Research ArticleClinical Studies

Mesonephric-like Adenocarcinoma of the Uterine Corpus: Comparison Between Mismatch Repair Protein Immunostaining and Microsatellite Instability Testing

HYUNJIN KIM and HYUN-SOO KIM
Anticancer Research April 2023, 43 (4) 1785-1795; DOI: https://doi.org/10.21873/anticanres.16332

Abstract

Background/Aim: The utility of mismatch repair (MMR) immunohistochemistry (IHC) and microsatellite instability (MSI) testing in uterine mesonephric-like adenocarcinoma (MLA) has seldom been reported. This study aimed to compare MMR IHC and MSI testing in uterine MLA. Patients and Methods: We analyzed the MMR protein expression of 25 patients with MLA and compared the results with the MSI status. Results: Of the cases, one (4.0%) was initially interpreted to have a loss of mutS homolog 2 (MSH2) and mutS homolog 6 (MSH6) expression, and eight (32.0%) to have a loss of MSH6 immunoreactivity. Upon re-evaluation of the slides and repeat IHC, all cases were revealed to demonstrate at least focal (5-20%) immunoreactivity for MSH2 or MSH6. MSI testing revealed all cases to be microsatellite stable (MSS). Conclusion: Uterine MLA is an MSS/MMR-proficient tumor. We observed complete concordance between MMR IHC and MSI testing. MMR IHC should be carefully interpreted, and discordant cases must be thoroughly reviewed. Repeat IHC and confirmatory MSI testing may be beneficial in resolving uncertain cases.

Key Words:

Endometrial carcinoma (EC) is a common malignancy of the female genital tract (1-6), with rising incidence and associated disease mortality. Most patients are diagnosed with EC early, which may be treated by surgery with or without adjuvant treatment (7, 8). Approximately 75% of patients with early-stage EC survive longer than five years. However, 10-20% of these patients will subsequently develop recurrence, often in distant sites (9). The prognosis of patients with advanced, recurrent, or metastatic EC remains unfavorable (10). The vast majority of cancer-related deaths is attributed to the failure to control recurrences and metastases (11).

Microsatellite instability (MSI) is caused by mismatch repair deficiency (MMRd), leading to the accumulation of mismatches, insertions, and deletions in repeated sequences (12). MMRd arises in the early stages of tumorigenesis (11). Approximately 30% of sporadic ECs arise from the MSI pathway (13). Therefore, a universal test for MSI is recommended for patients with EC to aid in the assessment of prognoses and determination of optimal treatments (14). Immunohistochemistry (IHC) is the standard method used to detect the loss of MMR protein expression in screening MMRd cases (12, 15, 16). Another standard yet less frequently used method is the polymerase chain reaction (PCR)-based MSI testing, which consists of a variable range of microsatellite markers, including the mononucleotide markers BAT-25 and BAT-26 as a minimum. MSI testing is a common alternative to MMR IHC, especially in cases with questionable IHC results (14, 17-20). The identification of MSI status is clinically important because MMRd in EC is predictive of the response to immune checkpoint inhibitors. According to the molecular classification of EC (21-23), the MSI status may be utilized to predict better prognosis and guide the choice of adjuvant therapy.

Mesonephric adenocarcinoma (MA) is a rare gynecological malignancy (24). It is typically located in the uterine cervix and vagina; however, several cases of malignant mesonephric lesions arising from the uterine corpus and ovary have been reported in the literature (25). MA originating from the upper female genital tract has been referred to as mesonephric-like adenocarcinoma (MLA) because of its nearly identical morphological and immunophenotypical features to MA (25). MLA of the uterine corpus was described in the 2020 World Health Organization (WHO) Classification of Female Genital Tumors (26). Uterine MLA has been shown to exhibit a more aggressive behavior and worse prognosis than other EC types (27-42).

MMR IHC and MSI testing are equally valid tools to screen MMRd in EC, and one or both may be used (43). However, few studies on MMRd screening have been reported in uterine MLA. Although MMR IHC and MSI testing yield highly concordant results in EC, it is unclear whether this holds true in uterine MLA. In this study, we aimed to compare MMR IHC and MSI status in uterine MLA and investigate the clinicopathological and prognostic significance of reduced mutS homolog 6 (MSH6) expression observed in a subset of cases.

Patients and Methods

Case selection and clinicopathological data collection. This study was approved by the Institutional Review Board of Samsung Medical Center (approval code: 2021-06-190; date of approval: July 7, 2021). Figure 1 shows the flowchart of this study. The pathology database was queried for uterine MLA cases, with the following inclusion criteria: (a) pathologically confirmed malignant mesonephric lesions and (b) tumor epicenter within the myometrium of the uterine corpus. The diagnosis of uterine MLA was established on the following histological, immunohistochemical, and molecular characteristics: (a) proliferation of small, closely packed, back-to-back tubules containing eosinophilic intraluminal secretions (Figure 2A); (b) diverse architectural patterns (Figure 2B; e.g., ductal, papillary, solid, spindle, retiform, glomeruloid, sieve-like, sex cord-like, comedonecrosis-like); and (c) either immunophenotypical (positive immunoreactivity for at least one of the mesonephric markers, including GATA-binding protein 3, transcription termination factor 1, cluster of differentiation 10, paired box 2, calretinin, and negative or focal positivity for hormone receptors) or molecular (pathogenic Kirsten rat sarcoma viral oncogene homolog mutation) confirmation (24, 25, 33, 42). We found 47 cases of malignant mesonephric lesions. Two tumors were in the uterine cervix, five in the ovary, and 40 in the uterine corpus. The following clinical and pathological information were obtained from the electronic medical records and pathology reports for each patient: age at initial diagnosis, initial International Federation of Gynecology and Obstetrics (FIGO) stage (44), initial treatment, post-operative treatment, lung metastasis, post-treatment recurrence, survival status, recurrence-free survival (RFS), overall survival (OS), and initial interpretation of MMR protein results. For each case, the most representative block was selected to perform PCR-based MSI testing and next-generation sequencing (NGS).

Figure 1.
Figure 1.

Study flowchart. IHC: Immunohistochemistry; MA: mesonephric adenocarcinoma; MLA: mesonephric-like adenocarcinoma; MMR: mismatch repair; MMRd: mismatch repair-deficient; MMRp: mismatch repair-proficient; MSI: microsatellite instability; MSS: microsatellite stable; NGS: next-generation sequencing; PCR: polymerase chain reaction.

Figure 2.
Figure 2.

Histological features and proficient mismatch repair protein expression in uterine mesonephric-like adenocarcinoma (MLA). (A and B) Characteristic histological features of uterine MLA: (A) Proliferation of compactly aggregated small tubules possessing densely eosinophilic intraluminal secretions and (B) architectural diversity. (C-F) Preserved nuclear immunoreactivities for (C) MLH1, (D) MSH2, (E) MSH6, and (F) PMS2. Original magnification: A, 100×; B, 20×; C-F, 100×.

Review of the immunostained slides. Two experienced gynecological pathologists (H.K. and H.-S.K.) reviewed the MMR-immunostained slides. We used primary antibodies against mutL homolog 1 (MLH1; prediluted, clone M1, Ventana Medical Systems, Roche, Oro Valley, AZ, USA), post-meiotic segregation increased, Saccharomyces cerevisiae 2 (PMS2; dilution 1:20, clone MRQ-28, Cell Marque, Rocklin, CA, USA), mutS homolog 2 (MSH2; dilution 1:500, clone G219-1129, Cell Marque), and MSH6 (dilution 1:500, clone 44/MSH6, BD Biosciences, Franklin Lakes, NJ, USA). The slides were evaluated and separated into three categories: preserved, loss, and subclonal loss of protein expression (45, 46). The loss of one or more MMR proteins was defined as MMRd, and preserved expression of all four MMR proteins was defined as mismatch repair-proficient (MMRp). Loss of protein immunoreactivity was classified as completely absent nuclear staining (0%) in the tumor cells with appropriate internal control staining (positive nuclear expression in the stromal non-neoplastic cells or lymphocytes) (12). Subclonal loss of expression was defined as abrupt regional loss of protein expression with intervening stromal positivity in the regions of absent tumor cell staining (46).

PCR-based MSI testing. MSI status was determined using multiplex PCR to amplify five quasi-monomorphic mononucleotide repeat markers (BAT-25, BAT-26, NR-21, NR-24, and NR-27) (47-50). Genomic DNA was isolated from the formalin-fixed, paraffin-embedded (FFPE) tumor tissue sections using QIAamp DNA Mini Kit (Qiagen, Hilden, Germany). Sense primers were labeled with fluorescent dyes. Amplicons were analyzed using an ABI PRISM 3130 Genetic Analyzer (Applied Biosystems, Foster City, CA, USA). Allelic sizes were estimated using GeneMapper Software v4.1 (Applied Biosystems). Tumors with allelic size variation in 0, 1, and ≥2 microsatellites were classified as microsatellite stable (MSS), MSI-low (MSI-L), and MSI-high (MSI-H), respectively.

NGS. Five-micrometer-thick FFPE tumor tissue sections were deparaffinized and hydrated through alcohol solutions with decreasing concentration gradients. The sections were manually microdissected using an ethanol-dipped scalpel point. The scraped material was washed in phosphate-buffered saline and digested in proteinase K overnight at 56°C in Buffer ATL (Qiagen). DNA was then isolated using a QIAamp DSP DNA FFPE Tissue Kit (Qiagen) (51). A Qubit 4 Fluorometer (Thermo Fisher Scientific, Waltham, MA, USA) was used for sample quantitation. The NGS library was prepared using extracted DNA and Ion AmpliSeq Library Preparation on the Ion Chef System (Thermo Fisher Scientific). Sequencing was performed on the Ion Torrent S5 XL platform, using an Oncomine Comprehensive Assay v3 (Thermo Fisher Scientific), an amplicon-based, targeted assay that enables the detection of relevant single-nucleotide variants, amplifications, gene fusions, and indels from 161 cancer-related genes. Genomic data were analyzed, and alterations were detected using Ion Reporter Software v5.6 (Thermo Fisher Scientific). We also reviewed the variant call format file and Integrative Genomics Viewer (Broad Institute, Cambridge, MA, USA). Only variants in coding regions, promoter regions, or splice variants were retained.

Statistical analysis. Fisher’s exact test or linear-by-linear association test was performed to examine whether MSH6 expression status was associated with clinicopathological characteristics of patients with uterine MLA. Univariate analysis with log-rank test and Kaplan–Meier plots was performed to examine the prognostic significance of reduced MSH6 expression. Statistical analyses were performed using IBM SPSS Statistics for Windows v23.0 (IBM Corporation, Armonk, NY, USA). Statistical significance was defined as a p-value <0.05.

Results

Baseline clinicopathological characteristics. We excluded nine cases in which both MMR IHC and MSI testing could not be performed and six patients whose MSI statuses were not available. Consequently, 25 patients with uterine MLA were included in this study. As shown in Table I, the mean age of the patients was 61 years (range=46-77 years). The initial FIGO stages were distributed as follows: stage IA (3/25; 12.0%), IB (1/25; 4.0%), II (3/25; 12.0%), IIIB (3/25; 12.0%), IIIC (4/25; 16.0%), IVA (1/25; 4.0%), and IVB (10/25; 40.0%). All, except two patients, (92.0%) underwent surgery as the initial treatment. Twenty-one patients (84.0%) received post-operative treatment including chemotherapy (10/25; 40.0%), concurrent chemoradiation (6/25; 24.0%), and radiation therapy (5/25; 25.0%). Fourteen patients (56.0%) experienced metastases to the lungs. Follow-up information was available in all except one patient who was lost to follow-up. Post-treatment recurrences were detected in 18 patients (72.0%). Nine patients (36.0%) died during the follow-up period. Median RFS and OS period were 10.2 (range=0.8-53.1 months) and 19.4 (range=4.6-93.8 months) months, respectively.

View this table:
Table I.

Baseline clinicopathological characteristics.

MMR IHC. Table II shows that 16 cases were confirmed to be MMRp tumors, exhibiting diffuse and strong nuclear immunoreactivities (i.e., preserved expression) in all four MMR proteins (Figure 2C-F). The staining proportion ranges for MLH1, PMS2, MSH6, and MSH2 were 90-100%, 90-100%, 95-100%, and 80-100%, respectively. Of the remaining nine cases, one (case 12) was initially interpreted to have a loss of MSH2 and MSH6 expression, and eight cases (cases 4, 7, 8, 10, 13, 17, 18, and 25) were diagnosed with MMRd tumors based on the initial interpretation of MSH6 as loss of expression. We reviewed the MMR-immunostained slides obtained from these nine patients. Five of the nine cases (cases 4, 8, 12, 17, and 18) showed adequate staining quality and exhibited uniform immunoreactivity for MMR proteins with moderate-to-strong intensity in the stromal cells and lymphocytes (internal positive control). The slide review of these cases revealed that some tumor cells at the tumor periphery displayed weak nuclear expression for MSH2 or MSH6 expression (Figure 3A-D), even though the majority of tumor cells were negative for these proteins. The staining proportion ranged from 5-20%, put differently, at least 5% of the tumor cells exhibited nuclear immunoreactivity in these five cases. In contrast, the remaining four cases (cases 7, 10, 13, and 25) had negative internal control staining. Repeat IHC for MSH6 was conducted using the same FFPE blocks in two cases (cases 7 and 25) and alternative blocks in the others (cases 10 and 13). Repeat staining in the four cases revealed low but preserved MSH6 expression (staining proportion range=5-25%), rendering a different interpretation. MLH1 and PMS2 were expressed in all nine cases (staining proportion range: 80-100% and 90-100%, respectively). Consequently, we found that the nine cases showing low but preserved MMR protein expression (i.e., MMRp tumors) were initially misinterpreted as MMRd tumors and none of the cases exhibited a subclonal loss of MMR protein expression.

View this table:
Table II.

Results of mismatch repair (MMR) immunohistochemistry (IHC), microsatellite instability (MSI) testing, and next-generation sequencing (NGS).

Figure 3.
Figure 3.

Reduced mismatch repair (MMR) protein expression in the uterine mesonephric-like adenocarcinoma. (A and B) Case 12 in which the initial MMR immunostaining was interpreted as loss of expression for (A) MSH2 and (B) MSH6; however, a slide review revealed preserved expression of both proteins. (C and D) Cases in which MSH6 immunostaining was initially interpreted as loss of expression, but a slide review revealed focal nuclear immunoreactivity for MSH6 at the periphery of the tumor. Original magnification: A-D, 100×.

Results of MSI testing and NGS. All 25 cases showed MSS using PCR (Table II). There was 100% concordance between the reviewed results of MMR IHC and MSI testing. No pathogenic mutation in MMR genes was detected using NGS.

Clinicopathological and prognostic significance of reduced MSH6 expression in uterine MLA. We noted that nine tumors (36.0%) exhibited preserved but significantly reduced nuclear MSH6 immunoreactivity, with a variable staining proportion range of 5-20%. We conducted statistical analyses to investigate whether reduced MSH6 expression was associated with clinicopathological characteristics and outcomes of patients with uterine MLA. However, no significant relationship was observed between reduced MSH6 expression and clinicopathological characteristics of uterine MLA, including patients’ age (p=0.688), initial FIGO stage (p=0.355), type of post-operative treatment (p=0.967), lung metastasis (p=0.678), and post-operative recurrence (p=0.635) (Table III). There was no significant difference in RFS (p=0.432) and OS (p=0.660) in patients with uterine MLA according to MSH6 expression status.

View this table:
Table III.

Relationship between mutS homolog 6 (MSH6) expression status and clinicopathological characteristics and outcomes.

Discussion

Patients with MSI-H/MMRd metastatic EC have recently gained approval for the use of pembrolizumab, a programmed cell death 1 inhibitor, after a failure of first-line chemotherapy (52). In those with EC that are not MSI-H/MMRd, a combination of lenvatinib, an oral multikinase inhibitor, and pembrolizumab have been approved for use if disease progression occurred following a prior platinum-based systemic therapy (53, 54). The paradigm shift in treatment options for MSS/MMRp advanced or recurrent EC patients was based on the 36% objective response rate and 16.4 months median OS in the combination therapy of lenvatinib plus pembrolizumab, with possible improvement of patient tolerance and quality of life, as compared to monotherapy with pembrolizumab (53). In this regard, MSI status is an important pathological parameter to determine combination therapy with lenvatinib as the second-line therapy of patients with advanced or recurrent EC.

The current WHO Classification designates uterine MLA as a rare histological type of EC (55). However, few studies have analyzed the frequency of MMRd, or the results and concordance of MMR IHC and MSI testing in uterine MLA. In this study, all 25 patients were eventually classified under MSS/MMRp uterine MLA. The initial MMR IHC interpretation and MSI testing results were conflicting in nine of the 25 cases. However, a thorough re-evaluation of the slides and repeat IHC showed that all nine cases had preserved MMR protein expression, although the staining proportion was low. Furthermore, we also demonstrated that all 25 cases of uterine MLA exhibited MSS using PCR-based MSI testing and that they did not harbor any pathogenic mutation in the MMR genes. Taken together, these results indicate that uterine MLA is an MSS/MMRp tumor, and that patients with recurrent or metastatic MLA can be treated with lenvatinib and pembrolizumab combination therapy. MSI status and MMR protein expression should be accurately evaluated for proper treatment of uterine MLA, as it has very aggressive biological behavior and high metastatic capability. In our case series, all except two patients experienced recurrence, metastasis, or both.

We further scrutinized the nine cases misinterpreted as having MMRd tumors during the initial diagnostic process. The immunostained slides of the nine cases, in which loss of expression of MSH2 and MSH6 was interpreted in one case and MSH6 in eight cases, were re-evaluated. In four of the nine cases, the internal control was not adequately stained, thus repeat IHC was performed. Although the cut-off criteria for loss of MMR protein expression vary among previous literature, a thorough investigation of this persistent issue was performed by Guyot D’Asnieres De Salins et al. (56). Therein, they analyzed 2,143 colorectal carcinoma cases to reach a final conclusion that 100% loss of nuclear expression should be observed to interpret MMRd. Concurring with their conclusion, we used a cut-off staining proportion of 0%; if any of the tumor cells expressed the protein and the internal control was properly stained, then the interpretation would be ‘preserved’ (56). We observed that in all nine cases, the four MMR proteins were expressed in at least 5% of tumor cells, with variable staining intensities. When interpreting MMR IHC, pathologists should scrutinize the entire slide before reporting them as ‘loss’ of expression. Some tumors may stain heterogeneously with areas that are negative and others with intense positivity. Considering the possibility of staining heterogeneity, repeat IHC may be prudent. It can also be beneficial to perform staining on preoperative biopsy or curettage specimens.

To date, no study has discussed the decrease in MSH2 and MSH6 expression in uterine MLA. Although we did not clarify the mechanism of reduced immunoreactivities for MMR proteins, we have speculated some possible reasons. First, technical problems including pre-analytic (tissue ischemia, fixation, age of the FFPE blocks) and analytic (staining artifacts due to fixation gradients, edge effect, chromogen draping, antibody specificity) factors can affect the performance of IHC. Second, poor fixation is a common problem in MMR IHC. It is of utmost importance that well-fixed areas are examined when reporting MMR IHC to avoid erroneous interpretation of one or more proteins as loss of expression. Third, we cannot exclude the possibility that the reduced MSH6 expression observed in eight of the 25 cases indicate a subset of uterine MLA with MSH6 deficiency. To the best of our knowledge, aberrant MSH6 expression has not been reported in uterine MLA. Furthermore, all cases were confirmed as MSS using the MSI test. Any pathogenic mutation was not identified in the MMR genes in NGS. Thus, we concluded that reduced MSH6 expression was not a distinguishing feature of the MLA immunophenotype. Furthermore, because the MSH6 expression status did not show any significant clinicopathological and prognostic significance in statistical analysis, we cannot assign any clinical relevance to this unusual observation.

Conversely, very weak or very focal expression of MMR proteins can be noted in a small subset of MMRd EC cases. Since the expression of MMR proteins is generally strong and diffuse, any deviation from this including weak or focal staining deserves attention. Repeat IHC on a different block or a biopsy specimen can resolve some of these problems. Co-testing with MSI test or NGS may also be an effective diagnostic strategy to confirm any genetic abnormalities.

This study had some limitations. First, there was no standardized cut-off value to determine the loss of protein expression when interpreting MMR IHC in both EC and uterine MLA. Second, we could not clarify the mechanism of reduced MSH6 and MSH2 expression in uterine MLA. Further investigations are warranted to explore the molecular mechanisms underlying the alterations of MMR protein expression in uterine MLA. Third, we did not analyze the therapeutic effects of pembrolizumab or pembrolizumab plus lenvatinib combination therapy in our patients, which would highlight the importance of differentiating the MSI status in uterine MLAs. Future studies into the clinical course and follow-up information of patients treated with pembrolizumab or dual therapy are warranted.

In conclusion, we investigated the immunohistochemical expression status of MMR proteins and MSI status in 25 patients with uterine MLA. We confirmed that uterine MLA is an MSS/MMRd tumor. Although there were several cases showing the discrepancies in MMR IHC interpretation between initial diagnosis and slide review, a thorough reevaluation and repeat staining led to a final consensus. In this study, low-staining levels of at least one MMR protein were observed in 36.0% of the cases. When very weak or localized immunoreactivity is observed, positive tumor cells should be meticulously examined, and the results should be cross-checked with MSI testing. Furthermore, we noted complete concordance between MMR IHC and MSI testing. Considering that the treatment of patients with advanced or recurrent uterine MLA may differ depending on the MSI status, MMR IHC requires careful interpretation in uterine MLA. Discordant cases must be thoroughly reviewed. Repeat IHC and cross-checking with MSI testing is beneficial in resolving challenging cases.

Footnotes

  • Authors’ Contributions

    All Authors made substantial contributions to the conceptualization and design of the study; acquisition, interpretation, and validation of the data; drafting and critical revision of the article; and have given their approval to the final version to be published.

  • Conflicts of Interest

    The Authors have no conflicts of interest or financial ties to declare.

  • Received January 11, 2023.
  • Revision received January 19, 2023.
  • Accepted January 20, 2023.

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Mesonephric-like Adenocarcinoma of the Uterine Corpus: Comparison Between Mismatch Repair Protein Immunostaining and Microsatellite Instability Testing
HYUNJIN KIM, HYUN-SOO KIM
Anticancer Research Apr 2023, 43 (4) 1785-1795; DOI: 10.21873/anticanres.16332
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