Peri-Treatment Endocrine Support in ACC

Endocrine Supportive Management

Peri-treatment endocrine support in adrenocortical carcinoma (ACC) refers to the prevention, recognition, and treatment of hormone-related complications caused either by the tumor itself or by ACC-directed therapies. It sits within endocrine supportive management but is closely linked to surgery, systemic therapy, locoregional treatment, and survivorship because ACC may produce biologically active steroids and because mitotane can disrupt multiple endocrine axes.¹² The topic is therefore broader than adrenal replacement alone and includes management of hypercortisolism, monitoring for treatment-induced adrenal insufficiency, and surveillance for thyroid, gonadal, metabolic, and skeletal effects.³⁴

The most consistently documented endocrine complication is adrenal insufficiency during mitotane therapy. Mitotane accelerates steroid metabolism, alters cortisol-binding proteins, and complicates interpretation of standard biochemical tests, so replacement approaches often differ from those used in conventional primary adrenal insufficiency.⁵⁶⁷ At the same time, some ACCs present with clinically significant cortisol excess, creating a peri-treatment setting in which severe hypercortisolism may require urgent suppression before surgery or systemic treatment, followed by rapid transition to glucocorticoid deficiency once tumor secretion falls or therapy becomes effective.⁸⁹

Evidence in this area is limited and is derived mainly from retrospective referral-center series, physiologic studies, pediatric cohorts, and case reports rather than prospective comparative trials.¹¹⁰ As a result, several management principles are widely accepted, but many details of monitoring, dose adjustment, and long-term surveillance remain based on expert practice patterns rather than validated ACC-specific algorithms.⁶⁷

Clinical context

Endocrine instability in ACC may begin before anticancer treatment starts. Functioning tumors can produce cortisol and other steroids, contributing to hypertension, hypokalemia, hyperglycemia, infection risk, catabolism, and impaired tolerance of surgery or systemic therapy.⁸⁹ Conversely, successful treatment of hormonally active disease, including surgery, mitotane, steroidogenesis inhibition, or embolization-based procedures, may abruptly reduce steroid exposure and unmask adrenal insufficiency.¹¹¹²

This longitudinal pattern explains why endocrine support in ACC usually extends across the full treatment course rather than being confined to a single intervention. The reliable conclusion is that endocrine complications may materially affect treatment tolerance and acute safety; what remains less certain is the optimal surveillance schedule for all patients. In practice, repeated reassessment and patient education about adrenal decompensation are supported more consistently than any single laboratory-driven protocol.⁷¹

Major endocrine support domains

Adrenal insufficiency during mitotane therapy

Adrenal insufficiency is the best-supported endocrine toxicity of ACC treatment and appears particularly common during mitotane exposure.⁷¹ Retrospective adult and pediatric data suggest that most treated patients require glucocorticoid replacement, often at higher-than-standard doses because mitotane induces hepatic steroid metabolism and increases hormone clearance.⁵¹²⁴

Assessment of replacement adequacy is difficult. Total serum cortisol may be misleading because mitotane increases cortisol-binding globulin, and physiologic studies suggest that no single biomarker reliably defines sufficient replacement in this setting.¹³⁶ The practical implication is that symptoms, blood pressure, electrolytes, illness burden, and treatment timing remain essential components of assessment, with laboratory data interpreted in context rather than used in isolation.¹³¹

Recovery of the hypothalamic-pituitary-adrenal axis after mitotane cessation may occur but is often delayed. Cohort data indicate that recovery can take many months to years, so continued replacement should be reassessed over time, but empiric withdrawal without structured follow-up is not well supported.⁷²

Mineralocorticoid support

Some patients also develop clinically relevant mineralocorticoid deficiency, with hypotension, hyponatremia, or hyperkalemia prompting fludrocortisone replacement.¹⁴⁷ Pediatric experience suggests that this burden may be substantial in some populations, whereas adult reports are more variable.⁴

The consistent point is that mineralocorticoid replacement is sometimes necessary but should not be assumed for every patient receiving mitotane. Individualized assessment based on electrolytes, blood pressure, and volume status appears more reliable than fixed routine supplementation.⁷⁴

Control of hypercortisolism in functioning ACC

In cortisol-secreting ACC, endocrine support may initially focus on reducing hormone excess rather than replacing deficient hormones. Available reports suggest that steroidogenesis inhibitors, and in selected situations glucocorticoid receptor blockade, may help stabilize patients with severe hypercortisolism before surgery or during systemic treatment.⁸⁹

Evidence for optimal sequencing is limited and largely case-based, so comparative effectiveness is uncertain. Still, the clinical implication is relatively clear: severe cortisol excess may require parallel endocrine treatment because uncontrolled hypercortisolism can worsen metabolic, cardiovascular, infectious, and thrombotic risk during cancer care.⁹¹⁰

Other endocrine and metabolic toxicities

Beyond adrenal dysfunction, mitotane may affect several endocrine and metabolic systems. Retrospective adult and pediatric series describe low free thyroxine or central hypothyroid patterns, dyslipidemia, gonadal dysfunction, and abnormalities of puberty or sexual development.²¹⁵⁴ These abnormalities often emerge early in therapy and are commonly managed with standard supportive interventions such as levothyroxine or lipid-lowering treatment, although ACC-specific long-term outcome data remain sparse.³²

Bone health is an additional concern during prolonged treatment. Retrospective morphometric data suggest an increased burden of vertebral fractures over time in patients exposed to mitotane-containing regimens.¹⁶ This association has not been tested in prospective fracture-prevention trials, but it is sufficiently consistent to support baseline risk assessment and preventive bone-health measures during long-term therapy.¹⁶

Taken together, these findings indicate that endocrine support in ACC is multisystem rather than adrenal-specific. The reliable message is that thyroid, gonadal, lipid, and skeletal complications may accompany mitotane; what remains uncertain is the ideal screening interval and whether aggressive correction changes oncologic outcomes.³²

Pitfalls and differential diagnosis

The principal acute endocrine hazard is adrenal crisis or significant adrenal decompensation, which may present with nonspecific fatigue, anorexia, gastrointestinal symptoms, hypotension, or electrolyte abnormalities.¹¹¹² This presentation overlaps with cancer progression, postoperative decline, infection, and general treatment toxicity, making delayed recognition a recurrent risk.¹

Hypercortisolism introduces additional complexity because it may increase susceptibility to thrombosis and infection. Retrospective ACC data identify venous thromboembolism as an important complication, particularly in advanced disease, but ACC-specific prophylaxis strategies remain insufficiently defined.¹⁰ Clinically, this supports individualized assessment during high-risk periods rather than reliance on a uniform protocol.

When the pattern of adrenal dysfunction is atypical, alternative mechanisms should be considered. Indirect oncology literature indicates that central adrenal insufficiency from checkpoint inhibitor-associated hypophysitis or, more rarely, primary adrenal failure from immune-mediated injury can mimic mitotane-related toxicity.^17181920 Similarly, persistent postoperative symptoms after unilateral adrenalectomy or unexplained symptoms during multikinase inhibitor therapy may justify broader endocrine evaluation rather than automatic attribution to mitotane.²¹²² Severe infection can also resemble endocrine decompensation, particularly in patients with cortisol excess or heavy prior treatment exposure.²³

Role in management and research

Peri-treatment endocrine support is a core component of ACC management because endocrine complications may limit tolerance of surgery, systemic therapy, and prolonged mitotane treatment.¹³ Compared with a purely tumor-directed approach, proactive endocrine management may reduce preventable crises and facilitate continuation of intended anticancer therapy, although direct comparative outcome evidence is limited.¹

Current literature most strongly supports several practical principles: anticipatory glucocorticoid replacement during mitotane therapy, readiness to use higher-than-standard doses when clinically indicated, selective mineralocorticoid replacement, active treatment of severe hypercortisolism, and continued reassessment after treatment cessation because recovery may be delayed but remains possible.⁷¹⁴ What is less reliable is the precision of available monitoring tools, since no single biomarker or algorithm has been validated as definitive for ACC-specific endocrine support.⁶

Research needs include prospective definitions of optimal replacement strategies during mitotane therapy, better biomarkers of treatment-induced adrenal insufficiency, and clearer supportive-care pathways for thrombosis prevention, thyroid and gonadal surveillance, and bone protection.⁶¹⁰¹⁶ Until stronger evidence is available, multidisciplinary endocrine follow-up remains the approach most consistent with the published literature.¹⁷

Included Articles

• PMID 2574647: This case report describes mitotane-associated hepatic microsomal enzyme induction in metastatic ACC, with accelerated metabolism of replacement steroids and recurrent adrenal crisis despite conventionally adequate dosing. It highlights that patients on mitotane may require unusually high glucocorticoid and mineralocorticoid replacement and close monitoring for adrenal insufficiency.⁵

• PMID 5933557: This case report describes hyperfunctioning metastatic ACC treated with op’-DDD plus fluorouracil, followed by biochemical and clinical adrenal insufficiency with hyponatremia, hyperkalemia, absent urinary steroid production, and steroid-responsive symptoms requiring prednisone and fludrocortisone replacement.¹⁴

• PMID 17966598: This case of functioning metastatic ACC highlights intensive endocrine supportive care for severe hypercortisolism, hypokalemia, hypertension, and hyperglycemia. Aminoglutethimide improved cortisol-related complications, while hydrocortisone replacement was required after combined mitotane and steroidogenesis inhibition caused adrenal insufficiency.⁸

• PMID 22908067: In ACC patients receiving mitotane, monitoring glucocorticoid replacement is complicated by increased cortisol-binding globulin, altered steroid clearance, and assay cross-reactivity. Salivary cortisol measured by LC-MS/MS appears more selective than immunoassay and may better guide hydrocortisone replacement during treatment-induced adrenal insufficiency.¹³

• PMID 28780517: In ACC patients receiving adjuvant mitotane after R0 resection, mitotane impaired the hypothalamic-pituitary-adrenal axis at multiple levels, with low serum and salivary cortisol, elevated cortisol-binding globulin, suppressed DHEAS, and lower ACTH responses than primary adrenal insufficiency controls. The study concludes that no single biomarker reliably assesses mitotane-induced adrenal insufficiency, complicating glucocorticoid replacement management.⁶

• PMID 30159150: This pediatric case report highlights that mitotane can cause severe, persistent endocrine toxicity in childhood ACC, including adrenal insufficiency requiring supraphysiologic hydrocortisone, probable central hypothyroidism responsive to levothyroxine, and peripheral precocious puberty with later secondary central precocious puberty.¹⁵

• PMID 32164326: In patients with resected stage I–III ACC treated with adjuvant mitotane, adrenal insufficiency requiring glucocorticoid replacement was universal during therapy, but complete hypothalamic-pituitary-adrenal axis recovery occurred in most patients after stopping mitotane and was often delayed for about 2.7 years. The study supports ongoing hormonal reassessment after mitotane cessation to guide withdrawal of glucocorticoid and, when used, mineralocorticoid replacement.⁷

• PMID 32996176: In a retrospective cohort of 50 ACC patients on mitotane, treatment commonly caused major metabolic and endocrine toxicities including hyperlipidemia, low T4/free T4 with unchanged TSH, gonadal hormone disruption, and adrenal insufficiency. Statins and thyroxine improved biochemical abnormalities, and adrenal function recovered in many patients months after stopping mitotane.²

• PMID 34621849: This case report describes acute adrenal hypofunction after TACE for hormone-secreting ACC liver metastasis, presenting with hypotension, fatigue, anorexia, hyponatremia, very low cortisol, and elevated ACTH. Symptoms improved with hydrocortisone, supporting post-TACE hormone monitoring and prompt glucocorticoid replacement when adrenal insufficiency is suspected.¹¹

• PMID 34905056: In ACC patients receiving prolonged mitotane with or without chemotherapy, morphometric vertebral fractures increased during treatment, and fracture progression was associated with baseline vertebral fractures and higher body mass index rather than glucocorticoid replacement dose. The study supports implementing preventive bone-protection measures during mitotane therapy.¹⁶

• PMID 35670031: This systematic review highlights adrenal insufficiency as a common, clinically significant complication of ACC treatment, especially mitotane, with onset often within weeks to months and prolonged effects after discontinuation. It emphasizes the need for higher glucocorticoid replacement doses, sick-day education, and caregiver support to prevent adrenal crisis and treatment-related morbidity.¹

• PMID 36447829: This case highlights urgent endocrine management of life-threatening hypercortisolism from metastatic ACC using steroidogenesis inhibition or glucocorticoid receptor blockade alongside mitotane and chemotherapy, with thrombosis and infection prophylaxis and later high-dose glucocorticoid replacement after mitotane-induced adrenal insufficiency.⁹

• PMID 38736192: This pediatric ACC case highlights that mitotane can markedly increase exogenous steroid requirements through accelerated steroid metabolism, with adrenal crisis occurring within 2 days of treatment initiation. Close monitoring and individualized glucocorticoid replacement, potentially around three times standard maintenance dosing, may be necessary during mitotane therapy.¹²

• PMID 38776552: A retrospective referral-center cohort found venous thromboembolism in 18.7% of adults with ACC, usually after diagnosis and predominantly in stage 3 or 4 disease, with pulmonary embolism common and substantial short-term mortality after events. The study highlights thrombosis as an important supportive-care issue and notes uncertainty about ACC-specific prophylaxis duration and risk stratification.¹⁰

• PMID 40793901: A six-patient ACC case series found that mitotane-related adverse events appeared early, usually within the first three months and often at low doses, with endocrine toxicities predominating. Adrenal insufficiency, hypothyroidism, hypercholesterolemia, and occasional hypogonadism were managed with prompt hormone replacement and CYP3A4-sparing statins.³

• PMID 40868483: In a 20-year retrospective pediatric ACC series, mitotane was associated with frequent endocrine toxicities including universal adrenal insufficiency requiring supraphysiologic hydrocortisone, frequent mineralocorticoid replacement, precocious puberty or gynecomastia, and central hypothyroidism. The report supports regular mitotane level monitoring plus proactive multidisciplinary endocrine surveillance and replacement management throughout therapy.⁴

• PMID 3400766: A 1988 case series of high-dose suramin in unresectable ACC reported bilateral vortex keratopathy in all six treated patients, with occasional corneal symptoms and lens epithelial opacities but no clinical retinopathy on short-term assessment. The article is indirectly relevant to endocrine support because it broadens supportive-care considerations to non-endocrine toxicities associated with older ACC systemic therapy.²⁴

• PMID 10526944: A case report of long-term high-dose fosfestrol therapy causing secondary adrenal insufficiency in prostate cancer extends the ACC supportive-care note by highlighting that treatment-related hypoadrenalism in oncology can rarely be central rather than purely adrenal or mitotane-related. Its relevance to ACC is indirect but supports broader diagnostic caution when symptoms are discordant with usual replacement expectations.²⁵

• PMID 15251609: A 1995 case report described autoimmune Addison’s disease emerging after IL-2/TIL immunotherapy for metastatic renal cell carcinoma, documented by conversion to positive adrenal antibodies and impaired cortisol and aldosterone responses. For ACC supportive care, this serves as indirect historical evidence that some anticancer immunotherapies can rarely cause primary adrenal failure with mineralocorticoid deficiency.²⁰

• PMID 18520491: A postoperative autopsy case showed rapidly falling cortisol levels and fatal acute adrenal insufficiency after near-total loss of functional adrenal tissue, despite initially nonspecific findings and normal electrolytes. For ACC, the report indirectly reinforces the risk of abrupt perioperative adrenal decompensation and the importance of stress-context interpretation of cortisol values.²⁶

• PMID 27398811: A veterinary retrospective series of bilateral adrenalectomy found that planned postoperative hypoadrenocorticism could be managed with immediate perioperative dexamethasone, ongoing prednisone, mineralocorticoid replacement, and scheduled electrolyte surveillance. Its relevance to ACC is indirect but supports anticipatory replacement strategies when adrenal function is lost after major adrenal intervention.²⁷

• PMID 29390437: A case report outside ACC described chronic primary adrenal insufficiency after unilateral adrenonephrectomy complicated by major postoperative stress and sepsis, suggesting that reduced adrenal reserve after unilateral resection may rarely become clinically important. Its relevance to ACC is indirect but supports postoperative diagnostic caution when symptoms persist after adrenalectomy.²¹

• PMID 34092725: A non-ACC case report described nivolumab-associated adrenal insufficiency with atypical systemic immune toxicity, illustrating that checkpoint inhibitors can produce central or mixed adrenal dysfunction and thereby complicate attribution of adrenal symptoms in oncology patients.¹⁷

• PMID 34285878: A 2021 case report describes pembrolizumab-associated secondary adrenal insufficiency due to isolated ACTH deficiency with pituitary atrophy/empty sella, illustrating a central mechanism of checkpoint inhibitor-related adrenal dysfunction. Its ACC relevance is indirect but supports broader endocrine differential diagnosis when immunotherapy is used.¹⁸

• PMID 36039252: A broad review of ocular toxicities from genitourinary cancer therapies includes agents used in ACC, notably cisplatin, carboplatin, and etoposide, and describes mostly rare but occasionally serious visual adverse effects. Its ACC relevance is indirect, adding a non-endocrine supportive-care consideration rather than changing current endocrine framing.²⁸

• PMID 38623179: A 2024 case report described suspected disseminated cutaneous Rhizopus infection in a patient with metastatic ACC, initially presenting with atypical skin lesions and no fever. For this note, its relevance is mainly differential-diagnostic caution: severe infection can mimic general treatment-related or cancer-related decline rather than a primary endocrine complication.²³

• PMID 39678875: A 2024 esophageal cancer case report describes adrenal insufficiency with very low ACTH and cortisol during PD-1 inhibitor rechallenge, with symptomatic improvement after hydrocortisone. Although not ACC-specific, it supports the note’s caution that immune checkpoint inhibitors can cause adrenal dysfunction that may mimic other treatment-related symptoms.¹⁹

• PMID 41188808: A retrospective study in metastatic renal cell carcinoma found that cabozantinib was associated with sustained ACTH elevation and a small number of ACTH stimulation test-confirmed cases of mild primary adrenal insufficiency, with symptom improvement after hydrocortisone. For ACC, the relevance is indirect and mainly concerns broader differential diagnosis during tyrosine kinase inhibitor therapy.²²

References

Footnotes

1. Lived experience of people with adrenocortical carcinoma and associated adrenal insufficiency.. Endocrinol Diabetes Metab. 2022. PMID: 35670031. Local full text: 35670031.md ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷ ↩⁸ ↩⁹ ↩¹⁰ ↩¹¹

2. Metabolic and hormonal side effects of mitotane treatment for adrenocortical carcinoma: A retrospective study in 50 Danish patients.. Clin Endocrinol (Oxf). 2021. PMID: 32996176. Local full text: 32996176.md ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶

3. Adverse events related to mitotane during treatment of adrenocortical carcinoma.. Medicina (B Aires). 2025. PMID: 40793901. Local full text: 40793901.md ↩ ↩² ↩³ ↩⁴ ↩⁵

4. Mitotane-Induced Endocrine Alterations in Children with Adrenocortical Carcinoma: Clinical Implications from a 20-Year Retrospective Study.. Children (Basel). 2025. PMID: 40868483. Local full text: 40868483.md ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷

5. Hepatic microsomal enzyme induction and adrenal crisis due to o,p’DDD therapy for metastatic adrenocortical carcinoma.. Clin Endocrinol (Oxf). 1989. PMID: 2574647. Local full text: 2574647.md ↩ ↩² ↩³

6. Effects of mitotane on the hypothalamic-pituitary-adrenal axis in patients with adrenocortical carcinoma.. Eur J Endocrinol. 2017. PMID: 28780517. Local full text: 28780517.md ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶

7. Recovery of Adrenal Insufficiency Is Frequent After Adjuvant Mitotane Therapy in Patients with Adrenocortical Carcinoma.. Cancers (Basel). 2020. PMID: 32164326. Local full text: 32164326.md ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷ ↩⁸ ↩⁹ ↩¹⁰

8. [Disseminated adrenocortical carcinoma: case report].. Pol Arch Med Wewn. 2007. PMID: 17966598. Local full text: 17966598.md ↩ ↩² ↩³ ↩⁴

9. Recurrent Cushing Syndrome From Metastatic Adrenocortical Carcinoma With Fumarate Hydratase Allelic Variant.. AACE Clin Case Rep. 2022. PMID: 36447829. Local full text: 36447829.md ↩ ↩² ↩³ ↩⁴ ↩⁵

10. Venous thromboembolism in adrenocortical carcinoma: a retrospective analysis.. Oncologist. 2024. PMID: 38776552. Local full text: 38776552.md ↩ ↩² ↩³ ↩⁴ ↩⁵

11. Rare complication of acute adrenocortical dysfunction in adrenocortical carcinoma after transcatheter arterial chemoembolization: A case report.. World J Clin Cases. 2021. PMID: 34621849. Local full text: 34621849.md ↩ ↩² ↩³

12. Exogenous steroid replacement in a pediatric patient with adrenocortical carcinoma receiving mitotane.. Pediatr Blood Cancer. 2024. PMID: 38736192. Local full text: 38736192.md ↩ ↩² ↩³ ↩⁴

13. Assessment of salivary free cortisol levels by liquid chromatography with tandem mass spectrometry (LC-MS/MS) in patients treated with mitotane.. Hormones (Athens). 2012. PMID: 22908067. Local full text: 22908067.md ↩ ↩² ↩³

14. Addison’s disease following combined chemotherapy for hyperfunctioning adrenocortical carcinoma.. Arch Intern Med. 1966. PMID: 5933557. Local full text: 5933557.md ↩ ↩²

15. Mitotane in the treatment of childhood adrenocortical carcinoma: a potent endocrine disruptor.. Endocrinol Diabetes Metab Case Rep. 2018. PMID: 30159150. Local full text: 30159150.md ↩ ↩²

16. Progression of Vertebral Fractures in Patients with Adrenocortical Carcinoma Undergoing Mitotane Therapy.. J Clin Endocrinol Metab. 2022. PMID: 34905056. Local full text: 34905056.md ↩ ↩² ↩³ ↩⁴

17. Nivolumab-induced Vogt-Koyanagi-Harada-like Syndrome and Adrenocortical Insufficiency with Long-term Survival in a Patient with Non-small-cell Lung Cancer.. Intern Med. 2021. PMID: 34092725. Local full text: 34092725.md ↩ ↩²

18. A case of secondary adrenocortical insufficiency due to isolated adrenocorticotropic hormone deficiency with empty sella syndrome after pembrolizumab treatment in a patient with metastatic renal pelvic cancer.. Urol Case Rep. 2021. PMID: 34285878. Local full text: 34285878.md ↩ ↩²

19. Long-survival of a patient with esophageal cancer benefited from comprehensive treatment and MDT: a case report.. J Thorac Dis. 2024. PMID: 39678875. Local full text: 39678875.md ↩ ↩²

20. Autoimmune Addison’s disease after treatment with interleukin-2 and tumor-infiltrating lymphocytes.. Endocr Pract. 1995. PMID: 15251609. Local full text: 15251609.md ↩ ↩²

21. Chronic primary adrenal insufficiency after unilateral adrenonephrectomy: A case report.. Medicine (Baltimore). 2017. PMID: 29390437. Local full text: 29390437.md ↩ ↩²

22. Effects of cabozantinib on plasma adrenocorticotropic hormone and serum cortisol levels in patients with metastatic renal cell carcinoma: a retrospective study.. BMC Endocr Disord. 2025. PMID: 41188808. Local full text: 41188808.md ↩ ↩²

23. Cutaneous mucormycosis with suspected dissemination in a patient with metastatic adrenocortical carcinoma.. Med Mycol Case Rep. 2024. PMID: 38623179. Local full text: 38623179.md ↩ ↩²

24. Suramin keratopathy.. Am J Ophthalmol. 1988. PMID: 3400766. Local full text: 3400766.md ↩

25. Adrenocortical insufficiency associated with long-term high-dose fosfestrol therapy for prostatic carcinoma.. Intern Med. 1999. PMID: 10526944. Local full text: 10526944.md ↩

26. Evaluation of serum cortisol in the postmortem diagnosis of acute adrenal insufficiency.. Am J Forensic Med Pathol. 2008. PMID: 18520491. Local full text: 18520491.md ↩

27. Perioperative Management and Outcome of Bilateral Adrenalectomy in 9 Dogs.. Vet Surg. 2016. PMID: 27398811. Local full text: 27398811.md ↩

28. Potential Ophthalmological Side Effects Induced by Anti-Neoplastic Regimens for the Treatment of Genitourinary Cancers: A Review.. Cureus. 2022. PMID: 36039252. Local full text: 36039252.md ↩