This document discusses numerous preneoplastic and neoplastic lesions across multiple organ systems. Preneoplastic lesions involve abnormal cells with an increased cancer risk, while neoplastic lesions are cancerous or precancerous. Examples mentioned include actinic keratosis and Bowen's disease of the skin; oral leukoplakia; Barrett's esophagus; colonic adenomas; cirrhosis-associated liver cell changes; asbestos-related lung changes; various breast lesions; cervical intraepithelial neoplasia; penile intraepithelial neoplasia; prostatic intraepithelial neoplasia; and monoclonal gammopathy of undetermined significance, which can progress to myeloma.

1. PRENEOPLASTIC
AND NEOPLASTIC
LESIONS.
DR. MOHAN MOHANTY
MODERATOR- DR.ROHAN AGRAWAL

2. Preneoplastic lesions:
A lesion involving abnormal cells , which are associated with an increased risk of developing into
cancer.

3. SKIN

4. ACTINIC KERATOSIS
 Sun exposed sites.
 Light pigmented individuals.
 May regress or stable or
transform to malignancy.
 0.1-10% to SCC

5. Dysplasia with hyperkeratosis and parakeratosis

6. BOWEN DISEASE:
 SCC in situ or squamous intraepithelial
neoplasia.
 Indolent scaly, erythematous plaques
 Site- non chronically sun exposured
skin.
 Atypical epithelial changes.
 Involve full thickness of epithelium.
 3-5% risk to develop SCC.

7. Arsenic keratosis:
 Cutaneous manifestation of chronic
arsenic toxicity.
 Corn like yellowish hyperkeratotic plaques
or papules.
 Affects palms and soles
 May progress to SCC.
 HP: Hyperkeratosis, parakeratosis,
acanthosis.

8. Chronic radiation keratosis:
 Change in skin appearance: Hypo and
hyperpigmentation, skin atrophy, loss of hair
appendages.
 HP: Hyperkeratosis.
 Occurs due to imbalance of proinflammatory
and profibrotic cytokines.
 Etiology: Radiotherapy inappropriate dose,
genetic factor, CT disorders.
 May occur after years of treatment.

9. GASTROINTESTINAL TRACT:

10. Oral cavity:

11. LEUKOPLAKIA WITH DYSPLASIA
 A white patch or plaque that cannot be scrapped off
 Lichen planus and candidiasis are not included
 3% world’s population;5-25% premalignant.
 Malignancy: Increased duration, increased size of lesion,
non homogenous appearance.
 Can occur throughout upper aerodigestive tract.
 HP: Keratinizing dysplasis, hyperkeratosis, parakeratosis,
basal cell hyperplasia.
 Risk of SCC.

12. ERYTHROPLAKIA
 Red, velvety, plaque like appearance.
 Incidence of malignancy 17 times more than leukoplakia.
 Red coloured due to submucosal blood vessels seen
through it.
 Biopsy is must.
 remains level with or may b slightly depressed relative to
the surrounding mucosa.
 90% display severe dysplasia,ca in situ or minimally
invasive carcinoma.
 HP: Dysplasia.
 Progresses to SCC.

13. Oral submucous fibrosis:
 Juxtaepithelial deposition of fibrous tissue.
 Associated with beetle nut chewing.
 Due to cell mediated immune respone to
arecoline.
 Localized collagen disorder/ autoimmune
process.
 C/F: Progressive trismus, failure to protrude
tongue.
 Malignancy in 3-8%.

14. Lichen planus:
 Usually self limiting, more in case of oral
lesions.
 Post inflammatory hyperpigmentation seen.
 Expression of altered antigen in basal
epidermal cells leads to T cell activation.
 White, reticular, net like appearance.
 Burning sensation.

15. Actinic cheliosis:
 Actinic keratosis of lips.
 May progress to SCC.

16. Plummer Vinson Syndrome:
 Esophageal webs , dysphagia, iron deficiency
anemia, glossitis, angular chelitis.
 Progresses to SCC.
 Common in females.
 HP: epithelial atrophy with dysplasia.

17. ESOPHAGUS AND STOMACH:

18. BARRETT ESOPHAGUS:
 Complication of chronic GERD
 Replacement of esophageal squamous
mucosa by metaplastic columnar
epithelium with goblet cells
 Subdivided in to
1. Long segment(classic form)
2. Short segment
 Risk of esophageal adenocarcinoma.

19. HP:
Abundant metaplastic goblet cells, atypical mitosis,
nuclear hyperchromasia.

20. Autoimmune atrophic gastritis
 Affects fundus with loss of partial cells
 Spares antrum
 Endocrine cell hyperplasia, with hypergastrinemia
 Vit B 12 deficiency
 Achlorhydria
 Intestinal metaplasia
 Precursor to adenocarcinoma and neuroendocrine
tumors (carcinoid).

21. Menetriers’s disease:
 Due to excessive secretion of TGF-alpha.
 Irregular arrangement of gastric ruggae.
 HP: Diffuse hyperplasia of foveolar
epithelium, elongated dilated corkscrew
glands.
 Hypoproteinemia, diarrohoea, weight loss.
 Risk of gastric adenocarcinoma.

22. Gastric adenoma:
 8 – 10% of all gastric polyps
 Precursor lesion of gastric adenocarcinoma
 Up to 30 – 40% contain focus of carcinoma at time
of diagnosis
 Risk higher in larger tumors, especially if > 2cm, flat
or depressed

23. COLON:

24. Adenoma-Carcinoma Sequence

26. Neoplastic polyps:
 Colorectal adenomas are characterized by presence of epithelial dysplasia.
 Hallmark-nuclear hyperchromasia, elongation and startifiaction.
 Reduction in number of goblet cells.
 Tubular,tubulovillous or villous.
 Sessile serrated lesions-lack typical cytologic features of dysplasia.
 Size is the most imp risk of malignancy.

27. Cont….

28. HNPCC (Lynch Syndrome):
 Type of cancer syndrome.
 Germline mutation in MMR gene
 80% of patients develop colorectal carcinoma
 Also risk for: endometrial cancer(33%),ovarian carcinoma(5%), upper
urinary tract, other GI cancers.
 More often right colon and arises from adenomas

29. FAP
 AD, defect in APC gene.
 Numerous colorectal adenomas as
teenagers.
 Atleast 100 polyps are necessary for
diagnosis –Classic FAP
 Colorectal adenocarcinoma
develops in 100% in untreated
cases,

30. Colitis associated neoplasia:
 Long term Ulcerative colitis and colonic crohn disease.
 Risk of dysplasia and subsequent cancer related to
1. Duration of the disease
2. Extent of the disease
3. Nature of inflammatory response

31. Liver:
PRECANCEROUS LESION

32. LIVER
 Chronic liver disease and
cirrhosis
 Noncirrhotic liver-15-20%
 Underlying diseases

33. Small cell changes
Large cell changes
Dysplastic
changes

34. Lungs & Pleura:
PRECANCEROUS LESIONS

35. Asbestos related diseases
Family of pro inflammatory crystalline hydrated silicates
Asso with pulmonary fibrosis and various cancers
Lung carcinoma
Malignant mesothelioma
Laryngeal, ovarian , other extrapulmonary neoplasm including colon
carcinoma
90%mesothelioma are asbestos related
Life time risk of developing mesothelioma 7-10%

36. Breast:
PRECANCEROUS LESION

37. BREAST

38. USUAL DUCTAL HYPERPLASIA
 Benign epithelial proliferation
 Polyclonal
 Cohesive proliferation with haphazard architecture,
irregular ,slit like lumina ,often peripherally located
streaming,syncytial pattern
 Variable sized cells with indistinct borders
 Overlapping nuclei

39. ATYPICAL DUCTAL HYPERPLASIA
(ADH)
 Resembling DCIS but less developed in architecture and extend
 Size- <2mm and <2duct spaces
 Cells-evenly spaced monotonous cells,round nuclei with dense chromatin

41. DUCTAL CARCINOMA IN SITU
 Often detected on mammography
 Clonal proliferation of epithelial cells limited to ducts and lobules by
basement membrane.
 Myoepithelial cells are preserved ,may diminished
 Graded based on nucleus morphology
 Low grade
 High grade

43. SCLEROSING ADENOSIS
 Incidental microscopic finding
 Gross:small mass with a disk like , multinodular
configuration that cuts with increase resistance

44. Female genital tract
PRECANCEROUS LESION

45. Nonatypical endometrial hyperplasia
 Low risk of progression to carcinoma (2-4%)
 Gross: irregular endometrial thickening
 Simple:normal tubular glands
 Complex: abnormal irregular glands
 Cytology: elongate,dense, polarized nuclei

46. Endometrial intraepithelial neoplasia
 38% risk of carcinoma
 Polypoid or thickened endometrial lining
 Crowded glands with a gland to stroma ratio >1:1
 Altered cytology of the crowded glands
 Must be >1mm with in single tissue fragment
 Cytologically altered nuclei: enlarged, rounded,
pleomorphic,loss of polarity, vesicular chromatin, nucleoli

47. Low grade squamous intraepithelial
neoplasm of cervix(CIN1):
 Not recognisable grossly
 Relatively normal basal cell layer,hyperplastic parabasal
layer
 Orderly maturation
 Mitotic activities and dysplasia confinded to the lower
third of epithelium.no abnormal mitosis
 Koilocytosis
 Will clear spontaneously or few wl progress to HSIL
 HPV 6&11- LSIL/condyloma
 HPV 16&18-HSIL/SCC

48. High grade squamous intraepithelial
neoplasm of cervix: (CIN 2/3)
 May be Seen macroscopically
 High N:C ratio in all layers of epithelium
 Nuclear atypia, prominent mitotic
activities with atypical mitosis
 Mitotic figures found in upper layers of
epithelium

49. Vulva

50. Penis
PRECANCEROUS LESION

51. Penile lesions
Lesions sporadically associated with SCC of the penis
 Cutaneous horn of penis
 Bowenoid papulosis of the penis
 Lichen sclerosus (balanitis xerotica obliterans)
Premalignant Lesions
 Giant condylomata
 Erythroplasia of queyrat
 Bowen’s disease
 Paget’s disease

52. Penile intraepithelial neoplasm (PIN):
 Early neoplastic lesion of squamous epithelium
 Subdivided in to
HPV associated PIN:
 Basaloid(undifferentiated)
 Warty(bowenoid)
 Warty –basaloid
 Non-HPV associated PIN
 Differentiated

53. Basaloid PIN:
 Glans penis
 Morphologically High grade squamous
Intraepithelial lesions of cervix
 Squamous maturation is not characteristic
 P16 diffuse positive

54. Warty PIN:
 Papillomatous surface
 Abundant surface keratin
 Well developed koilocytic
atypia
 Frequent squamous
maturation
 Strong p16 positive
Warty- basaloid PIN.

55. HPV unrelated PeIN
 Differentiated PeIN
 Foreskin
 Lichen sclerosus and other inflammatory conditions
 Thickened squamous epithelium, elongated rete
ridges ,may show bridging
 P16 negative

56. Germ cell neoplasia in situ(GCNIS):
 80%-Residual testis in organs harbouring an invasive germ cell malignancy
 5%-C/L testis.
 Restricted to seminiferous tubules,also rete testies-pagetoid appearance
 Atypical germ cell at base of seminiferous tubules.
 Spermatogenesis absent.

57. Prostate:
2 premalignant Lesions:
 Prostatic intraepithelial Neoplasia (PIN)
(Intraductal dysplasia, primary atypia hyperplasia, large acinar dysplasia
,acinar- ductal dysplasia)
 Atypical adenomatous hyperplasia (AAH)
(adenosis, small gland hyperplasia)

59. Urinary bladder:
2 precursor lesions:
 Non invasive papillary tumors
 Flat non-invasive urothelial carcinoma in situ

62. BONE:
 Genetic syndromes.
 Chronic osteomyelitis.
 Paget disease.
 Giant cell tumor
 Irradiation
 Use of metal orthopaedic devices.

63. Hematogenous:

64. MONOCLONAL GAMMOPATHY OF
UNDETERMINED SIGNIFICANCE:
 2% elderly over age 50,3% over age 75 years.
 Over a period of 25yr-25-30% transform into myeloma.

65. MYELODYSPLASTIC SYNDROMES:
 Clonal hematopoietic stem cell disorders characterized by cytopenias,
dysplasia in one or more of the major myeloid cell lines, ineffective
erythropoiesis with cellular marrow .
 Transformation to acute leukemia :30-35%