Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 411: A 3-year-old child presents with an abdominal mass originating from the right adrenal gland. Biopsy reveals sheets of small cells with hyperchromatic nuclei, forming occasional pseudorosettes with central young nerve fibers. Which oncogene is associated with this tumor?

A. erb-B2
B. c-myc
C. L-myc
D. N-myc (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. N-myc** **Concept:** The clinical presentation (3-year-old child, adrenal mass) [4] and histopathology (small round blue cells, pseudorosettes) [2] are classic for **Neuroblastoma**, the most common extracranial solid tumor of childhood. The "pseudorosettes" described are **Homer-Wright rosettes**, characterized by tumor cells arranged around a central space containing neuropil (fibrillar material) [2]. In Neuroblastoma, the **N-myc (MYCN)** proto-oncogene on chromosome 2 is frequently amplified [1]. This amplification is a critical prognostic marker; more than 10 copies of N-myc indicate an aggressive clinical course, poor prognosis, and resistance to therapy, regardless of the tumor stage [1]. --- **Analysis of Incorrect Options:** * **A. erb-B2 (HER2/neu):** This is a growth factor receptor gene. Its amplification is primarily associated with **Breast Cancer** and Gastric Adenocarcinoma, where it dictates the use of Trastuzumab. * **B. c-myc:** This oncogene is located on chromosome 8. It is the hallmark of **Burkitt Lymphoma** (typically via t(8;14) translocation), leading to constitutive activation of B-cells. * **C. L-myc:** This member of the myc family is specifically associated with **Small Cell Carcinoma of the Lung**. --- **High-Yield Clinical Pearls for NEET-PG:** * **Homer-Wright Rosettes:** Seen in Neuroblastoma, Medulloblastoma, and Retinoblastoma [2]. * **Biomarkers:** Elevated urinary catecholamine metabolites (**VMA and HVA**) are diagnostic [3]. * **Opsoclonus-Myoclonus Syndrome:** A high-yield paraneoplastic syndrome ("dancing eyes, dancing feet") associated with Neuroblastoma. * **Staging:** Stage 4S is a unique category in infants (<1 year) that often shows spontaneous regression despite metastasis to liver, skin, or bone marrow. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 486-487. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 484-485. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 486. [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. 211-212.

Question 412: Which of the following are oncogenic viruses in humans?

A. Human Papillomavirus (HPV)
B. Epstein-Barr Virus (EBV)
C. Hepatitis B Virus
D. All of the above (Correct Answer)

Explanation: **Explanation:** Oncogenic viruses are viruses capable of inducing tumors by integrating their genetic material into the host genome or by expressing viral oncoproteins that interfere with host cell cycle regulation (e.g., inhibiting p53 and RB proteins) [1], [2]. 1. **Human Papillomavirus (HPV):** High-risk strains (HPV 16 and 18) are strongly associated with **Cervical Carcinoma**, oropharyngeal, and anogenital cancers [1], [2]. They produce oncoproteins **E6** (which degrades p53) and **E7** (which inhibits RB) [3]. 2. **Epstein-Barr Virus (EBV):** A member of the herpesvirus family, EBV is linked to **Burkitt Lymphoma**, Nasopharyngeal Carcinoma, and Hodgkin Lymphoma [1], [2]. It infects B cells via the CD21 receptor and utilizes the **LMP-1** gene to mimic CD40 signaling, promoting B-cell proliferation [4]. 3. **Hepatitis B Virus (HBV):** Along with HCV, HBV is a leading cause of **Hepatocellular Carcinoma (HCC)** [2]. It promotes oncogenesis through chronic inflammation, hepatocyte regeneration, and the **HBx protein**, which disrupts growth control and induces genomic instability. Since all three viruses are established human carcinogens, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **HTLV-1:** The only RNA retrovirus directly linked to human cancer (Adult T-cell Leukemia/Lymphoma) [2]. * **HHV-8:** Associated with Kaposi Sarcoma, especially in HIV patients [1], [2]. * **HCV:** Unlike HBV (a DNA virus), HCV is an RNA virus that causes cancer primarily through chronic inflammation and cirrhosis rather than integration into the host genome [2]. * **Merkel Cell Polyomavirus:** Associated with Merkel cell carcinoma of the skin. **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] 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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1007-1008. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336.

Question 413: Which of the following is NOT a tumor suppressor gene?

A. APC
B. p53
C. Rb
D. C-myc (Correct Answer)

Explanation: ### Explanation The fundamental distinction in cancer genetics lies between **Proto-oncogenes** and **Tumor Suppressor Genes (TSGs)**. **Why C-myc is the correct answer:** **C-myc** is a **proto-oncogene**, not a tumor suppressor gene [1]. It encodes a transcription factor that promotes cell cycle progression (by activating cyclins) and cell growth [1]. When mutated or overexpressed (gain-of-function), it becomes an oncogene, leading to uncontrolled proliferation. It is classically associated with **Burkitt Lymphoma** via the **t(8;14)** translocation. **Why the other options are incorrect:** * **APC (Adenomatous Polyposis Coli):** A "Gatekeeper" TSG that downregulates the WNT signaling pathway by promoting the degradation of β-catenin. Mutations lead to Familial Adenomatous Polyposis (FAP). * **p53 (TP53):** Known as the "Guardian of the Genome," it is the most commonly mutated TSG in human cancers. It induces cell cycle arrest (via p21) or apoptosis (via BAX) in response to DNA damage. * **Rb (Retinoblastoma gene):** The "Governor of the Cell Cycle," it controls the G1/S checkpoint by sequestering the E2F transcription factor. It was the first TSG discovered, leading to Knudson’s "Two-Hit Hypothesis." **High-Yield Clinical Pearls for NEET-PG:** * **Two-Hit Hypothesis:** TSGs generally require **loss-of-function** in both alleles to promote cancer (recessive at the cellular level), whereas proto-oncogenes require only a **single "gain-of-function"** mutation (dominant). * **N-myc** is associated with Neuroblastoma; **L-myc** with Small Cell Carcinoma of the Lung. * **Li-Fraumeni Syndrome:** Germline mutation of **p53** leading to multiple diverse wheels (SBLA syndrome: Sarcoma, Breast, Leukemia, Adrenal). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 296-297.

Question 414: The paraneoplastic hypercalcemia in lymphoma is due to ectopic production of which of the following?

A. Parathyroid hormone-related protein
B. 1,25 dihydroxyvitamin D (Correct Answer)
C. Parathyroid hormone
D. Prostaglandin E2

Explanation: ### Explanation **Correct Answer: B. 1,25 dihydroxyvitamin D** The primary mechanism of paraneoplastic hypercalcemia in **lymphomas** (both Hodgkin and non-Hodgkin) is the extra-renal conversion of 25-hydroxyvitamin D to **1,25-dihydroxyvitamin D (Calcitriol)** [1]. This occurs because malignant lymphocytes and associated macrophages express the enzyme **1-alpha-hydroxylase**, which is normally regulated by the kidneys [1]. This autonomous production leads to increased intestinal calcium absorption and bone resorption, independent of PTH levels [1]. **Analysis of Incorrect Options:** * **A. Parathyroid hormone-related protein (PTHrP):** This is the most common cause of paraneoplastic hypercalcemia overall (Humoral Hypercalcemia of Malignancy) [2]. However, it is typically associated with **Squamous Cell Carcinomas** (lung, head, and neck), renal cell carcinoma, and breast cancer, rather than lymphoma [2]. * **C. Parathyroid hormone (PTH):** Ectopic production of authentic PTH by tumors is extremely rare. Hypercalcemia of malignancy usually suppresses endogenous PTH. * **D. Prostaglandin E2:** While PGE2 can stimulate osteoclast activity and was historically linked to hypercalcemia in certain solid tumors, it is not the primary mediator in lymphoma-associated hypercalcemia. **High-Yield Clinical Pearls for NEET-PG:** * **Sarcoidosis Connection:** The mechanism in lymphoma is identical to that in Sarcoidosis (granulomatous disease), where activated macrophages produce 1-alpha-hydroxylase [3]. * **Multiple Myeloma:** Hypercalcemia here is due to **Local Osteolytic Hypercalcemia** mediated by RANKL and OAFs (Osteoclast Activating Factors), not systemic hormones [3]. * **Diagnostic Clue:** In lymphoma-induced hypercalcemia, labs will show **↑ Calcium, ↓ PTH, and ↑ 1,25(OH)₂D.** * **Treatment:** Glucocorticoids are particularly effective in these cases as they inhibit the 1-alpha-hydroxylase enzyme. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Central Nervous System Synapse, pp. 446-448. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 338-339. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 667-668.

Question 415: Lynch syndrome is associated with which of the following conditions?

A. Hereditary nonpolyposis colorectal cancer (Correct Answer)
B. Gastric adenocarcinoma
C. Hepatoma
D. Familial adenomatous polyposis of the colon

Explanation: **Explanation:** **Lynch Syndrome**, also known as **Hereditary Nonpolyposis Colorectal Cancer (HNPCC)**, is an autosomal dominant condition caused by germline mutations in **DNA Mismatch Repair (MMR) genes** (most commonly *MLH1, MSH2, MSH6,* and *PMS2*) [1]. This leads to **microsatellite instability (MSI)**, resulting in an increased risk of colorectal cancer and various extracolonic malignancies [3]. * **Option A (Correct):** Lynch syndrome is synonymous with HNPCC. Unlike FAP, it is characterized by the development of colorectal cancer at a young age without the presence of hundreds of precursor polyps [1], [2]. * **Option B (Incorrect):** While Lynch syndrome increases the risk of gastric cancer, it is primarily defined by its association with HNPCC [1]. Gastric adenocarcinoma is more specifically linked to *CDH1* mutations (Hereditary Diffuse Gastric Cancer). * **Option C (Incorrect):** Hepatoma (Hepatocellular carcinoma) is typically associated with chronic Hepatitis B/C infections, cirrhosis, or aflatoxin exposure, not MMR gene mutations. * **Option D (Incorrect):** Familial Adenomatous Polyposis (FAP) is caused by a mutation in the **APC gene** (Wnt signaling pathway). It is characterized by thousands of adenomatous polyps, whereas Lynch syndrome is "nonpolyposis" [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Amsterdam II Criteria:** Used for clinical diagnosis (3-2-1 rule: 3 relatives, 2 generations, 1 diagnosed before age 50). * **Most Common Extracolonic Site:** Endometrial carcinoma (crucial for screening in females) [1]. * **Tumor Location:** Predominantly occurs in the **right colon** (proximal to the splenic flexure) [1], [3]. * **Pathology:** Often shows "medullary" growth patterns and prominent tumor-infiltrating lymphocytes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 817. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 821-822. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 819-821.

Question 416: What is the normal level of Prostate-Specific Antigen (PSA) in males?

A. Less than 4 ng/ml (Correct Answer)
B. 4-10 ng/ml
C. Greater than 10 ng/ml
D. PSA is not produced by normal males

Explanation: **Explanation:** **1. Why Option A is Correct:** Prostate-Specific Antigen (PSA) is a serine protease produced by the ductal and acinar epithelium of the prostate gland. Its physiological function is to liquefy the seminal coagulum. In a healthy male with an intact blood-prostate barrier, only minute amounts of PSA leak into the systemic circulation. The universally accepted upper limit of "normal" for serum PSA is **< 4 ng/ml** [1]. Values below this threshold indicate a low probability of significant prostatic pathology. **2. Analysis of Incorrect Options:** * **Option B (4-10 ng/ml):** This range is clinically referred to as the **"Gray Zone."** While levels in this range can occur in Prostate Cancer, they are frequently elevated due to benign conditions like Benign Prostatic Hyperplasia (BPH) or Prostatitis. * **Option C (> 10 ng/ml):** This is considered a high value with a significantly increased predictive value for malignancy. Approximately 50% of patients with PSA > 10 ng/ml are found to have prostate cancer on biopsy. * **Option D:** This is incorrect because PSA is an organ-specific (though not cancer-specific) marker produced by all normal prostatic tissue. **3. High-Yield Clinical Pearls for NEET-PG:** * **Organ Specificity:** PSA is organ-specific but **not cancer-specific**. It can be elevated in BPH, prostatitis, prostatic infarction, and even after digital rectal examination (DRE) or cystoscopy [2]. * **Age-Specific PSA:** Normal limits increase with age (e.g., <2.5 ng/ml for 40–49 years; <6.5 ng/ml for 70–79 years) due to increasing prostate volume [1]. * **Free-to-Total PSA Ratio:** A **lower ratio (<15-20%)** of free PSA to total PSA is more suggestive of malignancy, whereas a higher ratio suggests BPH [1]. * **PSA Velocity:** An increase of **>0.75 ng/ml per year** is highly suspicious for cancer, even if the total PSA is <4 ng/ml [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. 992-993. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 499-500.

Question 417: In carcinoma of unknown primary, if the tissue marker CDX-2 is positive, what does it indicate?

A. Bladder cancer
B. Gastrointestinal cancer (Correct Answer)
C. Lung cancer
D. Thyroid cancer

Explanation: **Explanation:** **CDX-2 (Caudal-type homeobox 2)** is a transcription factor essential for the development and differentiation of intestinal epithelial cells. In the context of **Carcinoma of Unknown Primary (CUP)**, CDX-2 serves as a highly specific and sensitive immunohistochemical (IHC) marker for adenocarcinomas of **gastrointestinal origin**, particularly colorectal cancer (positive in >90% of cases). It is also frequently expressed in gastric and pancreaticoduodenal malignancies. **Analysis of Options:** * **Option B (Correct):** CDX-2 is the "master regulator" of the intestinal phenotype. Its expression in a metastatic lesion strongly points toward a primary site in the GI tract (Colorectal > Gastric/Small bowel). * **Option A (Bladder):** The primary marker for Urothelial carcinoma is **GATA-3**. While some urachal adenocarcinomas may express CDX-2, it is not the standard marker for bladder cancer. * **Option C (Lung):** The hallmark markers for primary lung adenocarcinoma are **TTF-1** (Thyroid Transcription Factor-1) and **Napsin A**. * **Option D (Thyroid):** Thyroid malignancies are characterized by **TTF-1** and **Thyroglobulin** (for papillary/follicular) or **Calcitonin** (for medullary carcinoma). **High-Yield Clinical Pearls for NEET-PG:** * **CK7-/CK20+/CDX-2+:** Classic IHC profile for **Colorectal Adenocarcinoma** [1]. * **CK7+/CK20-/TTF-1+:** Classic profile for **Lung Adenocarcinoma**. * **CK7+/CK20-:** Seen in Breast, Lung, and Thyroid cancers. * **PAX-8:** Highly specific for Renal, Ovarian, and Thyroid tumors. * **SATB2:** A newer, highly specific marker for colorectal origin, often used alongside CDX-2. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 819-821.

Question 418: Which of the following statements regarding Carcinoembryonic Antigen (CEA) is false?

A. A prognostic indicator
B. A glycoprotein
C. Elevated in colorectal carcinoma
D. Elevated only when there is hepatic metastasis (Correct Answer)

Explanation: **Explanation:** **Carcinoembryonic Antigen (CEA)** is a complex oncofetal glycoprotein normally produced during fetal development in the gastrointestinal tract and pancreas [1]. In adults, it is a widely used tumor marker, primarily associated with colorectal carcinoma. **Why Option D is the correct (False) statement:** CEA is **not** specific to hepatic metastasis. While levels are often significantly higher when colorectal cancer spreads to the liver (due to impaired biliary excretion and high tumor burden), CEA can be elevated in localized primary tumors, other malignancies (pancreas, lung, breast), and even **non-neoplastic conditions** such as heavy smoking, cirrhosis, ulcerative colitis, and pancreatitis [1]. Therefore, the word "only" makes this statement incorrect. **Analysis of other options:** * **Option A (Prognostic indicator):** This is true. Pre-operative CEA levels correlate with tumor stage. More importantly, it is the gold standard for **monitoring recurrence** after surgery; a rising CEA level post-resection is a sensitive indicator of tumor return [1]. * **Option B (Glycoprotein):** This is true. Biochemically, CEA is a member of the immunoglobulin superfamily and functions as a cell adhesion molecule. * **Option C (Elevated in colorectal carcinoma):** This is true. It is the most classic marker for this malignancy, though it lacks the sensitivity and specificity required for population screening [1]. **NEET-PG High-Yield Pearls:** * **Screening:** CEA is **NOT** used for screening the general population. * **Best Use:** Monitoring response to therapy and detecting recurrence. * **Smoking:** Always remember that chronic smokers can have baseline CEA elevations (up to 5 ng/mL), which must be considered when interpreting results. * **Other Markers:** Compare with **CA 19-9** (Pancreatic CA) and **AFP** (Hepatocellular CA/Yolk sac tumor). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 319-320.

Question 419: Which of the following is NOT a premalignant ulcer?

A. Bazin's ulcer (Correct Answer)
B. Paget's disease of nipple
C. Marjolin's ulcer
D. Lupus vulgaris

Explanation: **Explanation:** The core concept behind this question is distinguishing between **premalignant conditions** (lesions that have a high risk of transforming into cancer) and **benign inflammatory conditions**. **Why Bazin's Ulcer is the correct answer:** **Bazin’s ulcer** (Erythema Induratum) is a form of panniculitis (inflammation of subcutaneous fat) associated with Type IV hypersensitivity to *Mycobacterium tuberculosis*. [1] It typically presents as recurrent, painful, bilateral nodules on the calves of young women that may ulcerate. It is a purely inflammatory/infectious condition and has **no inherent malignant potential**. **Analysis of Incorrect Options:** * **Paget’s Disease of the Nipple:** This is a premalignant/malignant condition where adenocarcinoma cells (Paget cells) infiltrate the epidermis of the nipple. [2] It is almost always associated with an underlying ductal carcinoma in situ (DCIS) or invasive carcinoma. * **Marjolin’s Ulcer:** This refers to a squamous cell carcinoma (SCC) arising in areas of chronic irritation, such as old burn scars, chronic osteomyelitis sinuses, or long-standing venous ulcers. [3], [4] It is a classic example of malignancy arising from chronic inflammation. * **Lupus Vulgaris:** This is a progressive form of cutaneous tuberculosis. If left untreated for years, it carries a significant risk of developing into **Squamous Cell Carcinoma** (the "lupus carcinoma"). **High-Yield Clinical Pearls for NEET-PG:** * **Marjolin’s Ulcer** is typically more aggressive than standard SCC and has a higher rate of metastasis. * **Bowen’s Disease** is another high-yield premalignant term; it represents SCC *in situ* of the skin. [4] * **Erythroplasia of Queyrat** is SCC *in situ* specifically involving the glans penis. * **Remember:** Chronic irritation and chronic non-healing ulcers are major risk factors for Squamous Cell Carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1176-1177. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1061-1062. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 647-648. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 644-645.

Question 420: Which of the following are expressed in breast cancer?

A. HER2/neu
B. P53
C. BRCA1
D. All of the above (Correct Answer)

Explanation: Breast cancer is a heterogeneous disease driven by a variety of genetic alterations, including the activation of oncogenes and the inactivation of tumor suppressor genes [1]. **Explanation of the Correct Answer:** The correct answer is **D (All of the above)** because breast tumorigenesis involves a complex interplay of these three specific biomarkers: 1. **HER2/neu (ERBB2):** This is a proto-oncogene located on chromosome 17q. It is overexpressed (via gene amplification) in approximately 15–20% of breast cancers [1]. It serves as both a prognostic marker (associated with aggressive disease) and a predictive marker (indicating response to Trastuzumab). 2. **P53 (TP53):** This is the "guardian of the genome" (tumor suppressor gene). Mutations in *TP53* are the most common genetic alterations in human cancer. In breast cancer, *p53* mutations are frequently seen, particularly in the aggressive "Triple Negative" and "HER2-enriched" subtypes [1]. 3. **BRCA1:** This is a tumor suppressor gene involved in DNA repair (homologous recombination) [1]. Germline mutations in *BRCA1* significantly increase the lifetime risk of breast and ovarian cancer. Even in sporadic cases, the *BRCA1* pathway may be functionally impaired. **High-Yield Clinical Pearls for NEET-PG:** * **Molecular Subtypes:** Luminal A (ER+/PR+, HER2-), Luminal B (ER+, HER2+/-), HER2-enriched, and Basal-like (Triple Negative) [1]. * **Li-Fraumeni Syndrome:** Characterized by germline *p53* mutations; breast cancer is a core component [1]. * **BRCA1 vs. BRCA2:** *BRCA1* is more commonly associated with Triple Negative Breast Cancer (TNBC), while *BRCA2* is more often ER-positive. * **Nottingham Grading System:** Uses tubule formation, nuclear pleomorphism, and mitotic count to grade breast carcinoma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1060.

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Neoplasia — MCQs

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