Neoplasia — MCQs

A 70-year-old male, a chronic tobacco chewer for 50 years, presents with a six-month history of a large, fungating, soft papillary lesion in the oral cavity that has penetrated the mandible. Lymph nodes are not palpable. Biopsies show benign-appearing papillomatosis with hyperkeratosis and acanthosis infiltrating the subjacent tissues. What is the most likely diagnosis?

Q478Easy

Syndrome of inappropriate Antidiuretic Hormone secretion (SIADH) is a characteristic paraneoplastic association of which of the following carcinomas?

Q479Easy

Which condition is associated with the S-100 marker?

Q480Easy

Smoking is a causative factor for all the following carcinomas, except:

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 471: AKT1 amplification is seen in which of the following cancers?

A. Cancer of the bladder
B. Cancer of the colon
C. Breast cancer
D. Gastric cancer (Correct Answer)

Explanation: **Explanation:** The **PI3K/AKT/mTOR pathway** is a critical signaling cascade involved in cell growth, proliferation, and survival. Dysregulation of this pathway is a hallmark of various malignancies. **AKT1** (also known as Protein Kinase B alpha) is a key downstream effector of PI3K. **Why Gastric Cancer is Correct:** While mutations in the PI3K pathway are common across many cancers, **AKT1 gene amplification** is a specific molecular signature frequently identified in **Gastric Cancer**. Studies have shown that AKT1 amplification leads to protein overexpression, which correlates with advanced tumor stage, lymph node metastasis, and poor prognosis in gastric adenocarcinoma patients. **Analysis of Incorrect Options:** * **A. Bladder Cancer:** While the PI3K pathway is often activated in bladder cancer, it is more commonly associated with **PIK3CA mutations** or **PTEN loss** rather than primary AKT1 amplification. * **B. Colon Cancer:** Colorectal cancers frequently exhibit **PIK3CA mutations** (found in ~15-20% of cases) and **PTEN deletions**, but AKT1 amplification is not a characteristic driver for this malignancy. * **C. Breast Cancer:** In breast cancer (particularly ER+), the most common alteration in this pathway is the **AKT1 E17K mutation** (a point mutation in the pleckstrin homology domain), not gene amplification. **High-Yield Clinical Pearls for NEET-PG:** * **AKT1 E17K Mutation:** Most commonly associated with **Breast, Endometrial, and Ovarian cancers**. * **PTEN:** A tumor suppressor gene that acts as a negative regulator of the PI3K/AKT pathway. Its loss is a major driver in **Endometrial and Prostate cancers**. * **mTOR Inhibitors:** Drugs like Everolimus and Temsirolimus target this pathway and are used in Renal Cell Carcinoma (RCC) and Breast Cancer.

Question 472: All of the following are features of borderline tumors except?

A. Occurs in younger age
B. Mitotic figures < 9/10 per high power field
C. Very good prognosis
D. Stromal invasion seen (Correct Answer)

Explanation: ### Explanation **Borderline Tumors** (also known as tumors of low malignant potential) are a distinct category of neoplasms, most commonly discussed in the context of ovarian epithelial tumors. They occupy an intermediate position on the spectrum between benign and malignant lesions [1]. #### Why "Stromal Invasion Seen" is the Correct Answer: The defining pathological hallmark that distinguishes a **borderline tumor** from a **carcinoma** is the **absence of destructive stromal invasion** [1]. While borderline tumors exhibit features of malignancy—such as cellular atypia, stratification, and increased mitotic activity—they do not breach the basement membrane to invade the underlying stroma [2]. If destructive stromal invasion is present, the tumor is reclassified as a carcinoma [1]. #### Analysis of Other Options: * **A. Occurs in younger age:** This is a characteristic feature. Borderline ovarian tumors typically present in women aged 30–50, which is significantly younger than the average age for invasive ovarian cancer (usually postmenopausal). * **B. Mitotic figures < 9/10 HPF:** Borderline tumors show increased mitotic activity compared to benign tumors, but it remains relatively low. High mitotic counts (typically >10 per 10 HPF) are more suggestive of frank malignancy. * **C. Very good prognosis:** Because they lack invasive potential, these tumors have an excellent 10-year survival rate (approx. 95%), even if they present with "peritoneal implants" (which are usually non-invasive) [2]. #### NEET-PG High-Yield Pearls: * **Microinvasion:** Some borderline tumors may show "microinvasion" (defined as <3 mm or <5% of the tumor), but this does not change the prognosis or the "borderline" classification. * **Psammoma Bodies:** These are frequently seen in serous borderline tumors. * **CA-125:** Often elevated, but less useful for diagnosis than in invasive cases. * **Key Distinction:** Benign = No atypia; Borderline = Atypia but **No Invasion**; Malignant = Atypia + **Invasion** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, p. 1030. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1030-1032.

Question 473: Multifocal tumour of vascular origin in a patient of AIDS is:

A. Kaposi's sarcoma (Correct Answer)
B. Astrocytoma
C. Gastric carcinoma
D. Primary CNS lymphoma

Explanation: **Explanation:** **Kaposi’s Sarcoma (KS)** is the correct answer because it is a classic AIDS-defining illness [1]. It is a **multifocal, low-grade vascular tumor** caused by **Human Herpesvirus 8 (HHV-8)**, also known as KSHV [1]. In the context of HIV, it typically presents as purple-red macules, plaques, or nodules on the skin, mucous membranes, and viscera [2]. The tumor cells are derived from vascular or lymphatic endothelial cells. **Analysis of Incorrect Options:** * **Astrocytoma:** While HIV patients are at risk for various CNS issues, astrocytomas are not specifically associated with AIDS nor are they typically multifocal tumors of vascular origin. * **Gastric Carcinoma:** Though HIV patients have an increased risk of certain GI malignancies, gastric adenocarcinoma is not an AIDS-defining illness and is epithelial, not vascular, in origin [1]. * **Primary CNS Lymphoma:** This is a common AIDS-defining malignancy (associated with **EBV**), but it is a tumor of **B-cell lymphoid origin**, not vascular origin [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for "slit-like vascular spaces" containing extravasated RBCs and spindle-shaped stromal cells [2]. * **Four Clinical Types:** Classic (European), Endemic (African), Iatrogenic (Transplant-related), and AIDS-associated (Epidemic). * **Pathogenesis:** HHV-8 encodes a G-protein coupled receptor that stimulates VEGF, leading to angiogenesis. * **Diagnosis:** Biopsy is definitive; HHV-8 immunostaining is highly specific. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 526-527. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 262-263.

Question 474: S100 is a marker for which of the following neoplasms?

A. Melanoma (Correct Answer)
B. Schwannoma
C. Histiocytoma
D. Hemangioma

Explanation: **Explanation:** **S100** is a calcium-binding protein primarily found in cells derived from the **neural crest**. It is a highly sensitive, though not highly specific, immunohistochemical (IHC) marker used in diagnostic pathology. **Why Melanoma is the Correct Answer:** Melanocytes are neural crest-derived cells. **Melanoma** is the classic neoplasm associated with S100 positivity. While newer markers like HMB-45 and Melan-A are more specific, S100 remains the most sensitive screening marker for melanoma; a negative S100 result almost always rules out a diagnosis of melanoma. **Analysis of Other Options:** * **Schwannoma:** While Schwannomas are also S100 positive (as Schwann cells are neural crest-derived), in the context of standard NEET-PG questions, **Melanoma** is the primary association taught and tested for S100. *Note: If this were a "Multiple Correct" type question, Schwannoma would also be technically correct.* * **Histiocytoma:** Fibrous histiocytomas are typically negative for S100. However, Langerhans Cell Histiocytosis (LCH) is S100 positive, but "Histiocytoma" usually refers to fibrohistiocytic tumors which are negative. * **Hemangioma:** This is a vascular tumor derived from endothelial cells. The characteristic marker for vascular tumors is **CD31** or **CD34**, not S100. **High-Yield Clinical Pearls for NEET-PG:** * **S100 Positive Tissues:** Melanocytes, Schwann cells, Chondrocytes (cartilage), Adipocytes (fat), and Langerhans cells. * **S100 Positive Tumors:** Melanoma, Schwannoma, Neurofibroma, Chondrosarcoma, and Lipoma. * **Specific Melanoma Markers:** HMB-45 (highly specific for premelanosomes) and Melan-A (MART-1). * **Rule of Thumb:** If a spindle cell tumor is S100 negative, it is very unlikely to be a nerve sheath tumor or melanoma.

Question 475: What is a Turban tumor?

A. Basal cell carcinoma
B. Squamous cell carcinoma
C. Cutaneous cylindroma (Correct Answer)
D. Dermatofibroma

Explanation: **Explanation:** **Cutaneous Cylindroma (Option C)** is a benign adnexal tumor, traditionally thought to arise from eccrine or apocrine sweat glands [1]. It is nicknamed a **"Turban Tumor"** because multiple nodules can enlarge and coalesce over the scalp, resembling a turban [1]. * **Histopathology (High-Yield):** On microscopy, it shows a characteristic **"Jigsaw puzzle" appearance** [1]. It consists of nests of basaloid cells surrounded by thick, eosinophilic, PAS-positive hyaline basement membrane material [1]. * **Genetics:** It is associated with mutations in the **CYLD gene**. When multiple, it is often part of **Brooke-Spiegler Syndrome** (along with trichoepitheliomas and spiradenomas) [1]. **Why other options are incorrect:** * **Basal Cell Carcinoma (A):** The most common skin cancer, typically presenting as a pearly papule with telangiectasia or a "rodent ulcer" [2]. It shows peripheral palisading on histology, not a jigsaw pattern [2]. * **Squamous Cell Carcinoma (B):** Presents as scaling, friable plaques or erosions [3]. Histology shows keratin pearls and intercellular bridges. * **Dermatofibroma (C):** A common benign fibrous nodule, usually on the legs, characterized by the "dimple sign" (invagination upon lateral pressure) [2]. **NEET-PG High-Yield Pearls:** 1. **Jigsaw puzzle pattern** = Cylindroma [1]. 2. **CYLD Gene mutation** = Cylindroma. 3. **Brooke-Spiegler Syndrome** = Multiple Cylindromas + Trichoepitheliomas [1]. 4. **Turban Tumor** = Clinical gross appearance of confluent scalp cylindromas [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1154-1156. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1160-1162. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, p. 1158.

Question 476: Squamous cell carcinoma of the lip is least likely to develop in which of the following individuals?

A. Scandinavian fisherman
B. Redheaded individual with a year-round tan
C. Man who smokes a clay pipe
D. Brunette individual who constantly drinks tea (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Brunette individual who constantly drinks tea.** This question tests the understanding of risk factors for **Squamous Cell Carcinoma (SCC) of the lower lip**, which is primarily driven by chronic ultraviolet (UV) radiation exposure and chemical irritation [1]. **1. Why Option D is Correct:** Brunette individuals have higher levels of **eumelanin**, which provides significant photoprotection against UV radiation compared to fair-skinned individuals [2]. Furthermore, **tea consumption** is not a recognized risk factor for lip cancer; in fact, some studies suggest the polyphenols in tea may have antioxidant properties. This individual lacks both the genetic predisposition (fair skin) and the environmental triggers (UV/tobacco) associated with the disease. **2. Analysis of Incorrect Options:** * **Option A (Scandinavian fisherman):** High-risk. They typically have fair skin (Type I/II phenotype) and experience chronic, occupational sun exposure [2], leading to **actinic cheilitis**, a precursor to SCC [1]. * **Option B (Redheaded individual):** High-risk. Redheads possess the **MC1R gene variant**, resulting in high pheomelanin levels which offer poor UV protection [2]. A "year-round tan" in such an individual indicates chronic solar damage. * **Option C (Clay pipe smoker):** High-risk. Chronic heat and chemical irritation from the pipe stem, combined with the carcinogenic effects of tobacco, are classic risk factors for lower lip SCC [1]. **Clinical Pearls for NEET-PG:** * **Location:** SCC of the **lower lip** is more common (due to sun exposure), while SCC of the **upper lip** is rarer and often more aggressive [1]. * **Precursor Lesion:** **Actinic cheilitis** (crusting, thickening, and eversion of the lip) is the most common premalignant condition. * **Metastasis:** Lip SCC typically metastasizes first to the **submental or submandibular lymph nodes**. * **Field Cancerization:** Chronic exposure to tobacco/UV can prime the entire mucosal surface for multiple primary tumors. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 738-739. [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. 220-221.

Question 477: A 70-year-old male, a chronic tobacco chewer for 50 years, presents with a six-month history of a large, fungating, soft papillary lesion in the oral cavity that has penetrated the mandible. Lymph nodes are not palpable. Biopsies show benign-appearing papillomatosis with hyperkeratosis and acanthosis infiltrating the subjacent tissues. What is the most likely diagnosis?

A. Squamous cell papilloma
B. Squamous cell carcinoma
C. Verrucous carcinoma (Correct Answer)
D. Malignant mixed tumor

Explanation: **Explanation:** The clinical presentation and histopathology are classic for **Verrucous Carcinoma (Ackerman’s tumor)**, a low-grade variant of squamous cell carcinoma (SCC). **Why Verrucous Carcinoma is correct:** 1. **Risk Factors:** It is strongly associated with long-term tobacco use (chewing/snuff), often called "Snuff dipper's cancer." In India and Asia, the chewing of betel quid and paan (containing tobacco) is a major regional predisposing influence for oral cavity SCC [2]. 2. **Clinical Features:** It typically presents as a slow-growing, large, fungating, exophytic "cauliflower-like" mass. Despite its aggressive local invasion (e.g., penetrating the mandible), it has a **low metastatic potential**, explaining the absence of palpable lymph nodes. 3. **Histopathology:** It is characterized by "deceptive" benign-looking cytology. Key features include marked hyperkeratosis, acanthosis, and a **"pushing" (rather than infiltrating) border** of well-differentiated squamous epithelium into the underlying stroma. **Why other options are incorrect:** * **Squamous cell papilloma:** A benign lesion that does not invade underlying tissues like the mandible. * **Squamous cell carcinoma (Conventional):** While common in tobacco users, it typically shows significant cellular atypia, pleomorphism, and frequent early lymphatic spread (palpable nodes), which are absent here [2]. * **Malignant mixed tumor:** Usually refers to salivary gland tumors (e.g., Carcinoma ex pleomorphic adenoma) and does not present with this specific papillary, hyperkeratotic morphology [1]. **NEET-PG High-Yield Pearls:** * **"Pushing margins"** is the buzzword for Verrucous Carcinoma. * It is most commonly found in the **buccal mucosa** and gingiva. * **Treatment:** Wide local excision. Radiotherapy is generally avoided as it may trigger **anaplastic transformation** into a more aggressive SCC. * **Differential:** Must be distinguished from "Florid Oral Papillomatosis." **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 751-753. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 738-739.

Question 478: Syndrome of inappropriate Antidiuretic Hormone secretion (SIADH) is a characteristic paraneoplastic association of which of the following carcinomas?

A. Lobular carcinoma of breast
B. Small cell lung carcinoma (Correct Answer)
C. Non-small cell lung carcinoma
D. Fibrosarcoma

Explanation: **Explanation:** **Small cell lung carcinoma (SCLC)** is the correct answer because it is a neuroendocrine tumor derived from Kulchitsky cells [2]. These cells have the metabolic machinery to synthesize and ectopically secrete polypeptide hormones [1]. **SIADH** occurs when the tumor secretes excessive Antidiuretic Hormone (Arginine Vasopressin), leading to water retention, dilutional hyponatremia, and concentrated urine [1]. SCLC is the most common cause of paraneoplastic SIADH, occurring in approximately 7–10% of patients. **Analysis of Incorrect Options:** * **Lobular carcinoma of breast:** While breast cancer can cause paraneoplastic syndromes (like hypercalcemia via PTHrP), it is not classically associated with SIADH. * **Non-small cell lung carcinoma (NSCLC):** Specifically, **Squamous Cell Carcinoma** of the lung is famously associated with hypercalcemia due to the secretion of Parathyroid Hormone-related Protein (PTHrP), not SIADH. * **Fibrosarcoma:** This mesenchymal tumor is more commonly associated with **hypoglycemia** due to the secretion of Insulin-like Growth Factor (IGF-2), a condition known as Doege-Potter syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **SCLC "3 Cs":** **C**ushing Syndrome (Ectopic ACTH), **C**onfusion (SIADH/Hyponatremia), and **C**arcinoid-like syndrome. * **Lambert-Eaton Myasthenic Syndrome (LEMS):** Another high-yield paraneoplastic association of SCLC involving antibodies against voltage-gated calcium channels. * **Rule of Thumb:** If the question mentions a lung mass + Hyponatremia = **Small Cell**; Lung mass + Hypercalcemia = **Squamous Cell**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 725-727. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 337-338.

Question 479: Which condition is associated with the S-100 marker?

A. Multiple myeloma
B. Malignant melanoma (Correct Answer)
C. Prostate carcinoma
D. Medullary carcinoma thyroid

Explanation: **Explanation:** **Malignant Melanoma (Correct Answer):** S-100 is a calcium-binding protein found in cells derived from the **neural crest**. Since melanocytes are neural crest-derived, S-100 is a highly sensitive (though not highly specific) immunohistochemical marker for malignant melanoma [1]. It is used clinically to differentiate amelanotic melanoma from other poorly differentiated tumors. Other neural crest markers for melanoma include HMB-45 and Melan-A (which are more specific). **Analysis of Incorrect Options:** * **Multiple Myeloma:** This is a plasma cell neoplasm. The characteristic markers are **CD138 (Syndecan-1)**, CD38, and monoclonal light chains (Kappa/Lambda). * **Prostate Carcinoma:** The primary diagnostic markers are **PSA (Prostate-Specific Antigen)** and Prostatic Acid Phosphatase (PAP). On IHC, loss of basal cell markers like p63 is diagnostic. * **Medullary Carcinoma Thyroid:** This tumor arises from parafollicular C-cells. The classic marker is **Calcitonin**. It is also associated with amyloid stroma (Congo Red positive) and is a component of MEN 2A and 2B syndromes. **High-Yield Clinical Pearls for NEET-PG:** * **S-100 Positive Tumors:** Remember the mnemonic "L-M-N-S": **L**angerhans cell histiocytosis [3], **M**elanoma [1], **N**eural tumors (Schwannoma, Neurofibroma) [2], and **S**alivary gland tumors (Pleomorphic adenoma). * **Melanoma Specificity:** While S-100 is the most sensitive marker, **HMB-45** is the most specific marker for melanoma. * **Chondrosarcoma:** S-100 is also positive in cartilaginous tumors, which is a common "trap" in pathology exams. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 649-650. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1249-1251. [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, pp. 629-630.

Question 480: Smoking is a causative factor for all the following carcinomas, except:

A. Esophageal carcinoma
B. Laryngeal carcinoma
C. Nasopharyngeal carcinoma (Correct Answer)
D. Urinary bladder carcinoma

Explanation: The correct answer is **Nasopharyngeal carcinoma (NPC)**. While smoking is a major risk factor for most squamous cell carcinomas of the upper aerodigestive tract, NPC has a distinct etiology. **1. Why Nasopharyngeal Carcinoma is the correct answer:** The primary causative agent for Nasopharyngeal Carcinoma (especially the undifferentiated type) is the **Epstein-Barr Virus (EBV)** [1], [2]. Other significant risk factors include dietary factors (consumption of salt-cured fish containing nitrosamines), genetic predisposition (HLA-A2, B17), and environmental exposures (wood dust) [2]. Unlike other head and neck cancers, tobacco smoking is not considered a primary driver for NPC. **2. Why the other options are incorrect:** * **Esophageal Carcinoma:** Smoking is a potent risk factor for both Squamous Cell Carcinoma (due to direct mucosal irritation) and Adenocarcinoma (often via promotion of GERD). * **Laryngeal Carcinoma:** There is a direct dose-response relationship between cigarette smoking and laryngeal cancer [5]. Tobacco smoke contains polycyclic aromatic hydrocarbons that cause field cancerization in the larynx. * **Urinary Bladder Carcinoma:** This is a high-yield fact. Smoking is the most common risk factor for **Urothelial (Transitional Cell) Carcinoma**. Carcinogens like **beta-naphthylamine** and polycyclic aromatic hydrocarbons are absorbed in the lungs, enter the bloodstream, and are concentrated in the urine, leading to DNA damage in the bladder epithelium [3]. **High-Yield Clinical Pearls for NEET-PG:** * **EBV Association:** EBV is also linked to Burkitt Lymphoma, Hodgkin Lymphoma (Mixed cellularity), and CNS Lymphoma in AIDS patients [1]. * **Bladder Cancer:** Besides smoking, exposure to **aniline dyes** and *Schistosoma haematobium* (squamous cell type) are classic examiners' favorites [3]. * **Field Cancerization:** This concept explains why smokers often develop multiple primary tumors in the oral cavity, esophagus, and lungs [4]. **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. Head and Neck, pp. 744-745. [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. 217-218. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 720-721. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 314-315.

Practice by Chapter

Nomenclature and Classification of Tumors

Practice Questions

Characteristics of Benign and Malignant Neoplasms

Practice Questions

Molecular Basis of Cancer

Practice Questions

Carcinogenesis and Carcinogens

Practice Questions

Tumor Progression and Metastasis

Practice Questions

Tumor Markers

Practice Questions

Paraneoplastic Syndromes

Practice Questions

Genetic Basis of Cancer

Practice Questions

Tumor Immunity

Practice Questions

Cancer Epidemiology and Prevention

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Neoplasia — MCQs

Neoplasia — MCQs

On this page

Practice by Chapter

Want unlimited practice?