-1 or GATA3 were not performed, the lack of any supportive systemic findings and the tumor`s immunophenotype aligned with a prostatic origin, not a metastasis. Carcinosarcoma was also excluded based on the absence of heterologous differentiation (e.g., osteoid, cartilage, or rhabdomyoblasts) and no history of prior prostate carcinoma or therapy, which are commonly associated with carcinosarcoma. Taken together, the biphasic morphology, immunoprofile, and clinical context make a compelling case for sarcomatoid carcinoma, while confidently ruling out its closest histological mimics.
The etiology of sarcomatoid carcinoma remains unclear. However, some studies suggest it may arise as a dedifferentiated variant of conventional prostate carcinoma, potentially driven by TP53 mutations, Rb1 loss, and epithelial- mesenchymal transition (EMT)[7,8]. Due to its rarity, there are no established treatment guidelines, and management is often based on case reports and small retrospective studies[6,9]. The prognosis of sarcomatoid carcinoma is generally poor, with a high likelihood of metastasis at presentation [2]. Most patients exhibit resistance to androgen deprivation therapy (ADT), particularly those with PSAnegative tumors[5]. Radical prostatectomy is an option for localized disease, but for advanced cases, a multimodal treatment approach is required, including chemotherapy and radiation therapy[9]. Histopathologically, sarcomatoid carcinoma must be distinguished from other spindle cell neoplasms of the prostate, including stromal tumors and sarcomas. IHC markers such as vimentin and pan-cytokeratin are essential for accurate diagnosis[3,8]. An epithelial component with glandular differentiation supports the diagnosis of sarcomatoid carcinoma rather than a primary sarcoma[7]. The absence of PSA expression further suggests a loss of typical prostate epithelial characteristics [5]. Regarding differential diagnosis, this tumor must be distinguished from other biphasic malignancies, including carcinosarcoma and prostatic stromal tumors of uncertain malignant potential (STUMP)[8]. While carcinosarcoma also exhibits epithelial and sarcomatoid components, it is typically associated with a prior history of prostate cancer treatment, which was not the case in our patient[8,9]. However, STUMP lacks the high-grade features and mitotic activity seen in sarcomatoid carcinoma[8].
Conflict of Interest
The authors have no conflict of interest.
Authorship Contributions
Concept: HS, RP, AK, Design: HS, RP, AK, Data collection and/
or processing: HS, RP, AK, Analysis and/or interpretation: HS, RP,
AK, Literature search: HS, RP, AK, Writing: HS, Approval: RP, AK.
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