119-137 dr agus sel squamosa carsinoma

8/14/2019 119-137 Dr Agus Sel Squamosa Carsinoma

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Were bigger than we ever dreamed| 119

NEOPLASMA MALIGNA

Squamous cell carcinoma Karsinoma epidermoid dengan pertandukan

Common, derived from keratinocytes in epidermal layer

Usually men, associated with sun exposure (UV light may induce p53 mutations and diminish

surveillance function of Langerhans cells in epidermis),

PUVA treatment for psoriasis, arsenic, tars/oils, chronic ulcers, draining osteomyelitis, old burn scars, necrobiosis lipoidica, hidradenitis suppurativa,

ORALBIOMEDIS PATOLOGI ANATOMI

By dr. Agus Suharto, Sp. PA, edited by CR #01

II. Diseases of the Salivary Glands

A. Sialadenitis

B. Acute parotitis

C. Sjogren syndrome

D. Mucocele

E. Ranula

F. Tumors of the salivary gland

I. Diseases of the Mouth & Jaw

A. Congenital DisordersB. Inflammatory disorders

C. Tumors and tumor-like conditions


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ionizing radiation Risk factors: immunosuppression (post-transplant or HIV), xeroderma pigmentosa (disorder with diminished capacity for

DNA repair after UV light exposure, due to gene at 9q22.3;

associated with squamous cell, basal cell carcinoma and

melanoma),

lack of pigmentation in skin, actinic keratosis (precursor lesion), epidermodysplasia verruciformis; very rare in blacks

5% are node positive at diagnosis; metastatic rate is 5-10% intransplant patients, who do poorly with metastatic disease

Slow growing, locally invasive but rarely metastasizes outside nodes(but see above); most common site is lung


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Metastases more likely in tumors that originate in scars or ulcers

Positive stains:

high molecular weight keratin,

SQUAMOUS CELL CARCINOMA

Prognosis : excellent; metastases uncommon if tumor < 1.5 cm deep; 5%metastasize if 2 cm or more and definite dermal invasion

Good prognostic factors :

low stage, no/superficial dermal invasion, small vertical tumor thickness (< 4 mm), well differentiated, short duration, location other than scalp, ears, lips, nose, eyelids or soft tissue (which

readily invade subcutaneous tissue)

Treatment:

surgical excision with adequate margins; also curettage, electrodesiccation,

cryotherapy, radiation therapy

Gross : often white plaque (leukoplakia); may have induration, ulceration,

hemorrhage

Micro :atypia at all levels of epidermis; 80% are well differentiated with keratin

pearls, intercellular bridges and no/rare keratohyaline granules; invade dermis by

definition;

may contain non-neoplastic melanocytes that transfer melanin to tumorcells; occasionally clear cells, rarely signet ring cells

Spindle, adenoid and verrucous variants are described separately Other variants are acantholytic (pseudoglandular, tumor clefts produed by

acantholysis of tumor cells) and pseudoangiosarcomatous (clefts separate

neoplastic lobules)Low grade (well differentiated) : cell differentiation, uniform cell size, intact

intercellular bridges, no/rare mitotic figures, no/mild pleomorphism

High grade (poorly differentiated): little cell differentiation, pleomorphism with

spindle cells, necrosis, marked mitotic activity, deep invasion


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EMA, involucrin, p53 (50%), variable CEA

Negative stains:

Ber-EP4, usually CK7 and CK20 (head and neck tumors, Mod Path2004;17:407)

Diagnosis Differential : keratoacanthoma (for well differentiated tumors)

Squamous Cell Ca

Squamous cell carcinoma (HE) x 75

Squamous cell carcinoma (HE) x 150


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Selected cases of squamous cell carcinoma: (a) a representative case of

moderately differentiated squamous cell carcinoma (H&E, X 40); (b)

intranuclear staining for human telomerase reverse transcriptase activity (X200); (c) intracytoplasmic COX-2 stain (X 200); (d) strong intranuclear p53

expression (X 400).

Selected cases of keratoacanthoma: (a) a representative case of earlykeratoacanthoma with overhanging lips and central horn-filled crater (H&E,

40); (b) negative for telomerase activity ( 400); (c) basal staining for p53 (

100); (d) negative COX-2 stain ( 200).


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Histopathologic criteria to differentiate early keratoacanthoma from a well

to moderately differentiated squamous cell carcinoma (Ackerman et al and

Cribier et al)

Keratoacanthoma Squamous cell carcinoma

Exoendophytic lesion with a central horn-

filled crater

Predominantly endophytic with

no horn-filled crater

Overhanging 'lips' of epithelium No epithelial 'lips'

Rarely ulcerated Commonly ulcerated

Abundant pale staining cytoplasm of

keratinocytes

Less common

Intraepithelial abscesses within the lesion Rare

Acantholytic cells within the

intraepithelial abscesses often

Acantholytic cells form without

associated neutrophils

Gland-like formations rare Pseudoglandular formations

often

Lack of anaplasia Common

Sharp outline between tumor nests and

stroma

Indistinct

Absence of stroma desmoplasia Present


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BASAL CELL CARCINOMA

Disebut basal cell carcinoma karenayang mengalami perubahan adalah sel

epitel basal, kan epitel itu ada

beberapa jenis (epitel propium,

granulosum, spinosum dan basale)

Most frequent form of skin cancer Usually sun exposed skin (not mucosal

surfaces), in proportion to number of

pilosebaceous units present

Rosai claims these tumors attempt todifferentiate toward pilosebaceous

units, but often this is not readily

apparent

Often multiple tumors Usually older adults Slow and indolent, untreated cases may invade subcutis, skeletal muscle

and bone; facial tumors may invade skull, nares, orbit or temporal bone;

only 100 metastatic cases described, often associated with basal cell

nevus syndrome or basosquamous histology, on sunlight-protected skin

Metastases are rare; 60% to regional lymph nodes, also lung, liver, bone Risk factors: fair skin, blue eyes, immunosuppression (higher incidence,

more aggressive tumors),

xeroderma pigmentosum

Basal cell carcinoma (HE) x 75

Basal cell carcinoma ini disebut juga

dengan karsinoma basoselulare.

Semua karsinoma basoselulare ini

sifatnya progresif, prognosisnya

jelek, dan membutuhkan terapi

radiasi (kemoterapi). Mudah

metastasis, namun untuk metastasis

membutuhkan banyak proses.

Metastasisnya dapat melalui limfe,

pembuluh darah, dll. Jikametastasisya di pembuluh darah,

maka akan membuat pembuluh

darah baru (neovaskularisasi) oleh

karena itu, saat ini banyak

dikembangkan obat-obatan untuk

mencegah pembentukan pembuluh

darah baru, yaitu Anti VEGF

(Vaskuler Endotelial Growth Faktor)


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Also associated with nevus sebaceus of Jadassohn, chronic venous stasis of lower leg, arsenic, X rays, skin injury, chickenpox scars, tattoos, hair transplant scars, immunosuppression

Less common in children or young adults, sunlight-protected skin; rarelycoexists with benign nevus

Basal cell carcinomaDisebut juga dengan ulkus rodent.

Gambaran histologis tepinya seperti pagar (palisade)

MALIGNANT MELANOMA

Melanoma

Pada dasarnya pewarnaan pada kulit itu disebabkan oleh dua factor ada

factor instrinsik dan ekstrinsik. Kalo yang ekstrinsik contohnya karena

paparan sinar UV, sedangkan kalo instrinsik adanya pigmen melanin.

Keabnormalan melanin ini mula-mula akan jinak (melanoma) tapi lama-

kelamaan akan berubah ganas dan menjadi malignan melanoma. Sel-selnya

banyak yang anaplasi (polimorfik dan atipi). Malignan melanoma yang terjadi

pada daerah sel yang tidak ada melaninnya disebut juga dengan amelanotic

melanoma. Keganasan malignat melanoma ini tergantung dengan

kedalaman invasinya.


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Incidence increasing worldwide - 48,000 cases and 9,200 deaths in US in2000

Usually due to sun (UV light) exposure

Warning signs : change in color of pigmented lesion, enlargement of existing

mole, itching or pain in preexisting mole, development of new pigmented

lesion in adult life, irregular borders in pigmented lesion, variegation of color

in pigmented lesion

Head and neck, lower extremities (particularly in women); rarelysubungual (melanotic whitlow), palm, sole. Also oral and anogenital

mucosa, esophagus, meninges, eye

Populations at higher risk: whites with fair skin, red hair, tendency toburn or freckle from sun exposure, large number of melanocytic nevi,

xeroderma pigmentosum, familial dysplastic nevi, melanosis, vitiligo,

possibly neurofibromatosis type I

Up to 10% may be familial due to CMM1 gene at 1p36 Blacks have low risk, their common melanoma sites are palms, soles, nail

beds or mucous membranes

Usually after puberty, occasionally children - all have same morphology 5% are multiple, although prognosis is related to type and stage of largest

lesion, not number of lesions; must distinguish multiple lesions from hot

nevi / nevus activation

Achilles tendon tumors are often spindled Tend to grow laterally and deep; common metastases to regional lymph

nodes, also liver, lungs, GI tract, bone, CNS, heart (50% at autopsy), skin

(satellite tumors within 2 cm of primary tumor), other sites

Overall 5 year survival is 60% Poor prognostic factors:


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increased Breslow (vertical) thickness in primary tumor, high stage (TNM), males (do worse than females), high mitotic rate, ulceration, microscopic satellites (tumor nests 50 microns or larger and

separated from main tumor mass),

deeper level of invasion for T1 tumors, higher % tumor area/volume in sentinel node, increased density of dendritic leukocytes in nodal paracortex

(associated with risk of tumor in non-sentinel nodes, recurrence and

death, Mod Path 2004;17:747)

Overall behavior is variable, with occasional late deaths or long survivaleven with widespread satellite nodules

Melanoma

S100:nuclear and cytoplasmic, 90%+ sensitive but not specific (although usually

negative in tumors considered in the differential)

HMB45:less sensitive but more specific than S100; negative in desmoplastic

melanoma

MelanA/Mart1:sensitive, but also stains steroid-producing cells in ovary, testis, adrenal

cortex

Tyrosinase:


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sensitive, but also stains peripheral nerve sheath and neuroendocrine tumors

Microphthalmia transcription factor:sensitive, but also stains dermatofibroma and smooth muscle tumors;

negative in spindle cell / desmoplastic melanoma

NKI-C3 and NSE: nonspecific Negative stains: p53

Malignant Melanoma

Lesions are irregular in contour and

pigmentation. Macular areas correlated with the

Nevus Pigmentosus

Melanomasteps of tumor progression in dysplastic nevi

Melanocytic hyperplsia, B. Junctional nevus, C. Dysplastic nevus (compound

nevus with abnormal architectural and cytologic freatures, D. early melanoma

(radial growth phase melanoma large dark cells in epidermis), E.advancedmelanoma (vertical growth phase)


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radial growth phase, while raised areas usually correspond to nodular

aggregation of malignant cells in the vertical cell growth

Malignant Melanoma

Irregular nested and single cell

growth of melanoma cells within

the epidermis and an underlying

inflammatory response within

the dermis.

Malignant Melanoma

vertical phase growth

Nodular aggregates of infiltrating cells

Beberapa gambar

disamping adalah

gambaran histologis

perbesaran lemah

maupun kuat, kan di

praktiukum udah yaa,

jadi recall aja materi

praktikum nya

Malignant Melanoma

radial growth phase of melanoma


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Malignant Melanoma

High-power view of malignant melanoma cells

Nodular malignant melanoma (HE) x 10

Superficial spreading melanoma (HE) X 100

MALIGNANT MELANOMA


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Undifferentiated carcinoma

Pada dasarnya, carcinoma terdapat tida macam differensiasi,

diferensiasi baik, sedang, dan buruk.Nasopharynx

Inflammation Acute Chronic

Neoplasm

Juvenile angiofibroma Undifferentiated carcinoma

a McIvor mouth gag is applied and a

left nasopharyngeal mass is visible

behind the soft palate and left

posterior pillar. The final diagnosiswas lymphoepithelioma


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Nasopharingeal Ca, non-keratinizing, undiff.

Sering disebut juga

NPC (Nasopharink

Carcinoma)

Sel ini murni berasal

dari sel epitel yang

mengalami

keabnormalan, tetapi

gambaran histologis

banyak terlihat

sebukan limfosit yang

berfungsi membunuh

sel-sel tumornya,

hiperkromatid


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EBV

(IH; LMP-1) x 600

Anaplastic (undifferentiated) Carcinoma

Metastasic tumor

LARYNX: benign vs malignant

Gambaran disamping adalah

gambaran histologis dari

undifferentiated carcinoma

yang terinfeksi Epstein Bar

Virus, dilihat dengan

menggunakan pewarnaan

LMP (Laten Membran

Protein)

Pada NPC ini, carcinomanya

tersembunyi, pada saat

pemeriksaan AJH (Aspirasi

Jarum Halus) dia tidak

terlihat, namun NPC ini

mudah bermetastasis

Pada gambaran histologis

terlihat gumpalan sel tumor

yang dikelilingi oleh limfosit

Pada penyanyi dengan suara

seriousa biasanya ada nodus

singer, sedangkan papilloma yang

terdapat diplica vokalis itu

merupakan infeksi dari HPV


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Adenoid cystic carcinoma

Most characteristic appearance consists of cribriform pattern with

masses of small, dark-staining cells arrayed arround cystic spaces

Laryngeal papillomatosisLaryngeal Carcinoma

Gross: fungating/papillar

Adenoid cystic carcinoma ini, memiliki gambaran histologis pada

otot luriknya terdapat abnormalitas/tumor. Tumor epithelial ini

tersusun Kribiformis seperti jaringan. Lumen ini memiliki massa

mucoid sehingga disebut mucoepidermoid tumor.


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Mucoepidermoid tumor (Palatal gland)

Mucoepidermoid tumor (Low grade)

Comprised of

mucus-producing and epidermoid omponents

and cells intermediate between the two

Mucoepidermoid tumor (moderate grade)

Mucoepidermoid tumor (High grade)

Jadii, jangan lupa yaa

teman-teman tentang

terminology pada tumor

dan kanker, kalo

ditulisan belakangnya :

..oma : jinak

.carcinoma : ganas dari

sel epitel

.sarkoma : ganas dari

sel mesenkimal

119-137 dr agus sel squamosa carsinoma

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