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|Year : 2014 | Volume
| Issue : 4 | Page : 403-405
Tumor to tumor metastasis: Adenocarcinoma of lung metastatic to meningioma
A Talukdar1, D Khanra1, S Mukhopadhay1, D Bose2
1 Department of General Medicine, Medical College and Hospital, Kolkata, West Bengal, India
2 Department of Pathology, Medical College and Hospital, Kolkata, West Bengal, India
|Date of Submission||18-Mar-2013|
|Date of Decision||10-Nov-2013|
|Date of Acceptance||23-Dec-2013|
|Date of Web Publication||5-Nov-2014|
Dr. A Talukdar
Department of General Medicine, Medical College and Hospital, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
Tumor-to-tumor metastasis (T2Tmets) is an established entity but often overlooked and underdiagnosed. Merely 84 such cases are reported in literature till date. The authors here describe a 65-year-old man presenting with first episode of focal seizure and incidentally turned out to be a case of adenocarcinoma of lung metastatic to a meningioma. The diagnosis of T2Tmets was based solely on histopathological criteria. Recent advent of brain imaging revolutionized its diagnosis and it has moved from the realm of thologists to that of radiologists. In our case, diagnosis was also established by immunohistochemistry.
Keywords: Histopathology, immunohistochemistry, meningioma, magnetic resonance imaging, (MRI), tumor to tumor metastasis, (T2Tmets)
|How to cite this article:|
Talukdar A, Khanra D, Mukhopadhay S, Bose D. Tumor to tumor metastasis: Adenocarcinoma of lung metastatic to meningioma. J Postgrad Med 2014;60:403-5
| :: Introduction|| |
Tumor-to-tumor metastasis (T2TMets) is an entity where malignancy of one organ metastasizes to another preexisting malignant lesion. Coexistence of two or more primary neoplasms in a patient is common but T2TMets is a rare phenomenon with fewer than 100 cases being reported till date. Clinical suspicion and precise diagnosis of such tumors are important as they will dictate flawless staging of malignancy and appropriate management strategies. The authors here describe a 65-year-old man presenting with first episode of focal seizure and incidentally turned out to be a case of adenocarcinoma of lung metastatic to meningioma. Our report highlights the need for histopathologists, surgeons, and oncologists to be aware of the existence of this phenomenon.
| :: Case Report|| |
A 65-year-old right-handed male patient was brought to emergency with focal seizure involving right side of body which was persistent for 3 h. There was neither history of preceding fever, altered sensorium nor it was associated with loss of consciousness, sphincter incontinence, or tongue bites. The seizure was terminated by intravenous lorazepam and phenytoin. There was no postictal confusion, amnesia of the event, or any residual neurodeficit. There was no similar episode in the past. The patient became had been a smoker for 45 years. He worked in battery factory over 45 years and underwent surgery for cataract in both eyes (30 years and 28 years ago). He was not a diabetic or hypertensive. However, he had history of chronic dry cough and weight loss in last couple of years. General examinations were within normal limits except grade III clubbing. Systemic examination including neurological and respiratory systems were normal.
A noncontrast computer tomography (CT) scan of brain showed intracerebral space occupying lesion in left parietal cortex with gross perilesional edema [Figure 1]a. His hematological and biochemical parameters were within normal limits. Magnetic resonance imaging (MRI) of brain showed an extraaxial soft tissue mass (29 × 18 × 17 mm) in left high parietal parafalcine region with gross perilesional edema favoring of meningioma [Figure 1]b-d. Presence of a ring enhancing lesion (yellow arrow) and dural tail (red arrow) are noted in association with the parafalcine mass [Figure 2]a and b. Chest radiograph of the patient showed irregular opacities seen at both upper zones [Figure 3]a. Contrast-enhanced CT (CECT) of chest revealed irregular, lobulated mass at both upper zones and mediastinal lymphadenopathy [Figure 3]b and c. Histopathological examination of left lung mass is suggestive of poorly differentiated adenocarcinoma [Figure 4]a and b. Tumor cells expressed TTF-1 and Napsin A and are immunonegative for P 63. Magnetic resonance spectroscpy (MRS) noted reduction in N-Acetyl acetic acid (NAA), increase in choline/creatine ratio, and presence of lactate peak in absence of alanine, lipid, or myoinositol peak suggestive of dual presence of meningioma and metastasis. He subsequently underwent a left frontal craniotomy and partial resection of the tumor. Brain biopsy from left parasagittal space occupying lesion confirmed metastatic adenocarcinoma on meningioma [Figure 5]a-c. Tumor cells express TTF1, vimentin, EMA, and cytokeratin and are immunonegative for P 63. The patient was advised external beam radiotherapy as a palliative treatment which he refused. He also refused chemotherapy for carcinoma of lung and was lost to follow-up.
|Figure 1: Intracerebral space occupying lesion in left parietal cortex with gross perilesional edema is noted in (a) noncontrast computer tomography scan of brain, (b) fluid attenuated inverse reconstruction, (c) axial T2-weighted, and (d) postcontrast axial T1-weighted magnetic resonance imaging of brain. There are other very small hyperintense lesions (red arrows) scattered throughout the brain parenchyma|
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|Figure 2: Postcontrast (a) axial T1- and (b) T2-weighted and (c) sagittal T1-weighted magnetic resonance imaging of brain showing extraaxial left parasagittal enhancing falx lesion. Presence of dural tail (red arrow) and a ring enhancing lesion (yellow arrow) are noted in association with the parafalcine mass|
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|Figure 3: Chest radiograph (a) showing irregular opacities seen at both upper zones. Contrast enhanced computer tomography of chest revealed irregular, lobulated mass at both upper zones and mediastinal lymphadenopathy in both mediastinal (b) and parenchymal window (c)|
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|Figure 4: Fine-needle aspiration cytology (a) and trucut biopsy (b) taken from left lung mass is suggestive of poorly differentiated adenocarcinoma on histopathological examination. [×400, H&E]|
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|Figure 5: Histopathological examination of left parasagittal space occupying lesion of brain showing metastatic adenocarcinoma (a) along with presence of whorl patterns (yellow arrow) and psammoma bodies (red arrow) suggestive of meningioma (c and d) [×400, H&E]|
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| :: Discussion|| |
The phenomenon of T2TMets has been described since Fried  published the first case of bronchogenic carcinoma metastatic to a meningioma in 1930. Out of 84 documented cases of this T2TMets, the donor neoplasm is most frequently lung carcinoma followed by breast carcinoma.  Meningioma is the most common benign host tumor, whereas renal cell carcinoma is the most frequent malignant recipient.  Meningiomas have been cited as the most common intracranial neoplasm to harbor T2TMets.  Some philosophies the event as a ''chance accident,'' while others probe into scientific theories related to epidemiology and biology of meningioma, such as higher incidence among intracranial neoplasm, slow growth rate, hypervascularity, and high collagen and lipid content.  Interactions between the meningothelial and metastatic tumor as well as high expression of E-cadherin render meningioma a rich "fertile" medium for acceptance of donor tumor cells. , In addition, the speculation that psammoma bodies exempt meningiomas from metastatic implants has been dethroned by the subversive phenomenon of T2Tmets. 
In any benign intracranial neoplasm with rapid growth or gross perilesional edema or features of increased intracranial pressure should be looked for secondary metastasis onto it. On CT scan of brain, metastasis within a meningioma may appear as a hyperdense area or, when associated with a necrotic component, as a hypodense area.  MRI of brain may demonstrate atypical signal changes suggesting the presence of another tumor within a meningioma.  Meningiomas having densely packed capillaries show a greater T2 signal intensity drop. On the contrary, adenocarcinomas due to their high mucin content have diffusely spaced capillaries conferred a smaller T2 signal intensity drop.  MRS may be useful methods in noninvasively in identifying metastatic cells within a meningioma. Increases in lipid/creatinine and alanine/creatinine ratios have been able to distinguish metastasis and meningiomas from other intracranial tumors, respectively.  Perfusion MRI or MRS can aid in locating area of T2Tmets and tissues can be taken for histopathology by means of image-guided biopsy. 
Histopathological examination remains the gold standard method of diagnosing this unique event. The terms "tumor-to-tumor metastasis" and "collision tumor" have often been confused with one another. When a primary tumor metastasizes to an organ involved with another neoplasm, without invading the substance of this neoplasm, the best term is "collision tumor" rather than "tumor-to-tumor" metastases.  The following criteria should be met for documentation of tumor-to-tumor metastasis:
- More than one primary tumor must exist;
- The recipient tumor must be a true benign or malignant neoplasm;
- The metastatic neoplasm must be a true metastasis with established growth in the host tumor, and not the result of contiguous growth, "collision tumor" or embolization of tumor cells; and
- Should not pertain to tumors that have metastasized to the lymphatic system, where lymphoreticular malignant tumors already exist.  Recently, the importance of the metastatic tumor epicenter is emphasized in evaluation of T2Tmets. 
As per the criteria proposed by Petraki et al., all the three features were present in our case. Features of metastatic adenocarcinoma of lung were present in the parafalcine meningioma, which is evidenced by ''psammoma bodies'' and ''whorled pattern'' in the histopathology of brain. Confirmations had been made radiologically and immunohistochemically as well parallel to the clinical suspicion. It is worth mentioning that no definite standardized criteria for diagnosis of T2TMets have been laid out. Management of T2TMets in the background of lung carcinoma is also not elucidated properly. This rare pathological reality highlights the lacuna of knowledge regarding its pathogenesis, diagnosis, and management to the oncologists, pathologists, and radiologists.
| :: Acknowledgment|| |
The authors are thankful to Dr. P. Samui, consultant radiologist, Medical College, Kolkata for indepth analysis of MRI brain.
| :: References|| |
Fried BM. Metastatic inoculation of a meningioma by cancer cells from a bronchiogenic carcinoma. Am J Pathol 1930;6:47-52.
Lanotte M, Benech F, Panciani PP, Cassoni P, Ducati A. Systemic cancer metastasis in a meningioma: Report of two cases and review of the literature. Clin Neurol Neurosurg 2009;111:87-93.
Fidler IJ. The pathogenesis of cancer metastasis: The 'seed and soil' hypothesis revisited. Nat Rev Cancer 2003;3:453-8.
Shimada S, Ishizawa K, Hirose T. Expression of E-cadherin and catenins in meningioma: Ubiquitous expression and its irrelevance to malignancy. Pathol Int 2005;55:1-7.
Watanabe T, Fujisawa H, Hasegawa M, Arakawa Y, Yamashita J, Ueda F, et al.
Metastasis of breast cancer to intracranial meningioma: Case report. Am J Clin Oncol 2002;25:414-7.
Gyori E. Metastatic carcinoma in meningioma. South Med J 1976;69:514-7.
Moody P, Murtagh K, Piduru S, Brem S, Murtagh R, Rojiani AM. Tumor-to-tumor metastasis: Pathology and neuroimaging considerations. Int J Clin Exp Pathol 2012;5:367-73.
Jun P, Garcia J, Tihan T, McDermott MW, Cha S. Perfusion MR imaging of an intracrania collision tumor confirmed by image-guided biopsy. AJNR Am J Neuroradiol 2006;27:94-7.
Petraki C, Vaslamatzis M, Argyrakos T, Petraki K, Strataki M, Alexopoulos, et al.
Tumor to tumor metastasis: Report of two cases and review of the literature. Int J Surg Pathol 2003;11:127-35.
Takei H, Powell SZ. Tumor-to-tumor metastasis to the central nervous system. Neuropathology 2009;29:303-8.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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