Molecular Pathology — MCQs

A 1-year-old girl with an inborn error of metabolism resulting in a lysosomal storage disease receives a hematopoietic stem cell transplant intended to replace her macrophage population. The gene of interest has a 'marker' small nucleotide polymorphism within a non-coding intron of the affected gene in which an A (patient gene) is substituted for a G (donor gene). She does quite well for the first 3 weeks. She tests positive for the missing enzyme, her previously abnormally enlarged organs begin to diminish in size, and assay of peripheral blood lymphocytes reveals increasing numbers of cells with the G polymorphism. However, the attending physicians are now concerned because repeated genetic testing reveals a progressive increase in lymphocytes with the A nucleotide polymorphism. Which of the following is the best explanation for this finding?

Molecular Pathology Indian Medical PG Practice Questions and MCQs

Question 21: What is the first manifestation in cell injury?

A. Pyknosis
B. Cell swelling (Correct Answer)
C. Nuclear fragmentation
D. Nuclear lysis

Explanation: **Explanation:** **1. Why Cell Swelling is the Correct Answer:** Cell swelling (also known as **hydropic change** or vacuolar degeneration) is the **earliest and most common manifestation** of almost all forms of reversible cell injury [1]. The underlying mechanism involves the failure of energy-dependent membrane pumps. When a cell is injured (e.g., via hypoxia), ATP production decreases, leading to the failure of the **Na+/K+-ATPase pump** [1]. This results in an accumulation of intracellular sodium and an efflux of potassium. The increased osmotic pressure causes an obligatory influx of water into the cell, leading to swelling of the cytoplasm and organelles like the mitochondria and endoplasmic reticulum. **2. Why the Other Options are Incorrect:** * **A, C, and D (Pyknosis, Karyorrhexis, Karyolysis):** These are the three hallmark stages of **nuclear changes in irreversible cell injury (Necrosis)** [1]. * **Pyknosis (A):** Nuclear shrinkage and increased basophilia. * **Karyorrhexis (C):** Fragmentation of the pyknotic nucleus. * **Karyolysis (D):** Fading of chromatin due to DNAse activity. Since cell swelling occurs during the *reversible* phase, it precedes these irreversible nuclear changes. **3. NEET-PG High-Yield Pearls:** * **Light Microscopy:** Cell swelling appears as "cloudy swelling" or small clear vacuoles within the cytoplasm (hydropic change) [1]. * **Gross Appearance:** Affected organs (liver, kidney, heart) show increased weight and pallor. * **Sequence of Reversible Injury:** Decreased ATP → Failure of Na+ pump → Influx of Na+ and H2O → Efflux of K+ → **Cell Swelling** [1]. * **Point of No Return:** Irreversibility is characterized by **severe mitochondrial damage** (vacuolization) and **membrane damage** (plasma and lysosomal membranes). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 49-50.

Question 22: Which of the following cellular components is capable of recognizing dead material?

A. NET (Neutrophil Extracellular Traps)
B. Inflammasome (Correct Answer)
C. Necrosis
D. Toll-like receptor

Explanation: ### Explanation **Correct Answer: B. Inflammasome** The **inflammasome** is a multi-protein cytoplasmic complex that serves as a key component of the innate immune system [1]. It is specifically designed to recognize both **PAMPs** (Pathogen-Associated Molecular Patterns) and **DAMPs** (Damage-Associated Molecular Patterns). * When cells die (necrosis), they release "danger signals" such as **uric acid crystals, extracellular ATP, and altered membrane lipids** [1]. * The inflammasome (most notably the **NLRP3** type) senses these products of cell death [1]. * Once activated, it triggers the enzyme **Caspase-1**, which cleaves precursor forms of cytokines into their active states (**IL-1β and IL-18**), leading to inflammation and a specialized form of programmed cell death called **pyroptosis** [1]. --- ### Why other options are incorrect: * **A. NETs (Neutrophil Extracellular Traps):** These are extracellular fibrillar networks of chromatin and antimicrobial proteins released by neutrophils to trap and kill **microbes** (bacteria/fungi), not primarily to recognize dead host material. * **C. Necrosis:** This is a **process** of uncontrolled cell death itself, characterized by membrane rupture and leakage of contents. It is the *source* of the dead material, not the *sensor* of it. * **D. Toll-like Receptors (TLRs):** While TLRs are crucial innate sensors, they are primarily located on **plasma membranes and endosomes** to detect microbial components (like LPS or viral RNA). While some TLRs can sense DAMPs, the inflammasome is the classic, specialized cytoplasmic machinery dedicated to recognizing metabolic products of cell injury and dead material [1]. --- ### NEET-PG High-Yield Pearls: * **NLRP3 Inflammasome:** Associated with clinical conditions like **Gout** (sensing uric acid), **Atherosclerosis** (sensing cholesterol crystals), and **Type 2 Diabetes** (sensing amyloid) [1]. * **Caspase-1:** The "Inflammatory Caspase" (unlike Caspase-3, which is the "Executioner Caspase" in apoptosis). * **Pyroptosis:** A pro-inflammatory form of programmed cell death uniquely mediated by the inflammasome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, p. 196.

Question 23: Why do fetal cells continue to divide while terminally differentiated adult cells do not?

A. Adult cells have many cyclin inhibitors that prevent entry into the S phase. (Correct Answer)
B. Phosphatase is absent in fetal cells.
C. Proteinase is absent in the fetus.
D. CD kinases are absent in fetal cells.

Explanation: ### Explanation **1. Why Option A is Correct:** The cell cycle is strictly regulated by **Cyclins** and **Cyclin-Dependent Kinases (CDKs)**. To transition from the G1 phase to the S phase (DNA synthesis), cells must overcome the "restriction point." [1] In **terminally differentiated adult cells** (like neurons or cardiac myocytes), the cell cycle is arrested in the **G0 phase**. [1] This is primarily due to the high expression of **Cyclin-Dependent Kinase Inhibitors (CDKIs)**, such as the **Cip/Kip family (p21, p27, p57)** and the **INK4 family (p16)**. [1] These inhibitors bind to and silence CDK-cyclin complexes, preventing the phosphorylation of the Retinoblastoma (Rb) protein. Without Rb phosphorylation, the E2F transcription factor remains bound and inactive, effectively blocking entry into the S phase. [2] In contrast, **fetal cells** have low levels of these inhibitors and high telomerase activity, allowing for rapid, continuous proliferation to support organogenesis. [3] **2. Why Other Options are Incorrect:** * **Option B (Phosphatase):** Phosphatases (like CDC25) are actually essential for activating CDKs by removing inhibitory phosphate groups. Their absence would stop cell division, not promote it. * **Option C (Proteinase):** Proteinases (like Caspases or Ubiquitin-proteasome enzymes) are present in both fetal and adult cells for apoptosis and protein turnover. They are not the primary regulators of the G1-S transition. * **Option D (CD Kinases):** CDKs are the "engines" of the cell cycle. If they were absent in fetal cells, the fetus could not grow or develop. Fetal cells have high CDK activity. [1] **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Governor" of the Cell Cycle:** The **RB Gene** (Retinoblastoma) is the key negative regulator. When hypophosphorylated, it stops the cycle. [2] * **The "Guardian" of the Genome:** **p53** acts by inducing **p21** (a CDKI), which halts the cell cycle to allow for DNA repair. * **Quiescent vs. Permanent Cells:** **Stable (Quiescent) cells** (e.g., hepatocytes) are in G0 but can re-enter the cycle; **Permanent cells** (e.g., neurons) have high CDKI levels and cannot re-enter the cycle. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 37-38. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 300-301. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 38-39.

Question 24: In the alveolar variant of rhabdomyosarcoma, the resultant fusion protein is believed to function as what?

A. Activated growth factor receptor
B. Chimeric transcription factor (Correct Answer)
C. Constitutively active kinase
D. Novel growth factor

Explanation: **Explanation:** The correct answer is **B. Chimeric transcription factor.** **Understanding the Mechanism:** Alveolar Rhabdomyosarcoma (ARMS) is characterized by specific chromosomal translocations, most commonly **t(2;13)(q35;q14)** and less frequently **t(1;13)(p36;q14)**. These translocations result in the fusion of the **PAX3** (or PAX7) gene with the **FOXO1** (formerly FKHR) gene. * **PAX3/7** are genes involved in muscle differentiation (transcription factors). * **FOXO1** is a transcription factor involved in cell cycle regulation. The resulting **PAX3-FOXO1** fusion protein is a **chimeric transcription factor**. It possesses the DNA-binding domain of PAX and the transactivation domain of FOXO1, making it a much more potent activator of myogenic genes than wild-type PAX3. This leads to dysregulated gene expression, promoting cell proliferation and inhibiting apoptosis. **Analysis of Incorrect Options:** * **A & D (Growth Factor/Receptor):** While many cancers (like GIST or HER2+ breast cancer) involve growth factors or their receptors, ARMS is driven by nuclear genetic rearrangement, not extracellular signaling molecules. * **C (Constitutively active kinase):** This mechanism is classic for **Chronic Myeloid Leukemia (BCR-ABL)**, where the fusion protein acts as a tyrosine kinase. In ARMS, the fusion protein acts directly on DNA in the nucleus. **High-Yield Clinical Pearls for NEET-PG:** * **Embryonal RMS:** Most common type; associated with **loss of heterozygosity (LOH) at 11p15.5** (IGF-2 gene). * **Alveolar RMS:** More aggressive; characterized by **t(2;13)** fusion. * **Histology:** ARMS shows small round blue cells arranged in clusters separated by fibrous septa, resembling pulmonary alveoli. * **IHC Markers:** Desmin, Myogenin (Myf4), and MyoD1 are positive. Myogenin expression is typically more diffuse in the Alveolar variant compared to the Embryonal variant.

Question 25: The SYT-SSX1 gene fusion is associated with which of the following neoplasms?

A. Liposarcoma
B. Rhabdomyosarcoma
C. Synovial sarcoma (Correct Answer)
D. Ewing sarcoma

Explanation: **Explanation:** The correct answer is **Synovial sarcoma**. This neoplasm is characterized by a highly specific reciprocal translocation, **t(X;18)(p11;q11)** [1]. This translocation results in the fusion of the **SS18** (formerly *SYT*) gene on chromosome 18 with one of the **SSX** genes (usually *SSX1*, *SSX2*, or rarely *SSX4*) on the X chromosome [1]. The resulting **SYT-SSX** fusion protein acts as an aberrant transcriptional regulator that disrupts chromatin remodeling (SWI/SNF complex), leading to oncogenesis. **Analysis of Incorrect Options:** * **Liposarcoma:** Most commonly associated with **t(12;16)** resulting in the **FUS-CHOP** fusion (Myxoid/Round cell subtype) or **MDM2** amplification (Well-differentiated/Dedifferentiated subtype). * **Rhabdomyosarcoma:** Alveolar rhabdomyosarcoma is characterized by **t(2;13)** or **t(1;13)**, involving the **PAX3-FOXO1** or **PAX7-FOXO1** gene fusions. * **Ewing sarcoma:** Classically associated with **t(11;22)(q24;q12)**, leading to the **EWS-FLI1** gene fusion. **High-Yield NEET-PG Pearls:** * **Synovial Sarcoma:** Despite the name, it does *not* arise from synovial cells; it originates from mesenchymal stem cells near joints [1]. * **Morphology:** Can be **biphasic** (epithelial glands + spindle cells) or **monophasic** (spindle cells only) [1]. * **Immunohistochemistry (IHC):** Positive for **TLE1**, Cytokeratin, and EMA. * **Prognostic Correlation:** The **SYT-SSX1** variant is more common in biphasic tumors and is generally associated with a poorer prognosis compared to the *SYT-SSX2* variant. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1225-1226.

Question 26: What is the function of peroxisomes?

A. Protein synthesis
B. Carbohydrate metabolism
C. Generating hydrogen peroxide (H2O2) (Correct Answer)
D. DNA replication

Explanation: ### Explanation **Correct Option: C. Generating hydrogen peroxide (H2O2)** Peroxisomes are specialized membrane-bound organelles containing oxidative enzymes (such as catalase and urate oxidase). Their primary function is the **beta-oxidation of very-long-chain fatty acids (VLCFA)** and the detoxification of various substances. During these oxidative reactions, peroxisomes generate **hydrogen peroxide (H2O2)** as a byproduct [1]. Subsequently, the enzyme **catalase** within the peroxisome decomposes this H2O2 into water and oxygen, protecting the cell from oxidative damage [1]. **Analysis of Incorrect Options:** * **A. Protein synthesis:** This is the primary function of **ribosomes** (either free-floating or attached to the Rough Endoplasmic Reticulum). * **B. Carbohydrate metabolism:** While some gluconeogenesis steps occur in the cytosol and mitochondria, the primary hub for carbohydrate metabolism (glycolysis, TCA cycle) is the **cytosol and mitochondria**. * **D. DNA replication:** This process occurs exclusively within the **nucleus** (and to a small extent in the mitochondria for mtDNA). **High-Yield Clinical Pearls for NEET-PG:** * **Zellweger Syndrome:** An autosomal recessive "peroxisome biogenesis disorder" caused by mutations in *PEX* genes. It leads to the accumulation of VLCFAs, resulting in hypotonia, seizures, hepatomegaly, and early death. * **X-linked Adrenoleukodystrophy (X-ALD):** A defect in the transport of VLCFAs into peroxisomes (ABCD1 mutation), leading to myelin breakdown and adrenal insufficiency. * **Key Enzyme:** **Catalase** is the marker enzyme for peroxisomes [1]. * **Plasmalogen Synthesis:** Peroxisomes are essential for the synthesis of plasmalogens, which are vital phospholipids in the myelin sheath of neurons. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 59.

Question 27: What genetic mutation leads to Duchenne Muscular Dystrophy?

A. Myasthenia gravis
B. Duchenne Muscular Dystrophy (Correct Answer)
C. Motor neuron disease
D. Poliomyelitis

Explanation: **Explanation:** **Duchenne Muscular Dystrophy (DMD)** is an X-linked recessive disorder caused by a mutation in the **DMD gene**, located on the short arm of the X chromosome (Xp21) [2]. This gene is the largest known human gene, making it highly susceptible to spontaneous mutations. The mutation typically involves **large deletions** (65% of cases) that result in a **frameshift**, leading to a complete absence of the protein **dystrophin** [1]. Dystrophin is crucial for anchoring the muscle cytoskeleton to the extracellular matrix; its absence leads to membrane instability, calcium influx, and progressive myofiber necrosis. **Analysis of Options:** * **Myasthenia Gravis:** This is an autoimmune neuromuscular junction disorder caused by antibodies against postsynaptic acetylcholine receptors (AChR), not a genetic mutation of muscle structural proteins. * **Motor Neuron Disease (MND):** These are neurodegenerative disorders (e.g., ALS) affecting upper and lower motor neurons. While some forms have genetic links (e.g., SOD1 mutations), they are not primary muscular dystrophies. * **Poliomyelitis:** This is an infectious disease caused by the Poliovirus, which destroys anterior horn cells in the spinal cord, leading to flaccid paralysis. **High-Yield Clinical Pearls for NEET-PG:** * **Gower’s Sign:** Patients use their hands to "climb up" their own thighs to stand due to proximal muscle weakness. * **Pseudohypertrophy:** The calves appear enlarged due to the replacement of muscle tissue with fat and connective tissue (fibrosis). * **Becker Muscular Dystrophy (BMD):** A milder form caused by **non-frameshift** mutations, resulting in truncated but functional dystrophin [1]. * **Diagnosis:** Elevated Serum Creatine Kinase (CK) levels are seen from birth; definitive diagnosis is via genetic testing or muscle biopsy (showing absent dystrophin) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151.

Question 28: Xeroderma pigmentosum is characterized by

A. Autosomal dominant inheritance
B. Inability to repair sunlight induced damage to DNA (Correct Answer)
C. Irregular accumulation of melanin in the basal cell layer
D. Acanthosis of epithelium with elongation of rete ridges

Explanation: **Explanation:** **Xeroderma Pigmentosum (XP)** is a rare genetic disorder characterized by an extreme sensitivity to ultraviolet (UV) radiation [1]. **1. Why the Correct Answer is Right:** The fundamental defect in XP is a mutation in the genes responsible for **Nucleotide Excision Repair (NER)** [1], [2]. Normally, UV light causes the formation of **pyrimidine dimers** (specifically thymine dimers) in DNA. In healthy individuals, the NER pathway identifies and excises these dimers [1]. In XP patients, this repair mechanism is non-functional, leading to the accumulation of mutations in keratinocytes, which rapidly progresses to skin malignancies (Basal Cell Carcinoma, Squamous Cell Carcinoma, and Melanoma) [1], [2]. **2. Analysis of Incorrect Options:** * **Option A:** XP follows an **Autosomal Recessive** inheritance pattern, not dominant [1]. Both parents must be carriers. * **Option C:** While pigmentary changes occur (freckling), the hallmark is not just melanin accumulation but rather cellular damage and atrophy. Irregular melanin in the basal layer is more characteristic of simple ephelides (freckles). * **Option D:** Acanthosis and rete ridge elongation are features of chronic inflammatory conditions or psoriasis; XP typically presents with epidermal atrophy and solar elastosis. **3. NEET-PG High-Yield Pearls:** * **Key Enzyme Defect:** UV-specific endonuclease (involved in the initial nicking of the DNA strand). * **Clinical Presentation:** Severe sunburn after minimal sun exposure, early-onset freckling (before age 2), and a **2000-fold increase** in the risk of skin cancer. * **Associated Conditions:** Some variants (e.g., De Sanctis-Cacchione syndrome) include neurological abnormalities like microcephaly and intellectual disability. * **Diagnosis:** Chromosomal breakage study or unscheduled DNA synthesis (UDS) assay. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 332-333.

Question 29: What is the immunohistochemical marker used to label basal cells in suspected prostate carcinoma?

A. Alpha Fetoprotein
B. Alpha-Methylacyl-coenzyme Racemase (Correct Answer)
C. Annexin
D. AgNOR

Explanation: **Explanation:** In the diagnosis of prostate carcinoma, the most critical histological feature is the **absence of a basal cell layer**. While benign prostatic glands possess a dual cell layer (inner secretory and outer basal), malignant glands consist of a single layer of neoplastic cells [1]. **Why the Correct Answer is Right:** * **Alpha-Methylacyl-coenzyme Racemase (AMACR/P504S):** This is a mitochondrial and peroxisomal enzyme involved in the beta-oxidation of branched-chain fatty acids. It is **overexpressed in prostatic adenocarcinoma** [1] but is typically absent or weakly expressed in benign glands. * *Note on the Question Context:* While the question asks for a marker used to "label" cells in suspected carcinoma, it is important to clarify that **AMACR labels the malignant cells**, whereas markers like **p63** or **High Molecular Weight Cytokeratin (HMWK/34̢E12)** are used to label the **basal cells**. In clinical practice, a "cocktail" (PIN4) containing AMACR and basal cell markers is used; a positive AMACR and negative p63/HMWK confirms malignancy. **Why the Incorrect Options are Wrong:** * **Alpha-Fetoprotein (AFP):** A marker for Yolk Sac Tumors and Hepatocellular Carcinoma. * **Annexin:** A group of proteins involved in apoptosis and cell signaling; not a specific diagnostic marker for prostate cancer. * **AgNOR (Argyrophilic Nucleolar Organizer Regions):** A silver staining technique used to assess cellular proliferation and malignancy grade, but it is non-specific and not a primary IHC marker for prostate basal cells. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard IHC for Prostate Cancer:** **AMACR (+)** and **p63/HMWK (-)** [1]. * **Most common site:** Peripheral zone (posterior lobe) [1]. * **Gleason Scoring:** Based on glandular **architecture**, not nuclear features [1]. * **PSA (Prostate Specific Antigen):** Organ-specific but not cancer-specific (elevated in BPH and prostatitis) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 990-994.

Question 30: A 1-year-old girl with an inborn error of metabolism resulting in a lysosomal storage disease receives a hematopoietic stem cell transplant intended to replace her macrophage population. The gene of interest has a 'marker' small nucleotide polymorphism within a non-coding intron of the affected gene in which an A (patient gene) is substituted for a G (donor gene). She does quite well for the first 3 weeks. She tests positive for the missing enzyme, her previously abnormally enlarged organs begin to diminish in size, and assay of peripheral blood lymphocytes reveals increasing numbers of cells with the G polymorphism. However, the attending physicians are now concerned because repeated genetic testing reveals a progressive increase in lymphocytes with the A nucleotide polymorphism. Which of the following is the best explanation for this finding?

A. Generalized immune complex formation
B. Graft-versus-host disease
C. Immune paralysis
D. Rejection of the stem cell transplant (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** The core of this question lies in understanding **chimerism** and **genetic markers** following a hematopoietic stem cell transplant (HSCT). * **The Setup:** The patient (Recipient) has an **'A'** nucleotide, while the donor has a **'G'** nucleotide at a specific locus. * **Initial Success:** After the transplant, the appearance of the 'G' polymorphism and the enzyme indicates successful engraftment—donor cells are producing the missing enzyme. [1] * **The Shift:** The subsequent progressive increase in the **'A'** nucleotide polymorphism signifies that the recipient's own cells (autologous recovery) are replacing the donor cells. In the context of HSCT, if donor-derived cells (G) are disappearing and being replaced by recipient cells (A), it indicates that the host's immune system is destroying the graft. [2] This is the definition of **Graft Rejection**. [3] **2. Why the Other Options are Wrong:** * **Graft-versus-host disease (GVHD):** In GVHD, the *donor* T-cells attack the *recipient's* tissues [4]. This would typically result in a dominance of donor cells (G), not an increase in recipient cells (A). * **Generalized immune complex formation:** This refers to Type III hypersensitivity (e.g., Serum Sickness). While it can occur post-transplant, it does not explain the shift in genetic polymorphisms from donor to recipient type. * **Immune paralysis:** This is a state of temporary anergy or non-responsiveness. It would likely lead to persistent engraftment or opportunistic infections, but not the active replacement of donor cells by host cells. **3. Clinical Pearls for NEET-PG:** * **Chimerism Analysis:** Monitoring donor vs. recipient DNA (using SNPs or Short Tandem Repeats/STRs) is the gold standard for assessing engraftment post-HSCT. * **Lysosomal Storage Diseases (LSDs):** HSCT is a therapeutic strategy for certain LSDs (like Hurler Syndrome) because donor-derived macrophages (microglia in the brain, Kupffer cells in the liver) provide a continuous source of the deficient enzyme to neighboring host cells—a process called **cross-correction**. * **Rejection vs. GVHD:** Remember, **Rejection** is Host-vs-Graft (Host T-cells vs. Donor HLA), whereas **GVHD** is Graft-vs-Host (Donor T-cells vs. Host HLA). [4] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 244-245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-240. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 180-181. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 182-183.

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