Aim: The aim of our study was to evaluate status of estrogen and progesteron hormone receptors (ER and PR), and HER2 receptors in diagnostic core biopsy specimens, compared to surgical resection specimens of the same patients after NAC regimens all including trastuzumab. Introduction: Neoadjuvant chemotherapy (NAC) is associated with phenotypic alteration in breast carcinoma, especially with the change of molecular phenotype through the modulation of hormone and HER2 receptors expression. Material and Methods: The study included 35 patients with HER2-amplified locally advanced breast carcinoma that were treated with NAC regimens that included trastuzumab, and which had receptors status determined on pre-NAC core biopsy, and on surgical specimen after the completion of the therapy. Results: Pathological complete response (pCR) was observed in 4 cases (11.4%), while partial response to therapy was noted in 31 cases (88.6%). Invasive breast carcinoma of no special type (NST) was the most common histological type in 27 cases (87.1%), while the most common histological grade (HG) was HG3 in 27 cases (87.1%). There were no noted changes in histological type or grade of the carcinoma. The rates of ER and PR receptors positivity on diagnostic core biopsy compared to post-NAC surgical resection specimens were 61.29% to 67.74% and 48.39% to 64,52%, respectively. HER2 receptors status changed from positive to negative in 2 cases (6,45%). Conclusion: Changes in status of the receptors in breast carcinoma after NAC is significant due to implications in tailored therapy approach, and subsequent modification of adjuvant therapy regimens.

Lung carcinoma is the leading cause of increases in the morbidity and mortality rates of malignant diseases worldwide. Adenocarcinoma has been the most common histological type in the last decades due to: changes in the tobacco industry, smoking habits and the use of immunohistochemistry. Among more than half of patients, lung adenocarcinoma is diagnosed in an advanced stage of the disease. The discovery of mutations in epidermal growth factor receptor (EGFR) in lung adenocarcinoma is a major advancement in molecular pathology and a new approach to the treatment of these patients. Patients with EGFR mutated lung adenocarcinoma receive a targeted therapy (Tyrosine Kinase Inhibitors-TKI) which leads to improvements in disease prognosis and quality of life. Real-time polymerase chain reaction (PCR) is the most widely used and most reliable method since it requires a minimum amount of starting material and allows the amplification of the desired DNA segment up to a billion times. In this way, deletions in exon 19 are detected in approximately 90% of cases, more often in women, non-smokers and in the territory of Asia. The following may be used for EGFR testing: fresh tissue, fast-frozen tissue, tissue molded into paraffin blocks after fixation in formalin and cytological material obtained by scraping from glass tiles. Tissue processed by decalcination, acid treated or heavy metal treated tissue should be avoided. Although surgical samples represent the golden standard in determining EGFR mutations, the results obtained are compatible with the results obtained by bronchoscopic biopsy and thus eliminate the need for invasive diagnostic procedures. Bronchoscopy is an invasive diagnostic method, whose objectives are to diagnose lung tumors, determine the endoscopic spread of the disease and assess tumor operability. The presence of a tumor may be indicated by a different bronchoscopic aspect of the endobronial mucosa. The sensitivity and specificity of this method depends on: bronchologist’s skills, endoscopic findings, the number of biopsy samples, the professional competence of pathologist-cytologist and the obtained tumor amount. The tumor amount is generally small and depends on the histological type, endoscopic findings, sampling technique and the presence of other cells. It is recommended to take three to five biopsy samples, used for diagnosing but also for molecular testing. Targeted therapy is applied based on the obtained results. Given that biopsy samples molded in paraffin are cut into multiple histological sections, and that the tumor amount decreases, it is necessary to minimize the “consumption”. The concentration of isolated DNA does not differ among patients with wt EGFR and mutated EGFR adenocarcinoma. To date, there has been no consensus regarding the number of tumor cells necessary to determine EGFR mutations, and it is recommended to take samples with a minimum of 200 to 400 tumor cells. Invalid results obtained by using the PCR method are most commonly the result of a small number of preserved tumor cells in a biopsy sample. Blood and necrosis may be limiting factors for molecular testing, but not exclusion factors for the same. Bronchoscopic biopsy sample is adequate for the determination of EGFR mutations because the majority of biopsy samples have more than 100 tumor cells, the difference between the concentration of isolated DNA in EGFR mutated and wt EGFR adenocarcinomas is not statistically significant, EGFR mutations are also detected in samples with a small number of tumor cells when using highly sensitive tests.

Lung cancers are the most common cause of morbidity and mortality from malignant tumors in the World. The neodjuvant therapy in patients with locally advanced (IIIA-IIIB) lung cancer and affected N2 lymph nodes is one of the modes of multimodal treatment of patients with non-small cell lung cancer (NSCLC) in order to improve the outcome of their treatment. This involves converting patients from a higher to a lower stage of the disease - “downstaging”. There has been no significant connection between some forms of tumor response and types of therapy. Given the importance of complete pathological responses and tumor regression in the prediction of treatment outcomes, finding this relationship is of importance for the design of future neoadjuvant trails. In determining the histological tumor regression is very important measurement of area of residual tumor (ART). As the size of the tumor is one of the prognostic factors in patients with NSCLC who did not receive neoadjuvant therapy so the measurement of ART, as opposed to the macroscopic size of the tumor, one of the prognostic factors in patients with NSCLC, who had received neoadjuvant therapy. The ultimate goal of neoadjuvant therapy should be resectability and “downstaging” that could provide overall oncology benefit in specific clinical situations. The main objectives of this research were: to objectively estimate the size of ART in tumor tissue of lung and lymph nodes; to estimate the relation between the surface of ART with the size of the tumor on postoperative surgical material after neoadjuvant therapy; to analyze and estimate the relation between histomorphological parameters in tumor regression induced by neoadjuvant therapy and spontaneous tumor regression in tumors of the lung and lymph nodes in the postoperative surgical material and depending on the histological type of cancer; to estimate the relation between clinical response to neoadjuvant therapy according to criteria of the World Health Organization and histological parameters in lung tumors and lymph nodes in the postoperative surgical material after neoadjuvant therapy; to estimate the correlation of the pathological ypTN with clinical ycTN stage of the disease and the degree of tumor regression induced by neoadjuvant therapy and pathological ypTN and estimation of the relation between clinical and pathological involvement of N2 lymph nodes after neoadjuvant therapy. Measurement of the total size of the preserved ART is the most important objective parameter in the assessment of the grade of tumor regression. Size of residual tumor did not correlate with the size of the tumor after neoadjuvant therapy. There was a significant difference in the histological picture of tumor regression induced by neoadjuvant therapy and spontaneous tumor regression. There was no significant difference between the histologic type of tumor and histological tumor regression. There is no significant correlation between clinical response and the grade of tumor regression after neoadjuvant therapy. There is no correlation between clinical and pathological staging of the diseaSPECIAL SESSION: DEPARTMENT OF PATHOLOGY, MEDICAL FACULTY, UNIVERSITY NOVI SAD, SERBIA 34 MATERIA MEDICA • Vol. 34 • Issue 1, suplement 1 • april 2018. se after neoadjuvant therapy. There is no correlation between the grade of tumor regression induced by neoadjuvant therapy and ypTN stage of the disease. There is no correlation between the clinical and the pathological involvement of the N2 lymph nodes to neoadjuvant therapy. The grade of tumor regression and measurement ART after neoadjuvant therapy determined by histopathological analysis of the resected tumor is the most objective criterion for evaluation of chemotherapeutic response and prediction of treatment outcome in patients.

In preparation for the 8th edition of the TNM classification for lung cancer the International Association for the Study of Lung Cancer (IASLC) collected data on 94,708 cases of lung cancer diagnosed between 1999 and 2010, donated by 35 institutions in 16 countries. After exclusions, 77,156 remained for analysis: 70, 967 cases of non-small cell lung cancer (NSCLC) and 6,189 cases of small-cell lung cancer (SCLC). Analysis of the cases of NSCLC has allowed proposals for revisions to the T, N and M descriptors and TNM Stage groupings. Size remained an important determinant and a descriptor for all of the T categories. A new cut points at 1 and 4 cm have been proposed and as a result new T categories have been created: T1a ≤1 cm, T1b > 1 to 2 cm, T1c > 2 to 3 cm, T2a > 3 to 4 cm, T2b > 4 to 5 cm, T3 > 5 to 7 cm and T4 > 7 cm. However, measuring precise tumor size can be challenging since it is known that tumor gross size depends on whether the size measurement is performed on fresh or formalin-fixed specimen. In about 10% of cases, formalin fixation can cause down-staging of pathologic T category as a result of tumor shrinking. Tumors invading the diaphragm have been reclassified as T4, and tumors extending within 2cms of the carina without its invasion, or tumors associated with collapse or consolidation of the whole lung have been down-staged to T2. Tis and T1mi were introduced for adenocarcinoma in situ, squamous cell carcinoma in situ and minimally invasive adenocarcinoma, respectively. Visceral pleural invasion, defined as the involvement of its elastic layer, remains unchanged as T2 category, but specific analysis of visceral pleural invasion, showed that there is two types of invasion: PL1 where tumor invades beyond the elastic layer and PL2 where tumor invades pleural surface and that these two had different prognosis, PL2 being associated with the worst outcome. Elastic stains are recommended to clarify the status of visceral pleural invasion for cases in which initial hematoxylin-and-eosin-stained slides failed to show presence of invasion. Mediastinal pleura invasion disappears as a T descriptor. N categories remained the same as in 7th edition. 8th did not bring guidelines about the minimum number of lymph nodes that should be assessed for pathohistological analysis. In M descriptor category M1a retained, while M1b has been reassigned to describe a form of limited disease with a single metastatic deposit in one distant organ. A new category of M1c has been proposed and it is reserved for situations in which there are multiple metastases in one or more distant sites. Assessment of multifocal lung tumors and the distinction of synchronous primary tumors from intrapulmonary metastases represent an important problem as this decision significantly influences tumor staging, as well as treatment approach. Four different clinical presentation of lung cancer with multifocal lung involvement are described: second primary cancer, intrapulmonary metastasis, multifocal lung adenocarcinoma with ground glass/lepidic features, and pneumonic-type lung adenocarcinoma. The tumors are considered second primary tumor if it have clearly a different histology or have a different radiographic appearance, metabolic uptake growth pattern or different biomarkers. Each tumor is staged separately based on current TNM staging system. The nodules are considered to be intrapulmonary metastasis if exact matching breakpoints are identified by genetic hybridization or have similar clinical features such as radiographic appearance, growth pattern or significant nodal and systemic SPECIAL SESSION: DEPARTMENT OF PATHOLOGY, MEDICAL FACULTY, UNIVERSITY NOVI SAD, SERBIA 32 MATERIA MEDICA • Vol. 34 • Issue 1, suplement 1 • april 2018. metastasis. TNM staging depends on location of the nodule relative to the primary tumor site. If it is in the same lobe, the tumor is designated as T3, if it is in the same lung, but in different lobe as T4, and it it is in the contralateral lung as M1a. Tumors are considered multifocal lung adenocarcinoma if there are multiple subsolid nodules with at least one suspected or proven to be a cancer. Ground glass nodule <5 mm or lesion suspected to be AAH is excluded. T stage is based on highest T lesion with indicating the multiplicity. Tumor is categorized as a pneumonic-type adenocarcinoma if there is a diffuse pneumonic infiltrate or consolidation with regional distribution. Stage IA is divided into IA1, IA2 and IA3 to accommodate T1a, T1b and T1cN0M0 tumors. All N1 disease is staged IIB except for T3-T4N1M0 tumors which are stage IIIA. A new stage IIIC is created for T3-T4N3M0 tumors and stage IV is divided into IVA (M1a and M1b) and IVB (M1c). In conclusion, multi-disciplinary approach and the close cooperation among medical and radiation oncologists, pulmonologists, surgeons, radiologists and pathologists is important in properly staging of lung cancer as well as, in treatment plans.

Pathologists often have a dilemma is a lymph node biopsy reactive or corresponds to a lymphoproliferative or other malignant disease. In everyday routine work, we rely on morphologic criteria and immunohistochemical analyzes. In better-equipped labs additional cytogenetic and molecular methods are used if morphology and immunohistochemical analyzes are not sufficient for getting correct diagnoses. It is important to know clinical presentation and the opinion of a clinician who runs the case. In reactive lymph nodes general morphology is mostly preserved. Distribution of B and T cells, histiocytes, dendritic cells and proliferation is adequate. Foreign cells are not present. Ways of reaction in lymph nodes are follicular hyperplasia, paracortical expansion, sinus histiocytosis and granuloma formation. If metastases are present, most often from carcinomas and melanomas, the initial deposits are usually sub capsular or less often in sinuses. One should be careful to differentiate sinus histiocytes and metastatic tumor cells, what can easily be verified by immunohistochemical stains.If it is a lymphoma, one should decide is it a Hodgkin or a non-Hodgkin lymphoma. In non-Hodgkin lymphomas, one should decide between small cell and large cell lymphomas. In non-Hodgkin lymphomas, tumor cells are dominant and background inflammation is scant and mostly consisted of small T cells and rare histiocytes. In T cell lymphomas background inflammation can be quite various. In Hodgkin lymphomas background inflammation most often is various and almost always outnumbers tumor cells. Tumor cells are large, with lobulated or multiple nuclei and conspicuous nucleoli. The immunophenotype is usually clearly different from non-Hodgkin lymphomas. The differentiation of small cell and large cell non-Hodgkin lymphomas is easily made by comparing cell sizes. If tumor cell size is closer to size of histiocytes or endothelium it is a large cell lymphoma, but if it SPECIJALNA SESIJA: KATEDRA ZA PATOLOGIJU MEDICINSKOG FAKULTETA, UNIVERZITETA NOVI SAD, SRBIJA 31 MATERIA MEDICA • Vol. 34 • Issue 1, suplement 1 • april 2018. is closer to small lymphocytes and red blood cells it is a small cell lymphoma. Differentiation of small cell lymphomas is based on morphology, distribution of cells and on immunophenotype. Differentiation of large cell non-Hodgkin lymphomas requires immunohistochemical analyzes because morphology is often very similar among entities. Correct diagnosis is important due to application of optimal therapy and reaching the best prognosis for the patient.

Pancreatic cancer is high aggressive malignant neoplasm with very poor prognosis and about only 5% a five-year survival. It is the fourth leading cause of cancer death in USA, as well in Serbia, although in terms of the incidence of this disease the mortality is rising and it takes seventh place. Speaking about the southern Backa, the mortality rate is slightly lower and it is the fifth place, according to the available literature. This can be explained by the lack of highly specific and sensitive diagnostic tests, which makes pancreatic cancer most often detected by an advanced, inoperable stage of the disease (>60%), although surgical resection is the only curative therapy. Analogous to other carcinomas, there is a gradual progression of the pancreatic duct epithelial cells, so every invasive carcinoma arises from the previous intraepithelial neoplasia. There are three different types of common precancerous lesions known for pancreatic cancer which clinical detection and treatment can stop the progression to invasive cancer and reduce mortality. The first one is Pancreatic Intraepithelial Neoplasia (PanIN), and the other two types of precancerous lesions are both larger fluid-filled types- Intraductal Papillary Mucinous Neoplasms (IPMNs) and Mucinous Cystic Neoplasms (MCNs). PanIN is an asymptomatic, small (usually <5 mm in diameter), nonfluid flat or papillary lesion arising in the small intralobular pancreatic ducts. It is the most common and important precursor of invasive pancreatic carcinoma. Histologically, it’s consisted of columnar to cuboidal cells with varying amounts of mucin. Accordingly to different degrees of cytological and architectural atypia, PanIN is classified into three grades- low, intermediate and high grade. PanIN-1A (flat) and PanIN-1B (papillary) are low grade lesions with minimal atypia, while PanIN-2 belongs to intermediate lesion showing mild to moderate atypia with frequent papillae. PanIN-3, also referred as “carcinoma in situ”, is characterized by severe cytological and architectural atypia amd it can be flat, papillary or cribriform pattern. The immunohistochemical profile of PanINs vary with the grade of dysplasia. Low grade lesions show positivity for gastric foveolar mucin MUC5AC, pyloric gland mucin MUC6, while MUC1 is almost exclusively expressed by high grade PanINs lesions. Among fluid-filled types of precancerous pancreatic lesions, IPMNs are the most common lesions. IPMNs vary in their location and size within the pancreas size, and these two features correlate with how dangerous they are. Because they can be detected by imaging procedures, it is possible to detect them before they become cancer. They are most often detected in patients who are routinely monitored due to a high familial risk, or incidentally in people who were imaged for another reason. Those lesions belong to group of the heterogeneous group of cystic pancreatic lesions because papillary epithelial proliferation and mucin production lead to cystic dilatation of involved ducts. SPECIJALNA SESIJA: KATEDRA ZA PATOLOGIJU MEDICINSKOG FAKULTETA, UNIVERZITETA NOVI SAD, SRBIJA 29 MATERIA MEDICA • Vol. 34 • Issue 1, suplement 1 • april 2018. Those lesions are slightly more common in the head and uncinate process (55%) compared with the body and the tail of the pancreas and about 30% of them are multifocal. IPMNs are subdivided into main duct IPMN (MD-IPMN) which are localized in the main pancreatic duct and measured ≥5 mm, while the other branch duct type (BD-IPMN) is >5 mm in diameter andcommunicates with the main pancreatic duct but it is uninvolved by the process. Mixed IPMN combines both types. Microscopically, the lining epithelial component is represented by tall mucin producing columnar cells but lack the “ovarian-type” seen in mucinous cystic neoplasms. Like PanINs, IPMNs are graded on the basis of the greatest degree of dysplasia into low grade, moderate and high grade dysplasia or carcinoma in situ and IPMN with associated invasive carcinoma. Many studies have showed that approximately one-third of patients with IPMN are associated with invasive carcinoma, so precise basement membrane micro analysis is an imperative. Accordingly to their histological characteristics there are intestinal, pancreatobiliary, oncocytic and gastric subtype of IPMN with different immunohistochemical profiles. Intestinal-type IPMN is characterized by tall columnar cells with elongated nuclei and amphophilic cytoplasm and MUC2, MUC5AC, MUC4 and CDX-2 positivity. In contrast, pancreatobiliary subtype of IPMN is characterised by branched papillae with high grade intraepithelial neoplasms and MUC1 And MUC5AC immuno positivity. The third are oncocytic type, predominantly occurs in main duct and presented with a complex branched papillary structures covered by oncocytic cells mixed with goblet cells and mucin-containing cells. This type shows diffuse positivity for MUC5AC, MUC6 and focal positivity for MUC1 or MUC2. The gastric subtype is low grade lesions mainly found in branched ducts and characterised by papillae covered by foveolar glandular epithelium with MUC5AC and sometimes MUC6 positivity. The last and the most infrequent type of pre-cancerous pancreatic lesions are MCNs. The principle difference between IPMNs and MCNs is how they look under a microscope, and how they behave in the patient. These cystic lesions are almost solitary, typically located in the pancreatic body and tail. Grossly, this lesion can grow very large, it is usually septated and with fibrous pseudocapsule often with calcifications. Histologically, the epithelium og noninvasive MCN is consisted of columnar cells with varying degree of dysplasia (low grade, moderate and high grade dysplasia) and underlying ovarian-like stroma. Immunohistochemically, thode epithelial cells are EMA, CEA, MUC5AC, MUC2, cytokeratins 7, 8/18 and 19 positive, while the underlying ovarian-like stroma shows ER, PR, vimentin and SMA immune reactivity. Precancerous lesions of the pancreas are important changes whose visualization and detection in a significant number would reduce the incidence of pancreatic cancer and, consequently, the mortality of this highly aggressive neoplasm with an unfavorable therapy outcome.

Assessment of relationship between density, perimeter and endothelial surface (“endothelial area”, EA) of vascular spaces (VS) using “ImageJ” analysis and morphological characteristics of adenocarcinoma. Introduction: Colorectal adenocarcinoma invasion involves complex reaction of tumor cells and stroma, whereas angiogenesis is essential for metastatic potential. Material and Methods: 70 resected specimens were reviewed. For each adenocarcinoma histological grade, pathological stage, lymphatic, venous and perineural invasion, growth pattern, metastases in lymph nodes and liver were determined. For visualization of vascular endothelial cells immunohistochemical staining CD31 antibody was used. From each tumor nine fields were photographed: three from invasive front, three from VS highest density and three selected randomly. Computer analysis of images was done using program “ImageJ”. For analysis of EA (EA representing surface area of CD31 positive endothelial cells) program recalculated them as percentage of tested fields (% area). VS density was shown as number VS per 1mm2, while perimeter of VS was shown in Results of all parameters were compared with all above described morphological characteristics. Results: There was no significant correlation between density and perimeter of VS and any of histopathological findings. EA from randomly chosen fields (minimum 0,69%, maximum 10,11%, p=0,016) correlates with the presence of venous invasion. There was no significant correlation between EA from the invasive front and areas of the highest density and any of the histopathological findings. Conclusion: Assessment of vascular endothelial surface area is only vascular parameter which positively correlates with prognostic parameters that could indicate worse outcome.

Aim: We present a rare case of simultaneous occurrence Concurrent occurrence of acute myeloid leukemia (AML) and monoclonal plasmacitosis (MP): Introduction: The simultaneous occurrence of acute myeloid leukemia (AML) and monoclonal plasmacytosis (MP) in bone marrow (BM) biopsy in patient without previous exposure to chemotherapy is very rare. Case report: We reported the case of a 45-year-old woman who presented with fatigue, fever, maculopapular rush, weight loss and bone pain. She was admitted to the Haematology Department of University CHC Bezanijska Kosa in November 2015. The complete blood count showed: white blood cell count 33x109/l (neutrophils 31%, myeloblasts 12%, monoblasts, promonocytes and monocytes 53%), hemoglobin 77gr/l, platelet count 34x109/l and 5% blastic cells in the peripheral smear. Serum immunoelectrophoresis showed increased monoclonal IgA (IgA 9,98, IgM 2,29, IgG 10,1), kappa/lambda 0,84, Beta2microglobulin 3,16. Biochemistry showed elevated creatinin level 93umol/l, uric acid 412 umol/l, high LDH 876U/l and sedimentation rate (50mm/h). Urine electrophoresis showed monoclonal heavy and light chains lambda type. Liquor immunophenotyping showed neuroleukemia. Skeletal survey showed no lytic lesions. The BM aspiration revealed around 10% plasma cells and BM biopsy showed infiltration by 20% monoclonal plasma cells (kappa-/lambda ) with 30% infiltration by cells with monocytes differentiation (without excess of blasts). Biopsy of skin lesion 17 MATERIA MEDICA • Vol. 34 • Issue 1, suplement 1 • april 2018. revealed myeloid sarcoma. Cytogenetic analysis detected normal karyiotype with FLT3 and NPM mutation. The patient was diagnosed as AML-M5, administered with induction therapy (DA Cytosar) and consolidation therapy (HiDAC) and she was successfully treated with allogenenic stem cell transplantation. She achieved and maintained complete remission. Conclusion: Monoclonal plasmacytosis of BM should be carefully examined due to possible association with other haematological malignancies

Aim: The aim of the study is to classify tumors into four main molecular subtypes using immunohistochemistry and in situ hybridisation methods, as well as to determine frequency of different carcinoma subtypes. Introduction: Four molecular subtypes of breast carcinoma can be identified: Luminal A and Luminal B (hormone receptors positive), HER2 enriched (HER2 overexpression) and Triple Negative / Basal-like (absence of HER2 amplification and steroid receptors expression). Materials and Methods: Cross-sectional study, conducted in Institute of pathology, Medical Faculty, University in Belgrade, during the ten months period in 2017, included 337 patients with diagnosed breast carcinoma. Using the methods of immunohistochemistry, all four markers (estrogen, progesteron, HER2, and Ki67) were evaluated on breast carcinoma tissues. As additional methods, “in situ” hybridisation (FISH, SISH) was used in cases if HER2 oncoprotein results on immunohistochemistry were equivocal. Results: Luminal A, Luminal B, HER2 enriched, and Triple Negative carcinomas were present in 133 (39,45%), 147 (43,62%), 22 (6,5%), 34 (10,08%) cases, respectively. For 55 (16,35%) cases, in situ hybridisation had been done in order to classify carcinomas in proper molecular subtype. Conclusion: Frequency of molecular subtypes of breast carcinomas in our study are similar to literature data for European countries. Breast carcinoma subtyping has prognostic and predictive values for further patient treatment, and should be done in institutions with adequately trained personnel and equipment, in order to achive best results in the shortest time.

Aim: We present an unusual case of malignant gastrointestinal stromal tumor filling the entire abdominal cavity. Introduction: Gastrointestinal stromal tumors are the most common mesenchymal neoplasms of the gastrointestinal tract. Small tumors are generally benign, but large tumors disseminate to the liver, omentum and peritoneal cavity. They rarely occur in other abdominal organs. Material and Metods: The operative material consisted of segment of ileum where a tumor mass of 8 cm was found originating from the wall and fragments of small intestinal serosa and omentum where multiple nodular tumor mases were found. Representative samples were taken, and were paraffin embedded and stained routinely with Hematoxyllin-Eosin. Additionally immunohistochemical analyses were performed using the antibodies c-kit, CD34, Vimentin, CKAE1/AE3, Ki67 and others. Results: Microscopic analysis revealed a malignant gastrointestinal stromal tumor with a high mitotic rate of 58/50 HPF mitoses. However clinical reports stated that an additional large 12 cm tumor mass was found in the liver that was not removed. Conclusion: Gastrointestinal stromal tumors are the most common gastrointestinal mesenchymal neoplasms but presence of multiple tumor masses on various organs and sites is rare. Presence of multiple tumors in various organs brings about the issues of possibility of multiple primaries or the proper detection of the original tumor mass.