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population_epidemiology_of_acc

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Population Epidemiology of ACC

Epidemiology and Risk Context

Adrenocortical carcinoma (ACC) is a rare primary malignant tumor of the adrenal cortex and an uncommon cause of adrenal mass, endocrine syndrome, or cancer mortality at the population level.123 Within adrenal oncology, it sits in clear contrast to the much larger population of benign adrenal adenomas and incidentalomas, which dominate routine imaging practice.4 Population-based studies consistently show that ACC is usually diagnosed in adults, has a slight female predominance, and often presents with regional invasion or metastatic disease, contributing to poor survival compared with many other endocrine neoplasms.526

The epidemiology of ACC is shaped as much by rarity as by tumor biology. Most available estimates come from retrospective registries, hospital databases, historical compilations, and selected referral cohorts, with variable pathology confirmation, incomplete endocrine and genetic annotation, and inconsistent separation of pediatric from adult disease.753 Older series may also be less reliable because they predate contemporary adrenal pathology standards.89 As a result, broad patterns such as rarity, age distribution, female predominance, and advanced stage at diagnosis are more dependable than precise estimates for temporal trends, environmental risks, or uncommon hereditary associations.

A further interpretive issue is referral context. ACC is rare even among patients with adrenal lesions, but its apparent frequency rises sharply in surgical and tertiary-center cohorts that are enriched for suspicious masses.410 This makes population-based estimates essential for pretest probability, while reminding clinicians and researchers that institutional case mixes may not reflect general practice.

Population frequency and demographic distribution

Across modern registry studies, ACC incidence is generally reported at about 0.1 per 100,000 persons per year, or roughly 1 case per million annually.21163 Some datasets suggest modest increases over time, whereas others show long-term stability; taken together, the evidence supports persistent rarity more strongly than a confirmed secular rise in biologic occurrence.1263 The reliable conclusion is that ACC remains an exceptionally uncommon cancer, and apparent incidence shifts may reflect coding, ascertainment, or diagnostic practice as much as true epidemiologic change.

Most adult cases are diagnosed in the fifth to sixth decade of life.2136 Historical literature has described a bimodal age pattern with a childhood peak, but this is more evident in pooled reviews than in adult-focused registries and should be interpreted in light of the distinct biology of pediatric ACC.8 Clinically, this supports treating pediatric and adult ACC as related but epidemiologically separate groups when considering risk and outcomes.

A slight female predominance is one of the more reproducible demographic observations.142156 However, not all cohorts show the same pattern, and male predominance in some institutional or historical datasets likely reflects small numbers or referral effects rather than a settled biologic rule.71610 Reported laterality differences, including a possible excess of left-sided tumors, remain of uncertain significance.15

Race and ethnicity analyses have so far suggested more similarity than difference in adjusted survival outcomes within U.S. registry data, although age at diagnosis and some local tumor features may vary between groups.1718 These findings are useful for broad epidemiologic description but are limited for mechanistic inference because registries do not capture endocrine phenotype, germline predisposition, or access-to-care detail comprehensively.

ACC in the broader adrenal-mass population

Population epidemiology of ACC is best understood against the background of adrenal incidentalomas, most of which are benign and nonmalignant.4 In incidentaloma cohorts, ACC accounts for only a small minority of lesions, whereas adrenalectomy series and tertiary referral cohorts substantially overrepresent malignancy because they selectively include larger, functional, or radiographically suspicious tumors.410 The practical implication is that the prevalence of ACC depends heavily on the population being sampled and should not be extrapolated across settings without adjustment for referral bias.

This broader diagnostic context also helps explain why increased use of cross-sectional imaging has not clearly translated into earlier ACC detection at the population level. Retrospective national data suggest no consistent reduction in tumor size, no major stage migration, and no clear survival improvement attributable to incidental imaging alone.5 What is reliable here is the continued tendency toward advanced presentation; what is less reliable is any assumption that rising imaging intensity by itself materially changes ACC outcomes.

Stage and clinical phenotype at presentation

A large proportion of patients with ACC present with regional extension or metastatic disease rather than organ-confined tumors.52136 This is among the strongest and most consistent findings in population studies. Its clinical importance is direct: epidemiologic survival patterns largely reflect the frequency with which ACC is unresectable or systemically advanced at diagnosis.

Hormonal presentation is more variable than stage distribution. Functional ACC is well recognized, but population-based evidence indicates that overt hormone excess characterizes only a subset of cases, and many patients do not present through classic endocrine syndromes.19 Historical summaries suggest that functional presentation may be more common in childhood and nonfunctional tumors more common in older adults, but this pattern is supported mainly by aggregated reviews rather than uniformly phenotyped registries.8 The practical implication is that absence of overt hormone excess does not substantially reduce concern for ACC when other clinical or imaging features are suspicious.

These phenotype patterns lead directly to population outcomes. Because advanced stage is common at diagnosis, overall survival for ACC remains poor in registry-based cohorts.2123

Hereditary and environmental risk context

Most ACC appears sporadic, but a minority occurs in the setting of inherited cancer predisposition. The best-supported hereditary contexts are TP53-related syndromes and Beckwith-Wiedemann spectrum, with Lynch syndrome increasingly recognized as an uncommon but plausible association.202122 These associations are sufficiently established to matter in clinical genetics, especially in children, younger adults, and patients with multiple primaries or suggestive family histories.

By contrast, evidence for other predisposition settings is much weaker. Reported associations with NF1, CHEK2, ATM, MEN1, congenital adrenal hyperplasia-related pathways, and ARMC5 rely largely on case reports, small series, or unresolved variant interpretation and do not yet support reliable population-level risk estimates.23242526272829 Familial adenomatous polyposis appears to increase detection of adrenal lesions, but available cohorts suggest that most of these lesions are benign and that ACC remains rare even in that population.3031 The clinical implication is that established hereditary syndromes should prompt targeted evaluation, whereas isolated reports should not be treated as evidence for broad screening programs.

Environmental risk data remain limited and methodologically fragile. Smoking has been associated with ACC in exploratory and retrospective studies, but residual confounding, rarity of disease, and possible case-classification issues make causality uncertain.932 Geographic analyses are similarly mixed, with some studies showing no clustering and others reporting regional variation that could reflect environment, rurality, socioeconomic differences, or ascertainment artifacts.1133 At present, no environmental exposure has evidence comparable in strength to the best-established hereditary risk settings.

Survival and population-level outcomes

Population outcomes for ACC are poor, with prognosis strongly associated with age, stage, local invasion, nodal disease, distant metastasis, and whether surgical treatment is performed.3423 These relationships are consistent across retrospective datasets and align with the central role of complete resection in potentially curative management. What is reliable is the broad prognostic gradient between localized operable disease and advanced unresectable disease; what is less reliable is any precise survival estimate for an individual patient derived from registry data alone.

Some studies also identify social and health-system correlates of outcome, such as marital status.34 These associations may reflect support, access, and treatment delivery rather than tumor biology, so they are better viewed as markers of care context than as intrinsic prognostic factors.

Interpretation and research implications

Taken together, population studies show ACC to be a rare adrenal malignancy that is uncommon even within the much larger population of adrenal masses and that often presents too late for favorable population-level outcomes.543 This epidemiologic framing is clinically useful for estimating pretest probability and for understanding why surgery remains central when disease is localized, while advanced disease drives much of the observed mortality burden.342

The main limitations of the field are persistent reliance on retrospective data, incomplete biologic annotation, variable pathology certainty in older literature, and inconsistent distinction between pediatric and adult disease.523 Future epidemiologic work is likely to be most informative when registry-scale incidence data are linked to standardized pathology review, endocrine phenotype, germline testing, and treatment detail.

Included Articles

  • PMID 1813685: A Japanese autopsy survey from 1973 to 1984 found 222 adrenocortical carcinomas and reported a male predominance, with age distributions of carcinoma and adenoma both peaking in the sixth decade. The authors also note that age at presentation did not reliably distinguish benign from malignant adrenocortical tumors.7
  • PMID 8242539: This review of 1,891 published ACC cases reports rarity, female predominance, a bimodal age distribution with peaks in the first and fifth decades, and age-related functional status patterns, with functional tumors common in children and nonfunctional tumors predominating in older patients. It also notes that most cases present at advanced stage.8
  • PMID 8621222: An exploratory adult case-control study of adrenal cancer, thought to be predominantly ACC, found a possible association between heavy smoking in men and oral contraceptive use in women, while alcohol, body size, and most dietary factors showed no clear relationship. The authors emphasize major histologic uncertainty and the need for further study.9
  • PMID 9293929: In a Cleveland Clinic familial adenomatous polyposis registry, adrenal incidentalomas detected by CT were more frequent than expected in the general population, while only one symptomatic ACC was identified among 15 adrenal masses. The authors conclude that incidental adrenal masses in FAP likely have limited clinical relevance and should be managed similarly to those in patients without FAP.30
  • PMID 11150379: A case report of ACC arising in a patient with a germline MSH2 mutation found the adrenal tumor was microsatellite stable and retained MSH2 and MLH1 expression, unlike the patient’s colorectal tumor. The authors therefore conclude this ACC was likely coincidental rather than part of the HNPCC/Lynch tumor spectrum.35
  • PMID 15170137: In a cohort of young patients with osteosarcoma and multiple primary cancers, one patient had adrenocortical carcinoma in infancy followed by osteosarcoma 10 years later, and this patient carried a germ-line p53 mutation. The report supports hereditary cancer predisposition as a relevant risk context for ACC.20
  • PMID 17848847: This review examines whether germline or somatic CYP21A2-related 21-hydroxylase deficiency predisposes to adrenal tumors, including rare ACC. It reports that CYP21A2 mutation carriers appear overrepresented among patients with adrenal masses, but mutation status does not correlate with endocrine testing or tumor features, arguing against a major tumorigenic mechanism.36
  • PMID 19494161: This U.S. epidemiologic review identifies adrenocortical carcinoma as one of the endocrine disorders with the lowest incidence and notes that data on adrenal disorders are sparse. The summary supports the rarity of ACC in population-based datasets.1
  • PMID 21788046: In a large National Cancer Database cohort of adults with ACC, fewer than half presented with localized disease, and increased cross-sectional imaging over more than two decades was not associated with smaller tumors, stage migration, or improved survival. The findings frame ACC as commonly advanced at diagnosis despite frequent incidental adrenal imaging.5
  • PMID 24369210: This review summarizes nine published ACC cases from Thailand reported between 1983 and 2012, noting sporadic occurrence, a marked male predominance, a broad age range from infancy to older adulthood, and that about two-thirds of cases were hormonally functional, most often producing cortisol or androgens.16
  • PMID 24474656: In adolescents and young adults aged 15 to 39 years, lack of insurance was associated with a higher risk of distant-stage cancer diagnosis overall, but this effect was substantially weaker for adrenocortical carcinoma than for cancers more amenable to early detection.37
  • PMID 25520849: This case report describes ACC arising in a patient with neurofibromatosis type 1 and notes that only a small number of NF1-associated ACC cases had been reported. Tumor loss of heterozygosity at the NF1 locus is presented as supportive, but not definitive, evidence that NF1 may contribute to ACC susceptibility.23
  • PMID 26742968: A SEER-based cohort study of 1,271 adults with ACC found that single, divorced, or widowed status was independently associated with worse overall and disease-specific survival versus married status. Older age, nodal involvement, higher T classification, and non-operative management also correlated with higher mortality.34
  • PMID 29377868: In a Canadian familial adenomatous polyposis cohort, adrenal masses were identified in 16% of patients, roughly higher than expected in the general population, but nearly all lesions were benign and no APC genotype-phenotype correlation for adrenal lesions was found. One ACC-related death occurred among 63 adrenal masses.31
  • PMID 29956810: In a TCGA-based pan-cancer analysis, adrenocortical carcinoma was reported to be more frequent in females than males and to show a relatively young age at initial pathologic diagnosis, with cases skewing toward patients in their 20s to 30s.14
  • PMID 29977421: A SEER-based U.S. population study found ACC incidence remained low and largely stable at 1.02 per million from 1973 to 2014, with predominance in females, White patients, and adults diagnosed at a median age of 55 years. Most tumors were unilateral and many patients presented with advanced, high-grade disease and poor survival.2
  • PMID 30561782: A SEER population analysis of primary adrenal malignancies found ACC to be the most common subtype after age 30 years, with a mean presentation age of 53 years. ACC incidence increased over time, most often presented with localized or regional rather than distant disease, and had a 5-year cancer-specific survival of 38% without clear survival improvement over four decades.12
  • PMID 30623166: This case report describes ACC in a 48-year-old woman with a pathogenic germline CHEK2 c.1100delC deletion, presented as the first reported association of this variant with ACC. The authors place it in the context of hereditary predisposition in a minority of ACC cases and note that causality and management implications remain uncertain.24
  • PMID 31094003: In a population-based Swedish cohort of endogenous Cushing’s syndrome diagnosed from 2002 to 2017, cortisol-producing adrenocortical carcinoma accounted for 5 of 82 cases, with an estimated annual incidence of 0.2 cases per million. Among 34 ACC cases identified in the region, only a minority had overt hypercortisolism meeting Cushing’s syndrome criteria.19
  • PMID 31958848: In a retrospective cohort of 755 adrenal incidentaloma patients, adrenocortical carcinoma was identified in 1.5% of cases. The study also describes the broader incidentaloma context, with most lesions nonfunctional and detected incidentally on CT in a predominantly female, middle-aged population.4
  • PMID 32451468: In a population-based German cohort of 321 children with molecularly confirmed Beckwith-Wiedemann spectrum, adrenocortical carcinoma occurred as a rare tumor within a markedly elevated overall childhood cancer risk. The highest cancer risk was associated with paternal uniparental disomy of 11p15.5, supporting Beckwith-Wiedemann spectrum as an ACC predisposition context.21
  • PMID 32871402: A nationwide multicenter analysis reported a positive association between smoking and ACC, including a state-level correlation between smoking prevalence and ACC incidence and higher tobacco-use prevalence among ACC cases than melanoma controls. The study frames smoking as a possible environmental or lifestyle risk factor for adrenal carcinogenesis.32
  • PMID 33185660: This review and retrospective Lynch syndrome cohort study supports ACC as a Lynch-associated tumor, with three nonsecreting ACC cases among 634 carriers, all in MSH2 mutation carriers, and an estimated markedly elevated standardized incidence ratio versus the general population. It also notes prior reports of about 3.2% Lynch syndrome prevalence among ACC cases.22
  • PMID 33836455: This case report describes a patient with ACC carrying a germline pathogenic ATM frameshift variant with tumor loss of heterozygosity, suggesting a possible hereditary risk association. The article places ATM alongside established hereditary contexts for ACC but emphasizes that the finding is preliminary and requires further validation.25
  • PMID 35976672: A Japanese hospital-based cancer registry study found ACC was the most common histologically confirmed adrenal malignancy overall, occurred mainly around the sixth decade, showed a slight female predominance, and was stage IV in 46.3% of cases with available staging data.13
  • PMID 36288855: A SEER-based comparison found that Hispanic adults with ACC were younger at diagnosis than Caucasians and had higher T3-4 primary tumor rates, but similar ENSAT stage distribution, treatment patterns, cancer-specific mortality, and other-cause mortality after adjustment.17
  • PMID 37043366: A SEER-based comparison of African American and Caucasian adults with ACC found no meaningful differences in stage, grade, treatment type, cancer-specific mortality, or other-cause mortality after propensity matching. The study suggests race/ethnicity was not associated with more advanced presentation or worse survival in this ACC cohort.18
  • PMID 37647861: In a multicenter cohort of 1,858 patients with adrenocortical carcinoma, ACC was more frequent in females than males, with a female predominance that was stronger in patients 18 years or younger. ACC also occurred more often in the left adrenal than the right, and women were slightly younger at diagnosis.15
  • PMID 37858722: A Texas cancer registry analysis from 2000 to 2018 found stable ACC incidence of about 0.104 per 100,000 persons per year, a slight female predominance, and no clear county-level geographic clustering. The findings argue against an obvious environmental hotspot signal in this dataset.11
  • PMID 38002081: This review of adrenal tumors in congenital adrenal hyperplasia notes that adrenocortical carcinoma is extremely rarely reported in CAH, and it remains unclear whether CAH confers a higher ACC prevalence than the general population. The article frames CAH as a possible but unproven risk context when evaluating adrenal masses.26
  • PMID 38370442: A Danish population-based cohort from 2003-2019 found an age-adjusted ACC incidence of 1.4 per million per year, with female predominance and a significant annual incidence increase observed only in women. The cohort also showed mean diagnostic age near 56 years and frequent presentation with advanced disease.6
  • PMID 39909739: This letter discusses germline risk interpretation in adult sporadic ACC, emphasizing that an ARMC5 c.2192C>G variant was enriched in an ACC cohort but remains of uncertain clinical significance. The authors state that carriers should not currently be managed as having an ACC-predisposing condition, while noting a possible but extremely rare progression from PBMAH to ACC.27
  • PMID 39915149: This letter argues that current evidence does not support ARMC5 as a germline predisposition gene for adrenocortical carcinoma. The discussed ARMC5 variants are considered likely benign by ACMG-style interpretation, lack consistent second-hit evidence, and have not been linked to ACC across reported PBMAH cohorts.28
  • PMID 39935491: This case report frames MEN1 as a rare hereditary context for ACC and notes that ACC incidence appears higher in MEN1-associated adrenal tumors than in sporadic adrenal incidentalomas. It emphasizes MEN1 mutation testing and family screening when ACC occurs in a syndromic endocrine setting.29
  • PMID 40206460: A Colorado retrospective and registry-based analysis found ACC incidence near 1 case per million overall, with a higher age-adjusted incidence in Western than Eastern Colorado across both institutional and state datasets. The authors suggest this geographic pattern may reflect environmental, socioeconomic, or rurality-related risk factors, while emphasizing data and diagnostic limitations.33
  • PMID 40851244: A retrospective Romanian tertiary-center adrenalectomy series found adrenocortical carcinoma in 11.2% of adrenal tumors, with a nonsignificant decrease from 16.3% in 2001–2011 to 7.4% in 2012–2022 despite increased overall adrenal surgeries. ACC cases were more frequent in men in this cohort, and two presented with metastatic disease at diagnosis.10
  • PMID 41394112: A population-based Zurich cancer registry study spanning 1980 to 2022 found that ACC incidence remained stable over four decades, with an age-standardized incidence rate of 0.2 per 100,000 in 2022 and no significant average annual increase. The cohort included 76 ACC cases, and reported median overall survival for ACC was 2.2 years.3

References

Footnotes

  1. Clinical review: Prevalence and incidence of endocrine and metabolic disorders in the United States: a comprehensive review.. J Clin Endocrinol Metab. 2009. PMID: 19494161. Local full text: 19494161.md ↩ ↩2

  2. The Characteristics and Trends in Adrenocortical Carcinoma: A United States Population Based Study.. J Clin Med Res. 2018. PMID: 29977421. Local full text: 29977421.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11

  3. Rising Incidence of Neuroendocrine Neoplasms in Northern Switzerland-Data From the Cancer Registry.. J Endocr Soc. 2026. PMID: 41394112. Local full text: 41394112.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9

  4. Clinical Characteristics and Follow-Up Results of Adrenal Incidentaloma.. Exp Clin Endocrinol Diabetes. 2021. PMID: 31958848. Local full text: 31958848.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6

  5. Effects of increased cross-sectional imaging on the diagnosis and prognosis of adrenocortical carcinoma: analysis of the National Cancer Database.. J Urol. 2011. PMID: 21788046. Local full text: 21788046.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7

  6. Incidence, Treatment, and Survival of Adrenocortical Carcinoma in Denmark 2003-2019.. J Endocr Soc. 2024. PMID: 38370442. Local full text: 38370442.md ↩ ↩2 ↩3 ↩4 ↩5 ↩6 ↩7

  7. Primary adrenocortical tumors in autopsy records—a survey of “Cumulative Reports in Japan” from 1973 to 1984.. Jpn J Surg. 1991. PMID: 1813685. Local full text: 1813685.md ↩ ↩2 ↩3

  8. Adrenal cortical carcinoma. Epidemiology and treatment with mitotane and a review of the literature.. Cancer. 1993. PMID: 8242539. Local full text: 8242539.md ↩ ↩2 ↩3 ↩4

  9. Risk factors for adrenal cancer: an exploratory study.. Int J Cancer. 1996. PMID: 8621222. Local full text: 8621222.md ↩ ↩2 ↩3

  10. Clinicopathological spectrum of adrenal tumors: a retrospective study from a Romanian tertiary referral center.. Rom J Morphol Embryol. 2025. PMID: 40851244. Local full text: 40851244.md ↩ ↩2 ↩3 ↩4

  11. Incidence and Geographical Distribution of Adrenocortical Carcinoma: Retrospective Analysis of a State Cancer Registry.. Endocr Pract. 2024. PMID: 37858722. Local full text: 37858722.md ↩ ↩2 ↩3

  12. The who, when, and why of primary adrenal malignancies: Insights into the epidemiology of a rare clinical entity.. Cancer. 2019. PMID: 30561782. Local full text: 30561782.md ↩ ↩2 ↩3

  13. Clinicopathological features of adrenal malignancies: Analysis of hospital-based cancer registry data in Japan.. Int J Urol. 2022. PMID: 35976672. Local full text: 35976672.md ↩ ↩2 ↩3

  14. Impact of sex, body mass index and initial pathologic diagnosis age on the incidence and prognosis of different types of cancer.. Oncol Rep. 2018. PMID: 29956810. Local full text: 29956810.md ↩ ↩2

  15. Asymmetric Adrenals: Sexual Dimorphism of Adrenal Tumors.. J Clin Endocrinol Metab. 2024. PMID: 37647861. Local full text: 37647861.md ↩ ↩2 ↩3

  16. Adrenal cortical carcinoma in Thailand: a review on the previous reported case.. Indian J Cancer. 2013. PMID: 24369210. Local full text: 24369210.md ↩ ↩2

  17. Hispanic vs. Caucasian Race/Ethnicity in Adrenocortical Carcinoma Patients.. Anticancer Res. 2022. PMID: 36288855. Local full text: 36288855.md ↩ ↩2

  18. African American vs Caucasian race/ethnicity in adrenocortical carcinoma patients.. Endocr Relat Cancer. 2023. PMID: 37043366. Local full text: 37043366.md ↩ ↩2

  19. The incidence of endogenous Cushing’s syndrome in the modern era.. Clin Endocrinol (Oxf). 2019. PMID: 31094003. Local full text: 31094003.md ↩ ↩2

  20. Multiple primary cancers in patients with osteosarcoma: influence of anticancer drugs and genetic factors.. Am J Clin Oncol. 2004. PMID: 15170137. Local full text: 15170137.md ↩ ↩2

  21. Cancer incidence and spectrum among children with genetically confirmed Beckwith-Wiedemann spectrum in Germany: a retrospective cohort study.. Br J Cancer. 2020. PMID: 32451468. Local full text: 32451468.md ↩ ↩2

  22. Characteristics of Adrenocortical Carcinoma Associated With Lynch Syndrome.. J Clin Endocrinol Metab. 2021. PMID: 33185660. Local full text: 33185660.md ↩ ↩2

  23. Adrenal cancer in neurofibromatosis type 1: case report and DNA analysis.. Endocrinol Diabetes Metab Case Rep. 2014. PMID: 25520849. Local full text: 25520849.md ↩ ↩2

  24. Case Report of an Adrenocortical Carcinoma Associated With Germline CHEK2 Mutation.. J Endocr Soc. 2019. PMID: 30623166. Local full text: 30623166.md ↩ ↩2

  25. Ataxia telangiectasia mutated germline pathogenic variant in adrenocortical carcinoma.. Cancer Genet. 2021. PMID: 33836455. Local full text: 33836455.md ↩ ↩2

  26. Landscape of Adrenal Tumours in Patients with Congenital Adrenal Hyperplasia.. Biomedicines. 2023. PMID: 38002081. Local full text: 38002081.md ↩ ↩2

  27. Response to letter to the editor on “Germline NGS targeted analysis in adult patients with sporadic adrenocortical carcinoma”.. Eur J Cancer. 2025. PMID: 39909739. Local full text: 39909739.md ↩ ↩2

  28. Letter Re: Germline NGS targeted analysis in adult patients with sporadic adrenocortical carcinoma.. Eur J Cancer. 2025. PMID: 39915149. Local full text: 39915149.md ↩ ↩2

  29. Multiple Endocrine Neoplasia Type 1 With Adrenal Cortical Adrenocortical Carcinoma: A 25-Year Follow-Up and Family Report.. JCEM Case Rep. 2025. PMID: 39935491. Local full text: 39935491.md ↩ ↩2

  30. Adrenal masses in patients with familial adenomatous polyposis.. Dis Colon Rectum. 1997. PMID: 9293929. Local full text: 9293929.md ↩ ↩2

  31. Characteristics of Adrenal Masses in Familial Adenomatous Polyposis.. Dis Colon Rectum. 2018. PMID: 29377868. Local full text: 29377868.md ↩ ↩2

  32. Smoking is associated with adrenal adenomas and adrenocortical carcinomas: a nationwide multicenter analysis.. Cancer Treat Res Commun. 2020. PMID: 32871402. Local full text: 32871402.md ↩ ↩2

  33. Geographical Variation in Adrenocortical Carcinoma Incidence Across Colorado.. J Endocr Soc. 2025. PMID: 40206460. Local full text: 40206460.md ↩ ↩2

  34. Beyond biology: the impact of marital status on survival of patients with adrenocortical carcinoma.. Int Braz J Urol. 2015. PMID: 26742968. Local full text: 26742968.md ↩ ↩2 ↩3 ↩4

  35. Adrenocortical adenocarcinoma in an MSH2 carrier: coincidence or causal relation?. Hum Pathol. 2000. PMID: 11150379. Local full text: 11150379.md ↩

  36. The role of 21-hydroxylase in the pathogenesis of adrenal masses: review of the literature and focus on our own experience.. J Endocrinol Invest. 2007. PMID: 17848847. Local full text: 17848847.md ↩

  37. Insurance status and distant-stage disease at diagnosis among adolescent and young adult patients with cancer aged 15 to 39 years: National Cancer Data Base, 2004 through 2010.. Cancer. 2014. PMID: 24474656. Local full text: 24474656.md ↩

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