Histopathologic findings in eyes treated with a ruthenium plaque for uveal melanoma

Messmer, Elmar P.; Bornfeld, Norbert; Foerster, Michael; Schilling, Hannah; Wessing, A

doi:10.1007/bf00165952

Cited by 59 publications

(33 citation statements)

References 18 publications

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“…Others believe that Table 4. Predictors of enucleation, tumor recurrence, and poor visual acuity in 51 patients with thick choroidal melanoma (7 mm ≤ thickness < 11 mm) after 106 Ru brachytherapy (poor visual acuity was defined as VA less than or equal to 20/200) indirect tumoricidal effects of radiation through obliterating tumor blood supply can justify lower doses to apex even when the tumor is very thick, and the apex of tumor will receive radiation less than the recommended dose [15,16,34]. Compatible with this theory, some authors [22] have recommended a minimal radiation dose of 300-400 Gy to the sclera for development of choroidal atrophy.…”

Section: Discussionmentioning

confidence: 99%

Ruthenium-106 brachytherapy for thick uveal melanoma: reappraisal of apex and base dose radiation and dose rate

Naseripour¹,

Jaberi²,

Sedaghat³

et al. 2016

jcb

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Purpose: To evaluate the outcomes of ruthenium-106 ( 106 Ru) brachytherapy in terms of radiation parameters in patients with thick uveal melanomas.Material and methods: Medical records of 51 patients with thick (thickness ≥ 7 mm and < 11 mm) uveal melanoma treated with 106 Ru brachytherapy during a ten-year period were reviewed. Radiation parameters, tumor regression, best corrected visual acuity (BCVA), and treatment-related complications were assessed.Results: Fifty one eyes of 51 consecutive patients including 25 men and 26 women with a mean age of 50.5 ± 15.2 years were enrolled. Patients were followed for 36.1 ± 26.5 months (mean ± SD). Mean radiation dose to tumor apex and to sclera were 71 (± 19.2) Gy and 1269 (± 168.2) Gy. Radiation dose rates to tumor apex and to sclera were 0.37 (± 0.14) Gy/h and 6.44 (± 1.50) Gy/h. Globe preservation was achieved in 82.4%. Preoperative mean tumor thickness of 8.1 (± 0.9) mm decreased to 4.5 (± 1.6) mm, 3.4 (± 1.4) mm, and 3.0 (± 1.46) mm at 12, 24, and 48 months after brachytherapy (p = 0.03). Four eyes that did not show regression after 6 months of brachytherapy were enucleated. Secondary enucleation was performed in 5 eyes because of tumor recurrence or neovascular glaucoma. Tumor recurrence was evident in 6 (11.8%) patients. Mean Log MAR (magnification requirement) visual acuity declined from 0.75 (± 0.63) to 0.94 (± 0.5) (p = 0.04). Best corrected visual acuity of 20/200 or worse was recorded in 37% of the patients at the time of diagnosis and 61.7% of the patients at last exam (p = 0.04). Non-proliferative and proliferative radiation-induced retinopathy was observed in 20 and 7 eyes.Conclusions: Thick uveal melanomas are amenable to 106 Ru brachytherapy with less than recommended apex radiation dose and dose rates.

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Section: Discussionmentioning

confidence: 99%

Ruthenium-106 brachytherapy for thick uveal melanoma: reappraisal of apex and base dose radiation and dose rate

Naseripour¹,

Jaberi²,

Sedaghat³

et al. 2016

jcb

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“…Thereafter, another 170 such pathological studies have been reported [24][25][26][27][28][29][30][31]. A substantial number of irradiated tumours are treated successfully, but the actual percentage of loss of proliferative capacity of all stem cells will never be known.…”

Section: Tumour Biology In Relation To Ionising Radiationmentioning

confidence: 99%

“…Appearances suggesting continuing tumour cell activity was noted in rutheniuml~ melanomas in 55 of 56 cases [24]. On the other hand, microscopically complete tumour necrosis was found in 10 out of 25 large melanomas, measuring > 7-8 mm in height after iodine125-brachytherapy [25].…”

Section: Tumour Biology In Relation To Ionising Radiationmentioning

confidence: 99%

Uveal melanoma: updated considerations on current management modalities

1995

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Published data on growth rates of uveal melanomas and effects of treatment modalities raise important considerations. Dissemination from uveal melanomas starts after the tumour is larger than 7 mm diameter; growth from 7 to 10 mm diameter increases the risk of metastases incrementally to approximately 16%. Estimations of turnout doubling times indicate that metastatic death before 8 years is nearly always due to pre-therapeutic dissemination so that the impact on survival by therapy can only be assessed thereafter. Histopathology on irradiated melanomas reveals that reproductive activity has not been suppressed and the anticipated (and unfavourable) risk of metastases is not balanced by poor post-irradiation visual acuity. Also the psychological well-being of a patient with a functional fellow eye is better after primary enucleation. Conservative management is most appropriate for: small melanomas, patients with a short life expectancy, melanomas in a single functioning eye, and patients refusing enucleation.Optimum treatment of any form of neoplastic disease by modern therapeutic modalities should ideally be based on an accurate knowledge of the biological behaviour of the specific neoplastic process. With regard to ocular melanomas, there are serious gaps in knowledge concerning growth rates in situ and in the documentation of the time intervals between the presentation of the primary tumour and the appearance of metastases. The rarity of the tumour necessitates careful accumulation of data, so that an adequate analysis can be made of the claimed success of cure rates. Equally important, the side effects and the complications of treatment should be the subject of careful scrutiny. In this communication the literature on the relevant aspects of melanoma biology and current treatment modalities is critically analysed. Tumour biology Tumour doubling timeInformation on tumour doubling time of uveal melanomas was introduced in 1980 [1] and updated reviews were provided in 1987 [2] and in 1992 [3]. From this data it was possible to estimate the risk of metastatic disease in relation to the dimensions of the tumour. The application of meta analysis provided by Diener-West and associates [4] and Markowitz et al. [5] has indicated that a radical reappraisal of the current philosophy of management is required. When do uveal melanomas metastasize ?In 1984, an editorial in the American Journal of Ophthalmology stated that 'it is unclear at what stage in its course a uveal melanoma develops the capacity to metastasize ' [6]. However an analysis of the data then available in the literature provided evidence which indicated that metastatic disease does not occur until

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“…These intratumoral macrophages often carried pigment and are called melanophages. In another study, two of the most prominent findings within tumors following ruthenium plaque therapy were tumor cell necrosis and an accumulation of pigmented macrophages [51]. Local treatment with thermotherapy also stimulated the influx of macrophages [52].…”

Section: Macrophage-influx After Therapymentioning

confidence: 99%

Uveal Melanoma: The Inflammatory Microenvironment

Bronkhorst

Jager²

2012

J Innate Immun

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Uveal melanoma is a highly malignant intraocular tumor with quite homogeneous tumor tissue and a diffuse leukocytic infiltration. In contrast with many other malignancies, the presence of infiltrating macrophages and T cells is associated with a poor prognosis rather than a good one. The clear link between inflammation and cancer in this malignancy provides a paradigm for macrophage plasticity and function. Macrophages in uveal melanoma have an M2-like phenotype and are associated with the loss of one specific chromosome – monosomy 3. The central players involved in this process and discussed in this review include macrophages, T lymphocytes, chemokines and cytokines, including the macrophage-attraction molecules. When a tumor acquires the ability to release significant amounts of macrophage-attraction molecules it causes the expansion of a population of myeloid immature cells that may not only help the tumor to suppress immune reactions but also aid in the construction of new blood vessels for tumor growth. A better understanding of the molecular basis of a local myelomonocytic cell population will bring a better understanding of the immunopathology of this disease and will lead to therapeutic interventions in uveal melanoma. This review focuses on the roles of the local inflammatory microenvironment in the development and progression of uveal melanoma.

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Histopathologic findings in eyes treated with a ruthenium plaque for uveal melanoma

Cited by 59 publications

References 18 publications

Ruthenium-106 brachytherapy for thick uveal melanoma: reappraisal of apex and base dose radiation and dose rate

Ruthenium-106 brachytherapy for thick uveal melanoma: reappraisal of apex and base dose radiation and dose rate

Uveal melanoma: updated considerations on current management modalities

Uveal Melanoma: The Inflammatory Microenvironment

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