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COLORECTAL CANCER - MORPHOLOGY

COLORECTAL CANCER - MORPHOLOGY. SBALO – Angel MILEV UMBAL St. ANN – Stefan PETROV 07 – 11 - 2009. H istory says : In the beginning was Duke 1 and 2 Afther that was Astler & Coller ( Annals of Surgery , June, 1 9 5 4 ). Astler & Coller RESULTS:.

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COLORECTAL CANCER - MORPHOLOGY

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  1. COLORECTAL CANCER - MORPHOLOGY SBALO – Angel MILEV UMBAL St. ANN – Stefan PETROV 07 – 11 - 2009

  2. History says : In the beginning was Duke 1 and 2 Afther that was Astler & Coller (Annals of Surgery, June, 1 9 5 4) • Astler & Coller RESULTS:

  3. GROSS MORPHOLOGYColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • Early carcinomas, i.e., tumors limitedto the submucosa, are mostly • polypoid • pedunculated • semipedunculated • sessile • flat lesions • flat with slight elevation • with lightcentral depression • Advanced carcinomas (invadingbeyond the submucosa) are four types, similar to the Borrmann categories ofgastric carcinoma: • * Polypoid (protuberant) • * Ulcerated, with sharply demarcated margins • * Ulcerated without definite borders • * Diffusely infiltrating • In contrast to gastric carcinomas, the latter twotypes are uncommon. • The most common type is the ulcerated type with sharply demarcated margins.

  4. GROSS MORPHOLOGYRosai and Ackerman’s SurgicalPathology, Juan Rosaj Edt., Vol. I, Mosby. (2004) Advanced carcinomas (invadingbeyond the submucosa) are four types, similar to the Borrmann categories ofgastric carcinoma: * Polypoid (protuberant)

  5. GROSS MORPHOLOGYRosai and Ackerman’s SurgicalPathology, Juan Rosaj Edt., Vol. I, Mosby. (2004) Advanced carcinomas (invadingbeyond the submucosa) are four types, similar to the Borrmann categories ofgastric carcinoma: * Ulcerated, with sharply demarcated margins

  6. GROSS MORPHOLOGYRosai and Ackerman’s SurgicalPathology, Juan Rosaj Edt., Vol. I, Mosby. (2004) Advanced carcinomas (invadingbeyond the submucosa) are four types, similar to the Borrmann categories ofgastric carcinoma: * Ulcerated without definite borders

  7. GROSS MORPHOLOGYRosai and Ackerman’s SurgicalPathology, Juan Rosaj Edt., Vol. I, Mosby. (2004) Advanced carcinomas (invadingbeyond the submucosa) are four types, similar to the Borrmann categories ofgastric carcinoma: * Diffusely infiltrating

  8. HISTOMORPHOLOGY - Histological TypingColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • Extremely uncommon carcinomas not listed in theWHO classification, • and reported in only a few cases, include microglandular goblet cell carcinoma, • clear cell carcinoma, adenosquamous carcinoma, spindle cell and • metaplastic carcinoma (carcinosarcoma), giant cell carcinoma, choriocarcinoma, • carcinomas arising in endometriosis, melanotic adenocarcinoma, and • Paneth cell rich papillary adenocarcinoma.

  9. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000CRC -1 • ADENOCARCINOMA – GRADING – 1 – TO 3

  10. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000CRC -2 • MUCINOUSADENOCARCINOMA

  11. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000CRC -3 • SIGNET RING-CELL CARCINOMA

  12. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000CRC -4 • PROGNOSTIC FACTORS IN CRC

  13. HISTOMORPHOLOGY - Histological GradingColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • Histopathological grading of tumors is performed to provide some indication • of their aggressiveness, which relates to prognosis and/or choice of • treatment. The traditional system of grading also used by the International • Union Against Cancer (UICC) tumor node metastasis (TNM) classification • distinguishes four grades: • G1: well differentiated • G2: moderately differentiated • G3: poorly differentiated • G4: undifferentiated • The WHO provides and recommends a grading system with two • classes: • Low-grade, encompassing G1 and G2 • High-grade, encompassing G3 and G4 • This latter grading system fulfills all clinical requirements, and can be • performed with higher reproducibility. We prefer this grading with only • two categories. When a carcinoma shows different grades of differentiation, • the higher grade should determine the final categorization. Thus a carcinoma • that shows both low- and high-grade areas should be classified as high-grade. • However, the disorganized glands seen commonly at the advancing edge of • the carcinoma should not be considered as high-grade malignancy. Highgrade • carcinomas account for 20% to 25% of resected carcinomas.

  14. HISTOMORPHOLOGY - Additional Histological ParametersColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • The character of the invasive margin (pushing or expanding, or • well-circumscribed vs. irregular diffusely infiltrating) • Peritumoral inflammation • The presence of peritumorous lymphoid aggregates • Invasion of lymphatic vessels (L classification): L0, no lymphatic • invasion, L1, lymphatic invasion; LX, lymphatic invasion cannot be • assessed • Venous invasion (V classification): V0, no venous invasion; V1, • microscopic venous invasion; V2, macroscopic venous invasion; • VX, venous invasion cannot be assessed. In case of microscopic • venous invasion, it is important to distinguish between involvement • of intramural veins (submucosa, muscularis propria) and that • of extramural veins (beyond muscularis propria) • Invasion of perineural spaces [Pn (perineural) classification]: • Pn0, no perineural invasion, Pn1, perineural invasion; PnX, • perineural invasion cannot be assessed.

  15. SPECIAL CLINICAL TYPES OF COLORECTAL CANCERColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • Hereditary Nonpolyposis Colon Cancer (HNPCC) - between 35 and 45 years), uncommon histological feature of medullary carcinoma (TILs), mucinous adenocarcinomas and high-grade tumors. An increased incidence of metachronous multiple primary tumors. HNPCC accounts for at least 4% to 6% of all colorectal carcinomas. • Carcinoma Arising in Familial Adenomatous Polyposis (FAP) & (HFAS) -usually with fewer than 100 adenomas, mostly of the flat type. The histological features are similar to those of sporadic cancers. High proportion of multiple synchronous primary tumors in symptomatic cases (up to a third of cases). • Carcinoma Developing in Inflammatory Bowel Disease -predominantly in extensive ulcerous colitis with a history of 10 years or longer, involving most of the large bowel (right-sided colitis) and with high activity of inflammation. Often synchronous multiple carcinomas. High-grade tumors, mucinous adenocarcinomas, and signet-ring cell carcinomas. Less than 1% of all colorectal carcinomas arise in inflammatory bowel disease.

  16. TUMOR SPREAD IN COLORECTAL CARCINOMAColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • Cases of high-grade tumors, required a 2 cm distal resection margin. • The bidirectional lymph drainage of tumors of the • splenic flexure and the adjacent left thirdof the transverse colon and upper • third of the descending colon requires an extended left hemicolectomy (left • and transverse colectomy) for radical resection.

  17. Colon Cancer, Adenocarcinoma: Differential Diagnoses & WorkupT Dragovich & VL TsikitisArizona Medical Center(2009) If he has already acquired - 1 If he has already acquired - 2 1 . pTNM STAGING causal treatment STAGING –pTNM & 5-year RELAPSE FREE SURVIVAL (short)

  18. The UICCTNM/pTNMClassification of Tumors of the Colon and RectumColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • T/pT—Primary tumor • TX/pTX Primary tumor cannot be assessed • T0/pT0 No evidence of primary tumor • Tis/pTis Carcinoma in situ: intraepithelial or invasionof lamina propriaa • T1/pT1 Tumor invades submucosa • T2/pT2 Tumor invades muscularis propria • T3/pT3 Tumor invades through muscularis propriainto subserosa or intononperitonealizedpericolic or perirectal tissue • T4/pT4 Tumor directly invades other organs or • structuresb,c and/or perforatesvisceral peritoneum • N/pN—Regional lymph nodesd • NX/pNX Regional lymph nodes cannot be assessed • N0/pN0 No regional lymph node metastasis • N1/pN1 Metastasis in 1–3 pericolic or perirectal lymphnodes • N2/pN2 Metastasis in 4 or more pericolic or perirectallymph nodes • M/pM—Distant metastasis • MX/pMX Distant metastasis cannot be assessed • M0/pM0 No distant metastasis • M1/pM1 Distant metastasis • Regional lymph nodes for each anatomical site or subsite the following are regional: Appendix Ileocolic Cecum Ileocolic, right colic Ascending colon Ileocolic, right colic, middle colic Hepatic flexure Right colic, middle colic Transverse colon Right colic, middle colic, left colic, inferior mesenteric Splenic flexure Middle colic, left colic, inferior mesenteric Descending colon Left colic, inferior mesenteric Sigmoid colon Sigmoid, left colic, superior rectal (hemorrhoidal), inferior mesenteric, and rectosigmoid Rectum Superior, middle, and inferior rectal (hemorrhoidal), inferior mesenteric, internal iliac, mesorectal (paraproctal), lateral sacral, presacral, sacral promontory (Gerota) • (extended edition) Ramifications (i.e., optional subdivisions of existing TNM/pTNM categories) pT3 pT3a Minimal: tumor invades through the muscularis propria into the subserosa or into nonperitonealized pericolic or perirectal tissues, not more than 1mm beyond the outer border of the muscularis propria pT3b Slight: tumor invades through the muscularis propria into the subserosa or into nonperitonealized pericolic or perirectal tissues, more than 1mm but not more than 5mm beyond the outer border of the muscularis propria pT3c Moderate: tumor invades through the muscularis propria into the subserosa or into nonperitonealized pericolic or perirectal tissues, more than 5mm but not more than 15mm beyond the outer border of the muscularis propria pT3d Extensive: tumor invades through the muscularis propria into the subserosa or into nonperitonealized pericolic or perirectal tissues, more than 15mm beyond outer border of the muscularis propria pT4 pT4a Invasion of adjacent organs or structures, without perforation of the visceral peritoneum pT4b Perforation of the visceral peritoneum (extended edition)

  19. The UICCTNM/pTNMClassification of Tumors of the Colon and RectumColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) (continued) • Note: The definitions of the clinical classification (TNM) correspond to those of the pathologicalclassification (pTNM). • Stage grouping is shown in Figure 2. • AThis includes cancer cells confined within the glandular basement membrane (intraepithelial)or lamina propria (intramucosal) with no extension through the muscularis mucosae intothe submucosa. • BDirect invasion in T47pT4 includes invasion of other segments of the colorectum by way of theserosa, e.g., invasion of the sigmoid colon by a carcinoma of the cecum. • CTumor that is adherent to other organs or structures, macroscopically, is classified as T4. However,if no tumor is present in the adhesion, microscopically, the classification should be pT3. • DA tumor nodule in the pericolic/perirectal adipose tissue without histological evidence ofresidual lymph node in the nodule is classified in the pN category as a regional lymph nodemetastasis if the nodule has the form and smooth contour of a lymph node. If the nodulehas an irregular contour, it should be classifies in the T category and also coded as V1(microscopicvenous invasion) or V2, if it was grossly evident, because there is a strong likelihood thatit represents venous invasion. Figure 2.

  20. MALIGNANT TUMORS OTHER THAN CARCINOMASColorecal cancer / edited by Jim Cassidy, Patrick Johnston, Eric Van Cutsem. (2007) • Traditionally, neuroendocrine tumors have been separated from epithelialtumors and classified in a special way. They are classified as: • Well-differentiated neuroendocrine tumor (formerly: carcinoid),ICD-O code 8240/1 • Well-differentiated neuroendocrine carcinoma (formerly: malignantcarcinoid), ICD-O code 8240/3 • Poorly differentiated neuroendocrine carcinoma (small cell carcinoma),ICD-O code 8041/3 • GIST (1% of malignomas) • Kaposi sarcoma(AIDS?) • Primarymalignant melanomas in the rectum (without involvement of the anal region) • Primary colorectal malignant lymphomas(involving the ileocecal region and the rectum) • The classification is not yet standardized • (for further details in noncarcinomatous • malignant tumors. ( ! )

  21. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -1 • Anatomy of the anal canal

  22. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -2 • WHO histological classification of tumours of the anal canal (2000)

  23. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -3 • TNM classification of tumours of the anal canal (STAGING)

  24. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -4 • SQUAMOUS CELL CARCINOMA - PURE

  25. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -5 • SQUAMOUS CELL CARCINOMA – COMBINED

  26. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -6 • MUCINOUS ADENOCARCINOMA >

  27. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -7 • ADENOCARCINOMA

  28. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -8 • MELANOMA MALIGNUM

  29. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -9 • PRECANCEROSES – HPV GENESIS

  30. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -10 • PRECANCEROSES – M. PAGET

  31. Pathology and Genetics of Tumours of the Digestive SystemWorld Health Organization Classification of Tumours2000AC -11 • Anal tumours - immunoreactivity profile

  32. The results of our study – cecum, colon ascendens(1988 June – 2008 June incl. )

  33. The results of our study – MPC of colon ascendens - 1 Fig. 2. MPC with chondroid ( C ) and osseous ( O ) metaplasia. Hematoxylin and Eosin. x 200. Fig. 3 High Power view of chondroid metaplasia chondroid ( C ) with a close connection between that foci and the border of carcinoma’s glandule (BM – basement membrane - arrow). Hematoxylin and Eosin. x 400

  34. The results of our study – MPC of colon ascendens - 2 • Fig. 4 High Power view of osseous metaplasia ( O ) with a close connection between that foci and the border of carcinoma’s glandule (BM – basement membrane - arrow). Hematoxylin and Eosin. x 400 Fig. 5. Metastases of adenocarcinoma only in lymphatic nodule. Hematoxylin and Eosin. x 100

  35. The results of our study – MPC of colon ascendens - 3 • Fig. 6. Diffuse ( 3 + ) Cytokeratin. Anti-HumanCytokeratinClones AE1/AE3 (Dako), x 150 Fig. 7. Focal staining for Vimentin. Monoclonal MouseAnti-VimentinClone VIM 3B4 (Dako), x 150

  36. The results of our study – MPC of colon ascendens - 4 • Fig. 8. S-100 immunoreactivity positive neuroendocrine cells and neuronal endings. PolyclonalRabbit Anti-CowS-100 (Dako), x 100 Fig. 9. VEGF (6p21,3) strongly positive in the stroma and perivascular. Monoclonal MouseAnti-HumanVascular Endothelial Growth FactorClone VG1 (Dako), x 200

  37. The results of our study – MPC of colon ascendens - 5 • Fig. 10. α-SMA positive in perineoplastic smooth muscle. Monoclonal MouseAnti-HumanAlpha Smooth Muscle ActinClone 1A4 (Dako), x 200 Fig. 11. HER2 focal positive ( 2 + ). Polyclonal RabbitAnti-Humanc-erbB-2 Oncoprotein (Dako), x 150

  38. The results of our study – MPC of colon ascendens - 6 • RESULTS • Clinical Findings • The Patients ranged in age from 39 to 84 years were with an average age of 68. The Proportion between the men and women are 44.68% / 55.32% (all 77 patients) – all white. The local distribution of the tumors are as follows: 36 colon ascendens; 41 cecum. Matrix production of cartilaginous and osseous substance was found in only one case. • In the current study were found MPC in a white man at the age of 78. The Patient had right-sided hemicolectomy. No metastases were found out intraoperatively or by CAT. • Gross Pathology • The MPC tumor was with diameter of 10 cm. Macroscopically this nodular protruded tumor had Invaded deep into the surrounding soft tissues. The Metastases were found in one of the two lymphonodules. No invasion was found in the resection borders and the omentum. Pathologically this case was • estimated as pTNM 9: T3N1Mx. • Histopathology • Microscopically (on the base of the histological estimation) we found G2 – G3. • Intestinal adenocarcinoma, in which, the most of the matrix foci were of cartilaginous and osseous mature tissues. None of them reaches to the intestinal inner surface. In the high magnification ( x 40 ) we found out a close connection between that foci and the border of carcinoma’s glandule. These foci were located only in the carcinoma, and not in the metastase.

  39. The results of our study – MPC of colon ascendens - 7 • DISCUSSION • This study describes a distinct subgroup of MPC of the human colon which hasn’t been described up till now. • In addition to the mayor criterion for a diagnosis of MPC, as follows: • the presence of overt carcinoma with direct transition to matrix-producing cells and cartilaginous / osseous matrix; • the matrix of MPC had to lack of intervening spindle cell or osteoclastic component (Wargotz, E.S, 1988),we propose to include the following: • 3. The foci of cartilage and osseous mature tissues in the matrix carcinoma must not reach the intestinal inner surface. • 4. They must be MULTIPLE. • 5. The MPC must be located only in the wall of the colon. • Cartilaginous and osseous metaplasia is an uncommon feature of tumors, arising in the human “overted” glands: mammary, salivary and others. They may occur in both: benign and malignant neoplasms. • In the colon they can be found in the so called “benign metaplastic polypus”, but their presence in malignant epithelial blastomas (carcinomas) was not recorded until now.

  40. What’s next? • Classification of colorectal cancer based on correlation of clinical, morphological and molecular features. • 1. The Vienna classification of gastrointestinal epithelial neoplasia – Gut 2000;47;251-255, Dixon, P Sipponn, AN Price & HWatanabe, T Hirota, Y Kato et all. 48 pathologists from 15 countries reviewed a circulating slide set and attend this workshop on 5 and 6 September 1998 - Vienna, Austria. In summary, this new classification is practical and should be useful for resolving many of the discrepancies between Western and Japanese pathologists in the diagnosis of gastrointestinal epithelial neoplastic lesions.

  41. And the next? • 1.Molecular Validation of the Modified Vienna Classification of Colorectal Tumors – Journal of Molecular Diagnostics, Vol. 4, No. 4, November 2002, T Sugai, W Habano, N Uesugi, Yu-Fei Jiao, • Shin-ichi Nakamura, K Sato, T Chiba, and Motohiro Ishii. Iwate Medical University – Morioka – Japan. • Based on Crypt Isolation Method and DNA Extraction, Analysis of DNA Ploidy Pattern, Analysis of Allelic Imbalances at ChromosomalLoci and Analysis of Microsatellite Instability, usingPolymerase Chain Reaction-Single-StrandConformation Polymorphism Analysis andSequencing,

  42. COLORECTAL CANCER - MORPHOLOGY SBALO – Angel MILEV UMBAL St. ANN – Stefan PETROV WELCOME TO: bpa-pathology.com The END

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