Chapter 16 images Flashcards

apthous ulcer

fibroma

pyogenic granuloma

Erythroplakia

leukoplakia

hyperkeratosis in the development of squmous cell carcinoma (earliest stage, no genetic causes known)

mild moderate dysplasia in the development of SCC, genetic mutations associated with this stage: p16 mutations on genes 9p21, 3p (9 and 3)
genes and diagnosis

Squamous cell carcinoma, mutations associated with this malignancy include gene translocation (11; 13) (Cyclin D mutation), and mutations on chroms 4, 6, 8, 13, 14.

severe displasia CIS, gene mutations associated with this condition include gene mutations 17p13 mutation effecting TP53

erythroplakia, almost always associated with severe dysplasia and/or invasive carcinoma (90%)

squamous cell carcinoma, 95% of head/neck tumors are SCCs. in the west, tobacco and alcohol are the most highly associated. genetic mutations (simplified):
Hyperplasia/Hyperkeratosis: 9 (p16; cyclin D inhibitor) + 3 –>
Moderate dysplasia: 17 (TP3: codes for p53) –>
Severe dysplasia CIS: 4, 6 ,8, 11 (cyclin D itself), 13, 14 —>
Squamosu Cell carcinoma

SCC: histo nests/islands of malignant keratinocytes invade underlying CT stroma and Skeletal muscle

mucocele, inflammatory sialadenitis, blocks salviary gland, lower lip common, xerostomia

mucocele, cystlike cavity filled with mucinous material and granulation tissue

pleom adenoma, high fraction ass with chrom rearrangements involving PLAG1, mostly no dysplasia or mitotic activity.

Pleo A, dominant histo is heterogeneity ductal cells myoepi cells, acini, tubules, stand, myxoid tissue, cartilage

Warthin, narrow cyst like spaces lined by double layer of neeoplas resting on dense lymphoid stroma with germinal centers

papillary cystadenoma lymphmatosum (warthin tumor): epithelial and lymphoid elements, germinal centers beneat the epithelium.
warthins arises exclusive in the parotid gland
10% multifocal, 10% bilateral
5th-7th decades of life, usually women
smokers 8x times the risk

Mucoepidermoid carcinoma
cricumscribed but not well defined all the same
MECT1 and MAML2 translocation via 11; 19
Noth signaling PW effected–> cAMP dependent signaling
most common form of primary malignant tumor of salivary gland
histo: cords, sheets, cystic config of squamous cells, mucous filled vacuoles. can appear both benign and malig. subclassified into low, intermediate, or high grade.
Dinstinguished from adenoid cystic carcinoma: ACC are smaller, have hyaline between the cells, take on a cribriform pattern, and often form around nerve endings “perineural invasion”

Where do these largely occur? How would you distinguish it from the “other” most common tumor?

adenoid cystic acarcinoma (distinct from muco carcin):
50% occur in the minor salivary glands (palatine especially), the biggers ones include parotid and and submandiblar. appear in nose, sinuses, upper airwaysm breast, elsewhere. “cribriform pattern enclosing secretions” and “perineural invasion” (invades around a nerve)
small, poorly encapsulated, infiltrative, compact nucleu, scan cyto, tubular, solid, or cribriform patterns spaces between cells filled with hyaline material (excess basement membrane)

adenoid cystic carcinoma: perineural invasion