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core_morphology_of_acc

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Core Morphology of ACC

Pathology, Classification, and Differential Diagnosis

Core morphology of adrenocortical carcinoma (ACC) refers to the gross and microscopic features used to recognize malignant adrenocortical neoplasia and to distinguish it from adrenocortical adenoma and from non-cortical adrenal or retroperitoneal mimics.12 Within adrenal pathology, morphology remains the primary basis for diagnosis because ACC is usually identified by a composite pattern of architectural disorder, proliferative activity, necrosis, and invasion rather than by a single pathognomonic feature.34

Typical ACC is a large, heterogeneous adrenal mass with hemorrhage, necrosis, and variegated cut surfaces, and histologically often shows diffuse or trabecular growth, decreased clear-cell content, eosinophilic or compact cells, increased mitotic activity, atypical mitoses, confluent necrosis, and capsular, sinusoidal, or venous invasion.567 These features are generally interpreted in structured systems such as Weiss-based approaches, especially for intra-adrenal tumors without overt metastatic disease or direct extension.24

The evidence base is constrained by the rarity of ACC. Most morphologic criteria were developed from retrospective surgical series and expert reviews, while unusual variants are often described only in small series or case reports.38 Diagnostic performance is therefore strongest in well-sampled resection specimens and less certain in biopsy material or in uncommon subtypes such as oncocytic, myxoid, and sarcomatoid tumors.794 In current practice, morphology is highly informative but not fully standalone, and it is interpreted alongside clinical, endocrine, imaging, and immunophenotypic data.1011

Diagnostic Context

The main morphologic task is to separate ACC from benign adrenocortical neoplasms and from other adrenal-region tumors, including pheochromocytoma, renal cell carcinoma, metastatic carcinoma, and rare mesenchymal or epithelioid lesions.121314 This distinction is most difficult in tumors confined to the adrenal gland that lack unequivocal malignant behavior such as recurrence, metastasis, or gross extra-adrenal extension.153

Gross findings may raise suspicion but are not definitive. ACC is often large and heterogeneous, with hemorrhage, necrosis, and cystic degeneration, but size and weight overlap with adenoma and cannot independently establish malignancy.158 The reliable implication is practical rather than categorical: grossly abnormal lesions warrant extensive sampling, whereas gross appearance alone does not resolve the diagnosis.164

This diagnostic context leads directly to the central role of histologic pattern recognition.

Core Histologic Pattern

Across reviews and comparative series, the most consistently useful microscopic findings are diffuse or trabecular architecture, reduced clear-cell proportion, eosinophilic or compact cell predominance, increased mitotic activity, atypical mitoses, confluent necrosis, and capsular, sinusoidal, or venous invasion.562 Retrospective data suggest that necrosis, atypical mitoses, and elevated mitotic counts are among the more discriminatory features when ACC is compared with adenoma.617

No single histologic feature is completely sensitive or specific. Some carcinomas may show limited overt atypia, while some adenomas may display hemorrhage, fibrosis, or focal atypical change without malignant behavior.1819 The practical implication is that morphology is most reliable when several adverse features converge in an adequately sampled specimen rather than when diagnosis rests on one abnormal finding.74

Invasion and necrosis

Among conventional findings, demonstrable invasion generally carries the greatest diagnostic weight. Capsular penetration, sinusoidal or venous invasion, local extension, recurrence, and metastasis are more persuasive evidence of carcinoma than cytologic atypia alone.2032

Confluent tumor necrosis also appears to be a relatively robust discriminator in contemporary retrospective data, although it should still be interpreted within the full morphologic context rather than as an isolated rule.174 Clinically, the most dependable conclusion is that true invasion strongly supports malignancy, whereas atypia without invasion is less secure, particularly in variant tumors.219

Histologic Variants and Pitfalls

Once the conventional pattern is established, the main interpretive challenges arise from variant morphologies. Current classifications continue to recognize oncocytic, myxoid, and sarcomatoid forms, but each may reduce the reliability of standard criteria if assessed without attention to variant-specific pitfalls.4

Oncocytic ACC

Oncocytic ACC is composed of cells with abundant granular eosinophilic cytoplasm and mitochondria-rich ultrastructure.2021 In this setting, pleomorphism and even some conventional scoring elements may overstate malignant potential, so greater emphasis is placed on invasion, necrosis, size, unresectability, or metastasis, often with use of Lin-Weiss-Bisceglia criteria.229 What is reliable is the presence of invasive or clinically aggressive behavior; what is less reliable is eosinophilic cytology by itself.2021

Myxoid and cystic patterns

Myxoid change is not specific for carcinoma and may be seen in both benign and malignant adrenocortical neoplasms.2324 Similarly, cystic or pseudocystic presentation may obscure focal viable carcinoma in the cyst wall.16 The practical implication is that these patterns should prompt broader sampling and renewed attention to mitotic activity, necrosis, and invasion rather than a diagnosis based on stromal appearance or cyst formation alone.164

Sarcomatoid and rhabdoid patterns

Sarcomatoid and rhabdoid ACC are rare but important because they may mimic retroperitoneal sarcoma, metastatic sarcomatoid carcinoma, or other epithelioid malignancies.25262728 Available evidence, largely from case reports, suggests aggressive behavior, but generalizability is limited by rarity and publication bias.2628 In practice, morphology alone is often insufficient, and diagnosis usually depends on extensive sampling plus supportive adrenal cortical immunophenotyping to confirm lineage and exclude mimics.144

These variants illustrate a broader principle: ACC morphology is most dependable when interpreted as a structured pattern, not as a checklist applied mechanically.

Differential Diagnosis and Ancillary Support

The principal differential diagnosis is between ACC and adrenocortical adenoma, but non-cortical mimics are also a recurring problem, particularly renal, neuroendocrine, vascular, and metastatic tumors.131029 Morphology can strongly suggest cortical malignancy, but lineage assignment may remain uncertain in unusual locations, ectopic adrenal rests, or highly pleomorphic tumors.3031

Immunohistochemistry is therefore primarily adjunctive. Markers of adrenal cortical differentiation may help separate ACC from renal cell carcinoma, pheochromocytoma, thyroid metastasis, and mesenchymal lesions, but they do not by themselves establish malignant behavior within a cortical neoplasm.221311 The reliable use of ancillary studies is to confirm cortical origin and narrow the differential; they are less reliable as substitutes for morphologic assessment of malignancy.104

Prognostic Associations and Role in Workflow

Some morphologic features associated with diagnosis also correlate with outcome. Retrospective series link higher mitotic activity, atypical mitoses, necrosis, and vascular or sinusoidal invasion with metastatic risk and more aggressive behavior.619 These associations are useful but imperfect, and morphology alone does not fully predict clinical course.194

Accordingly, core morphology is most dependable in resection pathology with adequate sampling.84 By comparison, core biopsy and especially fine-needle aspiration have limited ability to distinguish ACC from adenoma because of sampling constraints and cytomorphologic overlap.3233 The practical clinical implication is that pathology from limited specimens may suggest cortical malignancy or help exclude mimics, but definitive classification often still depends on the resection specimen and integrated clinicopathologic assessment.84

Limitations and Research Context

The main limitation of this field is that many widely used morphologic principles are derived from retrospective experience rather than prospective validation, and uncommon variants remain underrepresented outside case reports and small institutional series.38 Interobserver reproducibility also varies, especially in borderline lesions and in tumors with oncocytic or other unusual histology.94

Historical ultrastructural studies helped establish cortical differentiation by describing abundant smooth endoplasmic reticulum and mitochondria with tubular or lamellar cristae, but these observations now serve mainly as supporting context rather than routine diagnostic arbiters.3435 Current WHO-aligned practice continues to place morphology at the center of ACC diagnosis while emphasizing careful sampling, awareness of variant patterns, and integration with proliferation markers and ancillary studies rather than reliance on any single algorithm.174

Included Articles

  • PMID 208228: Two androgen-secreting ACC cases showed virilization with tumors composed mainly of compact eosinophilic cells resembling zona reticularis, plus capsular infiltration and, in one case, liver metastases. Ultrastructurally, abundant smooth endoplasmic reticulum, numerous mitochondria with lamellar or tubular cristae, scant lipid, and focal basement membrane discontinuity were described, with the latter proposed as a marker of malignancy versus virilizing adenoma.34
  • PMID 1129901: This clinicopathologic series compared adrenocortical carcinomas with adenomas and found that architectural disarray, pleomorphism, increased or bizarre mitoses, vascular invasion, hemorrhage, and necrosis were generally useful malignant features, while tumor size and weight correlated most consistently with outcome.1
  • PMID 3213509: This infant ACC case highlights pathology-based diagnosis of a nonfunctional pediatric adrenal tumor, with extensive necrosis, pleomorphism, occasional giant cells, and a mitotic rate just over 1 per 10 high-power fields despite absent capsular or vascular invasion. The report emphasizes that ultrastructural and immunohistochemical findings can help distinguish ACC from adenoma and histologic mimics.36
  • PMID 3576916: This veterinary case highlights morphologic and ultrastructural features supporting adrenocortical carcinoma, including sheets, cords, and nests of eosinophilic tumor cells with necrosis, vascular invasion, and metastases. Desmosome-like junctions and absence of electron-dense secretory granules were useful in distinguishing cortical carcinoma from pheochromocytoma.37
  • PMID 3609394: This pathology-focused review emphasizes the difficulty of diagnosing adrenocortical carcinoma on histology alone and describes morphologic clues linked to malignancy, including nodular growth of small atypical cells with atypical mitoses, necrosis, lobulated gross appearance, and occasional vascular invasion. It also notes that tumor weight and lectin staining with RCA may support malignant classification.15
  • PMID 6464758: This case report of estrogen-producing ACC documents feminization in a 35-year-old man and correlates estrone secretion with tumor morphology. The carcinoma showed necrosis, vascular invasion, and mixed histology, while ultrastructural features included abundant smooth endoplasmic reticulum, irregular mitochondria with tubular or lamellar cristae, and scant lipid droplets.35
  • PMID 8561092: In a 56-case series with at least 5 years of follow-up, adrenal cortical carcinomas were distinguished from adenomas mainly by higher mitotic activity, frequent necrosis, predominantly solid or trabecular architecture, eosinophilic cytoplasm, and occasional vascular or capsular invasion, while size alone showed overlap.5
  • PMID 9213185: This case report describes functioning black adrenal adenoma as a benign cortical tumor that can mimic adrenocortical carcinoma clinically and on imaging. Pathologic benignity was supported by a well-circumscribed pigmented lipofuscin-rich lesion lacking necrosis, mitoses, or vascular invasion.38
  • PMID 10716153: This series characterizes myxoid adrenocortical neoplasms as a rare histologic variant that can occur in both adenomas and carcinomas, so myxoid change alone should not be taken as proof of malignancy. Diagnosis should instead rely on conventional malignant features such as necrosis, vascular or extracapsular invasion, and increased mitotic activity.23
  • PMID 10790237: This case report describes oncocytic adrenocortical carcinoma as a rare adrenal cortical variant with large polyhedral cells, abundant granular eosinophilic cytoplasm, and mitochondria-rich ultrastructure. It emphasizes that malignancy in oncocytic adrenocortical tumors is best established by vascular or capsular invasion or metastasis rather than cytologic atypia, mitotic activity, or necrosis alone.20
  • PMID 12218215: This case series characterizes oncocytic ACC as a rare, usually nonfunctioning adrenal cortical carcinoma composed of diffuse polygonal oncocytic cells with abundant eosinophilic granular cytoplasm and mitochondria-rich ultrastructure. In this variant, malignancy is supported more by large size, necrosis, extracapsular or vascular invasion, metastasis, and unresectability than by cytologic atypia or low mitotic rate.21
  • PMID 12675769: This case report describes a nonfunctional adrenocortical adenoma with extensive fibrosis, hemorrhage, parenchymal loss, focal adipose tissue, and ossification that radiologically mimicked myelolipoma and carcinoma. Histology favored adenoma because there were no mitoses, necrosis, vascular invasion, or capsular invasion, and the architecture was non-diffuse.18
  • PMID 12920217: Comparative histopathologic review of adrenocortical adenomas and carcinomas found tumor necrosis, atypical mitoses, and more than 1 mitosis per 50 high-power fields to be highly specific for carcinoma. In ACC, metastatic risk was associated with necrosis, atypical mitoses, more than 5 mitoses per 50 high-power fields, sinusoidal invasion, and a high adverse morphologic index.6
  • PMID 15302503: This review and case report describes oncocytic adrenocortical carcinoma as a rare histologic variant defined by abundant granular eosinophilic cytoplasm and supported by malignant features including diffuse architecture, necrosis, vascular invasion, and increased mitotic activity. The report also notes immunoreactivity for synaptophysin, alpha-inhibin, and Melan A.22
  • PMID 15378490: Cystic adrenal lesions can harbor ACC despite a benign-appearing macroscopic cystic presentation, most often as pseudocysts with focal malignant cells in the cyst wall. Extensive pathologic sampling helps distinguish true adrenal cysts from cyst-associated ACC and identify malignant features such as vascular invasion, coagulative necrosis, mitotic activity, and pleomorphism.16
  • PMID 17222069: This five-case retrospective series emphasizes that ACC pathology commonly includes large tumor size, necrosis, capsular or vascular invasion, and higher mitotic activity, while also showing that some clinically aggressive tumors may display few overt malignant features, underscoring the need for careful integrated histopathologic assessment.19
  • PMID 17466160: This case report highlights that ACC may mimic a primary renal tumor radiologically and emphasizes gross and microscopic features supporting adrenal cortical malignancy, including large size, hemorrhage, necrosis, marked atypia, atypical mitoses, and oncocytic or trabecular areas, alongside the differential diagnosis of adult suprarenal masses.12
  • PMID 18006015: This article summarizes gross and microscopic features of adrenocortical carcinoma, including hemorrhage, necrosis, cystic degeneration, trabecular or nested architecture, lipid-depleted eosinophilic cells, and frequent atypical mitoses. It emphasizes the diagnostic difficulty in separating carcinoma from adenoma and notes that definitive malignancy rests on invasion, recurrence, or metastasis.3
  • PMID 18080137: This case report describes adrenal sarcomatoid carcinoma as an exceptionally rare biphasic ACC variant with spindle-cell sarcomatoid areas, extensive necrosis, high mitotic activity, capsular and vascular invasion, and very aggressive clinical behavior. It emphasizes generous sampling and adrenal cortical immunoprofiling to distinguish this subtype from retroperitoneal sarcoma and metastatic carcinoma.25
  • PMID 18515402: In a single-centre ACC review, standardized histopathology reporting using the Royal College of Pathologists minimum dataset identified more malignant features than original reports. Common findings included diffuse architecture, fewer than 25% clear cells, confluent necrosis, abnormal mitoses, and mitotic count at least 6 per 50 high-power fields.7
  • PMID 19089656: This review outlines the gross and microscopic features that support diagnosing adrenocortical carcinoma, including disordered trabecular or diffuse architecture, compact cell predominance, pleomorphism, atypical mitoses, confluent necrosis, and capsular, sinusoidal, venous, local, or metastatic invasion. It also notes diagnostic pitfalls such as oncocytic variants and the need to integrate clinical, biochemical, and histologic findings in borderline intra-adrenal lesions.2
  • PMID 19369012: Sarcomatoid carcinoma is presented as an extremely rare morphologic variant of adrenocortical carcinoma characterized by a biphasic tumor with adrenocortical carcinomatous areas and sarcomatoid spindle-cell proliferation, often with necrosis, atypical mitoses, vascular invasion, and aggressive clinical behavior. The review also discusses terminology, distinguishing sarcomatoid carcinoma from carcinosarcoma based on the presence or absence of heterologous sarcomatous elements.26
  • PMID 21897901: This case highlights the pathologic distinction of ACC from synchronous renal cell carcinoma using gross findings, Weiss criteria, and immunohistochemistry. The ACC showed necrosis, high mitotic activity, pleomorphism, vascular invasion, and six Weiss criteria, while RCC was separated by EMA and keratin positivity.13
  • PMID 21897902: Two ACC case reports emphasize morphologic features supporting malignancy and the need to distinguish ACC from adenoma, pheochromocytoma, and renal cell carcinoma using combined histology, immunohistochemistry, and clinicobiochemical correlation, including trabecular architecture, necrosis, vascular or capsular invasion, and high mitotic activity.10
  • PMID 22031318: This case series characterizes myxoid adrenocortical neoplasms as a rare histologic variant that can occur in both adenomas and carcinomas. In this subtype, carcinoma was associated with larger size, hemorrhage, necrosis, capsular or vascular invasion, and higher mitotic activity, helping distinguish malignant from benign lesions.24
  • PMID 23445527: This case series describes a rare rhabdoid variant of adrenocortical carcinoma characterized by predominant rhabdoid cells with eosinophilic cytoplasmic inclusions, eccentric vesicular nuclei, prominent nucleoli, necrosis, and a minor conventional ACC component. The authors emphasize including ACC in the differential diagnosis of tumors with rhabdoid morphology.27
  • PMID 23889916: This case highlights pathologic and immunohistochemical features supporting primary adrenocortical carcinoma in a nonfunctional adrenal mass, including high nuclear grade, necrosis, mitotic activity, capsular and sinusoidal vascular invasion, melan-A and inhibin positivity, and negative TTF-1 and thyroglobulin to distinguish it from thyroid metastasis.11
  • PMID 24602387: This case-based review highlights ACC pathologic features supporting malignancy, including solid and trabecular architecture, capsular and renal capsule invasion, necrosis, marked pleomorphism, vascular tumor thrombus, and high mitotic activity. It also emphasizes differential diagnosis support from an adrenal cortical immunophenotype and formal scoring with modified Weiss and Van Slooten systems.39
  • PMID 25190978: In a retrospective series of retroperitoneal masses, two adrenal lesions were diagnosed cytologically as adrenocortical carcinoma and later confirmed on histopathology. The aspirates were described as showing pleomorphic cells with vague acinar formation, irregular chromatin, mitoses, fragile vacuolated cytoplasm, and necrosis.32
  • PMID 25724713: This case report highlights that adrenal PEComa can closely mimic sarcomatoid adrenocortical carcinoma on gross and microscopic examination, including epithelioid and spindle-cell morphology, necrosis, and invasion. It emphasizes the differential diagnosis of unusual adrenal tumors and the need to distinguish non-ACC mimics from true ACC.14
  • PMID 26376405: This case report describes ACC with an unusual gastric submucosal metastasis that mimicked primary gastric carcinoma, emphasizing differential diagnosis based on gross and microscopic features plus supportive immunohistochemistry. The adrenal tumor showed diffuse architecture, necrosis, capsular, sinusoidal, and vascular invasion, high mitotic activity with atypical mitoses, and fulfilled all nine Weiss criteria.40
  • PMID 26612224: This review emphasizes the gross and microscopic hallmarks of adrenocortical carcinoma, including large size, necrosis, hemorrhage, invasive growth, high mitotic activity, and atypical mitoses. It also notes sampling limitations on core biopsy and key differential considerations when morphology overlaps with other tumors.8
  • PMID 28551383: This case report describes an adrenal collision tumor in which a nonfunctioning adrenocortical adenoma contained an epithelioid angiosarcoma component. It highlights microscopic and immunohistochemical features that distinguish this vascular malignancy from adrenocortical carcinoma and other epithelioid adrenal tumors.29
  • PMID 30269470: This case report highlights intrarenal adrenocortical carcinoma arising in an adrenal rest as a rare renal mass that can mimic renal cell carcinoma. Diagnosis relied on adrenal cortical-like tissue, malignant histology with necrosis and vascular invasion, Weiss criteria, and exclusion of renal and mesenchymal mimics.30
  • PMID 32288686: This veterinary case report describes adrenocortical carcinoma with myxoid differentiation, highlighting pathologic features including cords, sheets, nests, necrosis, hemorrhage, vertebral and spinal cord invasion, and mucinous matrix confirmed by periodic acid-Schiff and alcian blue staining. Melan-A positivity with negative synaptophysin and chromogranin-A supported cortical rather than medullary origin.41
  • PMID 33281410: In a single-center series of 837 adrenocortical tumors, all 32 tumors classified as ACC showed confluent tumor necrosis, while none of 805 benign tumors did. The study proposes confluent necrosis on routine histology as a highly reproducible feature that may distinguish malignant from benign adrenocortical neoplasms, with Ki-67 above 10% present in most but not all ACCs.17
  • PMID 33815299: This case report highlights that ectopic ovarian ACC can mimic neuroendocrine carcinoma and may require expanded immunohistochemical evaluation to establish the diagnosis. Pathologic features included necrosis, prominent lymphovascular invasion, high mitotic activity, Weiss score 8, and a very high Ki-67 index.31
  • PMID 35878423: This review emphasizes that adrenal FNA has limited ability to distinguish adrenocortical adenoma from ACC because of substantial cytomorphologic overlap. Features favoring ACC include larger heterogeneous lesions with necrosis on imaging and, on cytology, high-grade atypia, mitotic activity, necrosis, and intranuclear inclusions.33
  • PMID 36699174: This case report highlights oncocytic adrenocortical carcinoma as a rare histopathologic ACC variant characterized by eosinophilic granular cytoplasm, necrosis, mitotic activity, capsular and vascular invasion, and potential large-vessel extension. It also summarizes key differential diagnoses and notes use of Lin-Weiss-Bisceglia criteria to classify malignant potential in oncocytic adrenal neoplasms.9
  • PMID 36761025: This case report describes adrenocortical oncocytic carcinoma as a rare ACC subtype with pathologic features including abundant eosinophilic cytoplasm, atypical mitoses, adipose tissue invasion, necrosis, and nested architecture. The diagnosis was supported by a Weiss score of 3 and immunoreactivity for Melan A, inhibin, synaptophysin, and calretinin.42
  • PMID 41057662: This review summarizes the WHO 5th edition pathology approach to ACC, emphasizing that diagnosis remains anchored in combined histopathologic assessment of invasion, architecture, necrosis, mitotic activity, and atypical mitoses, with careful sampling needed because no single algorithm is fully sensitive, specific, or reproducible. It also outlines key gross and microscopic features and recognized histologic subtypes including oncocytic, myxoid, and sarcomatoid ACC.4
  • PMID 41643097: This case report describes sarcomatoid ACC as an exceptionally rare, highly aggressive histologic variant characterized by mixed epithelial and spindle-cell or pleomorphic sarcomatoid components. The report emphasizes major diagnostic difficulty in distinguishing it from extra-adrenal sarcomas or metastatic sarcomatoid carcinomas and highlights adverse pathologic features including necrosis, atypical mitoses, vascular invasion, and high proliferative activity.28

References

Footnotes

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  4. Diagnosis and grading of adrenal cortical carcinoma.. Virchows Arch. 2026. PMID: 41057662. Local full text: 41057662.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11 ↩12 ↩13 ↩14 ↩15 ↩16

  5. Adrenal cortical neoplasms. A study of 56 cases.. Am J Clin Pathol. 1996. PMID: 8561092. Local full text: 8561092.md ↩ ↩2 ↩3 ↩4

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  8. Adrenal Tumors in Adults.. Surg Pathol Clin. 2015. PMID: 26612224. Local full text: 26612224.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6

  9. ONCOCYTIC ADRENOCORTICAL CARCINOMA IN A YOUNG PATIENT.. Acta Endocrinol (Buchar). 2022. PMID: 36699174. Local full text: 36699174.md ↩ ↩2 ↩3 ↩4 ↩5

  10. Adrenocortical carcinoma: Report of two cases.. Indian J Endocrinol Metab. 2011. PMID: 21897902. Local full text: 21897902.md ↩ ↩2 ↩3 ↩4

  11. A rare coexistence of non-functional adrenocortical carcinoma and multicentric papillary thyroid microcarcinoma: a case report.. J Med Case Rep. 2013. PMID: 23889916. Local full text: 23889916.md ↩ ↩2 ↩3

  12. 1500 gram suprarenal mass: a case report.. Can J Urol. 2007. PMID: 17466160. Local full text: 17466160.md ↩ ↩2

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  16. Cystic adrenal neoplasms.. Cancer. 2004. PMID: 15378490. Local full text: 15378490.md ↩ ↩2 ↩3 ↩4

  17. Differentiating Benign from Malignant Adrenocortical Tumors by a Single Morphological Parameter-a Clinicopathological Study on 837 Adrenocortical Neoplasias.. Indian J Surg Oncol. 2020. PMID: 33281410. Local full text: 33281410.md ↩ ↩2 ↩3 ↩4

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  19. [Adrenocortical carcinoma. A retrospective analysis of five cases].. An Med Interna. 2006. PMID: 17222069. Local full text: 17222069.md ↩ ↩2 ↩3 ↩4

  20. Fine-needle aspiration cytology of a case of oncocytic adrenocortical carcinoma.. Diagn Cytopathol. 2000. PMID: 10790237. Local full text: 10790237.md ↩ ↩2 ↩3 ↩4

  21. Oncocytic adrenocortical carcinoma: a morphologic, immunohistochemical and ultrastructural study of four cases.. Mod Pathol. 2002. PMID: 12218215. Local full text: 12218215.md ↩ ↩2 ↩3 ↩4

  22. Oncocytic adrenocortical carcinoma.. Urology. 2004. PMID: 15302503. Local full text: 15302503.md ↩ ↩2 ↩3

  23. Myxoid neoplasms of the adrenal cortex: a rare histologic variant.. Am J Surg Pathol. 2000. PMID: 10716153. Local full text: 10716153.md ↩ ↩2

  24. Myxoid adrenocortical neoplasms: a study of the clinicopathologic features and EGFR gene status of ten Chinese cases.. Am J Clin Pathol. 2011. PMID: 22031318. Local full text: 22031318.md ↩ ↩2

  25. Primary adrenocortical sarcomatoid carcinoma: case report and review of literature.. Virchows Arch. 2008. PMID: 18080137. Local full text: 18080137.md ↩ ↩2

  26. Sarcomatoid carcinoma of the adrenal gland: A case report and review of literature.. Pathol Res Pract. 2010. PMID: 19369012. Local full text: 19369012.md ↩ ↩2 ↩3

  27. Primary rhabdoid adrenocortical carcinoma: a clinicopathological and immunohistochemical study of three cases.. Histopathology. 2013. PMID: 23445527. Local full text: 23445527.md ↩ ↩2

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  29. A exceptional collision tumor of primary adrenal angiosarcoma and non-functioning adrenocortical adenoma.. Pathol Res Pract. 2017. PMID: 28551383. Local full text: 28551383.md ↩ ↩2

  30. An Intrarenal Adrenocortical Carcinoma Arising in an Adrenal Rest.. J Pathol Transl Med. 2018. PMID: 30269470. Local full text: 30269470.md ↩ ↩2

  31. Case Report: Ectopic Adrenocortical Carcinoma in the Ovary.. Front Endocrinol (Lausanne). 2021. PMID: 33815299. Local full text: 33815299.md ↩ ↩2

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  41. Paraplegia in a Domestic Ferret (Mustela Putorius Furo) Secondary to Metastatic Adrenocortical Carcinoma with Myxoid Differentiation.. J Exot Pet Med. 2019. PMID: 32288686. Local full text: 32288686.md ↩

  42. Case Report: Surgery to remove adrenocortical oncocytic carcinoma from an Asian male.. Front Surg. 2023. PMID: 36761025. Local full text: 36761025.md ↩

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