Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 21: All of the following statements are true about tumour markers except?

A. screening of a cancer
B. follow up of a cancer patient
C. confirmation of cancer (Correct Answer)
D. for knowing about recurrence

Explanation: **Explanation:** Tumor markers are biochemical substances (hormones, enzymes, or proteins) produced by tumor cells or by the body in response to tumor growth. While they are invaluable in clinical oncology, they have specific limitations. **Why Option C is the Correct Answer (The Exception):** Tumor markers are **not** used for the definitive **confirmation of cancer**. The "Gold Standard" for cancer diagnosis is always **histopathology** (biopsy) or cytopathology. Tumor markers lack the 100% specificity required for diagnosis because they can be elevated in non-neoplastic inflammatory conditions (e.g., PSA in prostatitis or CA-125 in endometriosis) [2]. **Analysis of Other Options:** * **A. Screening:** While most markers are not specific enough for general screening, a few are used in high-risk populations (e.g., **AFP** for Hepatocellular Carcinoma in cirrhosis patients or **PSA** for prostate cancer in elderly men) [2]. * **B. Follow-up:** This is the primary use of tumor markers. A decline in marker levels post-treatment indicates a therapeutic response [1]. * **D. Recurrence:** Tumor markers are highly sensitive for detecting the return of a tumor before it becomes radiologically visible (e.g., rising **CEA** levels in colorectal cancer) [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Most Specific Tumor Marker:** Calcitonin (for Medullary Carcinoma of Thyroid). * **CA-125:** Associated with Ovarian cancer (Surface epithelial tumors). * **CA 19-9:** Associated with Pancreatic and Cholangiocarcinoma. * **AFP (Alpha-fetoprotein):** Elevated in HCC and Yolk Sac Tumors (Endodermal sinus tumors) [2]. * **hCG:** Elevated in Choriocarcinoma and Hydatidiform mole. * **S-100:** Marker for Melanoma, Schwannoma, and Langerhans Cell Histiocytosis. **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. 254-255. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 346.

Question 22: Which of the following statements about carcinogenesis is false?

A. Asbestos exposure increases the incidence of lung cancer
B. Exposure to aniline dyes predisposes to cancer of the urinary bladder
C. Papilloma viruses produce tumors in animals but not in humans (Correct Answer)
D. Hepatitis B virus has been implicated in hepatocellular carcinoma

Explanation: ### Explanation **1. Why Option C is the Correct (False) Statement:** Human Papillomavirus (HPV) is a well-established human carcinogen. While it does cause tumors in animals (e.g., Shope papilloma virus in rabbits), it is most clinically significant for its role in human oncology. High-risk strains, specifically **HPV 16 and 18**, are responsible for approximately 70% of **cervical carcinomas** globally [1], [3]. They also cause oropharyngeal, anal, vulvar, and penile cancers [2]. The oncogenic potential lies in the viral proteins **E6** (which degrades p53) and **E7** (which binds and inactivates Rb) [1]. **2. Analysis of Incorrect Options:** * **Option A:** Asbestos is a potent carcinogen. While it is the primary cause of **mesothelioma**, it is statistically more likely to cause **bronchogenic carcinoma** (lung cancer), especially in smokers due to a synergistic effect. * **Option B:** Aniline dyes (specifically containing **2-naphthylamine**) are classic occupational hazards. They are metabolized in the liver and excreted in the urine, leading to **transitional cell carcinoma (TCC)** of the urinary bladder. * **Option D:** Chronic infection with **Hepatitis B Virus (HBV)** and Hepatitis C Virus (HCV) accounts for 75-85% of **hepatocellular carcinomas** worldwide [3]. The mechanism involves chronic inflammation, hepatocyte regeneration, and the HBx protein which interferes with p53 [4]. **3. NEET-PG High-Yield Pearls:** * **HPV Low-risk (6, 11):** Cause Genital Warts (Condyloma acuminatum) [3]. * **HPV High-risk (16, 18):** Cause Squamous cell carcinoma [3]. * **Aflatoxin B1:** Produced by *Aspergillus flavus*; associated with HCC (p53 mutation at codon 249) [5]. * **Schistosoma haematobium:** Associated with Squamous cell carcinoma of the bladder (not TCC). * **Vinyl Chloride:** Associated with Angiosarcoma of the liver [5]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 334-335. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1006-1007. [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. 219-220. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 336-337. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 331-332.

Question 23: Predominant osteoblastic secondaries are seen in which of the following malignancies?

A. Prostate carcinoma (Correct Answer)
B. Breast carcinoma
C. Bone carcinoma
D. Stomach carcinoma

Explanation: **Explanation:** The nature of bone metastases depends on the interaction between tumor cells and the bone microenvironment. Metastatic lesions are classified as **osteoblastic** (bone-forming), **osteolytic** (bone-destroying), or mixed [2]. **1. Why Prostate Carcinoma is Correct:** Prostate carcinoma is the classic example of a malignancy causing **predominantly osteoblastic** (sclerotic) metastases [1]. Tumor cells secrete factors like **Wnt proteins** and **Bone Morphogenetic Proteins (BMPs)** that stimulate osteoblast differentiation and activity, leading to the deposition of dense, irregular new bone. On X-ray, these appear as radio-opaque (white) spots [1]. **2. Analysis of Incorrect Options:** * **Breast Carcinoma:** While breast cancer is the most common cause of bone secondaries in females, it typically produces **mixed** lesions (both osteolytic and osteoblastic) [2]. * **Bone Carcinoma (Osteosarcoma):** This is a primary bone tumor, not a secondary (metastatic) lesion [3]. While it produces osteoid, the question specifically asks for "secondaries" (metastases). * **Stomach Carcinoma:** Gastrointestinal malignancies generally produce **osteolytic** lesions. While some signet-ring cell carcinomas can rarely cause blastic responses, they are not the "predominant" cause compared to prostate cancer. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Osteoblastic Metastases:** "**P**rostate **C**an **B**e **S**clerotic" (**P**rostate, **C**arcinoid, **B**reast (sometimes), **S**mall cell lung cancer). * **Osteolytic Metastases:** Most common overall. Key examples include **Lung (NSCLC), Renal Cell Carcinoma (RCC), Thyroid, and Multiple Myeloma** (punched-out lesions) [2]. * **Imaging:** Osteoblastic lesions are best seen on X-ray/CT; Osteolytic lesions carry a higher risk of pathological fractures and hypercalcemia [1]. * **Biochemical Marker:** Elevated **Alkaline Phosphatase (ALP)** is often seen in osteoblastic metastases due to increased bone turnover [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 501-502. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 673-674.

Question 24: Breast carcinoma is associated with all except?

A. BRCA1
B. BRCA2
C. TP53
D. ATR (Correct Answer)

Explanation: **Explanation:** Breast carcinoma is a genetically heterogeneous disease [1]. The question asks for the gene **not** typically associated with a significantly increased risk of breast cancer. **1. Why ATR is the Correct Answer:** **ATR (Ataxia Telangiectasia and Rad3-related)** is a protein kinase involved in DNA damage signaling, specifically responding to replication stress and single-strand breaks. While it belongs to the same family as ATM, mutations in ATR are primarily associated with **Seckel Syndrome** (microcephaly and growth retardation), not breast carcinoma. In contrast, mutations in **ATM** (Ataxia-Telangiectasia Mutated) are well-documented risk factors for breast cancer. **2. Analysis of Incorrect Options:** * **BRCA1 & BRCA2:** These are the most common high-penetrance susceptibility genes [1]. They are involved in homologous recombination repair of double-strand DNA breaks. BRCA1 is strongly linked to Triple Negative Breast Cancer (TNBC) and ovarian cancer, while BRCA2 is associated with male breast cancer and prostate cancer. * **TP53:** Mutations in the TP53 gene cause **Li-Fraumeni Syndrome** [1]. This syndrome carries a very high lifetime risk of early-onset breast cancer, along with sarcomas, leukemia, and adrenocortical tumors. **3. Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** Think "SBLA" syndrome (Sarcoma, Breast, Leukemia, Adrenal). * **Cowden Syndrome:** Associated with **PTEN** mutations; presents with breast cancer, thyroid cancer (follicular), and endometrial cancer. * **Peutz-Jeghers Syndrome:** Associated with **STK11** mutations; carries an increased risk of breast and gastrointestinal cancers. * **CHEK2:** A moderate-penetrance gene also associated with increased breast cancer risk. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1060.

Question 25: Which of the following is known as the guardian of the genes?

A. Rb
B. p53 (Correct Answer)
C. p16
D. p73

Explanation: The correct answer is **p53 (Option B)**. Known as the **"Guardian of the Genome,"** the p53 protein (encoded by the *TP53* gene on chromosome 17p) is the most frequently mutated gene in human cancers [1]. It acts as a molecular sentry that monitors cellular stress, particularly DNA damage [2]. When DNA damage is detected, p53 triggers three key mechanisms: 1. **Quiescence:** Temporary cell cycle arrest (at the G1-S checkpoint via p21 induction) to allow time for DNA repair [2]. 2. **Senescence:** Permanent cell cycle arrest [3]. 3. **Apoptosis:** Programmed cell death (via BAX induction) if the damage is irreparable [3, 4]. **Analysis of Incorrect Options:** * **Rb (Retinoblastoma protein):** Known as the **"Governor of the Cell Cycle."** It controls the G1-S transition by binding to the E2F transcription factor [2]. While crucial, it regulates the "gate" rather than monitoring genomic integrity. * **p16 (INK4a):** A cyclin-dependent kinase inhibitor (CDKI) that reinforces the Rb checkpoint [5]. It is a tumor suppressor but not the primary "guardian." * **p73:** A structural homolog of p53. While it can induce apoptosis, it is not as universally critical or frequently mutated in cancers as p53. **High-Yield Clinical Pearls for NEET-PG:** * **Li-Fraumeni Syndrome:** A germline mutation in *TP53* leading to a high risk of multiple diverse tumors (SBLA: Sarcoma, Breast, Leukemia, Adrenal). * **MDM2:** The negative regulator of p53; it targets p53 for degradation via the ubiquitin-proteasome pathway. * **HPV E6 vs. E7:** In cervical cancer, HPV protein **E6** degrades p53, while **E7** inhibits Rb. **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. 226-227. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 302-303. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 303-304. [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. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-298.

Question 26: A 50-year-old female presented with a lump in the right breast and was diagnosed with Luminal A carcinoma. Which of the following statements about this cancer is FALSE?

A. Most common subtype
B. Best prognosis
C. Estrogen receptor/Progesterone receptor negative (Correct Answer)
D. Poor response to paclitaxel

Explanation: ### Explanation **Molecular Classification of Breast Cancer: Luminal A Subtype** The correct answer is **C (Estrogen receptor/Progesterone receptor negative)** because Luminal A carcinoma is characterized by being **ER (Estrogen Receptor) positive** and **PR (Progesterone Receptor) positive** [1]. **Why Option C is False:** Luminal A is the most "differentiated" molecular subtype. It mimics the normal luminal epithelium of the breast ducts, which expresses hormone receptors [1]. By definition, Luminal A is **ER+ and/or PR+**, and **HER2/neu negative**. It also has a low **Ki-67 index** (low proliferative rate), distinguishing it from Luminal B. **Analysis of Other Options:** * **A. Most common subtype:** True. Luminal A accounts for approximately 40–55% of all invasive breast cancers, making it the most frequent molecular subtype encountered in clinical practice [1]. * **B. Best prognosis:** True. Due to its low grade, slow growth (low Ki-67), and high responsiveness to endocrine therapy (like Tamoxifen or Aromatase inhibitors), it has the highest survival rates among all subtypes [2]. * **D. Poor response to paclitaxel:** True. Luminal A tumors are "chemo-insensitive" compared to Triple-Negative or HER2-enriched cancers. Because they have a low mitotic rate, they respond poorly to traditional cytotoxic agents like taxanes (paclitaxel). **High-Yield Clinical Pearls for NEET-PG:** * **Luminal B:** ER+, but often HER2+ or has a **high Ki-67 (>14-20%)**. It is more aggressive than Luminal A. * **HER2-Enriched:** ER negative, PR negative, and HER2 positive. * **Basal-like (Triple Negative):** ER-, PR-, HER2-. Associated with **BRCA1 mutations** and has the worst prognosis [2]. * **Gold Standard for Subtyping:** While Gene Expression Profiling (PAM50) is the gold standard, in routine practice, **Immunohistochemistry (IHC)** is used as a surrogate [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1059-1060. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1064-1066.

Question 27: Gleason's scoring is performed for which of the following malignancies?

A. Prostate cancer (Correct Answer)
B. Lung cancer
C. Bladder cancer
D. Hodgkin's lymphoma

Explanation: **Explanation:** **Gleason’s scoring** is the gold standard grading system used to determine the prognosis of **Prostate Adenocarcinoma** [1]. Unlike many other grading systems that rely on cellular atypia, the Gleason system is based solely on the **architectural patterns** of the tumor glands under low-power magnification. 1. **Why Option A is Correct:** The Gleason score is calculated by identifying the most common (primary) and second most common (secondary) architectural patterns, each graded from 1 to 5 [1]. The sum (e.g., 3+4=7) provides the score. In modern practice, the **ISUP Grade Groups (1–5)** are used to further categorize these scores for clinical decision-making. 2. **Why Other Options are Incorrect:** * **Lung Cancer:** Graded based on histological type (Small cell vs. Non-small cell) and differentiation (Well, moderately, or poorly differentiated). * **Bladder Cancer:** Primarily graded using the **WHO/ISUP classification**, which categorizes tumors into Low-grade or High-grade papillary urothelial carcinomas. * **Hodgkin’s Lymphoma:** This is **staged** (Ann Arbor Staging) rather than graded, as the prognosis depends on the anatomical extent of the disease rather than the degree of cellular differentiation. **High-Yield Clinical Pearls for NEET-PG:** * **Gleason Grade 1:** Small, uniform glands (closest to normal). * **Gleason Grade 5:** No gland formation; solid sheets, cords, or single cells (most aggressive). * **Prostate Specific Antigen (PSA):** Used for screening and monitoring, but Gleason score is the best predictor of prognosis following radical prostatectomy [1]. * **Site:** Most prostate cancers arise in the **Peripheral Zone** [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. 989-994.

Question 28: Which enzymatic mutation is responsible for immortality of cancer cells?

A. DNA reverse transcriptase
B. RNA polymerase
C. Telomerase (Correct Answer)
D. DNA polymerase

Explanation: ### Explanation **Correct Answer: C. Telomerase** **Mechanism of Immortality:** In normal somatic cells, chromosomes have repetitive DNA sequences at their ends called **telomeres**. With each cell division, telomeres progressively shorten (the "end-replication problem"). Once they reach a critically short length, the cell enters senescence or apoptosis (the **Hayflick Limit**). Cancer cells achieve immortality by bypassing this limit through the upregulation of **Telomerase**, an enzyme that adds TTAGGG repeats to the ends of chromosomes. Telomerase is a specialized **RNA-dependent DNA polymerase** (a type of reverse transcriptase). By maintaining telomere length, cancer cells avoid senescence and gain the capacity for indefinite replication [1]. **Analysis of Incorrect Options:** * **A. DNA reverse transcriptase:** While telomerase is technically a reverse transcriptase, this is a broad category. In medical exams, "Reverse Transcriptase" usually refers to the enzyme used by retroviruses (like HIV) to convert viral RNA into DNA. * **B. RNA polymerase:** This enzyme is responsible for transcribing DNA into RNA. While essential for protein synthesis in all cells, its mutation or activity does not directly confer replicative immortality. * **C. DNA polymerase:** This enzyme is responsible for DNA replication during the S-phase. While mutations here can lead to "mutator phenotypes" (e.g., Lynch Syndrome), it is not the primary mechanism for overcoming the Hayflick limit. **High-Yield NEET-PG Pearls:** * **Telomerase Activity:** Present in >90% of human cancers, germ cells, and stem cells; it is absent or very low in most adult somatic cells [1]. * **Alternative Lengthening of Telomeres (ALT):** A minority of cancers (5-10%) maintain telomeres via DNA recombination rather than telomerase [1]. * **Breakage-Fusion-Bridge Cycle:** Shortened telomeres lead to chromosomal instability, which can drive early oncogenesis before telomerase is eventually reactivated to "fix" the genome and allow the cancer to persist. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 311-312.

Question 29: Blood-borne spread is a characteristic feature of which of the following?

A. Carcinoma
B. Sarcoma (Correct Answer)
C. Dysplasia
D. Metaplasia

Explanation: **Explanation:** The spread of malignant tumors occurs primarily through three routes: lymphatic, hematogenous (blood-borne), and seeding of body cavities. **1. Why Sarcoma is Correct:** Sarcomas (malignant tumors of mesenchymal origin) characteristically spread via the **hematogenous route** [1]. Because mesenchymal tissues are highly vascular, malignant cells easily invade thin-walled venules [1]. These cells then travel through the systemic circulation, most commonly lodging in the **lungs and liver**, which act as the first capillary beds encountered [1]. **2. Analysis of Incorrect Options:** * **Carcinoma:** These are malignant tumors of epithelial origin. Their characteristic mode of spread is via the **lymphatic system** (e.g., breast cancer spreading to axillary nodes). *Note: Some carcinomas like Renal Cell Carcinoma and Hepatocellular Carcinoma are exceptions and prefer blood-borne spread.* [1] * **Dysplasia:** This refers to disordered growth and maturation of an epithelium. It is a **pre-malignant** condition, not a malignancy itself; therefore, it does not have the capability to metastasize. * **Metaplasia:** This is a reversible change where one adult cell type is replaced by another (e.g., Barrett’s esophagus). It is an **adaptation**, not a neoplasm, and does not spread. **NEET-PG High-Yield Pearls:** * **Exceptions to the rule:** Four carcinomas characteristically spread via blood (Hematogenous) rather than lymphatics: **F**ollicular carcinoma of thyroid, **R**enal cell carcinoma (RCC), **H**epatocellular carcinoma (HCC), and **C**horiocarcinoma (Mnemonic: **F**our **R**eal **H**ot **C**hicks). * **First site of metastasis:** For most hematogenous spreads, the **Lungs** are the most common site due to the vena caval drainage [1]. * **Sentinel Lymph Node:** The first node in a regional lymphatic basin that receives lymph flow from a primary tumor (crucial for staging carcinomas). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 282.

Question 30: Cancer cachexia is due to which of the following cytokines?

A. TNF-α (Correct Answer)
B. IL-5
C. IL-8
D. Phospholipase A2

Explanation: **Explanation:** **Cancer Cachexia** is a paraneoplastic syndrome characterized by progressive loss of body fat and lean muscle mass, accompanied by profound weakness, anorexia, and anemia [1]. Unlike simple starvation, the weight loss in cachexia cannot be reversed by increased caloric intake because it is driven by a systemic inflammatory response rather than a mere calorie deficit [1]. **Why TNF-α is the correct answer:** **TNF-α (Tumor Necrosis Factor-alpha)**, originally named **Cachectin**, is the primary mediator of cancer cachexia. It is produced by macrophages in response to tumor cells or by the tumor cells themselves. It promotes cachexia through several mechanisms: * **Appetite Suppression:** It acts on the hypothalamus to cause anorexia. * **Lipolysis:** It inhibits lipoprotein lipase (LPL), preventing the storage of triglycerides in adipose tissue. * **Proteolysis:** It activates the ubiquitin-proteasome pathway, leading to the breakdown of skeletal muscle proteins. * *Note:* Other cytokines like IL-1 and IL-6 also contribute to this process. **Why the other options are incorrect:** * **IL-5:** Primarily involved in the recruitment, activation, and survival of **eosinophils**. It is associated with type 2 helper T-cell (Th2) responses and asthma. * **IL-8:** A potent **chemotactic factor for neutrophils**. It plays a key role in acute inflammation and angiogenesis but not in systemic metabolic wasting. * **Phospholipase A2:** An enzyme that releases arachidonic acid from membrane phospholipids, serving as the initial step in the synthesis of prostaglandins and leukotrienes. It is a mediator of inflammation but not a primary driver of cachexia. **High-Yield Clinical Pearls for NEET-PG:** * **PIF (Proteolysis Inducing Factor):** A tumor-derived soluble protein that specifically causes skeletal muscle breakdown in cachexia. * **LMF (Lipid Mobilizing Factor):** Increases fatty acid oxidation. * **Basal Metabolic Rate (BMR):** In cancer cachexia, the BMR is typically **increased**, despite reduced food intake (unlike starvation where BMR decreases). **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. 235-236.

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Neoplasia — MCQs

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