eMedicine Specialties > Ophthalmology > Retina

Retinoblastoma

Author: Marichelle Aventura Isidro, MD, Consulting Staff, Department of Ophthalmology, Santo Tomas University Hospital of Manila, Philippine Heart Center
Coauthor(s): Manolette R Roque, MD, MBA, DPBO, FPAO, President and CEO, Chief of Service, Ocular Immunology and Uveitis, Consulting Staff, Cornea and Refractive Surgery, Eye Republic Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines Co; Consulting Staff, CME Liaison, Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center; Thomas M Aaberg, Jr, MD, Clinical Assistant Professor, Department of Surgery, Michigan State University College of Human Medicine; Consulting Staff, Department of Ophthalmology, Associated Retinal Consultants; Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, Eye Republic Ophthalmology Clinic
Contributor Information and Disclosures

Updated: Jan 21, 2009

Introduction

Background

Retinoblastoma is the most common primary ocular malignancy (eye cancer) of childhood.

Peter Pawius of Amsterdam provided the first description of a tumor resembling retinoblastoma. He wrote of a malignancy invading the orbit, the temporal region, and the cranium, a picture now strongly suggestive of untreated retinoblastoma. The tumor was described as filled with a "substance similar to brain tissue mixed with thick blood and like crushed stone."1

In 1805, William Hey coined the term fungus haematodes, which he used to describe a fungating mass affecting the globe of the eye and destroying its internal organization.2

In 1809, the Scottish surgeon James Wardrop pieced together the random isolated facts and observations of previous authors. Despite not having a microscope at his disposal, his meticulous dissection and astute interpretations of some of these eyes led him to conclude that in most instances, the tumor arose from the retina. Wardrop documented the extension of the tumor to the optic nerve and brain. Later, he described metastasis to different parts of the body.3

In 1836, Langenbech, Robin, and Nystin of Paris confirmed by microscopic studies that the tumor definitely arose from the retina.

In 1864, Virchow named the tumor a glioma of the retina, supporting glial cells as the cell of origin of the tumor.4

In 1891, Flexner of Johns Hopkins was first to notice rosettes within the tumor.5  A few years later in 1897, Wintersteiner concurred with Flexner and proposed the name neuroepithelioma noting its resemblance to rods and cones and traced one tumor to the photoreceptor cell layer.6 Presently, their names are attached to these rosettes.

Most cells comprising the tumor histologically resemble the cells of an undifferentiated retina of the embryo called retinoblasts. This resemblance prompted Verhoeff to coin the term retinoblastoma,7  which later was adopted by the American Ophthalmological Society in 1926 as a general term for this entity.

In 1970, Tso and colleagues established that the tumor arises from photoreceptor precursors.8,9

Most recently, in October of 2007, a team of investigators at St. Jude Children's Research Hospital (Memphis, Tenn) claimed to have identified the specific cell that gives rise to retinoblastoma.10 The major importance of this discovery is the idea that retinoblastoma can arise from fully matured nerves in the retina called horizontal interneurons, disproving the long-held scientific principle that fully formed, mature nerves cannot multiply like young immature cells. 

Pathophysiology

The most widely held concept of histogenesis of retinoblastoma holds that it generally arises from a multipotential precursor cell (mutation in the long arm of chromosome 13 band 13q14) that could develop into almost any type of inner or outer retinal cell. Intraocularly, it exhibits a variety of growth patterns, which have been described as outlined below. (See Causes for more information.)

Endophytic growth

Endophytic growth occurs when the tumor breaks through the internal limiting membrane and has an ophthalmic appearance of a white-to-cream mass showing either no surface vessels or small irregular tumor vessels. This growth pattern is typically associated with vitreous seeding, wherein small fragments of tissue become separated from the main tumor. In some instances, vitreous seeding may be extensive and allow tumor cells to be visible as spheroid masses floating in the vitreous and anterior chamber, simulating endophthalmitis or iridocyclitis, and obscuring the primary mass. Secondary deposits or seeding of tumor cells into other areas of the retina may be confused with multicentric tumors.

Exophytic growth

Exophytic growth occurs in the subretinal space. This growth pattern is often associated with subretinal fluid accumulation and retinal detachment. The tumor cells may infiltrate through the Bruch membrane into the choroid and then invade either blood vessels or ciliary nerves or vessels. Retinal vessels are noted to increase in caliber and tortuosity as they overlie the mass.

Diffuse infiltrating growth

This is a rare subtype comprising 1.5% of all retinoblastomas. It is characterized by a relatively flat infiltration of the retina by tumor cells but without a discrete tumor mass. The obvious white mass seen in typical retinoblastoma rarely occurs. It grows slowly compared with typical retinoblastoma.

Frequency

United States

An estimated 250-500 new cases of retinoblastoma occur in the United States yearly.

International

Worldwide, the incidence of retinoblastoma is recorded to be about 11 cases per million children younger than 5 years. A more commonly used estimate is 1 case of retinoblastoma per 18,000-30,000 live births, depending on the country.

In the Philippines, unpublished reports have estimated the incidence to be more than 1 case of retinoblastoma per 18,000 live births.

Mortality/Morbidity

Survival rates for patients with retinoblastoma range from a reported 86-92%. However, these figures must be kept in the context of the retinoblastoma cancers. In actuality, the survival rate drops with each decade of life for patients with the genomic mutation.

The genomic mutation is a gene mutation within every cell of the individual's body. These patients typically present with either bilateral disease or unilateral-multifocal (one eye with multiple distinctly separate tumor foci) disease. These individuals have a predisposition for developing second cancers later in life.

Mortality in these individuals is consequently much higher than rates for those with somatic mutations (ie, affecting one retinal cell only and unilateral-unifocal disease). The greatest predictor of death is extraocular extension, either directly through the sclera or via extension along the optic nerve.

Race

  • No racial predilection appears to exist for retinoblastoma.
  • No difference in incidence exists among blacks and whites.

Sex

  • Studies show no significant difference in the incidence of retinoblastoma by sex for children aged 0-14 years.
  • The estimated boy-to-girl ratio is reportedly 1.12:1.

Age

Retinoblastoma is diagnosed in patients at an average of 18 months, with 90% of cases diagnosed in patients younger than 5 years.

  • Children who are affected bilaterally are diagnosed at an average age of 13 months, while patients with unilateral retinoblastoma are diagnosed at an average age of 24 months.
  • When a known family history of retinoblastoma exists, patients with bilateral retinoblastoma are diagnosed at an average age of 11 months.
  • A few cases of retinoblastoma in adults (aged 20 y and older) have been reported in the literature. Some theorize that these lesions arise from a previously existing retinocytoma that underwent malignant transformation.

Clinical

History

At the time of initial examination, obtain a careful family history.

  • Specifically ask parents about the occurrence of retinoblastoma in the family.
  • Elicit a history of eye tumors, previous enucleation, or any malignancy in childhood in any of the family members.
  • Only about 5% of patients who develop this disease have a positive family history.
  • A large number of patients with retinoblastoma (95%) have no previous family history, including those who have the bilateral hereditary form of the disease.

Physical

The clinical findings in all the stages of retinoblastoma are numerous and varied. Image 10 presents an overview of the presenting signs in retinoblastoma.

Presenting signs or symptoms in retinoblastoma. (...

Presenting signs or symptoms in retinoblastoma. (This table is modified from Abramson DH, Frank CM, Susman M, et al. Presenting signs of retinoblastoma. J Pediatr 1998 Mar; 132(3 Pt 1): 505-8.)

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Presenting signs or symptoms in retinoblastoma. (...

Presenting signs or symptoms in retinoblastoma. (This table is modified from Abramson DH, Frank CM, Susman M, et al. Presenting signs of retinoblastoma. J Pediatr 1998 Mar; 132(3 Pt 1): 505-8.)


  • Leukocoria (white pupillary reflex or cat's eye reflex) is the most common presenting sign, accounting for about 56.1% of cases.
  • Strabismus, which occurs as a result of visual loss, is the second most common mode of presentation. Thus, funduscopic examination through a well-dilated pupil must be performed in all cases of childhood strabismus.
  • Retinoblastoma can cause secondary changes in the eye, including glaucoma, retinal detachment, and inflammation secondary to tumor necrosis.
    • Pseudouveitis, with a red eye and pain and associated hypopyon and hyphema, is a rare presentation. It is characteristic of an infiltrating type of retinoblastoma in which the tumor cells invade the retina diffusely without forming a discrete tumor mass.
    • Orbital inflammation mimicking orbital cellulitis may occur in eyes with necrotic tumors and does not necessarily imply extraocular extension.
  • Proptosis is a more common presenting symptom in most underdeveloped countries.

Causes

Retinoblastoma is caused by the so-called retinoblastoma gene, which is a mutation in the long arm of chromosome 13.
  • This gene name is actually a misnomer because the gene does not actively lead to retinoblastoma. The unaffected gene actually suppresses the development of retinoblastoma.
  • When both homologous loci of the suppressor gene become nonfunctional by either deletion error or by mutation, retinoblastoma develops.
  • A positive family history is present in 5-10% of children who develop this disease.

More on Retinoblastoma

Overview: Retinoblastoma
Differential Diagnoses & Workup: Retinoblastoma
Treatment & Medication: Retinoblastoma
Follow-up: Retinoblastoma
Multimedia: Retinoblastoma
References
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Further Reading

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Keywords

intraocular cancer, intraocular childhood malignancy, eye tumor, ocular tumor, ocular malignancy, RB gene, retinoblastoma gene, childhood cancer, eye cancer

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Contributor Information and Disclosures

Author

Marichelle Aventura Isidro, MD, Consulting Staff, Department of Ophthalmology, Santo Tomas University Hospital of Manila, Philippine Heart Center
Marichelle Aventura Isidro, MD is a member of the following medical societies: American Academy of Ophthalmology and International Society of Refractive Surgery
Disclosure: Nothing to disclose.

Coauthor(s)

Manolette R Roque, MD, MBA, DPBO, FPAO, President and CEO, Chief of Service, Ocular Immunology and Uveitis, Consulting Staff, Cornea and Refractive Surgery, Eye Republic Ophthalmology Clinic; General Manager, Ophthalmic Consultants Philippines Co; Consulting Staff, CME Liaison, Section Chief of Ocular Immunology and Uveitis, Department of Ophthalmology, Asian Hospital and Medical Center
Manolette R Roque, MD, MBA, DPBO, FPAO is a member of the following medical societies: American Academy of Ophthalmic Executives, American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, American Society of Ophthalmic Administrators, American Uveitis Society, International Ocular Inflammation Society, Philippine Medical Association, Philippine Ocular Inflammation Society, and Philippine Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.

Thomas M Aaberg, Jr, MD, Clinical Assistant Professor, Department of Surgery, Michigan State University College of Human Medicine; Consulting Staff, Department of Ophthalmology, Associated Retinal Consultants
Thomas M Aaberg, Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Medical Association, American Society of Retina Specialists, Michigan Society of Eye Physicians & Surgeons, and Retina Society
Disclosure: Novartis Consulting fee Consulting

Barbara L Roque, MD, Full Partner, Ophthalmic Consultants Philippines Co, Chief of Service, Pediatric Ophthalmology and Strabismus, Consulting Staff, Orbit and Eye Plastics, Eye Republic Ophthalmology Clinic
Disclosure: Nothing to disclose.

Medical Editor

Gerhard W Cibis, MD, Clinical Professor, Director of Pediatric Ophthalmology Service, Department of Ophthalmology, University of Kansas, Kansas City
Gerhard W Cibis, MD is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, and American Ophthalmological Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine
Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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