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Viral hepatitis

Carcinomas of the Alimentary tract. Gastric Carcinoma (GC). Esophageal Carcinoma (EC). Colorectal Carcinoma (CRC). Viral hepatitis. 1. 2. Preneoplastic disorders of these three tumors: EC: >90%-squamous cell carcinomas, <10%-adenocarcinomas.

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Viral hepatitis

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  1. Carcinomas of the Alimentary tract Gastric Carcinoma (GC) Esophageal Carcinoma (EC) Colorectal Carcinoma (CRC) Viral hepatitis 1

  2. 2 Preneoplastic disorders of these three tumors: • EC: >90%-squamous cell carcinomas, <10%-adenocarcinomas. • preceded by chronic esophagitis ---Squamous epithelial dysplasia --- intraepithelial neoplasia (carcinoma in situ)----preneoplastic disorder chronic esophagitis carcinoma in situ • Barrett esophagus (precursor of E-adenocarcinoma )

  3. 3 chronic esophagitis • Many causes may induce chronic esophagitis Uremia, prolonged gastric intubation, ingestion of corrosive or irritant substances, radiation, and so on • Morphologic change- on gross: Mild esophagitis: simple hyperemia, with no histologic abnormality. Severe esophagitis: epithelial erosion, or ulceration into the submucosa.

  4. 4 chronic esophagitis ( on microscope) • three histologic features: ① eosinophils, with or without neutrophils, in the epithelial layer; ② basal zone hyperplasia, ③ elongation of lamina propria papillae. intraepithelial neutrophils occur in more severe injury. chronic esophagitis

  5. 5 • Barrett esophagus: Replacement of esophageal squamous-epithelium with gastric epithelium (in book page 218) Gastroesophageal junction Normal condition Barrett esophagus metaplastic columnar gastric epithelium distal esophagus (pale pink) (salmon-pink) stomach (more lush light brown)

  6. 6 Preneoplastic disorders (precursor lesions) GC 1. Atrophic chronic gastritis with mucosal dysplasia 2. Adenoma: true neoplasm containing dysplastic epithelium

  7. 7 Preneoplastic disorders CRC 1. Adenoma (villous adenoma) 3. FAP（familial adenomatous polyposis)--- 2. Ulcerative colitis (in book page 236) (in book p237 ) (in book page 231-234)

  8. 8 Adenomas of colon Basis on the epithelial architecture, adenomas of colon is divided into three sub-types. tubular adenomas (most common) tubulovillous adenoma (5-10%), villous adenomas (only 1%) villous adenoma • On gross: sessile, velvety or cauliflower-like masses; • On microscope: frondlike villiform extension of the mucosa is covered by dysplastic epithelium. • Invasive carcinoma is found in up to 40% of these lesions. villous adenoma (in book page 236)

  9. 9 Ulcerative colitis (ulceroinflammatory disease) • affect the colon • limite to the mucosa and submucosa (except in the most severe cases) • a systemic disorder Morphologic features: On gross, mucosa hyperemia, edema, and granularity. (with easy bleeding) In severely active cases, broad-based ulceration. Histologic features: mucosal inflammation, ulceration of the mucosa, chronic mucosal damage. (in book page 231-234)

  10. 10 Three natural narrowofesophagus • Morphology • Favored Location: • EC three natural narrow areas • 20% of ～arise in upper third esophagus (5cm) • 50% in the middle third esophagus (18cm) • 30% in the lower thirdesophagus (1-2cm) GC Pylorus and antrum 50~60%; Cardia 25%; remainder in body/fundus Lesser curvature (about 40%) > greater curvature (12%) So,favored location of ～: lesser curvature of the antropyloric region CRC50% arise in rectum, and 25% in ascending colon.

  11. 11 2. Three gross pattern –take one of three forms EC ●Exophytic polypoid or fungating form: mass protrude into the lumen ●Endophytic ulcerative form : ulcerative cancermass extend deeply ●Diffuse infiltrative form: cancer mass impart thickening and rigidity to the wall and lead to narrowing of the lumen.

  12. 12 2. Gross appearance: base on invasive depth-early and advanced～ GC(1) Early Gastric Carcinoma (E-GC) : confined to the mucosa and submucosa, regardless of presence or absence of perigastric lymph node metastases. （basis on clinical data: 10％ of E-GC: lymph node metastases） Two gross patterns: elevated form depressed form Both have no obvious tumor mass in the mucosa (---) Elevated form of E-GC Depressed form of E-GC

  13. 13 2. Gross appearance GC (2) Advanced Gastric Carcinoma (A-GC) : tumor mass has extended below the submucosa into the muscular wall. In some cases, perhaps has spread more widely. A-GC have three gross forms: (2.1) Exophytic polypoid or fungating mass (form)

  14. 14 (2.2 ) Endophytic ulcerative form (2.3 )Diffuse infiltrative mass. This rigid and thickened stomach is called a “leather bottle” stomach—革囊胃 (cancer mass imparts thickening and rigidity to the wall, and lead to narrowing of the lumen)

  15. 15 (2.2 ) Endophytic ulcerative mass Gastric ulcerative carcinoma gastric peptic ulcer larger, more surface， significant elevated edges

  16. 16 Obvious differences between peptic ulcer and cancer ulcer: (list) gastric peptic ulcer gastric cancer ulcer Location the lesser curvaturethe lesser and greater～ Size / shape 1-2cm, round ＞２cm, irregular Basis of depth deeper more surface Margins sharply elevation or beading Surrounding mucosal folds radiate absent Base of crater clean necrotic gray Cut section an eroded arteryabsent Histologic appearance four zonesinvasion by malignancy peptic ulcer Cancer ulcer

  17. 17 2. Gross appearance CRC (1)Exophytic Polypoid or fungating form (2)Endophytic ulcerative form (3)Diffuse infiltrative form (4) Mucinous mass with a gel-colloid appearance. (mucinous adenocarcinoma)

  18. Microscopic appearance : carcinomas arise from superficial epithelium of mucosa or gland EC Squamous cell carcinoma constitute ＞90% 18 Well- moderately- poorly-differentiated Adenocarcinomas: (<10%), arise from dysplastic mucosa in Barrett esophagus. (Mucin-producing adenocarcinoma)

  19. 19 Microscopic appearance • GC Adenocarcinoma＞90% • Squamous cell carcinoma (<10%): locate in cardia. • Histologic: gastric adenocarcinoma --- two major types: • intestinal- type diffuse-type Malignant calls form neoplastic glands do not form glands Like glands of colonic-- permeate the gastric wall • There are some differences between these two types (in book page 226-227) • WHO Classification Method: well-, moderately-, poorly-differentiated.

  20. 20 Microscopic appearance GC signet-ring cell carcinoma Nucleous of tumor cell is squeezed to cell margin, like diamond in married-ring.

  21. 21 • Microscopic appearance • CRC • Adenocarcinoma ＞90% Special type: produce mucin Signet-ring cell carcinoma: Mucin present in tumor cells Mucinous adenocarcinoam: Mucin is secreted into gland lumina • Squamous cell carcinoma (arising anal zone）

  22. 22 CPC (clinico-pathological correlation) In onset: insidious In late stage－dysphagia and obstructiongradually Bleeding-hematemesis or melena Other: weight loss, anorexia, fatigue, weakness and pain (relate with swallowing) EC (食道癌) E-GC: asymptomatic A-GC:abdominal discomfort or weight loss Locate in cardia: dysphagia Locate in the pyloric canal: obstructive symptoms Other: melena, fatigue, weekness-- GC (胃癌) Most cases: remain asymptomatic for years To see doctor: Faeces with bright red blood, change in bowel habit, and abdominal discomfort Significant clinical features: Faeces with bright red blood Faeces like writing brush Alternation of obstruction and diarrhea CRC (大肠癌)

  23. 23 Bleeding: in these three tumors As blood quickly congeals and turns brown in the acid environment of the stomach lumen Vomited blood:coffee grounds in patients with GC bright red blood in EC Faeces:melena (black- faeces) in patients with EC or GC bright red blood in patients with CRC

  24. 24 • Invasion and metastasis (浸润和转移) • Spread by direct extension into adjacent structures • For EC: • Upper third larynx, trachea, thyroid (occurred) • Middle third bronchus • Lower third cardia贲门 into

  25. 25 Invasion and metastasis Spread by direct extension------ For GC:spread into greater omentum and pancreas For CRC:spread into urinary bladder or uterus

  26. 26 • Invasion and Metastasis • 2. Metastasis • （for EC) Lymphatic pathway: Spread to regional LN • late stage terminal LN - left supraclavicular L • （last region）胸导管－左锁骨上LN (Virchow LN) • Hematogenous pathway: to distant sites • favored organs: Lung, liverand bone. • Seeding within body cavities: • In females , tumor cells of GC seed to • both the ovaries, • krukenberg tumor (克氏瘤)

  27. 27 Diagnosis 1. Endoscopy biopsy 2. Digital rectal examination: for rectal cancer. Digital rectal examination

  28. 28 Prognosis: for all tumors The most important prognostic indicator is the tumor stage at the time of resection. at Early stage: 5-y survival rate 90 ～ 95%，removed atLate stage: 5-y survival rate 10 ～ 15% ，removed So the only hope for cure of tumor is early detection and surgical remove.

  29. 30 Related to gene alterations Many studies indicate: genesis and development of tumor relate to some genes. EC - p53, p16 GC - c-met, K-sam, erb CRC - APC DNA repair gene DCC（deleted in colon cancer) p53 K-ras

  30. 30 Colorectal carcinogenesis:two pathogenetically distinct pathways for the development of colon cancer. APC/β-catenin pathway (adenoma-carcinoma sequence, or chromosome instability) Mismatch repair pathway (microsatellite instability)

  31. 31 • Colorectal carcinogenesis: • both of these pathways involve the stepwise accumulation of multiple gene’mutations. • but the genes involved and the mechanisms are different.

  32. 32 APC/β-catenin pathway (p.239,Fig. 10-22) Carcinoma Normal colon Adenomas Mucosal at risk APC at 5 APC/β-catenin K-RAS at 12p12 Telomerase Many other genes P-53 at 17p13 LOH at 18q21 Mismatch repair pathway (p239, Fig.10-23) Carcinoma Normal colon Sessile serrated adenoma Alteration of second allele by LOH, mutation, or promoter methylation Mutations of BAX,TCF-4, et al Microsatellite instability MLH1, MSH2

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