papillary carcinoma

Saturday, May 15, 2010

Papillary Carcinoma in a Male Breast Cyst: A Diagnostic Challenge

Intracystic papillary breast carcinoma is a rare form of non-invasive carcinoma with an excellent prognosis. It accounts for less than 0.5% of breast cancers. We report the case of a 75-year-old man presenting with a painless cystic lump in the right breast. Ultrasonography showed a cystic lesion and aspiration revealed blood-stained fluid with suspicion of malignancy. Excisional biopsy was necessary to confirm the diagnosis and also indicated that local treatment was adequate.

Keywords: Intracystic, Papillary carcinoma, Male breast cancer

Male breast cancer is a rare disease and the incidence is 1% of all breast cancer. Intracystic papillary breast carcinoma is an extremely rare condition in men and represents only 5–7.5% of all male breast carcinomas. Diagnosis is often delayed because of the benign appearance on physical examination and radiological imaging. Such carcinomas have a better prognosis than other types of breast malignancy. Fine needle aspiration is often inaccurate and excision biopsy may be necessary for the diagnosis. We report a case of 75-year-old man presenting with a cystic lesion of the right breast which recurred after aspiration. An excisional biopsy confirmed the diagnosis and also indicated that local treatment was adequate.

A 75-year-old male presented with a painless mass in the right breast of 1-month duration. On examination, he had a well-defined 2 cm × 2 cm, firm, non-tender, non-adhering lump lateral to the right nipple. The left breast and both axillae were normal. Ultrasound showed a cyst. Aspiration of the lump revealed blood-stained fluid. Microscopic examination revealed foamy macrophages in addition to numerous epithelial cells arranged as three-dimensional papillary clumps with nuclear crowding. There was also variation of nuclear size and prominent nucleoli. The appearance was suspicious of malignancy, with the possibility of a papillary lesion being raised.

The cyst recurred 2 weeks later and the patient subsequently underwent a lumpectomy. Macroscopic examination of the specimen showed a cyst of 30 mm diameter with an intracystic fleshy papillary lesion in its wall. Multiple sections were taken for microscopic examination. The cyst wall was lined by a single layer of epithelial cells without atypia. The papillary lesion was a non-invasive papillary carcinoma. The carcinoma cells were round to polyhedral with mild atypia and rare mitoses. There was no evidence of stromal invasion. The tumour was diagnosed as intracystic papillary carcinoma, low grade. Excision margins were free of tumour. No other treatment was performed. He was doing well at 1-year follow-up.

Friday, May 14, 2010

adult T-cell lymphoma/leukemia papillary carcinoma of thyroid Rare association

Papillary carcinoma is the most common malignant tumor of the thyroid, especially in countries with adequate or excess iodine in diet. Many studies indicate that a sizable number of papillary cancer cases occur in a setting of chronic thyroiditis. But the tumor that arises more frequently in thyroiditis is malignant lymphoma. We report a rare association of papillary carcinoma of thyroid in an elderly lady with adult T-cell lymphoma/leukemia. Fine needle aspiration of the thyroid, neck nodes and evaluation of the bone marrow and peripheral blood helped in the diagnosis of papillary cancer coexisting with adult T-cell lymphoma/leukemia.
Adult T- cell leukemia/lymphoma (ATL), a mature T-cell derived neoplasm with leukemic lymphoma nature is characterized by massive leukemic cell infiltration into various organs.Cutaneous involvement and hepatosplenomegaly are common manifestations; thyroid involvement and its association with papillary thyroid carcinoma (PTC) are rare. Role of fine needle aspiration cytology (FNAC) in primary diagnosis of thyroid cancers, especially lymphoid neoplasms has been well documented. With the aid of immunocytochemistry, flow cytometry, deoxyribonucleic acid analysis and immunophenotyping, thyroid lymphoid neoplasms are treated with chemoradiation, bypassing the need for surgical intervention.However, the non-diagnostic sampling error rate is relatively high or remains undiagnosed as lymphocytic thyroiditis (LT).
A 55-year-old lady was admitted with a slowly progressing thyroid mass of 20 years duration associated with a recent onset of fever. There was no history of dysphagia, hoarseness of voice, weight loss or toxic symptoms. The mass was non-tender, 5cms x 5cms in size, nodular and hard. There was generalized lymphadenopathy involving bilateral cervical, axillary and inguinal nodes.

A fine needle aspiration of the thyroid mass and left cervical lymph node yielded blood tinged material. The thyroid aspiration smears showed follicular cells in papillary fronds, in groups, clusters and scattered singly. The nuclei were overlapping and had fine chromatin, grooves and intranuclear inclusionsa. The background was hemorrhagic with an infiltrate of lymphocytes, plasma cells and atypical cleaved lymphoid cells, similar to the reactive infiltrate of LT. The cytological features were of PTC accompanied by a suspicious lymphoma infiltrate. The cervical node aspiration smears were moderately cellular comprising of a monotonous population of atypical lymphoid cells, with scanty cytoplasm, clefted nuclei and coarse clumped chromatin consistent with lymphoma cells. Correlating both the cytological pictures, a diagnosis of combined PTC and thyroid lymphoma was made.

Investigating further, indirect laryngoscopy showed both the vocal cords moving with respiration and phonation. Ultrasonography of the neck revealed enlarged thyroid with heterogeneous echotexture and multiple large nodules with calcification and few cystic spaces and increased vascularity on Doppler scan. Bilateral level Ib, II, III, IV, V and VI nodes were enlarged with absent hilus, irregular borders and few showing necrosis, calcification and subcapsular vascularity. On computed tomography (CT) scan, the thyroid mass was predominantly in the isthmus and left lobe enlarged nodes were detected in the superior mediastinum, pretracheal, paratracheal, tracheobronchial, costopulmonary and subcarinal regions. A small nodule in the apical segment of left lower lobe of lung was suggestive of metastasis. The bone scan was normal and there was no hepatosplenomegaly or retroperitonal lymphadenopathy.

Laboratory investigations revealed hemoglobin of nine gm/dl and leukocytosis of 98,000cells/mm with 48% atypical lymphoid cells. Bone marrow aspiration and biopsy done showed diffuse involvement by cleaved lymphoma cells. Immunohistochemistry showed positivity with CD 45 and CD 3, confirming the T- cell origin; serological test for human T- cell leukemia virus type 1 (HTLV-1) antibody was negative. The patient was diagnosed as stage IV non-HTLV-1 ATL coexistent with PTC. She received chemotherapy comprising of six cycles of CHOP [cyclophosphomide, doxorubicin, vincristine, prednisolone]. During the course of treatment, she had pneumonia in the third month which was treated; the blood counts dropped to normal limits. At the end of the sixth cycle, the total leukocyte count was 9,800 cells /mm with platelet count of 2, 76,000 lakh /mm and hemoglobin of 11gm/dl. However, the repeat bone marrow aspiration and biopsy showed persistent lymphoma infiltration suggesting tumor progression; she is lost to follow-up since then.
Non-Hodgkin lymphoma involving the thyroid can be primary or secondary from local extension from adjacent neck nodes or metastasis from a distant site. These tumors are usually of B-cell lineage; T-cell lymphomas have also been described. ATL, caused by HTLV-1, is characterized by leukemic infiltration into various organs. The c-Met expression in ATL cells is considered significant in tumor invasion and metastasis.The frequency of superimposed cancers, such as gastrointestinal adenocarcinomas, larynx cancers, hepatoma and thyroid papillary adenocarcinoma in ATL is significantly high. PTC occurring in combination with HTLV unassociated ATL, in fact being the primary clinical presentation, is rarely reported. The underlying pathophysiology is presumed to be one of the molecular defects. The somatic Fas mutations described in lymphoid neoplasms, including ATL, have been recently found significant in the pathogenesis of PTC.

Preoperative diagnosis of thyroid lymphoma/leukemia infiltrate is difficult on cytology owing to its resemblance to LT. Fewer numbers of follicular cells, Hürthle cells, tingible body macrophages and plasma cells favor a diagnosis of lymphoma. Lymphoid infiltrate per se has no statistical significance in differentiating the two conditions. Small, large and activated lymphoid cells with lymphoglandular bodies and plasma cells of LT can also be seen in mucosa associated lymphoid tissue (MALT) lymphomas while large cell lymphomas have a large monotonous population of neoplastic cells. The rate of false negative results with FNAC is frequent in lymphomas complicating LT due to sampling error or due to paucicellular aspirates. Diagnostic accuracy is more when neck nodes are involved. Other differential diagnoses include small cell variant of medullary carcinoma, metastatic small cell carcinoma of lung and anaplastic thyroid carcinoma. High grade lymphomas can be misinterpreted for anaplastic carcinomas resulting in unnecessary surgical intervention. In case of carcinomas, tumor cells are seen in clusters, staining positively with cytokeratin when compared to the dispersed pattern of lymphoma cells positive for lymphoid markers in the background of lymphoglandular bodies.

Autoimmune thyroiditis is considered the predisposing factor for PTC with risk rate of 10 to 40%, as evidenced by the presence of RET/PTC rearrangement in almost 95% of cases of Hashimoto thyroiditis.RET/PTC-1 activation either activates the follicular cells or provokes autoimmune responses that contribute to malignancy. A synchronous occurrence of PTC and non-HTLV-1 ATL as in the present case is very rare.

It was difficult to distinguish the primary or secondary thyroid involvement based on cytology alone. A thorough clinicoradiological examination for organomegaly and a complete hematological work-up is mandatory to identify the secondary lymphoma/leukemic infiltration. In our patient, it was the secondary involvement by adult T-cell leukemic infiltration. It was difficult to assess the nature of the background lymphoid infiltrate on cytology in the absence of prior history of LT or a systemic disease such as ATL.

For the diagnosis of thyroid lymphoma, surgery has limited value; most patients are treated by chemotherapy or radiation therapy. In the present case, a correct diagnosis obtained on FNAC avoided an unnecessary surgical intervention. Management of this patient was focused on thyroid lymphoma (stage IV) which has a worse prognosis compared to PTC with a relatively indolent course. Six cycles of chemotherapy normalized the peripheral blood cell counts. However, the overall prognosis is poor as evidenced by the persistent lymphoma infiltration of the marrow.

To summarize, critical evaluation of the lymphocyte-rich infiltrate of LT associated with PTC is important to identify rare T-cell lymphomas, primary or secondary, and distinguish them from the more frequent MALT lymphomas with better prognosis. FNAC is an easy, minimally invasive reliable initial diagnostic modality for thyroid lymphoid neoplasms and complementary cytopathologic techniques can increase the diagnostic accuracy bypassing surgery-asociated morbidity.

How to cite this article:
Khadilkar UN, Mathai AM, Chakrapani M, Prasad K. Rare association of papillary carcinoma of thyroid with adult T-cell lymphoma/leukemia. Indian J Pathol Microbiol 2010;53:125-7

How to cite this URL:
Khadilkar UN, Mathai AM, Chakrapani M, Prasad K. Rare association of papillary carcinoma of thyroid with adult T-cell lymphoma/leukemia. Indian J Pathol Microbiol [serial online] 2010 [cited 2010 May 14];53:125-7. Available from: http://www.ijpmonline.org/text.asp?2010/53/1/125/59202

Thursday, May 13, 2010

Variants of papillary carcinoma of the thyroid

Papillary carcinoma of the thyroid is now further subclassifiable into its different variants. We report incidence, clinical behaviour and outcome of rare variants of papillary thyroid cancers at Asir Central Hospital, Saudi Arabia. These variants differ from each other not only on a morphometric basis, but also in clinical behaviour. Accordingly, we report our experience of different variants in a series of 35 papillary carcinomas. These cases were received in the surgical pathology laboratory of Asir Central Hospital from January 1987 to December 1994. We have reviewed clinical charts, microscopic slides and pathological reports of these carcinomas. The following results have been obtained: 20 cases were classical (usual) papillary thyroid carcinomas; seven were follicular variants; three were tall cell columnar variants; two were oxyphilic variants; and one was a diffuse sclerosing variant. There were two de-differentiated papillary carcinomas (anaplastic carcinomas with foci of well-differentiated papillary carcinomas). These variants were also correlated with clinical parameters such as age, sex and nationality of the patients, aggressiveness of the tumours, types of surgery required, and follow-up when available.
Keywords: papillary carcinoma of thyroid, thyroid cancer.
Until recently, papillary carcinoma of the thyroid was regarded as a single group with indolent clinical course and excellent prognosis. This view is now changing. Recent reports¹ emphasize that papillary carcinoma should be further subclassified into its variants because of prognostic implications. These variants include follicular,²tall cell,³columnar cell,⁴diffuse sclerosing, oxyphilic (Hurthle cell), cribriform,⁵trabecular,⁶muco-epidermoid,⁷papillary carcinoma with nodular fasciitis-like stroma,⁸and de-differentiated papillary Accordingly, in this report, we have determined the incidence of different types of papillary thyroid neoplasms at Asir Central Hospital, and have correlated this with the clinical findings.
MATERIAL AND METHODS
We searched surgical pathology files that related to goitre specimens received in Asir Central Hospital during a period of 8 years from January 1987 to December 1994. We reviewed only those cases in which a diagnosis of papillary carcinoma was made. The microscopic slides were examined and papillary carcinomas were further subclassified into the following groups based on histological pattern: usual papillary carcinomas; follicular variants of papillary carcinomas; tall cell/columnar variants; diffuse sclerosing variants; oxyphilic variants; and de-differentiated papillary carcinomas. We also reviewed clinical charts to determine such parameters as age, sex and nationality of these patients, aggressiveness of the tumours, types of surgery required and follow-up when available.

Wednesday, May 12, 2010

Intracystic papillary carcinomas of the breast: a reevaluation using a panel of myoepithelial cell markers.

Abstract

Intracystic papillary carcinomas (IPC) of the breast have traditionally been considered to be variants of ductal carcinoma in situ (DCIS). However, it is not clear if all lesions categorized histologically as IPC are truly in situ carcinomas, or if some such lesions might represent circumscribed or encapsulated nodules of invasive papillary carcinoma. Given that the demonstration of a myoepithelial cell (MEC) layer around nests of carcinoma cells is a useful means to distinguish in situ from invasive carcinomas of the breast in problematic cases, assessment of the presence or absence of a MEC layer at the periphery of the nodules that comprise these lesions could help resolve this issue. We studied the presence and distribution of MEC at the periphery of the nodules of 22 IPC and, for comparison, 15 benign intraductal papillomas using immunostaining for 5 highly sensitive markers that recognize various MEC components: smooth muscle myosin heavy chain, calponin, p63, CD10, and cytokeratin 5/6. All 22 lesions categorized as IPC showed complete absence of MEC at the periphery of the nodules with all 5 markers. In contrast, a MEC layer was detected around foci of conventional DCIS present adjacent to the nodules of IPC. Furthermore, all benign intraductal papillomas, including those of sizes comparable to those of IPC, showed a MEC layer around virtually the entire periphery of the lesion with all 5 MEC markers. In conclusion we could not detect a MEC layer at the periphery of the nodules of any of 22 lesions categorized histologically as IPC. One possible explanation for this observation is that these are in situ lesions in which the delimiting MEC layer has become markedly attenuated or altered with regard to expression of these antigens, perhaps due to their compression by the expansile growth of these lesions within a cystically dilated duct. Alternatively, it may be that at least some lesions that have been categorized as IPC using conventional histologic criteria actually represent circumscribed, encapsulated nodules of invasive papillary carcinoma. Regardless of whether these lesions are in situ or invasive carcinomas, available outcome data indicate that they seem to have an excellent prognosis with adequate local therapy alone. Therefore, we believe it is most prudent to continue to manage patients with these lesions as they are currently managed (ie, similar to patients with DCIS) and to avoid categorization of such lesions as frankly invasive papillary carcinomas. Given our observations, we favor the term "encapsulated papillary carcinoma" over "intracystic papillary carcinoma" for circumscribed nodules of papillary carcinoma surrounded by a fibrous capsule in which a peripheral layer of MEC is not identifiable.

What’s the connection between dysplasia and neoplasia? : papillary thyroid carcinoma

Q. What is the connection between dysplasia and neoplasia? I understand that dysplasia is a precancerous condition. Grades I and II are not neoplastic. But grade III dysplasia, also called carcinoma in situ, is neoplastic, right? But is it a true carcinoma, or is it not at that point malignant?
A. Dysplasia is not a neoplastic process. While it is often a precursor to neoplasia, not all cases will evolve into malignancy (e.g., mild cervical dysplasia usually does not progress to carcinoma. We watch patients who have it carefully, though, to catch those patients that do go down that path.).
Carcinoma in situ is neoplastic. The cells in carcinoma in situ have the potential to invade (and definitely will, if left alone and untreated). They have acquired enough genetic mutations to have the characteristics of malignant cells (they are able to invade, able to grow on their own without growth signals, insensitive to growth-inhibiting signals, able to metastasize, etc).

Some classification schemes equate grade III dysplasia with carcinoma in situ, while others leave carcinoma in situ in its own category at the far end of the nastiness spectrum. Personally, I prefer the latter way of looking at things, because keeps the separation between dysplasia and neoplasia intact. The important thing to remember, no matter what semantics you choose, is that the chances of evolution into overt carcinoma rise with the degree of dysplasia. Mild dysplasia usually does not evolve into carcinoma, whereas severe dysplasia usually does.
The image above shows a portion of cervical epithelium that has undergone dysplastic change. The right hand side of the image shows normal squamous epithelium, and the left hand side of the image shows moderately dysplastic epithelium. The dysplastic epithelial cells are pleomorphic (varying in size and shape) and hyperchromatic (darkly-staining) nuclei. Their architecture is also disrupted. Instead of the nice basal layer and orderly maturation and flattening-out of cells that you see in normal epithelium, much of the epithelial thickness resembles the basal layer.

Renal Cell Carcinoma (RCC) Kidney Cancer

1 The kidney: The kidneys are two bean-shaped organs fixed to the back wall of the abdominal cavity. One kidney is to the left and the other is to the right of the backbone. Both are protected by the lower ribcage. The kidneys' function is to filter the blood and eliminate the body of excess fluid, salt and waste products. Filtered blood (urine) leaves the kidney through a long tubular structure called a ureter. The ureters connect the kidneys to the bladder. Urine is stored in the bladder until urination. All of the important functions of kidney can be handled with one kidney and that's why many people are living normal healthy lives with just one kidney. Kidney cancers may start within the kidney (primary) or have spread from another organ/source. Primary kidney cancers may include renal cell carcinoma, transitional cell carcinoma (renal pelvic tumor), sarcomas and collecting duct tumors.

2. Renal cell carcinoma (RCC): RCC is the most common type of kidney cancer. RCC begins small and grows larger over time, like many other cancers. Based on limited observations, renal cancers appear to grow approximately 1 cm (1/2 inch) in diameter per year. RCC usually grows as a single mass. Sometimes, a kidney may contain more than one tumor or tumors may be found in both kidneys at the same time. Patients with bilateral tumors, early onset of disease, or multiple tumors may suggest a genetic predisposition to form RCC as occurs in patients with Von Hippel-Lindau disease. In the past, RCCs were diagnosed only after they have become quite large or symptoms of flank pain, blood in the urine, or palpable mass in the abdomen developed. But fortunately, most RCC are now found incidentally (during evaluation of unrelated medical problems) by imaging studies such as ultrasound, CAT scan, or MRI. The recently observed rising incidence of RCC may not be solely due to increased use of imaging studies but a trend toward increased detection of small lesions that are surgically curable has been noted. RCC is difficult to treat and rarely cured once it has spread beyond the kidney and current therapies have limited efficacy. Researchers are beginning to understand ways that cause these kidney cells become cancerous. Much research is now focused on how mutations of genes on chromosome 3, 7, 17 result in kidney tumors. Other researchers are studying how different genetic changes seen in RCC affect how the cancer looks under the microscope and how likely it is to grow and spread aggressively. Doctors hope to use this information to treat RCC more effectively in new ways that cause fewer side effects.

placentoid bullous lesion of the lung : Papillary adenocarcinoma case file part 1

We report the case of a 52-year-old man with papillary adenocarcinoma arising in placentoid bullous lesion of the lung, which is a rare cystic lung disease. Macroscopically, the cyst contained a soft villous tumor closely resembling the placental chorionic villi of early gestation. Histologic examination revealed the tumor to be papillary adenocarcinoma with an abundant stromal core, which comprised vascular and lymphatic vessels, lymphocytes, fat cells, and smooth muscle. Immunohistochemically, adenocarcinoma cells were positive for CAM 5.2, epithelial membrane antigen, and PE10 (antisurfactant apoprotein A antibody). These results indicate that the adenocarcinoma was derived from the component epithelial cells of the cyst. Based on the tumor's macroscopic and microscopic appearance and on the results of the immunohistochemical studies, we conclude that the cystic tumor in our case arose in a placentoid bullous lesion of the lung.

(Arch Pathol Lab Med. 1998;122:915-919)

Epithelial malignancy is known to arise in association with cystic diseases of the lung. In most reported cases in which the type of cyst was described, the underlying cystic diseases were various congenital cysts or bullous lesions of the lung.1-12 Recently, we examined an autopsy case of lung carcinoma arising in a placentoid bullous lesion of the lung (PBLL)13-15 in a 52-year-old man. Placentoid bullous lesion of the lung is an unusual cystic lesion whose histogenesis has not yet been sufficiently established. This rare tumor was studied histologically and immunohistochemically.

REPORT OF A CASE

A 52-year-old man was admitted on November 30, 1995, for further evaluation of cervical lymphadenopathy and an abnormal shadow on chest roentgenogram. The abnormal shadow had first been noted by a family physician 6 years before admission. Computed tomography at that time indicated that the shadow represented a giant bulla in the right middle lobe. No findings suggestive of malignancy were found. The patient remained well until cervical lymphadenopathy was noted. The patient had a history of treatment with antituberculous drugs for pulmonary tuberculosis at the age of 9. He had smoked 25 cigarettes a day for 35 years.

Results of radiologic, pathologic, and laboratory examinations on and after admission were as follows. Chest roentgenogram demonstrated a large homogeneous shadow with a sharp border in the middle field of the right lung (Figure 1). Computed tomography showed a cystic lesion with an inner low-density area (Figure 2). A percutaneous biopsy specimen of the cystic lesion suggested a diagnosis of adenocarcinoma, and biopsy of a cervical lymph node revealed metastatic adenocarcinoma. A ^sup 99m^Tc bone scintigraphy also suggested metastases to the thoracic vertebrae and left parietal bone. Results of routine blood examination on admission were within normal limits. Only the serum level of CA125 was moderately elevated.

Although neck irradiation was performed for relief of pain and an anticancer drug (doxorubicin) was injected locally into the right pleural space to counter gradual accumulation of pleural fluid, systemic chemotherapy could not be given because of the patient's poor general condition. The patient died of respiratory insufficiency due to massive pleural effusion and pulmonary edema 4 months after admission. Autopsy was performed approximately 10 hours after death.

AUTOPSY FINDINGS

The left lung weighed 400 g, and the right weighed 680 g. The right pleura demonstrated marked thickening and fibrinous adhesion due to pleuritis carcinomatosa. There was also a fluid-filled loculated area in the pleural space. The surface of the pleura of the left lung was almost completely intact macroscopically, but microinvasion of the pleura by carcinoma cells was found histologically. Pleural fluid compressing the lungs measured 1500 mL on the left and 600 mL on the right. The lungs were edematous, but were almost completely expanded.

The central portion of the middle lobe with atelectasis was occupied by a sharply defined cystic tumor, measuring 4.5 x 3.0 x 2.5 cm, which was away from the loculated area mentioned above. The cyst contained a soft villous mass mimicking placental chorionic villi of early gestation, which was partially attached to the slightly shaggy inner surface of the thin wall (Figure 3). Although the bronchi of the middle lobe ran near the tumor, they were not connected to it. Microscopically, the mass was composed of papillary structures with round, oval, and trabecular shapes similar to chorionic villi at low magnification (Figure 4). The mass was a papillary adenocarcinoma with a wide stromal core. Carcinoma cells lining the stroma showed round, oval, or occasionally irregularly shaped and vesicular nuclei with relatively abundant eosinophilic cytoplasm (Figure 5). The apical margins of carcinoma cells were stained with Alcian blue. Most of the cyst wall was also covered with carcinoma cells. It was peculiar that the wide stromal core of the papillary structures comprised fat cells, infiltrating or aggregated lymphocytes, foam cells, and smooth muscle cells as well as vascular channels that frequently showed mural hyalinization (Figure 6). Preexisting cuboidal epithelial cells without atypia were seen on the surface of the papillary structures and in some parts of the cyst wall (Figure 7). The macroscopic and microscopic placenta-like appearance and the characteristic features of the stroma of the papillary structures were very similar to those of PBLL in areas not composed of adenocarcinoma. Therefore, the structure may be interpreted as carcinoma cells spreading superficially in PBLL, resulting in a papillary growth pattern. The carcinoma invaded the cyst wall and the surrounding lung tissue. Invasion of blood and lymphatic vessels was seen frequently.

papillary carcinoma

Saturday, May 15, 2010