Diagnostic Pathology: Open Access
Open Access

TROP2: Trophoblast Cell Surface Antigen 2; CNS: Central Nervous System; ADCs: Antibody-Drug Conjugates; SG: Sacituzumab Govitecan; OS: Overall Survival; TNBC: Triple-Negative Breast Cancer; BBB: Blood-Brain Barrier; IBC-NST: Invasive Breast Carcinoma of No Special Type.

The human trophoblast cell surface antigen 2 (TROP2) is a transmembrane glycoprotein that acts as an intracellular calcium signal transducer, driving self-renewal, cell proliferation, invasion and survival [1,2]. It is overexpressed in various solid tumors, including breast, Colorectal, lung, gastric, skin and pancreatic cancers, with expression reported in 55%-75% of cases [3-9]. Overexpression of TROP2 is generally associated to poor prognosis, increased tumor aggressiveness and higher metastatic potential [10,11].

Metastatic solid tumors remain a significant unmet medical challenge, particularly Central Nervous System (CNS) metastases, which are associated with extremely poor outcomes. While targeted therapies, such as monoclonal antibodies and Antibody-Drug Conjugates (ADCs), have improved outcomes in advanced cancer, their efficacy against CNS metastases is limited. Sacituzumab Govitecan (SG), a TROP2-directed ADC, has demonstrated significant Overall Survival (OS) benefits in patients with Triple-Negative Breast Cancer (TNBC) but showed no OS improvement for those with CNS metastases [12,13]. The prevailing explanation attributes this limitation to the inability of these therapies to effectively penetrate the Blood-Brain Barrier (BBB) [14]. However, the distinct molecular and genomic features of CNS metastases, which often diverge from those of the primary tumor, must also be considered [15]. Research on TROP2 heterogeneity between primary and metastatic lesions, particularly in the CNS, remains scarce. Based on this context, this study aims to evaluate TROP2 expression in brain metastases from various solid tumors and compare it with expression in primary tumors.

Case selection

After the approval from the institutional review board (approval number: 2024AN0580), A total of 61 surgically resected brain metastasis specimen between 2015 to 2023 were retrieved for the pathology database of the Department of Pathology at the Anam Hospital, Korea University College of Medicine, Seoul, Republic of Korea. When available, corresponding primary tumor tissues were also collected. Clinical data, including the patient’s age, sex and origin of tumor was reviewed in the electronic medical records.

Tissue microarray construction

Tissue Microarrays (TMAs) were constructed from formalin-fixed, paraffin-embedded tissue blocks by using a manual tissue microarrayer (UNITIMA, Seoul, South Korea). Areas occupied for >75% of tumor cells without accompanying tumor necrosis were selected and two representative cores were punched out from a donor block and transferred into a new recipient block with a punch of a 3mm diameter.

Immunohistochemical staining

 The Immunoshistochemical (IHC) staining was performed as follows. Briefly, 4-μm tissue sections from TMAs were subjected to IHC using a Ventana auto-stainer and an ultra-Vies DAB Detection Kit (Ventana, Tucson, Arizona), according to the manufacturer’s instruction. Primary antibodies for TROP2 (EPR20043, catalog No. ab214488, rabbit monoclonal, 1:2000, Abcam, Cambridge, UK) were used. The TROP2 IHC staining was evaluated by two pathologists (YNS and YSK) and classified into 3 categories (Figure1): Diffuse positive (>95%), focal positive (>0% and <95%) and negative.

Figure 1: Representative images of TROP2 Immunohistochemical (IHC) staining in metastatic brain tumor. (A) Metastatic invasive breast carcinoma, no special type showing diffuse TROP2 positivity (× 200, × 40 inlet). (B) Metastatic adenocarcinoma from the colon showing TROP2 focal positivity (× 400, × 40 inlet). (C) Metastatic follicular carcinoma from the thyroid showing TROP2 negativity (× 200, × 40 inlet).

Statistical methods

The R software (version 4.02, Vienna, Austria) was used. The association between TROP2 expression pattern and tumor origin, as well as between TROP2 expression pattern and pathologic diagnosis, was evaluated using the χ2 and/or fisher’s exact tests. Survival analysis based on expression levels was performed using log rank test and Kaplan-Meier analysis. P-values less than 0.05 were considered statistically significant.

Clinicopathological characteristics of cases

A total of 61 surgically resected brain metastasis specimens were available for analysis. Table 1 summarizes the characteristics of cases. The mean age of the patients was 61.5 ± 10.0 years (range, 37 to 82 years) with a male-to-female ratio of 1.1. Metastatic brain tumors originating from various organs were included. The most common primary site was lung (23 cases, 37.7%), followed by the breast (11 cases, 18.0%) and the colorectum (10 cases, 16.4%). Other primary sites included the bladder and skin (3 cases each, 4.9%), kidney and ovary (2 cases each, 3.3%) and well as less common sites such as the ear, gallbladder, hypopharynx, thymus and thyroid, each contributing 1 case (1.6%). In terms of pathologic diagnosis, adenocarcinoma was the most frequently observed type, with 27 cases (44.3%), followed by invasive ductal carcinoma with 11 cases (18.0%), Squamous cell carcinoma with 6 cases (9.8%) and undifferentiated carcinoma in 4 cases (6.6%). Melanoma and urothelial carcinoma were found in 3 cases each (4.9%). Less common diagnoses included clear cell carcinoma and high-grade serous carcinoma (2 cases each, 3.3%), along with adenoid cystic carcinoma, follicular carcinoma and thymoma each present in 1 case (1.6%) as shown in Table 1.

Table 1: Clinicopathological characteristics of the analyzed cases.

TROP2 expression in metastatic and primary tumor

Among the 61 metastatic brain tumors, TROP2 expression was diffusely positive in 38 cases (62.3%), focally positive in 10 cases (16.4%) and negative in 13 cases (21.3%, Figure 2A). Of the tumors with diffuse positive TROP2 expression, the most common site of origin was the lung (18 cases, 47.4%), followed by the breast (11 cases, 28.9%), bladder (3 cases, 7.9%) and ovary (2 cases, 5.3%). Single cases originated from colorectal, ear, gallbladder and hypopharyngeal primaries. Among the tumors with focal TROP2 expression, 8 cases (80%) originated from colorectum and 2 cases (20%) were from the lung. In the TROP2-negative cases, lung and skin tumors accounted for 3 cases each (23.1%), kidney and tumors of unknown origin accounted for 2 cases each (15.4%) and colorectal, thyroid and thymic tumors each accounted for 1 case (7.7%, Figure 2B). The distribution of TROP2 expression according to pathologic diagnosis is illustrated in Figure 2C.

Figure 2: TROP2 expression in metastatic brain and primary tumors. (A) Pie chart showing TROP2 expression pattern in metastatic brain tumors. (B and C) Bar chart showing TROP2 expression in metastatic brain tumor according to origin and diagnosis. (D) Pie chart showing TROP2 expression pattern in primary tumors. (E and F) Bar chart showing TROP2 expression in primary tumor according to origin and diagnosis.

Notably, in the most common tumor type, adenocarcinoma, TROP2 expression was diffusely positive in 15 cases (55.6%), focally positive in 9 cases (33.3%) and negative in 3 cases (11.1%). In contrast, all 11 cases of Invasive Breast Carcinoma of No Special Type (IBC-NST) showed diffuse TROP2 positivity. Similarly, in primary tumors, TROP2 expression was diffusely positive in 10 cases (71.4%), focally positive in 2 cases (14.3%) and negative in 2 cases (14.3%, Figure 2D). Among the TROP2 diffuse positive cases, 3 cases (30%) originated from the lung, 2 cases (20%) each from the bladder and colorectum and 1 case (10%) each from the hypopharynx, kidney and ovary. For the focal TROP2 positive cases, both originated from colorectal primaries (100%). Among the TROP2-negative cases, 1 case (50%) originated from the colorectum and 1 case (50%) from the thyroid (Figure 2E).

The distribution of TROP2 expression by pathologic diagnosis showed a pattern similar to that of brain metastatic lesions, with adenocarcinoma being the most common tumor type. In adenocarcinomas, TROP2 expression was diffusely positive in 4 cases (57.1%), focally positive in 2 cases (28.6%) and negative in 1 case (14.3%). All cases of squamous cell carcinoma, urothelial carcinoma, clear cell carcinoma and high-grade serous carcinoma demonstrated diffuse TROP2 positivity, while follicular carcinoma was TROP2-negative. Detailed TROP2 expression according to tumor origin and pathologic diagnosis for both brain metastatic lesions and primary tumors are provided in (Supplementary Tables 1 and 2) and as well as shown in Figure 2A-2E.

Differences in TROP2 expression based on clinical characteristics

We analyzed whether differences in TROP2 expression were associated with characteristics of CNS metastases or patient survival. Patients were categorized into two groups based on the presentation of CNS metastases at the time of diagnosis: Single vs. multiple metastases. When stratified by TROP2 expression levels, the distribution was as follows: Among patients with diffuse positive expression, 21 had single CNS metastasis and 16 had multiple metastases. In the focal positive group, 8 had single CNS metastasis and 2 had multiple metastases. Among patients with negative expression, 7 had single CNS metastasis and 6 had multiple metastases. Fisher’s exact test did not reveal a significant association (p=0.454).

The median survival post-CNS metastasis was: Diffuse positive, 76.4 months (95% CI: 46.8-NA); focal positive, 18.5 months (95% CI: 13.5-NA); and negative, 43.0 months (95% CI: 19.0-NA). The log-rank test again showed no significant differences (p=0.218). HRs were 2.93 (95% CI: 0.72-11.94, p=0.134) for focal positive relative to diffuse positive and 1.97 (95% CI: 0.64-6.08, p=0.237) for negative relative to diffuse positive as shown in Figure 3.

Figure 3: Kaplan–Meier analysis for post-CNS survival stratified by TROP2 expression levels.

Comparison of TROP2 Expression in paired primary and brain metastatic tumor

Among the 14 cases where both primary tumors and corresponding brain metastases were available for paired TROP2 expression analysis, three cases (21.4%) showed differences in TROP2 expression between the primary and metastatic sites (Figure 4, Supplementary Table 3). Specifically, in colorectal adenocarcinoma, one case shifted from diffuse positive in the primary lesion to focal positive in the metastasis and another case showed negative expression in the primary lesion but focal positivity in the metastasis. Additionally, a case of kidney clear cell carcinoma exhibited diffuse positive TROP2 expression in the primary tumor but was negative in the brain metastasis. The remaining 11 cases (78.6%) displayed consistent TROP2 expression patterns between the primary and metastatic lesions Supplementary Table 3 and as shown in Figure 4.

Figure 4: Sankey diagram illustrating the flow of TROP2 expression between primary and metastatic tumors.

This study provides important insights into the TROP2 expression in brain metastases across various primary tumor origins. Notably, the high prevalence of diffuse TROP2 positivity (62.3%) in brain metastases, particularly those originating from lung and breast cancers, highlights the potential role of TROP2 in the pathogenesis and progression of CNS metastasis.

Anti-cancer therapies targeting TROP2 have predominantly focused on the development of ADC. A representative TROP2 ADC, Sacituzumab Govitecan (SG), consists of a TROP2-targeting antibody linked to the topoisomerase I inhibitor SN-38 via a cleavable linker, with a drug-antibody ratio of 1:8, demonstrating potent anti-cancer effects [16]. In the ASCENT phase 3 clinical trial, SG significantly improved median progression-free survival (mPFS; HR 0.41, 95% CI 0.32-0.52, P<0.001) and median overall survival (mOS; HR 0.48, 95% CI 0.38-0.59, P<0.001) in patients with advanced TNBC, leading to FDA approval. In the TROPiCS-02 trial, targeting HR+/HER2- breast cancer, SG also demonstrated a significant mOS benefit compared to the control group (HR 0.79, 95% CI 0.65-0.96, P=0.020) [17]. Additionally, SG has shown therapeutic potential in minor cancer types, such as endometrial cancer, small cell lung cancer and castration-resistant prostate cancer [18]. Based on these findings, numerous combination therapy clinical trials are currently underway [19].

Datopotamab Deruxtecan (Dato-DXd) is another ADC that combines a TROP2 antibody with DXd, featuring a drug-to-antibody ratio of 1:4 [20]. In HR+/HER2- breast cancer, it demonstrated a significant improvement in mPFS compared to the control group (HR 0.63, 95% CI 0.52-0.76, P<.0001) [21]. In a phase 3 clinical trial for patients with advanced NSCLC, it also showed a significant mPFS benefit over docetaxel (HR 0.75, 95% CI 0.62-0.91, P=.004) [22]. Promising results have recently been reported in endometrial and ovarian cancer cohorts [23]. Additionally, other TROP2-targeting ADCs, such as SKB264, SHR-A1921 and LCB84, are undergoing early clinical trials based on encouraging preclinical data [24-26].

Preclinical studies suggest a potential correlation between TROP2 expression and the efficacy of ADCs. In breast cancer cell lines, increased TROP2 expression was associated with enhanced therapeutic activity of SG [27]. Similarly, clinical trials targeting TNBC demonstrated the greatest efficacy in patients with medium to high TROP2 expression, with objective response rates of 44%, 38% and 22% for high, medium and low expression levels, respectively [28]. However, clinical data across various cancer types remain limited and due to the bystander effect of ADCs and the heterogeneity of TROP2 expression, definitive conclusions cannot yet be drawn.

As cancer survival improves, recurrent CNS metastases following local treatment have become increasingly common, highlighting the need for effective systemic therapies. In cancers with high rates of brain metastases, such as breast and lung cancer, clinical trials now frequently include CNS-specific endpoints. Systemic treatment for CNS metastases remains challenging due to the BBB. While small molecules like TKIs have demonstrated CNS efficacy [29,30], larger agents like SG (160 kDa) face limited BBB penetration [31]. However, local BBB disruptions from metastases or radiotherapy may enable larger molecules to access CNS lesions, making target expression a critical determinant of efficacy. Our study supports this concept, with 78.7% of 61 brain metastases exhibiting diffuse or focal TROP2 expression. Consistency in TROP2 expression between primary and CNS lesions was observed in 78.6% of matched cases. These findings suggest a potential association between TROP2 expression and the efficacy of anti-TROP2 ADCs in CNS metastases, warranting further investigation.

This study represents the largest cohort of brain metastases evaluated for TROP2 expression using standardized IHC. All staining was performed in a single center, with a single pathologist ensuring consistency and the analysis was blinded to treatment data to minimize bias. Previous studies evaluating TROP2 expression in various cancers, including breast [3,32,33], colorectal [4,5], skin [8,34] and pancreas [9], primarily used semi-quantitative assessment methods such as H-score to evaluate TROP2 expression levels. These studies often relied on specific scoring thresholds to categorize TROP2 expression. In contrast, our study demonstrated a relatively clear differentiation of TROP2 expression into diffuse, focal and negative patterns, allowing for straightforward analysis without the need for further intensity or area-based categorization. It is important to note that factors such as the type of antibody used and the application of Tissue Microarrays (TMAs) may have influenced the observed TROP2 expression patterns. While TMAs are valuable for high-throughput analysis, they may not fully capture the tumor heterogeneity present in whole-tumor sections. Therefore, future studies examining cases with changes in TROP2 expression between primary and metastatic lesions, or those showing focal positivity, would benefit from evaluating TROP2 expression using whole-slide sections to better reflect the full spectrum of tumor heterogeneity. Comprehensive clinical data enabled robust correlations with TROP2 expression. However, the inclusion of diverse tumor types limited subgroup analyses and the lack of data from visceral metastases prevents conclusions about the specificity of TROP2 expression to CNS lesions. Furthermore, as samples were collected before TROP2 ADCs became available, intracranial efficacy based on TROP2 expression could not be assessed. Further studies are required to validate these findings.

In conclusion, this study demonstrated variable TROP2 expression in 61 brain metastasis samples and confirmed high consistency of TROP2 expression between primary and brain metastatic lesions. While promising, further research is required to validate the clinical efficacy of anti-TROP2 therapies in patients with CNS metastases.

Ethics Approval and Consent to Participants

The study protocol was approved by the institutional reEthics Approval and Consent to Participants The study protocol was approved by the institutional review board of each site, including Korea University Anam Hospital (No. 2024AN0580).

Competing Interest

 The authors have no conflict of interest in the study.

Funding

 No funding was received for this study.

Author Contributions

 The concept of the study was designed by JWK. JWL, JHK, SHL, YJC and KHP. JS and HO collected data for the study. YNS and JWK analyzed and visualized the data. YNS and JWK drafted the manuscript. All the authors have reviewed and approved the submitted data.

 Data Availability

 The dataset generated and/or analyzed during this study is available from the corresponding author upon reasonable request.view board of each site, including Korea University Anam Hospital (No. 2024AN0580).

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