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structured_reporting_and_molecular_integration_in_acc

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Structured Reporting and Molecular Integration in ACC

Immunohistochemistry and Molecular Pathology

Structured reporting and molecular integration in adrenocortical carcinoma (ACC) refers to the standardized pathology description of tumor morphology, extent, and validated prognostic features together with selected immunohistochemical and molecular findings that may refine diagnosis or risk assessment.1 Within ACC care, this approach sits at the interface of surgical pathology and molecular pathology and supports downstream staging, multidisciplinary prognostic assessment, and research classification.

In current practice, the most established components remain conventional histopathology and structured reporting of factors such as tumor extent, capsular and vascular invasion, necrosis, mitotic activity, margin status, nodal involvement, pathologic stage, and Ki-67 proliferative index.21 Immunohistochemical markers are primarily used to support adrenocortical lineage in difficult cases, while broader molecular assays have been studied mainly as adjuncts for differential diagnosis or prognostic stratification rather than as stand-alone diagnostic tools.3456

The evidence base is uneven. Structured reporting recommendations are supported by expert consensus and clinicopathologic experience, but many proposed molecular biomarkers in ACC derive from retrospective single-center series, small cohorts, isolated case reports, or pan-cancer bioinformatic analyses without robust ACC-specific validation.1789 As a result, many reported molecular associations may reflect biologic heterogeneity without yet demonstrating reproducible incremental value over established pathology variables in routine management.

Diagnostic context

ACC is a rare endocrine malignancy in which pathology reporting has unusual clinical importance because postoperative risk assessment and adjuvant decision-making often depend on the combined weight of several adverse features rather than any single defining test.1 Structured datasets are intended to reduce variability in how these features are captured across institutions, improving completeness and comparability in a disease where much of the clinical literature is retrospective and multicenter aggregation is often necessary.1

This is one of the more reliable advances in the field: standardization improves communication and data quality even when it does not introduce new biologic markers. The practical implication is that a complete structured report remains more dependable for routine care than an unstandardized expansion of optional molecular findings.1

Core structured reporting elements

The ICCR dataset provides the clearest framework for ACC resection reporting and emphasizes documentation of tumor size and extent, invasion patterns, necrosis, mitotic activity, resection margins, lymph node status, pathologic stage, and Ki-67 index.1 These elements align with the clinicopathologic variables that currently carry the strongest relevance for prognosis and multidisciplinary management.21

Among biologically informed measurements, Ki-67 has the most established role in routine ACC workflows and is already integrated into reporting and treatment discussions.21 However, Ki-67 assessment may be limited by intratumoral heterogeneity and technical variation in hotspot selection and counting, which has motivated digital image-analysis approaches to improve reproducibility.2 The practical message is that careful standardization of an already accepted marker may currently offer more clinical value than adding multiple exploratory biomarkers.

From these core reporting elements, molecular integration is most relevant when pathology must answer a specific diagnostic or biologic question.

Immunohistochemical and molecular diagnostic integration

Confirming adrenocortical lineage

A well-established use of immunohistochemistry in ACC is confirmation of adrenocortical origin when morphology is ambiguous. Earlier work with D11 and subsequent studies of SF-1 showed that these markers may help distinguish adrenocortical tumors from pheochromocytoma, metastatic carcinoma, and other adrenal-region mimics.34

This application is more reliable than most newer molecular proposals because it addresses a focused differential-diagnostic problem. Its limitation is that lineage confirmation does not establish malignancy; clinically, it narrows the diagnostic field rather than replacing histologic assessment of carcinoma.34

Distinguishing adenoma from carcinoma

Molecular adjuncts have also been studied for separating adrenocortical adenoma from carcinoma, particularly in borderline or diagnostically challenging tumors. Retrospective data suggest that ACC tends to show a greater burden of chromosomal copy-number alterations than adenoma, and KIAA0101 overexpression has shown discriminatory potential in tissue-based series.56 By contrast, some biologically plausible markers, such as components of the adrenomedullin pathway, have not clearly separated malignant from benign adrenocortical tumors.10

The reliable conclusion is that molecular differences between adenoma and carcinoma exist and may be detectable in selected settings. The less reliable conclusion is that any single assay has sufficient validation to supplant established morphologic systems, so these tests remain supplemental rather than routine stand-alone solutions.56

Unusual phenotypes and rare presentations

Integrated immunohistochemical and molecular approaches may also help characterize uncommon ACC phenotypes, including oncocytic tumors or unusual hormone production.11 Historical and isolated reports also suggest that rare molecular alterations may illuminate mechanisms of tumorigenesis in individual cases, but these observations are mainly hypothesis-generating because they derive from single cases or very small numbers.1211

The practical implication is that such findings may be informative for case interpretation and research classification, but they have limited generalizability for routine reporting standards.

Molecular patterns and prognostic signals

Beyond diagnosis, the molecular literature in ACC is dominated by candidate prognostic markers. Recurrent abnormalities involving loci or regulators such as ACTHR, GATA-family factors, and TERT support the view that ACC is biologically heterogeneous and that some tumors may acquire molecular features associated with aggressive behavior.131415 These findings are biologically plausible, but most are not standardized for routine pathology reporting.

A larger body of work reports associations between outcomes and expression of markers linked to proliferation, chromatin regulation, RNA processing, membrane trafficking, and developmental signaling, including FSCN1, FOXM1, HOXC11, YAP1, MSH6, HMGA1, DDX1, YKT6, B56ε, RPN1, ADRA2C, DHX34, and DDX39.161718192021222324252627 Other markers, including AR, MEIS1, STEAP1, PDCD10, SPAG6, and DR3, show context-dependent or internally complex relationships with stage or survival, underscoring that directionality and biologic interpretation are not always consistent across datasets.72829303132

What is reasonably reliable is the broader pattern: ACC shows measurable molecular heterogeneity, and many molecular readouts correlate with prognosis in retrospective data. What remains less reliable is whether any one of these markers adds enough reproducible information beyond stage, invasion, margins, necrosis, mitotic activity, and Ki-67 to justify universal incorporation into standard pathology templates.21

Evidence limitations and interpretation pitfalls

The main limitations in this field arise from study design and disease rarity. Much of the literature is based on retrospective cohorts, heterogeneous tissue processing, variable scoring thresholds, small discovery sets, or pan-cancer computational analyses that include ACC only as a minor subgroup.78923 These constraints make external validation difficult and may overstate apparent biomarker performance.

Accordingly, prognostic association should not be equated with clinical utility. A marker may correlate with survival, immune signatures, or mutational features without demonstrating that it improves diagnosis, changes treatment selection, or outperforms established clinicopathologic assessment in real-world ACC care.892426 The practical implication is that most molecular findings should be interpreted as supportive or investigational unless they answer a narrowly defined diagnostic question.

Role in management and research

In current clinical practice, structured reporting has a clearer and more established role than broad molecular integration. Standardized pathology datasets improve communication of the adverse features that inform prognosis estimation, postoperative surveillance planning, and discussion of adjuvant or investigational strategies.21

Molecular integration currently has its strongest roles in confirming cortical lineage, assisting selected difficult differentials, and organizing biologic research rather than replacing standard pathology workflows.345 Future progress will likely depend on ACC-specific validation studies that demonstrate analytical reproducibility and clinically meaningful incremental value, ideally allowing successful markers to be incorporated into standardized reporting frameworks rather than remaining isolated research observations.1

Included Articles

  • PMID 2114700: This study reports that monoclonal antibody D11 showed strong nuclear with variable cytoplasmic staining in benign and malignant adrenocortical tumors, while adrenomedullary lesions and most examined non-cortical mimics were negative. D11 immunocytochemistry helped distinguish cortical tumors from pheochromocytoma and adrenal metastases, including renal carcinoma.3
  • PMID 7629233: This study reports that Ad4BP, also known as SF-1, shows nuclear expression in more than 90% of examined adrenocortical carcinoma cells, including poorly differentiated and bizarre-nuclei tumor cells, while remaining restricted to adrenocortical parenchymal elements rather than medulla or capsule.4
  • PMID 8640304: This study reports constitutive SCP2 mRNA expression across human adrenocortical tissues, with relatively lower expression in two of three ACC samples than in other adrenal specimens. SCP2 levels correlated with mitochondrial free cholesterol content but not with cholesterol side-chain cleavage activity, suggesting a role in cholesterol transport rather than steroidogenic enzyme activity.33
  • PMID 15241732: This article describes a novel intronic ACTHR microsatellite marker, ACTHRint1, and reports loss of heterozygosity at the ACTHR locus in 4 of 10 adrenocortical carcinomas versus 1 of 57 adenomas. ACTHR locus loss was associated with reduced ACTHR expression, earlier recurrence, and poorer clinical course, while its direct biological role remained uncertain.13
  • PMID 17207921: This review summarizes altered GATA transcription factor expression in adrenocortical tumors, noting that human adrenal tumors may occasionally express GATA-4 while GATA-6 is usually reduced, with lower GATA-6 levels in carcinomas than adenomas except in virilizing tumors. It also notes reports linking GATA-4 expression to aggressive behavior.14
  • PMID 18460550: This study found adrenomedullin 2/intermedin and adrenomedullin expression in adrenocortical carcinomas by immunocytochemistry, with AM2/IMD and its receptor components CRLR and RAMP1-3 also detected by RT-PCR in adrenal tumor tissues. Expression did not significantly distinguish adrenocortical carcinoma from benign adrenocortical adenomas in the reported series.10
  • PMID 20364258: Comparative genomic hybridization distinguished adrenocortical carcinomas from adenomas in this small retrospective series, with chromosomal alterations present in all carcinomas versus a minority of adenomas and a much higher alteration burden in carcinomas. Several losses, including 1p, 1q, 6p, 6q, 9q, 10q, 13q, 15q, and 18q, were reported as frequent or exclusive in carcinoma.5
  • PMID 20454499: A case report of virilizing ACC in an AIP germline mutation carrier found loss of the wild-type AIP allele in the tumor, reduced AIP mRNA expression, and complete loss of AIP immunoreactivity, supporting possible AIP tumor-suppressor involvement in adrenocortical tumorigenesis.12
  • PMID 22096502: This study found marked KIAA0101 overexpression at mRNA and protein levels in ACC compared with normal adrenal cortex and benign adrenocortical tumors, with reported 84% diagnostic accuracy for distinguishing malignant from benign lesions. In ACC cell models, KIAA0101 knockdown reduced anchorage-independent growth and invasion, supporting a biologically relevant proliferative marker.6
  • PMID 25421287: This article describes an open-source digital pathology workflow for automated Ki67 hotspot detection and labeling index quantification in ACC, addressing intratumoral heterogeneity and reproducibility of scoring. It supports the importance of standardized Ki67 assessment because Ki67 is a key prognostic parameter incorporated into pathology reporting and treatment flow charts.2
  • PMID 31759122: A TCGA pan-cancer analysis reported that in adrenocortical carcinoma, higher androgen receptor mRNA expression was associated with favorable overall survival, and tumor-free ACC patients showed higher AR expression. The study frames AR as a molecular correlate rather than an ACC-specific validated biomarker.7
  • PMID 31783819: In ACC, FSCN1 and FOXM1 are overexpressed versus adenoma and normal adrenal tissue, detectable by immunohistochemistry, and their high expression is associated with worse overall and disease-free survival. The study also links these markers to immune-related signatures, supporting their relevance as prognostic molecular pathology markers.16
  • PMID 31923422: A pan-cancer TCGA-based analysis reported that higher HOXC11 mRNA expression was associated with worse overall survival in ACC across multiple datasets. The study presents HOXC11 as a potential prognostic molecular marker in ACC, although its functional validation was performed in other tumor types rather than ACC.17
  • PMID 33058949: This ICCR guideline article outlines a standardized pathology reporting dataset for ACC resection specimens, emphasizing structured documentation of prognostically relevant pathologic variables including Ki-67 proliferative index alongside invasion, mitotic activity, necrosis, margins, nodal status, and pathologic stage.1
  • PMID 33285287: In a pan-cancer clinical sequencing cohort, adrenocortical carcinoma showed TERT amplification more often than TERT promoter mutation, with reported frequencies of 13.6% and 4.5%, respectively. The study frames TERT alteration as a recurrent molecular event in ACC and notes that amplification may be associated with higher TERT expression.15
  • PMID 33937395: A TCGA-based pancancer bioinformatics study reported that NRP1 expression in ACC was associated with overall survival and positively correlated with tumor mutational burden. The analysis also linked NRP-family expression across cancers to immune checkpoint expression, immune infiltration, and tumor microenvironment features.8
  • PMID 34719224: Pan-cancer TCGA-based analyses reported that in adrenocortical carcinoma, higher YAP1 expression was associated with worse overall and disease-free survival, despite lower YAP1 mRNA expression in ACC than in non-tumor tissue. The study also frames YAP1 as a molecular biomarker linked to telomerase-related gene expression across cancers.18
  • PMID 34941572: A pan-cancer TCGA and GEO analysis reported that higher MSH6 expression in adrenocortical carcinoma was associated with worse overall and disease-free survival, and that MSH6 expression varied across ACC pathological stages. The study frames MSH6 as a potential molecular prognostic marker rather than an ACC-specific diagnostic tool.19
  • PMID 35117422: TCGA-based analysis reported that adrenocortical cancer cases with higher HMGA1 mRNA expression had significantly worse overall survival than low-expression cases. The excerpt presents HMGA1 as a candidate molecular prognostic biomarker across multiple cancers, including ACC.20
  • PMID 35313641: A pan-cancer transcriptomic analysis reported that STEAP1 expression is downregulated in adrenocortical carcinoma relative to normal tissue, yet higher STEAP1 expression within ACC correlates with advanced pathological stage and worse overall, disease-specific, and progression-free outcomes.28
  • PMID 36276268: A pan-cancer bioinformatics study reported that lower PDCD10 expression in adrenocortical carcinoma was associated with more favorable overall survival and progression-free interval. The analysis frames PDCD10 as a candidate prognostic molecular marker, while mechanistic conclusions for ACC remain indirect and exploratory.29
  • PMID 36836180: A pan-cancer bioinformatics study reported that MEIS1 is downregulated in ACC and that lower MEIS1 expression is associated with worse overall survival. In ACC, MEIS1 expression also varied by pathologic stage, immune subtype, and molecular subtype, suggesting possible biologic and prognostic relevance.30
  • PMID 36869749: This case report describes an oncocytic adrenocortical carcinoma with immunohistochemical and mRNA evidence of ectopic PTH production, alongside steroidogenic marker expression. Double-labeling suggested two intermixed tumor cell populations, with PTH-producing cells distinct from 3β-HSD- and aromatase-positive steroid-secreting cells.11
  • PMID 36939765: A pan-cancer TCGA and GTEx analysis reported that higher DDX1 expression was associated with worse overall survival in ACC. The study also linked DDX1 to immune-related features across tumors, but did not establish an ACC-specific clinical role beyond prognostic association.21
  • PMID 37058019: A TCGA- and GEO-based pan-cancer analysis reported that YKT6 is upregulated in ACC, varies by ACC pathologic stage, and that higher YKT6 expression is associated with worse overall and disease-free survival. The study also noted relatively frequent YKT6 amplification in ACC and a positive correlation between YKT6 expression and tumor mutational burden.22
  • PMID 38234609: A pancancer bioinformatic analysis reported that lower NRP1 expression was associated with longer overall survival in adrenocortical carcinoma, suggesting NRP1 may function as an unfavorable prognostic marker in ACC. The study did not provide ACC-specific tissue validation or mechanistic data.9
  • PMID 38425404: A pan-cancer bioinformatic analysis reported that B56ε expression is increased in ACC and that higher expression was associated with worse prognosis in ACC. The article also links B56ε expression across tumors with immune infiltration and immune checkpoint or HLA-related gene expression, although mechanistic validation was performed in hepatocellular carcinoma rather than ACC.23
  • PMID 38881923: A pan-cancer bioinformatics study reported that higher RPN1 mRNA expression was associated with worse overall survival in ACC. The article frames RPN1 as an emerging molecular biomarker linked to tumor biology, immune-related pathways, and potential immunotherapy relevance, though ACC-specific validation is not shown.24
  • PMID 39015705: A pan-cancer bioinformatics study reported that SPAG6 is upregulated in ACC relative to normal tissue, shows higher expression in female ACC patients, and that lower SPAG6 expression was associated with worse disease-free interval in ACC. The findings are exploratory and derive from retrospective database analysis rather than ACC-specific validation.31
  • PMID 39308687: A TCGA-based pan-cancer analysis reported that higher ADRA2C expression in adrenocortical carcinoma was associated with worse overall, disease-specific, and progression-free outcomes. The study also noted that ACC had the highest reported ADRA2C alteration frequency in the dataset, mainly mutations, suggesting possible biomarker relevance.25
  • PMID 39668816: A pan-cancer bioinformatics study reported that high DHX34 expression is associated with poor prognosis in adrenocortical carcinoma. The article frames DHX34 as a potential molecular biomarker linked to immune infiltration, mutational burden, microsatellite instability, and cell-cycle-related cancer pathways, but without ACC-specific mechanistic validation.26
  • PMID 40155034: The article notes prior reported findings that DDX39 is significantly upregulated in adrenocortical carcinoma tissues and that higher expression is associated with worse patient survival, placing DDX39 as a potential adverse molecular prognostic marker in ACC.27
  • PMID 41605339: A pan-cancer review reports that DR3 expression is downregulated in adrenocortical carcinoma relative to normal tissue datasets, yet higher DR3 expression within ACC is associated with worse survival. The review frames DR3 as a context-dependent biomarker linked broadly to immune infiltration and tumor biology.32

References

Footnotes

  1. Data set for reporting of carcinoma of the adrenal cortex: explanations and recommendations of the guidelines from the International Collaboration on Cancer Reporting.. Hum Pathol. 2021. PMID: 33058949. Local full text: 33058949.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11 ↩12 ↩13

  2. Automated Selection of Hotspots (ASH): enhanced automated segmentation and adaptive step finding for Ki67 hotspot detection in adrenal cortical cancer.. Diagn Pathol. 2014. PMID: 25421287. Local full text: 25421287.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7

  3. Immunocytochemical differential diagnosis of adrenocortical neoplasms using the monoclonal antibody D11.. Virchows Arch A Pathol Anat Histopathol. 1990. PMID: 2114700. Local full text: 2114700.md ↩ ↩2 ↩3 ↩4 ↩5

  4. Ad4BP in the human adrenal cortex and its disorders.. J Clin Endocrinol Metab. 1995. PMID: 7629233. Local full text: 7629233.md ↩ ↩2 ↩3 ↩4 ↩5

  5. Improvement of histopathological classification of adrenal gland tumors by genetic differentiation.. World J Urol. 2010. PMID: 20364258. Local full text: 20364258.md ↩ ↩2 ↩3 ↩4 ↩5

  6. KIAA0101 is overexpressed, and promotes growth and invasion in adrenal cancer.. PLoS One. 2011. PMID: 22096502. Local full text: 22096502.md ↩ ↩2 ↩3 ↩4

  7. The androgen receptor expression and association with patient’s survival in different cancers.. Genomics. 2020. PMID: 31759122. Local full text: 31759122.md ↩ ↩2 ↩3 ↩4

  8. Pancancer Analysis of Neurovascular-Related NRP Family Genes as Potential Prognostic Biomarkers of Bladder Urothelial Carcinoma.. Biomed Res Int. 2021. PMID: 33937395. Local full text: 33937395.md ↩ ↩2 ↩3 ↩4

  9. Comprehensive analysis and immunohistochemistry localization of NRP1 expression in pancancer and normal individual tissues in relation to SARS‑CoV‑2 susceptibility.. Exp Ther Med. 2024. PMID: 38234609. Local full text: 38234609.md ↩ ↩2 ↩3 ↩4

  10. Expression of adrenomedullin 2/intermedin in human adrenal tumors and attached non-neoplastic adrenal tissues.. J Endocrinol. 2008. PMID: 18460550. Local full text: 18460550.md ↩ ↩2

  11. Immunohistochemical characterization of a steroid-secreting oncocytic adrenal carcinoma responsible for paraneoplastic hyperparathyroidism.. Eur J Endocrinol. 2023. PMID: 36869749. Local full text: 36869749.md ↩ ↩2 ↩3

  12. Isolated familial somatotropinoma: 11q13-loh and gene/protein expression analysis suggests a possible involvement of aip also in non-pituitary tumorigenesis.. Clinics (Sao Paulo). 2010. PMID: 20454499. Local full text: 20454499.md ↩ ↩2

  13. The role of the ACTH receptor in adrenal tumors: identification of a novel microsatellite marker.. Horm Metab Res. 2004. PMID: 15241732. Local full text: 15241732.md ↩ ↩2

  14. GATA transcription factors in adrenal development and tumors.. Mol Cell Endocrinol. 2007. PMID: 17207921. Local full text: 17207921.md ↩ ↩2

  15. A Pan-Cancer Study of Somatic TERT Promoter Mutations and Amplification in 30,773 Tumors Profiled by Clinical Genomic Sequencing.. J Mol Diagn. 2021. PMID: 33285287. Local full text: 33285287.md ↩ ↩2

  16. Expression of FSCN1 and FOXM1 are associated with poor prognosis of adrenocortical carcinoma patients.. BMC Cancer. 2019. PMID: 31783819. Local full text: 31783819.md ↩ ↩2

  17. HOXC11 functions as a novel oncogene in human colon adenocarcinoma and kidney renal clear cell carcinoma.. Life Sci. 2020. PMID: 31923422. Local full text: 31923422.md ↩ ↩2

  18. Yes-associated protein 1 as a prognostic biomarker and its correlation with telomerase in various cancers.. Osong Public Health Res Perspect. 2021. PMID: 34719224. Local full text: 34719224.md ↩ ↩2

  19. An integrative pan-cancer analysis reveals the oncogenic role of mutS homolog 6 (MSH6) in human tumors.. Aging (Albany NY). 2021. PMID: 34941572. Local full text: 34941572.md ↩ ↩2

  20. High-mobility group A1 (HMGA1) gene expressions in various colorectal cancer cell lines and correlation with prognosis.. Transl Cancer Res. 2020. PMID: 35117422. Local full text: 35117422.md ↩ ↩2

  21. Pan-cancer analysis identifies RNA helicase DDX1 as a prognostic marker.. Phenomics. 2022. PMID: 36939765. Local full text: 36939765.md ↩ ↩2

  22. A pan-cancer analysis of the oncogenic role of YKT6 in human tumors.. Medicine (Baltimore). 2023. PMID: 37058019. Local full text: 37058019.md ↩ ↩2

  23. Comprehensive analysis of the protein phosphatase 2A regulatory subunit B56ε in pan-cancer and its role and mechanism in hepatocellular carcinoma.. World J Gastrointest Oncol. 2024. PMID: 38425404. Local full text: 38425404.md ↩ ↩2 ↩3

  24. RPN1: a pan-cancer biomarker and disulfidptosis regulator.. Transl Cancer Res. 2024. PMID: 38881923. Local full text: 38881923.md ↩ ↩2 ↩3

  25. Pan-cancer analysis of the role of α2C-adrenergic receptor (ADRA2C) in human tumors and validation in glioblastoma multiforme models.. J Cancer. 2024. PMID: 39308687. Local full text: 39308687.md ↩ ↩2

  26. DHX34 as a promising biomarker for prognosis, immunotherapy and chemotherapy in Pan-Cancer: A Comprehensive Analysis and Experimental Validation.. J Cancer. 2024. PMID: 39668816. Local full text: 39668816.md ↩ ↩2 ↩3

  27. Increased Expression of DDX39 in Uveal Melanoma Is Associated With Patient Prognosis.. Anticancer Res. 2025. PMID: 40155034. Local full text: 40155034.md ↩ ↩2

  28. The Prognostic Value and Immunological Role of STEAP1 in Pan-Cancer: A Result of Data-Based Analysis.. Oxid Med Cell Longev. 2022. PMID: 35313641. Local full text: 35313641.md ↩ ↩2

  29. Pan-Cancer Analysis on the Oncogenic Role of Programmed Cell Death 10.. J Oncol. 2022. PMID: 36276268. Local full text: 36276268.md ↩ ↩2

  30. A Systematic Pan-Cancer Analysis of MEIS1 in Human Tumors as Prognostic Biomarker and Immunotherapy Target.. J Clin Med. 2023. PMID: 36836180. Local full text: 36836180.md ↩ ↩2

  31. A comprehensive pan-cancer analysis revealing SPAG6 as a novel diagnostic, prognostic and immunological biomarker in tumor.. Gland Surg. 2024. PMID: 39015705. Local full text: 39015705.md ↩ ↩2

  32. Death receptor 3: A paradoxical biomarker and therapeutic target in pan-cancer.. Crit Rev Oncol Hematol. 2026. PMID: 41605339. Local full text: 41605339.md ↩ ↩2

  33. Expression of sterol carrier protein 2 (SCP2) in human adrenocortical tissue.. Eur J Endocrinol. 1996. PMID: 8640304. Local full text: 8640304.md ↩

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