Neoplasia — MCQs

A 15-year-old boy presents with pain and swelling in his right thigh. A biopsy of the mass demonstrates osteosarcoma. His mother was diagnosed with breast cancer one year ago, and his maternal grandmother died of breast cancer ten years ago. The child has three younger siblings. Siblings are at an increased risk of developing which of the following cancers?

Q220Easy

Which of the following functions is associated with the oncogenic MYC in lung cancer?

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 211: Which of the following is true about p53?

A. Tumor suppressor gene
B. Proto-oncogene
C. Pro-apoptotic
D. Encodes 53 kDa protein (Correct Answer)

Explanation: **Explanation:** The **TP53 gene**, located on chromosome **17p13.1**, is the most frequently mutated gene in human cancer [1]. It is often referred to as the "Guardian of the Genome." **Why Option D is Correct:** The name "p53" is derived directly from its molecular weight. The gene encodes a nuclear phosphoprotein that weighs **53 kilodaltons (kDa)**. This is a fundamental biochemical fact frequently tested in basic pathology. **Analysis of Incorrect Options:** * **Option A (Tumor Suppressor Gene):** While p53 functions as a tumor suppressor [2], the question asks what is "true" about the protein itself in a specific context. In many competitive exams, if a protein is named after its weight, that biochemical definition is considered the most definitive "identity" of the molecule. However, in most clinical contexts, p53 is indeed the prototypical tumor suppressor [3]. * **Option B (Proto-oncogene):** This is incorrect. Proto-oncogenes (like RAS or MYC) promote cell growth. p53 acts as a "brake" on the cell cycle; its loss of function leads to neoplasia [3]. * **Option C (Pro-apoptotic):** While p53 induces apoptosis (via BAX and PUMA) if DNA damage is irreparable [1], it also mediates **quiescence** (temporary cell cycle arrest) and **senescence** (permanent arrest) [1]. Calling it purely "pro-apoptotic" is a functional description, but not its defining structural characteristic. **NEET-PG High-Yield Pearls:** * **Mechanism:** p53 triggers **p21** (a CDK inhibitor), which arrests the cell cycle in the **G1 phase** to allow for DNA repair [1]. * **Li-Fraumeni Syndrome:** A germline mutation in TP53 leading to a high risk of multiple tumors (Sarcoma, Breast, Leukemia, Adrenal - SBLA syndrome). * **Degradation:** Under normal conditions, p53 has a short half-life because it is degraded by **MDM2**. * **Aflatoxin B1:** Specifically associated with a mutation in codon 249 of p53, leading to Hepatocellular Carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-304. [2] 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. 226-228. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-298.

Question 212: Which of the following is seen in African children with Burkitt's lymphoma?

A. Absence of EBV
B. T cell neoplasia
C. Deletion of C-myc gene
D. Chromosome 8q24 to chromosome 14q32 translocation (Correct Answer)

Explanation: **Explanation:** **Burkitt’s Lymphoma (BL)** is a highly aggressive B-cell non-Hodgkin lymphoma. The hallmark of this condition is the **t(8;14)(q24;q32)** translocation, which is present in approximately 85% of cases [4]. 1. **Why Option D is Correct:** The translocation involves the **c-MYC proto-oncogene** on chromosome 8 and the **IgH (Immunoglobulin heavy chain) gene** on chromosome 14 [4]. This moves c-MYC to a transcriptionally active site, leading to its constitutive overexpression. c-MYC is a potent transcription factor that drives rapid cell proliferation and metabolism, resulting in the characteristic "starry sky" appearance on histology [3]. 2. **Why Other Options are Incorrect:** * **Option A:** In the **Endemic (African) variant**, Epstein-Barr Virus (EBV) is found in nearly **100% of cases** [1]. It plays a critical role in the pathogenesis by immortalizing B-cells. * **Option B:** BL is a **B-cell neoplasm** (specifically of germinal center origin), expressing markers like CD19, CD20, and CD10 [2]. It is not a T-cell malignancy. * **Option C:** There is **overexpression/amplification** of the c-MYC gene, not a deletion [4]. Deletion would typically result in a loss of function, whereas BL requires a gain of oncogenic function. **High-Yield Facts for NEET-PG:** * **Variants:** Endemic (African; involves jaw), Sporadic (Abdominal/Ileocecal), and Immunodeficiency-associated (HIV) [2]. * **Morphology:** "Starry sky" pattern (Tingible body macrophages amidst a sea of malignant B-cells) [3]. * **Genetics:** Other translocations include t(2;8) and t(8;22), involving kappa and lambda light chains respectively [4]. * **Ki-67 Index:** Typically **>99%**, reflecting the highest proliferation rate among human tumors. **References:** [1] 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. 219-220. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 605-606. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 606. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.

Question 213: Which of the following is considered as a high-risk susceptibility gene for malignant melanoma?

A. CDKN1A
B. CDKN2A (Correct Answer)
C. CDKN3A
D. CDKN4A

Explanation: **Explanation:** **CDKN2A** (located on chromosome 9p21) is the most important high-risk susceptibility gene for hereditary malignant melanoma [1]. It is a complex locus that encodes two distinct tumor suppressor proteins via alternative splicing: **p16/INK4a** and **p14/ARF** [3]. * **p16/INK4a** inhibits Cyclin-Dependent Kinases (CDK4 and CDK6), maintaining the Retinoblastoma (Rb) protein in its active state to block cell cycle progression from G1 to S phase [1]. * **p14/ARF** stabilizes p53 by inhibiting MDM2 [3]. Germline mutations in CDKN2A are found in approximately 20-40% of families with a high incidence of melanoma (Melanoma-Pancreatic Cancer Syndrome) [2]. **Analysis of Incorrect Options:** * **CDKN1A (p21):** This gene encodes p21, a potent CDK inhibitor regulated by p53. While crucial for cell cycle arrest, germline mutations are not a primary driver for familial melanoma. * **CDKN3A:** This gene encodes a dual-specificity phosphatase that interacts with CDK2. It is not associated with melanoma susceptibility. * **CDKN4A:** This is a distractor; there is no clinically significant gene by this nomenclature in the context of melanoma pathogenesis. **High-Yield Pearls for NEET-PG:** 1. **Most common mutation in Sporadic Melanoma:** **BRAF** (specifically V600E mutation), seen in ~50-60% of cases [1]. 2. **Familial Melanoma:** Associated with **CDKN2A** (p16) and **CDK4** mutations [4]. 3. **Pathway:** Melanoma often involves the **RAS/MAPK** signaling pathway and the **PI3K/AKT** pathway [1]. 4. **Clinical Association:** Patients with CDKN2A mutations are also at a significantly increased risk for **Pancreatic Carcinoma** [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1150-1151. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-298. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 305-306. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1152-1153.

Question 214: Women carrying the BRCA1 gene have a higher likelihood of developing which type of breast carcinoma?

A. Medullary (Correct Answer)
B. Lobular
C. Colloid
D. Secretory

Explanation: **Explanation:** **1. Why Medullary Carcinoma is the Correct Answer:** The **BRCA1 mutation** is strongly associated with a specific phenotype of breast cancer [1]. Approximately 10-15% of BRCA1-associated breast cancers are **Medullary Carcinomas** [1]. These tumors are characterized by a "triple-negative" profile (ER, PR, and HER2/neu negative) and distinct histopathological features: solid sheets of large pleomorphic cells, high mitotic rate, and a prominent **lymphoplasmacytic infiltrate** [2]. Despite their aggressive histological appearance, they often have a better prognosis than poorly differentiated infiltrating ductal carcinomas [2]. **2. Analysis of Incorrect Options:** * **B. Lobular Carcinoma:** This is primarily associated with the loss of **E-cadherin** (CDH1 gene mutation) [1]. It is not specifically linked to BRCA1. * **C. Colloid (Mucinous) Carcinoma:** This subtype typically occurs in older women and is characterized by abundant extracellular mucin. It is usually ER/PR positive and not associated with BRCA1. * **D. Secretory Carcinoma:** A rare subtype often seen in children (juvenile breast cancer), characterized by the ETV6-NTRK3 gene fusion, not BRCA1. **3. High-Yield Clinical Pearls for NEET-PG:** * **BRCA1 vs. BRCA2:** BRCA1 is associated with Medullary Carcinoma and Serous Ovarian Carcinoma [1]. BRCA2 is more commonly associated with **Male Breast Cancer** and Pancreatic Cancer. * **Histology Keyword:** Look for "pushing margins" and "lymphocytic host response" in descriptions of Medullary Carcinoma [2]. * **Molecular Subtype:** Most BRCA1-related cancers fall under the **Basal-like** molecular subtype. * **Prophylaxis:** Bilateral salpingo-oophorectomy reduces the risk of both ovarian and breast cancer in BRCA carriers [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1069. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 455-456.

Question 215: Which of the following conditions is characterized by a Zellballen pattern?

A. Carotid body tumor (Correct Answer)
B. Lymphoepithelial cyst
C. Cholesteatoma
D. Thyroglossal cyst

Explanation: **Explanation:** The **Zellballen pattern** is the hallmark histological feature of **Paragangliomas**, of which the **Carotid body tumor** is the most common head and neck variant [1]. 1. **Why Carotid Body Tumor is Correct:** Paragangliomas are neuroendocrine tumors derived from extra-adrenal chromaffin cells. Microscopically, they consist of nests or clusters of polygonal chief cells (containing neurosecretory granules) surrounded by a vascular stroma and peripheral sustentacular cells. These characteristic nests are termed "Zellballen" (German for "cell balls"). 2. **Why the Other Options are Incorrect:** * **Lymphoepithelial cyst:** Typically found in the lateral neck (Branchial cleft cyst) or parotid, these are characterized by a lining of stratified squamous or columnar epithelium surrounded by dense lymphoid tissue with germinal centers. * **Cholesteatoma:** This is a non-neoplastic keratinizing squamous epithelial collection in the middle ear. Histology shows laminated layers of keratin debris and cholesterol clefts, not cellular nests [2]. * **Thyroglossal cyst:** A midline neck swelling lined by respiratory or squamous epithelium, often containing thyroid follicles within the cyst wall. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Carotid body tumors occur at the bifurcation of the Common Carotid Artery (CCA), leading to the **Lyre Sign** on angiography (splaying of ICA and ECA) [1]. * **Fontaine’s Sign:** The mass is mobile horizontally but fixed vertically due to its attachment to the carotid bifurcation. * **Staining:** Chief cells are positive for **Synaptophysin/Chromogranin**, while sustentacular cells are highlighted by **S-100**. * **Rule of 10s:** Traditionally associated with Pheochromocytoma, but remember that familial paragangliomas are often linked to **SDH (Succinate Dehydrogenase) gene mutations** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 748-749. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 747-748.

Question 216: Which of the following is not a cyclin-dependent kinase (CDK) inhibitor?

A. p21
B. p27
C. p53 (Correct Answer)
D. p57

Explanation: **Explanation:** The cell cycle is strictly regulated by **Cyclin-Dependent Kinases (CDKs)** and their inhibitors (**CDKIs**). CDK inhibitors are categorized into two families based on their structure and targets: the **CIP/KIP family** and the **INK4 family** [3]. **Why p53 is the Correct Answer:** **p53** is a tumor suppressor protein (often called the "Guardian of the Genome"), but it is **not** a direct CDK inhibitor [4]. Instead, p53 acts as a transcription factor. When DNA damage occurs, p53 levels rise and trigger the transcription of **p21** [1]. It is the p21 protein that then binds to and inhibits CDKs to halt the cell cycle [1]. Therefore, p53 is an upstream regulator, not a CDKI itself. **Analysis of Incorrect Options:** * **p21 (Option A):** A member of the **CIP/KIP family**. It is induced by p53 and inhibits a wide range of CDKs (CDK1, 2, 4, and 6), leading to cell cycle arrest in the G1 phase [1]. * **p27 (Option B):** A member of the **CIP/KIP family**. It responds to growth inhibitory signals like TGF-β and helps maintain the cell in the quiescent (G0) state. * **p57 (Option D):** A member of the **CIP/KIP family**. It is particularly important during embryogenesis. Mutations in the p57 gene (*CDKN1C*) are associated with **Beckwith-Wiedemann syndrome**. **High-Yield Clinical Pearls for NEET-PG:** 1. **INK4 Family:** Includes **p15, p16, p18, and p19** [3]. These specifically inhibit CDK4 and CDK6 (selective for the G1 phase) [2]. 2. **p16 Link:** Loss of p16 is commonly seen in many cancers, including pancreatic carcinoma and melanoma [2]. 3. **RB Protein:** The ultimate target of CDK activity. CDKs phosphorylate RB to release E2F, allowing the cell to progress from G1 to S phase. CDKIs prevent this phosphorylation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 305-306. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 37-38. [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. 227-228.

Question 217: What is the origin of the Pindborg tumour?

A. Reduced enamel epithelium
B. Stratum intermedium (Correct Answer)
C. Dental lamina
D. All of the above

Explanation: **Explanation:** The **Pindborg tumor**, medically known as **Calcifying Epithelial Odontogenic Tumor (CEOT)**, is a rare, benign but locally aggressive odontogenic neoplasm. **Why Option B is correct:** The tumor cells in CEOT histologically resemble the cells of the **stratum intermedium** of the enamel organ. This is supported by the presence of high alkaline phosphatase activity and the characteristic polyhedral epithelial cells with prominent intercellular bridges (desmosomes) seen on histopathology. **Analysis of Incorrect Options:** * **Option A (Reduced Enamel Epithelium):** This is the origin of the **Dentigerous cyst** and is also associated with the Adenomatoid Odontogenic Tumor (AOT), but not CEOT. * **Option C (Dental Lamina):** Remnants of the dental lamina (Rests of Serres) are typically the origin of the **Odontogenic Keratocyst (OKC)** and Ameloblastoma [1]. * **Option D:** Since the origin is specifically linked to the stratum intermedium, "All of the above" is incorrect. **NEET-PG High-Yield Pearls for Pindborg Tumor:** 1. **Radiology:** Classically presents as a unilocular or multilocular radiolucency with a **"Driven Snow" appearance** (radiopaque foci due to calcification). 2. **Histopathology:** Characterized by **Liesegang rings** (concentric calcifications) and **Liesegang-like amyloid-containing areas** that stain with Congo Red and show **apple-green birefringence** under polarized light. 3. **Location:** Most commonly occurs in the **posterior mandible** (molar-ramus area) and is often associated with an impacted tooth. 4. **Nature:** It is a slow-growing, painless swelling but has a recurrence rate of about 14%. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 741-742.

Question 218: Arrange the following in increasing order for risk of malignancy: Fibroadenoma, Sclerosing adenosis, Atypical ductal hyperplasia, Lobular carcinoma in situ.

A. Sclerosing adenosis, Fibroadenoma, Atypical ductal hyperplasia, Lobular carcinoma in situ
B. Fibroadenoma, Sclerosing adenosis, Atypical ductal hyperplasia, Lobular carcinoma in situ (Correct Answer)
C. Fibroadenoma, Sclerosing adenosis, Lobular carcinoma in situ, Atypical ductal hyperplasia
D. Sclerosing adenosis, Fibroadenoma, Lobular carcinoma in situ, Atypical ductal hyperplasia

Explanation: This question tests the understanding of the **Relative Risk (RR)** of developing invasive breast cancer associated with various benign and pre-malignant breast lesions. The risk is categorized based on histological findings [1]: 1. **Non-proliferative lesions (RR ~1.0x):** These carry no increased risk. Examples include **Fibroadenoma** (without complex features) [2], cysts, and mild hyperplasia. 2. **Proliferative lesions without atypia (RR 1.5–2.0x):** These show cellular proliferation but no architectural distortion or nuclear atypia [1]. Examples include **Sclerosing adenosis**, radial scars, and ductal hyperplasia of the usual type. 3. **Proliferative lesions with atypia (RR 4.0–5.0x):** These show some features of carcinoma in situ but are limited in extent [1]. **Atypical Ductal Hyperplasia (ADH)** and Atypical Lobular Hyperplasia (ALH) fall here. 4. **Carcinoma in situ (RR 8.0–10.0x):** **Lobular Carcinoma In Situ (LCIS)** and DCIS represent a significantly high risk for future invasive cancer. **Analysis of Options:** * **Option B is correct** because it follows the hierarchy: Fibroadenoma (No risk) < Sclerosing adenosis (Slight risk) < ADH (Moderate risk) < LCIS (High risk). * **Options A, C, and D** are incorrect because they misplace the risk hierarchy. Specifically, Sclerosing adenosis carries a higher risk than a simple Fibroadenoma, and LCIS carries a significantly higher risk than ADH. **High-Yield NEET-PG Pearls:** * **LCIS** is often an incidental finding and is considered a **risk factor** (marker) for bilateral breast cancer, rather than a direct precursor. * **Complex Fibroadenomas** (containing cysts >3mm, sclerosing adenosis, or calcifications) increase the RR to ~3.1x. * **Most common benign tumor of the breast:** Fibroadenoma [2]. * **Most common cause of bloody nipple discharge:** Intraductal papilloma (RR 1.5–2.0x). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1052-1056. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 448-449.

Question 219: A 15-year-old boy presents with pain and swelling in his right thigh. A biopsy of the mass demonstrates osteosarcoma. His mother was diagnosed with breast cancer one year ago, and his maternal grandmother died of breast cancer ten years ago. The child has three younger siblings. Siblings are at an increased risk of developing which of the following cancers?

A. Wilms tumor
B. Neuroblastoma
C. Hepatoblastoma
D. Glioma (Correct Answer)

Explanation: ### Explanation **Concept: Li-Fraumeni Syndrome (LFS)** The clinical presentation describes a classic case of **Li-Fraumeni Syndrome**. This is an autosomal dominant condition caused by a germline mutation in the **TP53 tumor suppressor gene** (located on chromosome 17p) [1]. The syndrome is characterized by a strong family history of early-onset cancers. **Why Glioma is Correct:** The "core" cancers associated with LFS are remembered by the mnemonic **SBLA**: **S**arcoma (Osteosarcoma/Soft tissue), **B**reast cancer, **L**eukemia, and **A**drenal cortical carcinoma. However, the spectrum also significantly includes **Brain tumors (specifically Gliomas)**. Since the siblings share the same genetic risk, they are at a high risk for these specific malignancies. **Why Other Options are Incorrect:** * **Wilms tumor (A):** Associated with WAGR syndrome, Denys-Drash, or Beckwith-Wiedemann syndrome (WT1/WT2 mutations), not typically TP53. * **Neuroblastoma (B):** Most common extracranial solid tumor in children; associated with N-MYC amplification, but not a core component of LFS. * **Hepatoblastoma (C):** Associated with Familial Adenomatous Polyposis (FAP) and Beckwith-Wiedemann syndrome, but not LFS. **High-Yield Clinical Pearls for NEET-PG:** * **TP53:** Known as the "Guardian of the Genome." It regulates the cell cycle at the G1-S checkpoint. * **LFS Criteria:** Proband diagnosed with sarcoma <45 years + First-degree relative with any cancer <45 years + Another first/second-degree relative with any cancer <45 years or sarcoma at any age. * **Most Common Cancer in LFS:** Breast cancer (females) and Sarcomas (males/children). * **Choroid Plexus Carcinoma:** In a child, this specific brain tumor is highly suggestive of a TP53 mutation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300.

Question 220: Which of the following functions is associated with the oncogenic MYC in lung cancer?

A. Protein kinase
B. GTP binding protein
C. Nuclear binding protein (Correct Answer)
D. Growth factor

Explanation: **Explanation:** **Why the correct answer is right:** The **MYC** gene (specifically *c-MYC*, *n-MYC*, and *l-MYC*) encodes a **nuclear transcription factor** [1] that plays a central role in cell cycle progression, metabolism, and apoptosis. Once synthesized, the MYC protein translocates to the nucleus, where it binds to specific DNA sequences (E-box sequences) via a basic helix-loop-helix leucine zipper domain. In lung cancer (particularly Small Cell Lung Cancer), *L-MYC* amplification leads to the constitutive expression of these nuclear proteins, driving uncontrolled cellular proliferation [1], [2]. **Why the other options are wrong:** * **A. Protein Kinase:** This function is characteristic of oncogenes like **ABL** (non-receptor tyrosine kinase) or **ERBB1/EGFR** (receptor tyrosine kinase) [1]. * **B. GTP Binding Protein:** This describes the **RAS** family of oncogenes (K-RAS, H-RAS, N-RAS). RAS proteins act as molecular switches by cycling between GDP-bound (inactive) and GTP-bound (active) states [2]. * **C. Growth Factor:** This refers to oncogenes like **PDGF-̢** (SIS oncogene), which act as extracellular signals to trigger cell growth. **High-Yield Clinical Pearls for NEET-PG:** * **MYC Family Associations:** * **c-MYC:** Burkitt Lymphoma (t[8;14]). * **N-MYC:** Neuroblastoma (Double minute chromosomes). * **L-MYC:** Small Cell Carcinoma of the Lung [2]. * **Mechanism:** MYC upregulates **Cyclin-Dependent Kinases (CDKs)** and downregulates CDK inhibitors, effectively "pushing" the cell through the G1/S checkpoint [2]. * **Warburg Effect:** MYC is a key mediator in reprogramming cell metabolism to aerobic glycolysis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 292-293. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 296-297.

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