Neoplasia — MCQs

Neoplasia Indian Medical PG Practice Questions and MCQs

Question 201: A 27-year-old man with AIDS develops a reddish, slightly raised rash on his face, neck, and mouth, consistent in appearance with Kaposi's sarcoma. Microscopically, the proliferating cells in this malignancy most closely resemble which of the following?

A. Angiosarcoma (Correct Answer)
B. Carcinosarcoma
C. Lymphoma
D. Malignant fibrous histiocytoma

Explanation: ### Explanation **1. Why Angiosarcoma is Correct:** Kaposi’s Sarcoma (KS) is a low-grade vascular malignancy caused by **Human Herpesvirus 8 (HHV-8)**, frequently seen in immunocompromised patients (AIDS-defining illness) [1]. Microscopically, KS is characterized by the proliferation of **spindle-shaped cells** of **endothelial origin** [2]. These cells form slit-like vascular spaces containing extravasated red blood cells [2]. Since **Angiosarcoma** is also a malignant tumor of vascular endothelial cells, it shares the closest histogenetic and morphological resemblance to KS, particularly the spindle cell morphology and the formation of irregular vascular channels [3]. **2. Why the Other Options are Incorrect:** * **Carcinosarcoma:** This is a "collision tumor" containing both malignant epithelial (carcinoma) and mesenchymal (sarcoma) components. It does not specifically resemble a vascular endothelial malignancy. * **Lymphoma:** These are malignancies of lymphoid cells (B-cells or T-cells). While AIDS patients are at high risk for Non-Hodgkin Lymphoma (e.g., DLBCL or Burkitt lymphoma), the morphology consists of sheets of lymphoid cells, not spindle-shaped vascular cells [4]. * **Malignant Fibrous Histiocytoma (now Undifferentiated Pleomorphic Sarcoma):** This is a high-grade soft tissue sarcoma characterized by extreme pleomorphism and a storiform pattern, lacking the specific endothelial markers and vascular slits seen in KS. **3. NEET-PG High-Yield Pearls:** * **HHV-8 (KSHV):** The essential causative agent for all four types of KS (Classic, Endemic/African, Iatrogenic, and AIDS-associated) [1]. * **Histology Hallmark:** "Slit-like spaces" with extravasated RBCs and **hyaline droplets** (representing degenerated RBCs) [2]. * **Marker:** **LANA-1** (Latent Nuclear Antigen) is a highly specific immunohistochemical marker for HHV-8 in tissue sections. * **Clinical Clue:** KS lesions do not blanch under pressure because the blood is trapped in tissue slits rather than functional vessels. **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 Infancy and Childhood, pp. 527-528. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 262-263.

Question 202: Duchenne's muscular dystrophy is inherited in which pattern?

A. X-linked dominant
B. X-linked recessive (Correct Answer)
C. Autosomal dominant
D. Autosomal recessive

Explanation: **Explanation:** **Duchenne Muscular Dystrophy (DMD)** is the most common and severe form of muscular dystrophy. It is caused by a mutation in the **DMD gene** located on the **short arm of the X chromosome (Xp21)**. 1. **Why X-linked Recessive (XLR) is correct:** The DMD gene is the largest known human gene, making it highly susceptible to spontaneous mutations. Because it is located on the X chromosome, the disease primarily affects males (XY), who have only one copy of the gene [1]. Females (XX) are typically asymptomatic carriers unless they exhibit "skewed lyonization" (inactivation of the normal X chromosome). 2. **Why other options are incorrect:** * **X-linked Dominant:** These disorders (e.g., Alport syndrome, Vitamin D-resistant rickets) affect both sexes, and an affected father would pass the trait to all his daughters but no sons. * **Autosomal Dominant:** These require only one mutant allele on a non-sex chromosome (e.g., Huntington’s disease, Marfan syndrome) [2]. * **Autosomal Recessive:** These require two mutant alleles (e.g., Cystic Fibrosis, Sickle Cell Anemia) [2]. Becker Muscular Dystrophy (BMD), a milder variant of DMD, is also XLR. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** DMD is caused by a **frameshift mutation** leading to a total absence of **Dystrophin**, a protein that anchors the muscle cytoskeleton to the extracellular matrix [2]. * **Clinical Signs:** **Gower’s sign** (using hands to "climb up" the body to stand) and **Pseudohypertrophy of calves** (muscle replaced by fat and fibrosis). * **Diagnosis:** Elevated Serum Creatine Kinase (CK) levels; Muscle biopsy shows variation in fiber size and absent dystrophin staining. * **Cause of Death:** Usually respiratory failure or dilated cardiomyopathy in the second decade of life. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151. [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. 57-58.

Question 203: Spontaneous regression, though rare, is seen in which of the following conditions?

A. Burkitt's lymphoma
B. Wilms tumor
C. Neuroblastoma (Correct Answer)
D. Melanoma

Explanation: **Explanation:** **Neuroblastoma** is a classic example of a tumor that can undergo **spontaneous regression** [1] or spontaneous maturation into a benign form (ganglioneuroma) [1]. This phenomenon is most frequently observed in **Stage 4S** (S for Special), which occurs in infants under one year of age. Despite widespread dissemination to the liver, skin, and bone marrow, these tumors often regress with minimal or no treatment due to mechanisms like cellular apoptosis or differentiation. **Analysis of Options:** * **Burkitt’s Lymphoma (A):** This is one of the fastest-growing human tumors with a very high proliferation index (Ki-67 near 100%). It is highly aggressive and requires intensive chemotherapy; it does not regress spontaneously. * **Wilms Tumor (B):** While it is a common pediatric renal tumor, it typically requires surgical resection and chemotherapy. Spontaneous regression is not a recognized feature. * **Melanoma (D):** Although rare instances of partial regression (often immune-mediated) are documented in melanoma, **Neuroblastoma** is the classic, high-yield textbook answer for spontaneous regression in the context of pediatric pathology and NEET-PG. **High-Yield Clinical Pearls for NEET-PG:** * **Neuroblastoma:** Derived from **neural crest cells** [1]. Most common extracranial solid tumor of childhood. * **Markers:** Elevated urinary catecholamines (VMA and HVA) [1]. * **Genetics:** **N-myc amplification** is the most important poor prognostic indicator [1]. * **Homer-Wright Rosettes:** Characteristic histological finding (also seen in Medulloblastoma and Retinoblastoma) [1]. * **Other tumors showing regression:** Choriocarcinoma and Renal Cell Carcinoma (rarely). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 483-487.

Question 204: All the following MALT lymphomas are related to a specific organism except:

A. MALT lymphomas of stomach - Helicobacter pylori
B. MALT lymphomas of skin - Bartonella henselae (Correct Answer)
C. MALT lymphomas of eye - Chlamydophila psittaci
D. MALT lymphomas of small intestine - Campylobacter jejuni

Explanation: **Explanation:** MALT (Mucosa-Associated Lymphoid Tissue) lymphomas, also known as extranodal marginal zone B-cell lymphomas, are frequently driven by chronic antigenic stimulation resulting from persistent bacterial or viral infections [1]. **Why Option B is correct:** MALT lymphomas of the **skin** (Borrelia-associated B-cell lymphoma) are associated with **_Borrelia burgdorferi_** (the causative agent of Lyme disease), particularly in European populations. **_Bartonella henselae_** is the causative agent of Cat Scratch Disease and Bacillary Angiomatosis, but it is not a recognized driver for cutaneous MALT lymphoma. **Analysis of incorrect options:** * **Option A (Stomach - *H. pylori*):** This is the most common association. Chronic infection leads to the recruitment of lymphoid tissue to the gastric mucosa [1]. Eradication of *H. pylori* with antibiotics can lead to complete regression of the lymphoma in early stages. * **Option C (Eye/Ocular Adnexa - *C. psittaci*):** Ocular adnexal MALT lymphomas (involving the conjunctiva or orbit) have a strong documented association with *Chlamydophila psittaci*. * **Option D (Small Intestine - *C. jejuni*):** Immunoproliferative Small Intestinal Disease (IPSID), a variant of MALT lymphoma primarily seen in the Mediterranean, is associated with chronic *Campylobacter jejuni* infection. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Hallmark:** The most common translocation in MALT lymphoma is **t(11;18)(q21;q21)**, involving the *API2-MALT1* fusion gene [2]. * **Treatment Note:** Gastric MALTomas that harbor the t(11;18) translocation are generally **unresponsive** to *H. pylori* eradication therapy. * **Other Associations:** MALT lymphoma of the **Salivary gland** is associated with **Sjögren’s syndrome**, and **Thyroid** MALT lymphoma is associated with **Hashimoto’s thyroiditis** [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 356-357. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 566-567. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 235-236.

Question 205: Burkitt's lymphoma is associated with which of the following gene anomalies?

A. t(9:22)
B. del. 5q
C. t(8:14) (Correct Answer)
D. t(17:15)

Explanation: Burkitt’s Lymphoma is a highly aggressive B-cell non-Hodgkin lymphoma characterized by the overexpression of the **c-MYC oncogene** [1]. The hallmark genetic anomaly is the **t(8;14)** translocation, which occurs in approximately 80% of cases [1]. In this translocation, the *c-MYC* gene on chromosome 8 is moved to the **Immunoglobulin Heavy Chain (IgH)** locus on chromosome 14 [1]. Because the IgH promoter is highly active in B-cells, it leads to the constitutive expression of c-MYC, a potent transcription factor that drives rapid cell proliferation and growth. **Analysis of Incorrect Options:** * **A. t(9;22):** Known as the **Philadelphia Chromosome**, this results in the *BCR-ABL1* fusion gene [2]. It is the diagnostic hallmark of **Chronic Myeloid Leukemia (CML)** and is also seen in some cases of ALL [2]. * **B. del. 5q:** This deletion is characteristic of **Myelodysplastic Syndromes (MDS)**, specifically the "5q-minus syndrome," which typically presents with macrocytic anemia and thrombocytosis. * **D. t(15;17):** This translocation involves the *PML-RARA* fusion and is diagnostic for **Acute Promyelocytic Leukemia (APL/AML-M3)** [3]. It is clinically significant because it responds to All-Trans Retinoic Acid (ATRA) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Classically described as a **"Starry Sky Appearance"** (tingible body macrophages acting as "stars" against a "sky" of dark neoplastic B-cells). * **Variants:** Endemic (African, associated with EBV, involves the jaw), Sporadic (abdominal involvement), and Immunodeficiency-associated. * **Other Translocations:** While t(8;14) is most common, variant translocations **t(2;8)** and **t(8;22)** involving kappa and lambda light chains can also occur in Burkitt’s [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [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. 225-226. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 326.

Question 206: What is the most common abnormality of a proto-oncogene in human tumors?

A. p53 point mutations
B. Point mutation in RAS family gene (Correct Answer)
C. Point mutation in C-kit gene
D. Overexpression of RET proto-oncogene

Explanation: ### Explanation The correct answer is **Point mutation in RAS family gene**. **1. Why RAS is correct:** The **RAS gene family** (HRAS, KRAS, NRAS) represents the most frequently mutated group of **proto-oncogenes** in human cancers. Approximately 30% of all human tumors harbor a RAS mutation. The underlying mechanism is a **single nucleotide point mutation**, most commonly at codons 12, 13, or 61. This mutation interferes with the GTPase activity of the RAS protein, trapping it in a "constitutively active" GTP-bound state, leading to continuous pro-growth signaling to the nucleus [2]. **2. Analysis of Incorrect Options:** * **p53 point mutations:** While *TP53* is the most commonly mutated gene in human cancer overall, it is a **tumor suppressor gene**, not a proto-oncogene [2]. The question specifically asks for a proto-oncogene. * **Point mutation in C-kit:** While mutations in *c-KIT* are characteristic of Gastrointestinal Stromal Tumors (GIST) and mastocytosis, they are not as ubiquitous across all human cancers as RAS mutations. * **Overexpression of RET:** *RET* mutations/rearrangements are specific to conditions like MEN 2A/2B and Medullary Thyroid Carcinoma [1]. It is a tissue-specific abnormality rather than the most common global proto-oncogene defect. **3. High-Yield Clinical Pearls for NEET-PG:** * **KRAS:** Most common RAS mutation; associated with **Pancreatic adenocarcinoma** (90%+) and **Colon cancer**. * **NRAS:** Associated with **Melanomas** and Hematologic malignancies (AML). * **HRAS:** Associated with **Bladder tumors**. * **Mechanism:** RAS mutations result in the failure of **GTP hydrolysis** (loss of GAP function), keeping the molecular switch "ON." **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 292. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 291-292.

Question 207: Carcinoid syndrome is due to:

A. Adrenaline
B. Noradrenaline
C. Serotonin (Correct Answer)
D. Dopamine

Explanation: **Explanation:** **Carcinoid syndrome** is a paraneoplastic syndrome associated with neuroendocrine tumors (Carcinoid tumors), most commonly arising in the ileum [1]. The syndrome occurs when these tumors secrete bioactive amines directly into the systemic circulation, bypassing hepatic metabolism. * **Why Serotonin is correct:** The primary mediator of carcinoid syndrome is **Serotonin (5-HT)**. In these tumors, dietary tryptophan is diverted toward the synthesis of 5-HT. When serotonin reaches the systemic circulation (typically after the tumor has metastasized to the liver), it causes the classic triad of symptoms: **flushing, diarrhea, and bronchospasm.** [1] Its metabolite, **5-HIAA**, is excreted in the urine and serves as a diagnostic marker. * **Why other options are incorrect:** * **Adrenaline & Noradrenaline:** These catecholamines are secreted by **Pheochromocytomas** (tumors of the adrenal medulla). While they cause hypertension and palpitations, they are not the primary mediators of carcinoid syndrome. * **Dopamine:** While a precursor to catecholamines, it is not associated with the clinical manifestations of carcinoid tumors. **High-Yield Clinical Pearls for NEET-PG:** 1. **Carcinoid Heart Disease:** Characterized by **fibrous plaque-like thickening** of the endocardium, primarily affecting the **Right Side** (Tricuspid insufficiency and Pulmonary stenosis). The left side is spared because the lungs contain monoamine oxidase (MAO), which inactivates serotonin. 2. **Diagnosis:** The most specific screening test is the **24-hour urinary 5-HIAA** (5-hydroxyindoleacetic acid) level. 3. **Pellagra Risk:** Patients may develop **Niacin (Vitamin B3) deficiency** because tryptophan is diverted to serotonin production instead of niacin synthesis. 4. **Rule of 1/3rds:** Carcinoid tumors are famous for being 1/3rd multicentric, 1/3rd metastatic, and 1/3rd associated with a second malignancy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 780-782.

Question 208: Sacrococcygeal teratoma tumor cells consist of cells from which germ layer(s)?

A. Ectoderm
B. Endoderm
C. Mesoderm
D. All of the above (Correct Answer)

Explanation: ### Explanation **Concept Overview:** A **teratoma** is a germ cell tumor composed of tissues derived from more than one germ cell layer—and frequently all three: **ectoderm, mesoderm, and endoderm** [1]. These tumors arise from totipotent germ cells (typically found in the gonads) or embryonic rests. Sacrococcygeal teratoma is the most common congenital tumor in newborns, arising from the **Hensen’s node** (primitive knot) at the distal end of the spine [2]. **Why "All of the above" is Correct:** By definition, a true teratoma must contain elements from multiple germ layers [1]. In a sacrococcygeal teratoma, you will find: * **Ectoderm:** Skin, hair follicles, and brain tissue [3]. * **Mesoderm:** Muscle, fat, bone, and cartilage [3]. * **Endoderm:** Gut epithelium, respiratory lining, and thyroid tissue [3]. **Analysis of Incorrect Options:** * **Options A, B, and C** are individually incorrect because selecting only one would imply the tumor is a simple hamartoma or a monodermal tumor. While these layers are present, the defining characteristic of a teratoma is the **co-existence** of all three. **NEET-PG High-Yield Pearls:** * **Most Common Site:** The sacrococcygeal region is the most common site for extragonadal teratomas in neonates. * **Gender Predilection:** It is significantly more common in **females** (approx. 4:1 ratio), though most are benign in this group. * **Malignancy Risk:** Most neonatal sacrococcygeal teratomas are mature (benign). However, the risk of malignancy (usually **Yolk Sac Tumor** components) increases if the surgical resection is delayed beyond 4 months of age [2]. * **Classification:** Often classified using the **Altman Criteria** based on their location (intrapelvic vs. extrapelvic). * **Tumor Marker:** Elevated **Alpha-fetoprotein (AFP)** levels may indicate a malignant yolk sac component within the teratoma. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 480-481. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 979-980. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1033-1034.

Question 209: Which of the following genes has been most closely associated with familial cases of ovarian cancer?

A. BRCA1 (Correct Answer)
B. WT1
C. NF2
D. VHL

Explanation: **Explanation:** **Correct Option: A (BRCA1)** The **BRCA1** (Breast Cancer 1) gene, located on chromosome **17q21**, is a tumor suppressor gene involved in DNA repair via homologous recombination. Mutations in BRCA1 are the most common cause of hereditary breast and ovarian cancer syndromes. Women with a BRCA1 mutation have a significantly higher lifetime risk of developing epithelial ovarian cancer (approx. 40%) compared to those with BRCA2 mutations (approx. 15%) [1]. These cancers are typically high-grade serous carcinomas. **Incorrect Options:** * **B. WT1 (Wilms Tumor 1):** Located on chromosome 11p13, this gene is primarily associated with **Wilms tumor** (nephroblastoma) in children and certain syndromes like WAGR and Denys-Drash syndrome. * **C. NF2 (Neurofibromin 2):** Located on chromosome 22q12, mutations lead to **Neurofibromatosis Type 2**, classically characterized by bilateral acoustic neuromas (vestibular schwannomas) and meningiomas. * **D. VHL (Von Hippel-Lindau):** Located on chromosome 3p25, this gene is associated with VHL syndrome, which presents with **Renal Cell Carcinoma (clear cell type)**, hemangioblastomas, and pheochromocytomas [2]. **High-Yield Clinical Pearls for NEET-PG:** * **BRCA1 vs. BRCA2:** BRCA1 is on Chromosome **17**; BRCA2 is on Chromosome **13**. * **Male Breast Cancer:** More strongly associated with **BRCA2** than BRCA1. * **Prophylaxis:** Bilateral salpingo-oophorectomy is often recommended for mutation carriers after completion of childbearing to reduce risk [1]. * **Treatment:** Ovarian cancers with BRCA mutations are particularly sensitive to **PARP inhibitors** (e.g., Olaparib) due to "synthetic lethality." **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1058-1059. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300.

Question 210: Oncogenes can be best studied by which of the following methods?

A. Transfection (Correct Answer)
B. Transduction
C. Transformation
D. Conjugation

Explanation: **Explanation:** The identification and study of oncogenes rely on the ability to introduce foreign DNA into a host cell to observe phenotypic changes, such as malignant transformation. **Why Transfection is the Correct Answer:** **Transfection** is the process of deliberately introducing naked or purified nucleic acids into eukaryotic cells (usually via chemical methods like calcium phosphate precipitation or physical methods like electroporation). In cancer research, DNA from tumor cells is "transfected" into a reporter cell line (commonly **NIH/3T3 mouse fibroblasts**). If the donor DNA contains an oncogene (e.g., *RAS*), the fibroblasts will lose contact inhibition and form colonies (foci), proving the presence of a transforming gene. This method was pivotal in discovering the first human oncogene, *HRAS*. **Analysis of Incorrect Options:** * **B. Transduction:** This involves the transfer of genetic material via a **bacteriophage** (virus). While retroviruses can carry oncogenes (v-onc), "transduction" as a laboratory method is less specific for the primary study of genomic oncogenes compared to transfection. * **C. Transformation:** In microbiology, this is the uptake of DNA by bacteria. In oncology, it refers to the *result* (a normal cell becoming cancerous), not the laboratory *method* used to study the genes themselves. * **D. Conjugation:** This is a process of horizontal gene transfer between bacterial cells via direct cell-to-cell contact (pili). It has no application in the study of human oncogenes. **High-Yield Clinical Pearls for NEET-PG:** * **NIH/3T3 Assay:** The classic transfection assay used to identify the *RAS* oncogene. * **Proto-oncogenes vs. Oncogenes:** Proto-oncogenes are normal cellular genes; they become oncogenes through **point mutations** (e.g., *RAS*), **amplification** (e.g., *HER2/neu*), or **translocation** (e.g., *BCR-ABL*) [1]. * **RAS Mutation:** The most common abnormality of proto-oncogenes in human tumors (found in ~30% of all cancers). **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. 228-230.

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