{"id":6585,"date":"2026-05-11T13:56:44","date_gmt":"2026-05-11T13:56:44","guid":{"rendered":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/?p=6585"},"modified":"2026-05-11T16:11:26","modified_gmt":"2026-05-11T16:11:26","slug":"when-prostate-cancer-reaches-the-orbit-a-case-report","status":"publish","type":"post","link":"https:\/\/journalofmedicaloptometry.com\/vol4issue2\/volume-4-issue-2\/when-prostate-cancer-reaches-the-orbit-a-case-report\/","title":{"rendered":"When Prostate Cancer Reaches the Orbit: A Case Report"},"content":{"rendered":"

ABSTRACT<\/strong><\/h2>\n

BACKGROUND<\/strong><\/h3>\n

The Global Cancer Observatory report ranks prostate cancer as the fourth highest incidence of cancer and the eighth leading cause of cancer death .[1]<\/sup><\/a> Most prostate adenocarcinomas are slow growing, whereas aggressive subtypes can be resistant to androgen-deprivation therapy and lethal.[2]<\/sup><\/a> According to the National Cancer Institute, 2021 data show that approximately 19 percent of men will be diagnosed with prostate cancer during their lifetime and about four percent will die from the disease.[3]<\/sup><\/a> Bone is a common site of metastasis from hematogenous spread, direct extension from adjacent tumors, or perineural spread; however, orbital metastasis is rare.[4]<\/sup><\/a>,[5]<\/a><\/sup><\/p>\n

CASE REPORT<\/strong><\/h3>\n

A 63-year-old man with a history of prostate cancer presented with recent-onset blurred vision in the left eye of 7 days\u2019 duration. Examination revealed decreased visual acuity, impaired color vision, and mild edema of the left optic nerve. He was urgently referred to the emergency department for magnetic resonance imaging of the brain and orbits to evaluate for structural optic nerve compromise. Imaging detected multiple cranial bone metastases, including a lesion involving the left anterior clinoid process, causing crowding of the left orbital apex and compression of the left optic nerve.<\/p>\n

CONCLUSION<\/strong><\/h3>\n

In this case of optic nerve compression from an orbital apex mass, the patient\u2019s oncologic history raised suspicion for metastatic disease. Axial tumor spread was likely hematogenous, with secondary orbital involvement from direct local extension. The presence of unilateral optic nerve edema prompted urgent neuroimaging, with giant cell arteritis remaining in the differential diagnosis. Once the space-occupying lesion was identified, oncology initiated systemic corticosteroids and local radiation to preserve vision.<\/p>\n

Keywords<\/strong>: orbital apex carcinoma, metastatic prostate cancer, prostate adenocarcinoma, bone metastasis, optic nerve edema, vision loss, optic nerve compression, orbital mass, androgen deprivation therapy<\/em><\/p>\n

 <\/p>\n

INTRODUCTION<\/strong><\/h2>\n

Prostate cancer is the most frequently diagnosed cancer among men in over one-half (105 of 185) of the countries of the world.[6]<\/sup><\/a> In North America, the incidence in 2022 was 255,800 and is projected to rise to 345,600 by 2050.6<\/sup> The same source projected a mortality increase from 39,600 cases in 2022 to 83,500 cases in 2050.6<\/sup> According to the National Cancer Institute, 2021 data indicate that approximately 19 percent of men will be diagnosed with prostate cancer during their lifetime, and 4 percent will die from the disease.3<\/sup><\/p>\n

Most prostate adenocarcinomas are slow-growing, yet aggressive types can be lethal and require intensive treatment.2,[7]<\/a><\/sup> Bone is a common site of metastasis, partly due to a direct connection via the valveless prostate venous system.[8]<\/sup><\/a> The bone microenvironment supports tumor growth, leading to osteoblastic lesions commonly seen in prostate cancer metastasis.8<\/sup> Meanwhile, molecular transformations allow tumor cells to attach, proliferate, and survive in bone.8<\/sup> Cancer cells may also produce pro-angiogenic and bone-resorbing factors, such as receptor activator of nuclear factor kappa-B ligand (RANKL) and vascular endothelial growth factor (VEGF), to modify the bone microenvironment and promote their growth.[9]<\/sup><\/a><\/p>\n

Orbit involvement occurs in less than one percent of prostate cancer patients, even among men with known metastatic disease.5<\/sup> Cases of metastasis to the orbital apex have been reported in the literature with variable presentations, including optic nerve edema, optic nerve compression, extraocular muscle thickening, ophthalmoplegia, ptosis, and proptosis.[10]<\/sup><\/a>,[11]<\/a>,[12]<\/a><\/sup> Wada et al. reported that the biopsy specimen from an orbital soft-tissue mass showed atypical cells with an increased nuclear-to-cytoplasmic ratio on hematoxylin and eosin staining, confirming the diagnosis of adenocarcinoma. Additionally, the immunohistochemical analysis of tumor tissue staining with pancytokeratin was consistent with prostate cancer metastasis.11,[13]<\/a><\/sup> Treatment modalities for orbital apex metastases include primary cancer-directed combination medical therapy and local radiation, though survival prognosis remains poor.13<\/sup><\/p>\n

CASE REPORT<\/strong><\/h2>\n

A 63-year-old man presented for an urgent evaluation with a one-week history of blurred vision in the left eye. He denied any eye trauma, headache, scalp tenderness, jaw claudication, malaise, or stroke symptoms. His medical history was notable for prostate cancer diagnosed in 2021, currently stage IV, previously treated with six cycles of docetaxel chemotherapy and currently managed with leuprolide-based androgen deprivation therapy. His medications included atorvastatin, apixaban, amlodipine, losartan, and metformin.<\/p>\n

On examination, visual acuity was 20\/20 in the right eye and 20\/70 in the left eye, compared to a previous low plus refraction of 20\/20 in both eyes seven months earlier. He was considered a pseudophakic emmetrope and was not using glasses. Generalized dyschromatopsia in the left eye was detected using Ishihara pseudoisochromatic plates, consistent with an afferent conduction deficit. His color vision was normal in the right eye, with all plates correctly identified. An afferent pupillary defect was not observed during this initial assessment, but was noted during a subsequent inpatient examination. Oculomotor function was intact, showing the full range of motion of the extraocular muscles in both eyes. Biomicroscopic examination of the anterior segment revealed typical anatomical structures without pathology. Both eyes had centered posterior chamber intraocular lenses. Intraocular pressures were within normal limits. A gross cranial nerve evaluation showed that CN I and CN III-XII were intact.<\/p>\n

Dilated fundus examination revealed a well-perfused optic nerve with a 0.20 cup-to-disc ratio in both eyes. The left optic nerve had a small inferior temporal optic disc hemorrhage and diffuse 1+ edema. Optic nerve pallor was not detected. The macula was flat with uniform pigmentation and no edema in either eye. Retinal vasculature exhibited moderate-severe arterial sclerosis, and no emboli were detected. Both the vitreous and peripheral retina were unremarkable. Structure and functional image analysis of both eyes, including color fundus photography, optic nerve optical coherence tomography (OCT), and Humphrey 24-2 Sita Standard visual field testing (Figure 1), revealed mild optic nerve edema in the left eye without retinal nerve fiber layer defects. Visual field testing demonstrated mild central defects in the right eye, a temporal defect, and dense inferior-nasal depression in the left eye with a mean deviation of -14.32 dB.<\/p>\n

\"pc<\/a>

Figure 1. Structure-function analysis correlating the color optic nerve photos, optical coherence tomography-derived optic nerve structural metrics, and Humphrey 24-2 SITA- Standard visual field results.<\/p><\/div>\n

 <\/p>\n

There was concurrent concern for arteritic anterior ischemic optic neuropathy and a space-occupying lesion given the patient\u2019s cancer history; therefore, he was sent to the emergency department for urgent laboratory evaluation, including erythrocyte sedimentation rate, C-reactive protein, complete blood count, chemistry panel, and neuroimaging. Magnetic resonance imaging (MRI) revealed cranial bone lesions, including a left temporal convexity dural lesion consistent with metastatic disease (Figure 2). Additionally, coronal T2-weighted sequences showed a hyperintense, reverse-C-shaped metastatic lesion arising from the anterior clinoid process, compressing the left optic nerve (Figures 3-4). Figures 5-6 illustrate coronal and axial views of metastatic bone lesions and orbital apex involvement, respectively. Laboratory studies demonstrated an elevated sedimentation rate (ESR) of 40 mm\/hr, and C-reactive protein (CRP) of 5.9 mg\/dL, findings consistent with new osteolytic activity. Alkaline phosphatase (ALP) was also elevated compared to prior values, suggesting bone or hepatic involvement.<\/p>\n

\"pc<\/a>

Figure 2. Axial T2-weighted fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging demonstrating hyperintense metastatic adenocarcinoma lesions involving the inner table of the skull (yellow arrows).<\/p><\/div>\n

 <\/p>\n

\"pc<\/a>


Figure 3. Coronal T2-weighted magnetic resonance imaging demonstrating thickening of the anterior clinoid process at the left orbital apex entry, consistent with bone metastasis from prostate adenocarcinoma (orange arrow).<\/p><\/div>\n

 <\/p>\n

\"pc<\/a>

Figure 4. Coronal T2-weighted magnetic resonance imaging demonstrating a hyperintense, reverse C-shaped metastatic lesion of the anterior clinoid process (white arrow) extending into the left orbital apex and compressing the left optic nerve (red arrow).<\/p><\/div>\n

 <\/p>\n

\"pc<\/a>


Figure 5. Coronal T2-weighted MRI demonstrating metastatic prostate adenocarcinoma in the left calvarium (white arrow) in relation to the orbits (blue arrows). This slice is 6.5 mm anterior to the orbital apex and shows normal orbital contents.<\/p><\/div>\n

 <\/p>\n

\"pc<\/a>

Figure 6. Axial T2-weighted fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging demonstrating metastatic osteoblastic lesion of the left orbital apex compressing the left optic nerve (green arrow). The normal right optic nerve is indicated by the white arrow.<\/p><\/div>\n

 <\/p>\n

He was diagnosed with metastatic bone cancer, admitted under oncology care, and treated with intravenous steroids. A comparison sodium fluoride positron emission tomography (PET) scan, which is specific for bone metastases, demonstrated extensive axial (skull) and appendicular skeletal involvement with prostate-specific membrane antigen (PSMA) avidity. Radiology also noted avid nodal disease involving the bilateral mediastinum, abdomen, and pelvis. Despite ongoing androgen deprivation therapy (ADT) with combined abiraterone acetate and prednisone to control disease progression, the patient developed metastatic disease. Notably, his medical history revealed that he had previously declined systemic chemotherapy with docetaxel during an earlier stage of treatment, at a time when his prostate-specific antigen (PSA) levels were rising.<\/p>\n

During admission, he received left orbital ionizing radiation at a dose of 3,000 centigray and was enrolled in the MAVERICK trial for progression of stage IV castration-resistant prostate cancer (CRPC). The MAVERICK trial[14]<\/sup><\/a> is a Phase 2 study evaluating abivertinib, a bone marrow kinase on chromosome X (BMX) inhibitor, in combination with abiraterone. This regimen targets a genetic vulnerability that allows cancer cells to synthesize androgens despite hormone therapy and improves progression-free survival.[15]<\/sup><\/a> The primary endpoint of the study is six-month radiographic progression-free survival.15 <\/sup><\/p>\n

DISCUSSION<\/strong><\/h2>\n

Distribution<\/strong><\/h4>\n

According to the Centers for Disease Control and Prevention, U.S. cancer statistics show that 255,395 new prostate cancer cases were reported in the United States in 2022.[16]<\/sup><\/a> The CDC mortality data recorded 33,881 deaths from prostate cancer in 2023.16<\/sup> The distribution of prostate cancers diagnosed from 2018 to 2022 was 70 percent at a localized stage, where the malignancy was confined to the prostate.16<\/sup> Fourteen percent were diagnosed at a regional stage, where the malignancy was detected in nearby lymph nodes, tissues, or organs.16<\/sup> Nine percent were diagnosed at a distant stage, where the malignancy had metastasized to distant sites.16 <\/sup>The remaining cases were unstaged or had an unknown stage due to insufficient information or patient refusal of diagnostic procedures and treatment.16 <\/sup><\/p>\n

Anatomy<\/h4>\n

Anatomically, the prostate is a dense fibromuscular gland of the male reproductive system located in the pelvis and enclosed by a thin fibrous capsule.[17]<\/sup><\/a> It consists of approximately two-thirds glandular tissue and one-third fibromuscular stroma.17<\/sup> The posterior peripheral zone accounts for about 65 percent of the prostatic volume and represents the most common site of prostatic carcinoma.17<\/sup> The central zone surrounds the ejaculatory ducts, whereas the transitional zone encircles the proximal urethra and is the principal site of benign prostatic hyperplasia.17\u00a0 <\/sup>The prostatic venous plexus (plexus of Santorini) communicates with the internal vertebral venous plexus (Batson plexus).[18]<\/sup><\/a> These valveless veins permit retrograde blood flow, providing a direct pathway for hematogenous dissemination of prostate cancer cells to the vertebral column and other skeletal sites.17,5 <\/sup><\/p>\n

The orbital apex is the posterior, narrowest part of the orbit, where the orbit communicates with the middle cranial fossa. The bony anatomy of the orbital apex consists of the sphenoid lesser wing, comprising the roof, the greater wing lateral wall, and the sphenoid body medial wall.[19]<\/sup><\/a> The orbital apex is anterior and inferior to the anterior clinoid process. The anterior clinoid process is a medial projection of the lesser wing of the sphenoid bone overhanging the optic canal.[20]<\/sup><\/a> It forms a critical boundary between the orbital apex and the intracranial compartment and is a key radiologic landmark.20<\/sup> The orbital apex transmits cranial nerve II, the ophthalmic artery, and sympathetic nerve fibers.19<\/sup> The soft tissue structures at the orbital apex consist of the annulus of Zinn and the origins of the four rectus muscles.19<\/sup> Through the superior orbital fissure within the annulus of Zinn at the orbital apex pass the superior and inferior divisions of the oculomotor nerve (CN III), the trochlear nerve (CN IV), the abducens nerve (CN VI), branches of the ophthalmic division of the trigeminal nerve (CN V1)\u2014including the nasociliary, frontal, and lacrimal nerves\u2014and the superior ophthalmic vein.19<\/sup> Orbital apex metastasis results from hematogenous spread, direct extension, or perineural spread of malignancy.21<\/sup> Hematogenous spread is most common, with tumor cells traveling through the bloodstream and seeding the orbit’s arterial supply via the ophthalmic artery.[21]<\/sup><\/a> Direct extension tumors that arise from adjacent structures may spread into the orbital apex when widespread skeletal metastasis occurs. Perineural tumor spread occurs along the cranial nerves and can reach the orbital apex via the superior orbital fissure or optic canal.21<\/sup><\/p>\n

Treatment<\/h4>\n

Orbital apex metastasis is a sight-threatening event, and steroids are initiated to reduce mass effect in the tumor microenvironment, though not as a cancer therapy.[22]<\/sup><\/a> Treatment modalities for the extension of metastatic lesions within the orbit and orbital apex from prostate cancer include systemic primary cancer-directed androgen deprivation therapy plus abiraterone acetate and prednisone combination therapy.[23]<\/sup><\/a> The proven effectiveness of therapies was evaluated in The Systemic Therapy in Advancing or Metastatic Prostate Cancer: Drug<\/p>\n

Evaluation (STAMPEDE) clinical trial, a multi-arm, multi-stage, randomized controlled trial in high-risk, locally advanced disease.[24]<\/sup><\/a> The LATITUDE study investigated ADT together with abiraterone acetate and prednisone and found improved radiographic progression-free survival.[25]<\/sup><\/a> Enzalutamide inhibits cancer growth by shutting down the androgen receptor pathway for advanced prostate cancer, delaying skeletal events, and improving survival in metastatic hormone-sensitive prostate cancer.[26]<\/sup><\/a> Meanwhile, six cycles of the mitotic inhibitor agent docetaxel at the start of androgen deprivation therapy for metastatic prostate cancer resulted in prolonged overall survival compared to that with ADT alone.[27]<\/sup><\/a><\/p>\n

Local radiation is the mainstay of palliation of orbital apex metastatic disease.22,[28]<\/a> <\/sup>External-beam radiation and stereotactic radiotherapy offer targeted, high-dose precision, thereby minimizing collateral damage when the optic nerve is involved.22<\/sup> Intensity-modulated radiation therapy (IMRT) is conformal radiation that spares normal tissues while treating the tumor.28<\/sup> Surgical intervention options includes biopsy, palliative resection, or orbitotomy. In cases of severe pain or blindness, orbital exenteration is performed to remove the contents of the orbit.28 <\/sup><\/p>\n

CONCLUSION<\/strong><\/h2>\n

This case of orbital apex metastasis from prostate adenocarcinoma underscores the importance of maintaining a high index of suspicion for space-occupying lesions in patients with a history of cancer. The axial tumor spread likely occurred through the bloodstream, with orbital involvement resulting from direct extension from a nearby metastasis. A notable aspect was the subtlety of optic nerve edema, despite decreased vision attributable to compression. In older patients, giant cell arteritis is a critical ocular emergency and a leading consideration in cases of acute vision loss; however, other prechiasmal and orbital pathologies should also be considered in the differential diagnosis. In this context, the patient\u2019s oncologic history strongly suggested metastatic disease, necessitating urgent neuroimaging.<\/p>\n

 <\/p>\n

REFERENCES<\/strong><\/p>\n

\u00a0<\/strong>[1]<\/sup><\/a> Bray F, Laversanne M, Sung H, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2024;74(3):229-263. doi:10.3322\/caac.21834<\/p>\n

[2]<\/sup><\/a> Harryman W, Hinton JP, Sainz R, et al. Intermediate risk prostate tumors contain lethal subtypes. Front Urol. 2024,4:1487872<\/p>\n

[3]<\/sup><\/a> SEER Cancer Stat Facts: Prostate Cancer. National Cancer Institute. Updated 2025. Available from: https:\/\/seer.cancer.gov\/statfacts\/html\/prost.html<\/p>\n

[4]<\/sup><\/a> Ito K, Tamura T, Urabe F, Sakamoto S, Kimura T, Egawa S, Ochiya T. Significance of EVs in prostate cancer bone metastases. Int J Mol Sci. 2025;26(24):12160 doi:10.3390\/ijms262412160<\/p>\n

[5]<\/sup><\/a> Long MA, Husband JE. Features of unusual metastases from prostate cancer. Br J Radiol. 1999;72(862):933-941 doi:10.1259\/bjr.72.862.10673935<\/p>\n

[6]<\/sup><\/a> Ferlay J EM, Lam F, Colombet M, Mery L, Pineros M, Znaor A, Soerjomataram I. et al. Global cancer observatory: cancer tomorrow. Lyon, France: International Agency for Research on Cancer. Available from: https:\/\/gco.iarc.fr\/tomorrow<\/p>\n

[7]<\/sup><\/a> Narod SA. Prostate cancer: A review of the epidemiology and biology. Nat Rev Urol. 2018;15(11):623-637 doi:10.1038\/s41585-018-0087-0<\/p>\n

[8]<\/sup><\/a> Ye L, Kynaston HG, Jiang WG. Bone metastasis in prostate cancer: molecular and cellular mechanisms (Review). Int J Mol Med. 2007 Jul;20(1):103-11<\/p>\n

[9]<\/sup><\/a> Park SH, Keller ET, Shiozawa Y. Bone marrow microenvironment as a regulator and therapeutic target for prostate cancer bone metastasis. Calcif Tissue Int. 2018 Feb;102(2):152-162 doi: 10.1007\/s00223-017-0350-8<\/p>\n

[10]<\/sup><\/a> Miranda AB, Guantay CD, Esp\u00f3sito E, Urrets\u2011Zaval\u00eda JA. Visual loss as the initial manifestation of an ignored disseminated prostate cancer: A case report. Am J Ophthalmol Case Rep. 2022;28:101748 doi:10.1016\/j.ajoc.2022.101748<\/p>\n

[11]<\/sup><\/a> Wada K, Tsuda T, Hanada Y, et al. A rare case of prostate carcinoma metastasis in the orbital apex. Ear Nose Throat J. 2022;101(9):571\u2013574 doi:10.1177\/0145561320973783<\/p>\n

[12]<\/sup><\/a> Mashrafi A, Begum T. Orbital metastasis from prostate cancer. BMJ Case Rep. 2015;2015:bcr2015211447 doi:10.1136\/bcr-2015-211447<\/p>\n

[13]<\/sup><\/a> Uluocak N, Parlaktas BS, Deniz FE, Erdemir F, Koseoglu RD, Gedar MO. Orbital metastasis of prostate cancer: a case report. Kaohsiung J Med Sci. 2007;23(4):199-202 doi: 10.1016\/s1607-551x(09)70398-5<\/p>\n

[14]<\/sup><\/a> MAVERICK Trial. ClinicalTrials.gov Identifier: NCTXXXXXXX. Available from: https:\/\/clinicaltrials.gov<\/p>\n

[15]<\/sup><\/a> Meeting abstract J Clin Oncol 41, TPS5106(2023) Volume 41, Number 16_suppl doi: 10.1200\/JCO.2023.41.16_suppl.TPS5106<\/p>\n

[16]<\/sup><\/a> U.S. Cancer Statistics Prostate Cancer Stat Bite. Centers for Disease Control and Prevention. Updated June 2, 2025. Available from: https:\/\/www.cdc.gov\/united-states-cancer-statistics\/publications\/prostate-cancer-stat-bite.html<\/p>\n

[17]<\/sup><\/a> McNeal JE. Normal histology of the prostate. Am J Surg Pathol. 1988;12(8):619\u2013633 doi:10.1097\/00000478-198808000-00003<\/p>\n

[18]<\/sup><\/a> McNeal JE. Anatomy of the prostate and morphogenesis of benign prostatic hyperplasia. Urol Clin North Am. 1990;17(3):477-486<\/p>\n

[19]<\/sup><\/a> Standring S, ed. Gray\u2019s Anatomy: The Anatomical Basis of Clinical Practice. 42nd ed. Elsevier; 2021<\/p>\n

[20]<\/sup><\/a> Tanriover N, Ulm AJ, Rhoton AL Jr. Microsurgical anatomy of the anterior clinoid process and optic strut. Neurosurgery. 2003;53(2):315-327<\/p>\n

[21]<\/sup><\/a> Goldberg RA, Rootman J. Clinical characteristics of metastatic orbital tumors. Ophthalmology. 1990;97(5):620\u2013624 doi:10.1016\/S0161-6420(90)32618-1<\/p>\n

[22]<\/sup><\/a> Gopishetty S, Singh L, Aqil M, Elhalis A, Ezekwudo D. Prostate cancer with orbital metastasis. Cureus. 2025;15(3):e80727 doi:10.7759\/cureus.80727<\/p>\n

[23]<\/sup><\/a> James ND, de Bono JS, Spears MR, et al; STAMPEDE Investigators. Abiraterone for prostate cancer not previously treated with hormone therapy. N Engl J Med. 2017;377(4):338-351 doi:10.1056\/NEJMoa1702900<\/p>\n

[24]<\/sup><\/a> STAMPEDE ClinicalTrials.gov number, NCT00268476 Available at: https:\/\/clinicaltrials.gov\/study\/NCT00268476<\/p>\n

[25]<\/sup><\/a> Fizazi K, Tran N, Fein L, et al; LATITUDE Investigators. Abiraterone plus prednisone in metastatic, castration-sensitive prostate cancer. N Engl J Med. 2017;377(4):352-360 doi:10.1056\/NEJMoa1704174<\/p>\n

[26]<\/sup><\/a> Davis ID, Martin AJ, Stockler MR, et al; ENZAMET Trial Investigators. Enzalutamide with standard first-line therapy in metastatic prostate cancer. N Engl J Med. 2019;381(2):121-131 doi:10.1056\/NEJMoa1903835<\/p>\n

[27]<\/sup><\/a> Sweeney CJ, Chen YH, Carducci M, Liu G, Jarrard DF, Eisenberger M, et al. Chemohormonal Therapy in Metastatic Hormone-Sensitive Prostate Cancer. N Engl J Med. 2015 Aug 20;373(8):737-46 doi: 10.1056\/NEJMoa1503747<\/p>\n

[28]<\/sup><\/a> Palmisciano P, Ferini G, Ogasawara C, Wahood W, Bin Alamer O, Gupta AD et al. Orbital metastases: A systematic review of clinical characteristics, management strategies, and treatment outcomes. Cancers (Basel). 2021;14(1):94 doi: 10.3390\/cancers14010094<\/p>\n","protected":false},"excerpt":{"rendered":"

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