Past Exams & Altucci Lecture Atlas
55 past oral-exam questions plus Prof. Altucci's lecture compendium — exam July 9, 2026
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Altucci FilesProf. Altucci — Lecture Notes Compendium
Structured transcription of Prof. Lucia Altucci's pathology & oncology lectures: tumor biology, classification, oncogenes, tumor suppressors, metastasis, BRCA, and hemodynamics — with high-yield FAQs and vocabulary for the July 9, 2026 oral exam.
6 sections · 43 FAQs · 10 terms
High-Yield
- ▸Tumor = autonomous, aggressive, atypical proliferation independent of physiological signals.
- ▸Monoclonal origin demonstrated by the classical G6PD isoenzyme study (single inactivated X in all tumor cells).
- ▸William Hahn: ~7–10 sequential mutations required to transform a normal cell into a fully malignant one.
Detail Bullets
- •Hyperplasia = ↑ cell NUMBER, physiologic/reversible (e.g., endometrium under estrogen).
- •Hypertrophy = ↑ cell SIZE (e.g., cardiac muscle in hypertension).
- •Metaplasia = reversible replacement of one differentiated cell type by another (Barrett's: squamous → columnar).
- •Dysplasia = disordered growth with atypia; PRE-neoplastic, still reversible.
- •Neoplasia = irreversible, clonal, autonomous proliferation.
- •Morphologic atypia: ↑ nuclear/cytoplasmic ratio, irregular nuclei, prominent nucleoli, dilated ER, abnormal mitochondria, atypical mitoses.
- •Tumor heterogeneity arises during clonal evolution — subclones with differing metastatic potential coexist.
Exam Pearls
- ★Altucci's trap: 'p53 is the guardian of the genome' is correct but INSUFFICIENT — always follow with WHY (DNA damage sensor → MDM2, p21, GADD45, BAX, FAS, IGF-BP3).
- ★Know the difference between TF (binds DNA directly) vs enhancer (acts via bound proteins, not direct DNA binding).
Q: Define a tumor in three words.
A: Autonomous, aggressive, atypical proliferation — clonal in origin, requiring 7–10 driver mutations (Hahn).
Q: Why is p53 called the guardian of the genome — and what does it actually DO?
A: It senses DNA damage; rising levels and tetramer assembly activate transcription of MDM2 (feedback), p21 (G1 arrest), GADD45 (S arrest via PCNA/DNA-pol-α inhibition), and BAX/FAS/IGF-BP3 (apoptosis). If repair fails, it directs the cell to apoptosis.
Q: Which RAS codon is most aggressive and why?
A: Codon 12 (especially G12C/G12D) — locks RAS in GTP-bound state, resists GAP-mediated hydrolysis, drives constitutive MAPK and PI3K signaling; poor response to standard therapy.
Q: Explain Burkitt lymphoma translocation.
A: t(8;14)(q24;q32) — c-MYC moves next to IgH enhancer → constitutive MYC expression; variants t(2;8) κ-light chain and t(8;22) λ-light chain.
Q: How does p16 differ from p21?
A: p16 (INK4 family) selectively inhibits CDK4/6 by COMPETING for the RB-binding site; p21 (CIP/KIP) inhibits a broad range of CDKs and is a direct p53 transcriptional target.
Q: What is the rate-limiting step of metastasis?
A: Colonization of the distant organ — most CTCs die in transit; only seed-compatible microenvironments allow micrometastasis outgrowth.
Q: Why do BRCA carriers benefit from PARP inhibitors?
A: Synthetic lethality: BRCA-deficient cells already lack HR repair; PARP inhibition blocks BER → unrepaired SSBs become DSBs → tumor-selective death.
Q: Why does diabetes predispose to gangrene?
A: Combined microangiopathy (basement-membrane thickening, ischemia), neuropathy (unrecognized trauma), and immunosuppression (impaired neutrophil function, hyperglycemic milieu) — wet gangrene from bacterial superinfection.
Q: NEW · What are oncosuppressor genes?
A: Recessive loss-of-function 'brake' genes (RB, p53, p16, APC, BRCA1/2, PTEN, NF1, VHL) requiring BIALLELIC inactivation (Knudson 2-hit). Split into gatekeepers (cell-cycle/apoptosis: RB, p53, p16) and caretakers (genome integrity: BRCA1/2, MMR, NER).
Q: NEW · Mechanism of action of p53?
A: DNA damage → ATM/ATR phosphorylate p53 (Ser15) → escapes MDM2 → stabilizes as homotetramer → transcribes p21 (G1 arrest), GADD45 (S arrest via PCNA/DNA-pol-α block), BAX/FAS/IGF-BP3 (apoptosis), MDM2 (negative feedback). HPV E6 degrades it; MDM2 amplification (sarcomas) functionally inactivates it.
Q: NEW · What is ATM (full name)?
A: Ataxia-Telangiectasia Mutated — PI3K-like Ser/Thr kinase on 11q22 that senses double-strand DNA breaks via the MRN complex (MRE11-RAD50-NBS1), then phosphorylates p53, CHK2, BRCA1 and γH2AX. Biallelic loss = Ataxia-Telangiectasia (cerebellar ataxia, telangiectasias, immunodeficiency, lymphoma).
Q: NEW · What is edema?
A: Excess interstitial fluid from imbalance of Starling forces: ↑ hydrostatic pressure (CHF, portal HTN), ↓ oncotic pressure (hypoalbuminemia), lymphatic obstruction, Na/H2O retention, or ↑ permeability (inflammation). Transudate (protein <3) vs exudate (protein >3) per Light's criteria.
Q: NEW · Most important cause of transudate formation?
A: LIVER CIRRHOSIS — portal hypertension ↑ sinusoidal hydrostatic pressure + hypoalbuminemia ↓ oncotic pressure → ascites with SAAG ≥ 1.1 g/dL. Other key causes: CHF, nephrotic syndrome, severe malnutrition.
Q: NEW · What is necrosis?
A: Unprogrammed cell death from severe injury — ATP depletion, Ca²⁺ overload, mitochondrial permeability transition, membrane rupture, lysosomal enzyme leak → INFLAMMATION. Patterns: coagulative (MI), liquefactive (brain, abscess), caseous (TB), fat (pancreatitis), fibrinoid (vasculitis), gangrenous (diabetic foot).
Q: NEW · Tumor histogenetic classification (Altucci)?
A: By tissue of origin + behavior: EPITHELIAL benign = adenoma/papilloma, malignant = carcinoma / adenocarcinoma / squamous-cell / transitional; MESENCHYMAL benign = -oma (lipoma, leiomyoma, osteoma), malignant = sarcoma; HEMATOPOIETIC = leukemia and lymphoma (ALWAYS malignant); mixed = pleomorphic adenoma, teratoma. Malignant 'sounding' benign-suffix tumors: melanoma, lymphoma, glioblastoma, mesothelioma, seminoma.
Q: NEW · What is atherosclerosis and what causes it?
A: Chronic inflammatory disease of large/medium arteries driven by LDL CHOLESTEROL infiltration of injured endothelium → ox-LDL → macrophage scavenger uptake → foam cells → fatty streak → SMC migration + collagen → fibrous-cap atheroma. Plaque rupture exposes thrombogenic core → MI/stroke. Risks: LDL, HTN, smoking, diabetes, age, male, family history.
Q: NEW · What is a granuloma?
A: Focal collection of activated epithelioid macrophages ± Langhans multinucleated giant cells, surrounded by lymphocytes, in response to a persistent indigestible antigen — a Type IV hypersensitivity reaction driven by CD4+ Th1 cells and IFN-γ. May be caseating (central necrosis) or non-caseating.
Q: NEW · Which disease is most associated with granulomas?
A: TUBERCULOSIS (Mycobacterium tuberculosis) — classic CASEATING granulomas with Langhans giant cells and acid-fast bacilli. Other granulomatous diseases: sarcoidosis (non-caseating), leprosy, fungi (histoplasma, blasto), Crohn disease, cat-scratch, foreign body, GPA, berylliosis.
Q: NEW · What is acute inflammation?
A: Rapid (minutes-days) stereotyped response to injury: vascular phase (histamine/bradykinin → vasodilation + ↑ permeability → exudate) + cellular phase (neutrophil margination, rolling on selectins, firm adhesion via integrins/ICAM-1, transmigration, chemotaxis to C5a/LTB4/IL-8, phagocytosis, ROS). Five cardinal signs: rubor, calor, tumor, dolor, functio laesa.
Q: NEW · Different types of exudate?
A: (1) SEROUS — thin, protein-poor (burn blister, viral pleurisy). (2) FIBRINOUS — fibrin-rich (uremic / post-MI pericarditis, 'bread-and-butter'). (3) PURULENT/SUPPURATIVE — pus, neutrophil-rich (abscess, empyema). (4) HEMORRHAGIC — RBCs (TB, malignancy, PE infarct, severe pancreatitis). (5) FIBRINOID — fibrin + necrosis in vessel walls (vasculitis, malignant HTN).
Q: NEW · What is in pus?
A: Degenerated/dying NEUTROPHILS ('pyocytes'), liquefied necrotic tissue, edema fluid (plasma proteins), cellular debris, and viable or dead microorganisms (typically pyogenic bacteria — S. aureus, S. pyogenes, E. coli). Yellow-green color = myeloperoxidase.
Q: NEW · Breast cancer — key subtypes?
A: Molecular IHC subtypes: LUMINAL A (ER+/PR+/HER2-/Ki67-low — best prognosis), LUMINAL B (ER+/HER2±/Ki67-high), HER2-ENRICHED (ERBB2 amp — trastuzumab + pertuzumab), TRIPLE-NEGATIVE/BASAL-LIKE (BRCA1, chemo-sensitive, pembrolizumab if PD-L1+). Treatment matched to subtype: endocrine (tamoxifen/AI), anti-HER2, chemo, PARPi for BRCA, surgery + RT.
Q: NEW · Nervous-system tumors — adults vs children?
A: ADULTS supratentorial: glioblastoma (IDH-wt, pseudopalisading necrosis), meningioma (psammoma, NF2), schwannoma, primary CNS lymphoma, and METASTASES (lung > breast > melanoma — most common overall). CHILDREN infratentorial: pilocytic astrocytoma (BRAF fusion, Rosenthal fibers), medulloblastoma (Homer-Wright rosettes), ependymoma (perivascular pseudorosettes), brainstem DIPG (H3K27M).
Q: NEW · Classification of anemia?
A: By MCV: MICROCYTIC (<80) — iron deficiency, thalassemia, ACD, sideroblastic, lead; NORMOCYTIC (80–100) — acute blood loss, hemolysis, marrow failure, CKD; MACROCYTIC (>100) — B12/folate deficiency, alcohol, hypothyroid, MDS. By kinetics: reticulocyte index >2 = hyperproliferative (hemolysis/blood loss); <2 = hypoproliferative.
Q: NEW · How do you recognize anemia clinically?
A: Symptoms of tissue hypoxia: fatigue, dyspnea on exertion, palpitations, headache, dizziness, syncope. Signs: pallor (conjunctiva, palmar creases, nail beds), tachycardia, systolic flow murmur, glossitis, koilonychia (Fe-def), jaundice (hemolysis), neurologic signs (B12). Confirm with CBC: Hb below age/sex cutoff.
Q: NEW · Normal hemoglobin levels?
A: Adult MEN 13.5–17.5 g/dL · Adult WOMEN 12.0–15.5 g/dL · Pregnant ≥ 11 · Children ~11–14. WHO anemia cutoff: <13 (M), <12 (F non-pregnant), <11 (pregnant, children 6 mo–5 yr). Hematocrit ≈ 3 × Hb.
Q: NEW · How does the RAS oncogene work (RAS-RAF pathway)?
A: RAS is a membrane GTPase switch. RTK (e.g., EGFR) → GRB2-SOS (GEF) loads RAS-GTP → binds RAF (Ser/Thr kinase) → phosphorylates MEK1/2 → phosphorylates ERK1/2 → translocates to nucleus → activates MYC, ELK-1, cyclin D1 → G1→S. RAS also activates PI3K-AKT-mTOR. GAPs (NF1) hydrolyze RAS-GTP to RAS-GDP. Oncogenic mutations (codons 12, 13, 61) lock RAS-GTP, resist GAP, drive constitutive MAPK.
Q: NEW · What is Src?
A: First proto-oncogene discovered (v-Src in Rous sarcoma virus, 1976). Non-receptor tyrosine kinase normally autoinhibited by Csk-mediated phosphorylation of C-terminal Tyr530. Phosphorylates FAK/paxillin (focal adhesions), cortactin (cytoskeleton), STAT3 (proliferation). Overactivation in colon/breast/pancreatic cancer drives motility and invasion. Targeted by dasatinib and bosutinib.
Q: NEW · Complications of diabetes?
A: MICROVASCULAR — retinopathy (microaneurysms, hemorrhages, neovascularization → blindness), nephropathy (Kimmelstiel-Wilson, microalbuminuria → ESRD), neuropathy (stocking-glove, autonomic). MACROVASCULAR — CAD, stroke, PAD, diabetic GANGRENE (combined ischemia + neuropathy + immunosuppression, typically WET liquefactive). Plus: infections, cataracts, NAFLD.
Q: NEW · How do ROS damage the diabetic retina?
A: Hyperglycemia drives mitochondrial superoxide overproduction + polyol pathway (sorbitol osmotic stress) + AGE/RAGE NF-κB activation + PKC-induced VEGF and endothelin-1. Result: pericyte loss, basement-membrane thickening, capillary microaneurysms, dot/blot hemorrhages, cotton-wool spots, neovascularization with vitreous hemorrhage and retinal detachment → diabetic RETINOPATHY.
Q: NEW · What is chronic inflammation?
A: Prolonged (weeks-months) inflammation with simultaneous tissue injury, repair, and immune infiltration. Dominated by MACROPHAGES (M1 IFN-γ→TNF/IL-1, M2 TGF-β→fibrosis), lymphocytes, plasma cells. Outcome = fibrosis. Triggers: persistent infection (TB, HCV, H. pylori), autoimmunity (RA, IBD), prolonged toxin (silica, asbestos, ox-LDL).
Q: NEW · What happens in type 2 diabetes (and what type of necrosis)?
A: Insulin resistance + relative β-cell failure → hyperglycemia → AGEs/ROS → endothelial dysfunction + microangiopathy. Diabetic foot ulcers progress to GANGRENOUS NECROSIS — typically WET gangrene (coagulative ischemic necrosis + superimposed liquefactive necrosis from polymicrobial bacterial infection). Treatment: debridement, broad-spectrum antibiotics, revascularization, glycemic control.
Q: NEW · What is fibrosis?
A: Excess deposition of type I/III collagen by activated MYOFIBROBLASTS (from resident fibroblasts, hepatic stellate cells, pericytes, or EMT) in response to chronic injury. Master cytokine = TGF-β (from M2 macrophages). TIMPs inhibit MMPs → matrix accumulates. End-result = scar replacing functional parenchyma (cirrhosis, IPF, keloid, scleroderma).
Q: NEW · What cells are involved in acute inflammation?
A: PRIMARY effector = NEUTROPHIL (PMN) — first responder at 6–24 h via margination, selectin rolling, integrin adhesion (LFA-1/ICAM-1), transmigration, chemotaxis (IL-8, C5a, LTB4, fMLP), phagocytosis with ROS/NETs. Supporting: tissue MAST CELLS (histamine), ENDOTHELIAL CELLS (P/E-selectin, ICAM-1, VCAM-1), MACROPHAGES (later), and PLATELETS.
Q: NEW · How many types of granulomas do you know?
A: By histology: CASEATING (central necrosis — TB, fungi) vs NON-CASEATING (sarcoidosis, Crohn, leprosy tuberculoid form, foreign body, berylliosis, cat-scratch, syphilis gumma). By mechanism: immune (Th1-driven, classic) vs foreign-body (no T-cell mediation, around inert material). Always contain epithelioid macrophages ± Langhans giant cells + lymphocyte rim.
Q: NEW · What is an atheroma and what is the role of LDL?
A: Atheroma = mature atherosclerotic plaque with soft lipid/necrotic core + fibrous cap (SMCs, collagen, foam macrophages). LDL is the central pathogenic driver: penetrates dysfunctional endothelium → oxidized to ox-LDL → engaged by macrophage scavenger receptors (CD36, SR-A, LOX-1) bypassing LDL-R feedback → unrestricted cholesterol uptake → FOAM CELLS → release IL-1, TNF, MCP-1 → recruitment + SMC proliferation. Lower LDL → fewer events (statins, PCSK9i).
Q: NEW · Role of oncogenes in cell transformation?
A: Dominant gain-of-function mutations of proto-oncogenes (point mutations, amplification, translocation) → constitutive growth-factor / receptor / signal-transducer / transcription-factor / cell-cycle activation → bypass of normal proliferation checkpoints, survival, angiogenesis, invasion. Examples: RAS, MYC, HER2, BCR-ABL, BRAF, EGFR, Cyclin D1, BCL-2.
Q: NEW · What is chemotaxis?
A: Directed leukocyte movement along a chemical gradient toward injury/infection. Chemoattractants (C5a, LTB4, IL-8/CXCL8, bacterial fMLP, CCL2 for monocytes) bind GPCRs → PI3K + Rac/Rho/Cdc42 → actin polymerization at leading edge, integrin activation (LFA-1) for firm adhesion. Defects: LAD-1 (β2-integrin), Chédiak-Higashi (LYST) → recurrent bacterial infections.
Q: NEW · BRCA1 vs BRCA2?
A: Both = caretaker tumor suppressors required for HOMOLOGOUS RECOMBINATION repair of double-strand breaks; interact with ATM, CHK2, RAD51, MRN complex, PCNA, H2AX. BRCA1 (17q21) → triple-negative basal-like breast + ovarian + ↑ male breast risk. BRCA2 (13q12) → ER+ breast + ovarian + male breast + pancreatic + prostate. Both → PARP inhibitor (olaparib) synthetic lethality.
Q: NEW · Most common metastatic sites?
A: LUNG, LIVER, BONE (axial > long bones — vertebrae, pelvis, ribs), BRAIN (grey-white junction), adrenal. Carcinomas favor LYMPHATIC spread; sarcomas favor HEMATOGENOUS. Organ-tropism (seed & soil — Paget): breast → bone, prostate → osteoblastic bone, colon → liver, lung → brain/adrenal, melanoma/RCC → anywhere.
Q: NEW · Mechanism of pRb?
A: Hypophosphorylated pRb binds and sequesters E2F → blocks transcription of S-phase genes (cyclin E, DNA-pol α, thymidine kinase, dihydrofolate reductase) → cell arrested in G1. Growth-factor signaling → cyclin D-CDK4/6 phosphorylates pRb → releases E2F → S-phase entry. p16-INK4a competitively inhibits CDK4/6, keeping pRb active. HPV E7 binds pRb constitutively → unopposed E2F → cervical/oropharyngeal cancer. Both alleles must be lost (Knudson) — retinoblastoma.
Q: NEW · Liver cirrhosis and liver fibrosis — same thing?
A: Liver fibrosis = excess collagen deposition by activated hepatic stellate cells in response to chronic injury (HCV, alcohol, NASH) — REVERSIBLE early. CIRRHOSIS = end-stage, IRREVERSIBLE: diffuse bridging fibrosis + regenerative nodules that distort vasculature → portal HTN (varices, splenomegaly, transudative ascites), hepatic failure (coagulopathy, hyperestrogenism, hyperammonemia), and ↑ HCC risk. Score with Child-Pugh / MELD.
Q: NEW · Type 1 vs Type 2 diabetes — pathology contrast?
A: T1DM: AUTOIMMUNE (HLA-DR3/4, anti-GAD65, anti-IA2, anti-ZnT8) → CD8+ T-cell destruction of β-cells → absolute insulin deficiency → childhood onset, lean, prone to DKA. T2DM: insulin RESISTANCE + relative β-cell failure → adult, obese, prone to HHS, islet amyloid (IAPP), polyp/PCOS associations. Both → micro/macrovascular complications via AGEs, polyol, PKC, hexosamine, ROS.
Monoclonality
All tumor cells arise from a single transformed progenitor — proven historically by G6PD isoenzyme analysis in heterozygous women.
Anaplasia
Loss of differentiation; hallmark of high-grade malignancy.
Desmoplasia
Dense fibrous stromal response surrounding an invasive carcinoma (classic in pancreatic and breast ca).
Cachexia
Paraneoplastic wasting — TNF-α, IL-6, IL-1, PIF-mediated muscle and fat catabolism.
Tumor Mutation Burden (TMB)
Number of somatic mutations per megabase; predicts response to PD-1/CTLA-4 immunotherapy.
Knudson two-hit
Two inactivating events needed in a tumor-suppressor locus; germline mutation provides the first hit in familial cancer syndromes.
Synthetic lethality
Simultaneous loss of two genes is lethal while loss of either alone is tolerated — basis for PARPi in BRCA-mutant cancers.
E-box (CACGTG)
DNA motif bound by MYC/MAX heterodimer to drive transcription of proliferation and metabolic genes.
Caretaker vs Gatekeeper
Caretakers (BRCA1/2, MMR) maintain genomic integrity; Gatekeepers (RB, p53, p16) directly regulate cell-cycle entry and apoptosis.
TAFs
Tumor Angiogenic Factors — FGF, VEGF, TGF-α/β, angiogenin, TNF-α, IL-1α — drive the avascular→vascular switch.
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Questions
01
What is the difference between apoptosis and necrosis?
medium
Cell Injury
Prof. Banfi
2025
02
What are the types of necrosis? Which is accompanied by inflammation?
medium
Cell Injury
Prof. Banfi
2025
03
Why does diabetes predispose to gangrene?
hard
Cell Injury
Prof. Banfi
2025
04
Describe the signaling cascade of apoptosis. Role of mitochondria?
hard
Cell Injury
Prof. Banfi
2026
05
What is the main difference between acute and chronic inflammation?
easy
Inflammation
Prof. Banfi
2025
06
What is the mechanism of fever? Role of prostaglandins?
medium
Inflammation
Prof. Banfi
2025
07
What leukocytes are involved in acute vs chronic inflammation?
medium
Inflammation
Prof. Banfi
2026
08
What proteins are expressed on endothelial cells during leukocyte recruitment?
hard
Inflammation
Prof. Banfi
2025
09
Difference between benign and malignant neoplasia?
easy
Neoplasia
Prof. Di Donato
2025
10
Explain multistep carcinogenesis. Name two driver mutations.
hard
Neoplasia
Prof. Di Donato
2026
11
What is the role of p53? What happens when it is mutated?
hard
Tumor Suppressors
Prof. Di Donato
2025
12
Explain Knudson's two-hit hypothesis using retinoblastoma.
medium
Tumor Suppressors
Prof. Castoria
2025
13
Describe the metastatic cascade. Rate-limiting step?
hard
Metastasis
Prof. Di Donato
2026
14
Define EMT. Which transcription factors drive it?
medium
Metastasis
Prof. Di Donato
2025
15
How does PTEN loss cause immunotherapy resistance?
hard
Tumor Suppressors
Prof. Castoria
2026
16
What is the tumor microenvironment? Role of CAFs?
hard
Tumor Microenvironment
Prof. Di Donato
2026
17
Pathophysiology of T1DM vs T2DM.
medium
Diabetes
Prof. Banfi
2025
18
Describe microvascular complications of diabetes.
hard
Diabetes
Prof. Banfi
2025
19
Compare AD and AR inheritance with examples.
easy
Genetics
Prof. Migliaccio
2025
20
Explain genomic imprinting using Prader-Willi and Angelman.
hard
Genetics
Prof. Migliaccio
2026
21
Chromosomal disorders: Down, Turner, Klinefelter — main features.
medium
Genetics
Prof. Migliaccio
2025
22
Describe Fragile X syndrome — molecular basis.
hard
Genetics
Prof. Migliaccio
2025
23
Compare AML, ALL, CML, CLL.
medium
Lymphoma/Leukemia
Prof. Banfi
2025
24
Differentiate Hodgkin from non-Hodgkin lymphoma.
medium
Lymphoma/Leukemia
Prof. Banfi
2026
25
What are exosomes? Role in cancer progression?
hard
Exosomes
Prof. Castoria
2026
26
Endocrine therapy of ER+ breast cancer.
medium
Hormone Malignancies
Prof. Castoria
2025
27
Mechanism of tamoxifen. Side effects?
medium
Hormone Malignancies
Prof. Castoria
2026
28
Compare aromatase inhibitors and GnRH agonists in breast cancer.
hard
Hormone Malignancies
Prof. Castoria
2025
29
Define hypertrophy, hyperplasia, metaplasia, atrophy.
easy
Cell Biology
Prof. Banfi
2025
30
Explain Barrett's esophagus — metaplasia and risk.
medium
Cell Biology
Prof. Banfi
2026
31
What is autophagy? Dual role in cancer?
hard
Cell Biology
Prof. Castoria
2026
32
Mechanism of ROS-mediated cell injury.
hard
Cell Injury
Prof. Banfi
2025
33
Explain the four mechanisms of diabetic microangiopathy.
hard
Diabetes
Prof. Banfi
2026
34
Compare Graves and Hashimoto thyroiditis.
medium
Cell Biology
Prof. Castoria
2025
35
Classify anemias by MCV.
easy
Cell Biology
Prof. Banfi
2025
36
Explain RAS oncogene activation.
hard
Neoplasia
Prof. Di Donato
2025
37
What is the role of NF-κB in inflammation and cancer?
hard
Inflammation
Prof. Banfi
2026
38
Describe the complement system pathways.
medium
Inflammation
Prof. Banfi
2025
39
Mechanism of wound healing — phases and key cells.
medium
Inflammation
Prof. Banfi
2025
40
Compare granulomatous inflammation in TB and sarcoidosis.
hard
Inflammation
Prof. Banfi
2026
41
Describe BCR-ABL and the Philadelphia chromosome.
hard
Lymphoma/Leukemia
Prof. Banfi
2026
42
Pathophysiology of sickle cell anemia.
medium
Genetics
Prof. Migliaccio
2025
43
Mitochondrial inheritance — features and example diseases.
hard
Genetics
Prof. Migliaccio
2026
44
Mechanism of carcinogenesis by HPV.
hard
Neoplasia
Prof. Di Donato
2025
45
What is angiogenesis in cancer? Therapeutic targets?
medium
Neoplasia
Prof. Di Donato
2025
46
What is the Warburg effect?
hard
Neoplasia
Prof. Di Donato
2026
47
Describe atherosclerosis pathogenesis.
medium
Diabetes
Prof. Banfi
2025
48
What is amyloidosis? Classification and stain.
medium
Cell Biology
Prof. Banfi
2026
49
Pathophysiology of Cushing syndrome.
medium
Cell Biology
Prof. Castoria
2025
50
Difference between hyperplasia and dysplasia.
easy
Cell Biology
Prof. Banfi
2025
51
What is paraneoplastic syndrome? Give examples.
hard
Neoplasia
Prof. Di Donato
2026
52
Describe immune checkpoint inhibitors mechanism.
hard
Tumor Suppressors
Prof. Castoria
2026
53
Explain DNA mismatch repair and Lynch syndrome.
hard
Tumor Suppressors
Prof. Di Donato
2025
54
Mechanism of action of GnRH agonists in prostate cancer.
medium
Hormone Malignancies
Prof. Castoria
2026
55
What is the role of miRNAs in disease?
hard
Genetics
Prof. Migliaccio
2026