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Pathology - Testicular Germ Cell Tumors
Risk factors comprise cryptorchidism, genetic factors, and testicular dysgenesis.
Seminoma(S) is the most prevalent type and is similar to ovarian dysgerminoma.
Embryonal carcinoma (EC) is the second most prevalent kind.
Endodermal sinus tumor (yolk sac tumor) (EST) is more prevalent in newborns and children.
Teratoma (T) accounts for 30% of all testicular tumors.
Choriocarcinoma (CC) is the most aggressive kind of cancer.
Seminoma consists of uniform cells with well-defined cell membranes, transparent cytoplasm, and a prominent nucleus.
Embryonal Carcinoma : Glandular or tubular cell patterns with papillary folds.
There is a mesodermal core with layers that resemble those found in primitive glomeruli (Endodermal sinus ( yolk tumor /EST)
Teratoma (T): Teratomas derived from many embryonic layers are usually malignant, unlike ovarian dermoid cysts.
Choriocarcinoma (CC): Sheets/cords of cells resembling syncytiotrophoblasts and cytotrophoblasts with transparent cytoplasm.
Symptom and Signs
Seminoma: Pain-free testicular swelling or lump that does not allow light to pass through upon inspection with a flashlight.
Embryonal Carcinoma : Painful testicular tumor frequently associated with metastases.
Endometrial Sinus Tumor :Testicular mass appears before the age of 3.
Teratoma :Symptoms include a painful bulge in the testes and gynecomastia.
Choriocarcinoma:Chief Complaint: Pain-free, nodular swelling in the testicles; development of breast tissue in males; presence of enlarged lymph nodes above the collarbone (if cancer has spread). Laboratory results show elevated levels of hCG in (S,EC,T,CC) samples, as well as elevated levels of AFP in (EST and T)
Therapy
Treatment options include radiotherapy, chemotherapy, and radical inguinal orchectomy. Testicular cancers predominantly affect Caucasian males aged 15 to 34.
Risk factors comprise cryptorchidism, genetic factors, and testicular dysgenesis.
Seminoma(S) is the most prevalent type and is similar to ovarian dysgerminoma.
Embryonal carcinoma (EC) is the second most prevalent kind.
Endodermal sinus tumor (yolk sac tumor) (EST) is more prevalent in newborns and children.
Teratoma (T) accounts for 30% of all testicular tumors.
Choriocarcinoma (CC) is the most aggressive kind of cancer.
Seminoma consists of uniform cells with well-defined cell membranes, transparent cytoplasm, and a prominent nucleus.
Embryonal Carcinoma : Glandular or tubular cell patterns with papillary folds.
There is a mesodermal core with layers that resemble those found in primitive glomeruli (Endodermal sinus ( yolk tumor /EST)
Teratoma (T): Teratomas derived from many embryonic layers are usually malignant, unlike ovarian dermoid cysts.
Choriocarcinoma (CC): Sheets/cords of cells resembling syncytiotrophoblasts and cytotrophoblasts with transparent cytoplasm.
Symptom and Signs
Seminoma: Pain-free testicular swelling or lump that does not allow light to pass through upon inspection with a flashlight.
Embryonal Carcinoma : Painful testicular tumor frequently associated with metastases.
Endometrial Sinus Tumor :Testicular mass appears before the age of 3.
Teratoma :Symptoms include a painful bulge in the testes and gynecomastia.
Choriocarcinoma:Chief Complaint: Pain-free, nodular swelling in the testicles; development of breast tissue in males; presence of enlarged lymph nodes above the collarbone (if cancer has spread). Laboratory results show elevated levels of hCG in (S,EC,T,CC) samples, as well as elevated levels of AFP in (EST and T)
Therapy
Treatment options include radiotherapy, chemotherapy, and radical inguinal orchectomy. Testicular cancers predominantly affect Caucasian males aged 15 to 34.
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Pathology - Testicular Sex Cord–Gonadal Stroma Tumors
Primarily benign tumors originating from sex cord stroma.
Similar to Sertoli-Leydig cell ovarian cancers.
Typically observed in individuals aged 20 to 60.
Pathology
Leydig cell tumor is characterized by small yellowish-brown nodules made up of polygonal cells with eosinophilic cytoplasm and round nucleus. It also contains distinctive intracytoplasmic Reinke crystals, which are rod-shaped crystalloids. These tumors typically generate androgens and estrogens.
Sertoli cell tumor is a solid mass made up of tumor cells organized in trabeculae and cord structures resembling seminiferous tubules.
Clinical Symptoms and Signs
Testicular swelling or nodule that does not show light passing through during a flashlight examination.
Leydig cell tumors can cause early puberty in children or breast enlargement in adults.
Therapy
Treatment options include radiotherapy, chemotherapy, and radical inguinal orchectomy.
Testicular lymphomas make about 5% of testicular neoplasms and are the most prevalent type of testicular cancer in men over the age of 60.
Primarily benign tumors originating from sex cord stroma.
Similar to Sertoli-Leydig cell ovarian cancers.
Typically observed in individuals aged 20 to 60.
Pathology
Leydig cell tumor is characterized by small yellowish-brown nodules made up of polygonal cells with eosinophilic cytoplasm and round nucleus. It also contains distinctive intracytoplasmic Reinke crystals, which are rod-shaped crystalloids. These tumors typically generate androgens and estrogens.
Sertoli cell tumor is a solid mass made up of tumor cells organized in trabeculae and cord structures resembling seminiferous tubules.
Clinical Symptoms and Signs
Testicular swelling or nodule that does not show light passing through during a flashlight examination.
Leydig cell tumors can cause early puberty in children or breast enlargement in adults.
Therapy
Treatment options include radiotherapy, chemotherapy, and radical inguinal orchectomy.
Testicular lymphomas make about 5% of testicular neoplasms and are the most prevalent type of testicular cancer in men over the age of 60.
Sertoli Cell Tumor
Leydig Cell Tumor
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Pathology - Acute Bacterial Prostatitis
Primarily caused by gram-negative rods such as E. coli, Proteus mirabilis, Klebsiella, or Enterobacter, as well as N. gonorrhoeae or Enterococcus.
Risk factors comprise urinary tract infection, Foley catheterization, and recent transurethral surgery or cystoscopy.
Pathology: The prostate gland is enlarged due to edema and congestion.
Microscopic examination reveals an inflammatory infiltration, typically lymphocytic, in the prostate stroma that may extend into the glandular regions.
Manifests with fever, dysuria, and perineal discomfort. Experiencing pain with a noticeable sensitive prostate upon examination. May sometimes be linked to urinary retention.
Possible complications involve the formation of a prostatic abscess or the presence of chronic prostatitis.
Laboratory results: Leukocytes detected in urinalysis; urine culture shows positive results.
Antibiotic treatment targeting the responsible bacterium often lasts for 30 days to prevent problems.
Chronic bacterial prostatitis can occur as a consequence of inadequate treatment of acute bacterial prostatitis. Patients exhibit genitourinary discomfort, dysuria, frequent urination, and recurring UTIs. Diagnosis is confirmed by detecting bacteria in produced prostatic secretions or urine culture following prostatic massage, comparable to those found in acute bacterial prostatitis. Treatment involves a 4- to 12-week regimen of antibiotics.
Primarily caused by gram-negative rods such as E. coli, Proteus mirabilis, Klebsiella, or Enterobacter, as well as N. gonorrhoeae or Enterococcus.
Risk factors comprise urinary tract infection, Foley catheterization, and recent transurethral surgery or cystoscopy.
Pathology: The prostate gland is enlarged due to edema and congestion.
Microscopic examination reveals an inflammatory infiltration, typically lymphocytic, in the prostate stroma that may extend into the glandular regions.
Manifests with fever, dysuria, and perineal discomfort. Experiencing pain with a noticeable sensitive prostate upon examination. May sometimes be linked to urinary retention.
Possible complications involve the formation of a prostatic abscess or the presence of chronic prostatitis.
Laboratory results: Leukocytes detected in urinalysis; urine culture shows positive results.
Antibiotic treatment targeting the responsible bacterium often lasts for 30 days to prevent problems.
Chronic bacterial prostatitis can occur as a consequence of inadequate treatment of acute bacterial prostatitis. Patients exhibit genitourinary discomfort, dysuria, frequent urination, and recurring UTIs. Diagnosis is confirmed by detecting bacteria in produced prostatic secretions or urine culture following prostatic massage, comparable to those found in acute bacterial prostatitis. Treatment involves a 4- to 12-week regimen of antibiotics.
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Pathology - Benign Prostatic Hyperplasia
Resulting from elevated estradiol levels associated with aging.
Prevalent in males over 50 years old (impacts 90% of men by age 70).
Pathophysiology: Elevated estradiol levels stimulate the expression of receptors for DHT, resulting in prostate enlargement.
Prostate enlargement characterized by a rubbery, nodular growth in the periurethral and transurethral zones (middle and lateral lobes).
Microscopic: Both glandular and fibromuscular stromal components exhibit hyperplasia.
Manifests with frequent urination, nighttime urination, painful urination, and challenges initiating and stopping urine flow due to nodules compressing the urethra.
Complications may involve urinary blockage resulting in kidney failure, enlarged bladder, kidney swelling, ureter swelling, and urinary tract infections.
Laboratory results: Elevated total prostate-specific antigen (PSA) levels with a corresponding rise in the percentage of free PSA.
Treatment includes finasteride, a 5-alpha-reductase inhibitor; tamsulosin, a 1 blocker; and transurethral resection of the prostate (TURP) for severe instances.
Benign prostatic hyperplasia (BPH) is the most common cause of urinary tract blockage in men and is not considered a condition that leads to cancer.
Resulting from elevated estradiol levels associated with aging.
Prevalent in males over 50 years old (impacts 90% of men by age 70).
Pathophysiology: Elevated estradiol levels stimulate the expression of receptors for DHT, resulting in prostate enlargement.
Prostate enlargement characterized by a rubbery, nodular growth in the periurethral and transurethral zones (middle and lateral lobes).
Microscopic: Both glandular and fibromuscular stromal components exhibit hyperplasia.
Manifests with frequent urination, nighttime urination, painful urination, and challenges initiating and stopping urine flow due to nodules compressing the urethra.
Complications may involve urinary blockage resulting in kidney failure, enlarged bladder, kidney swelling, ureter swelling, and urinary tract infections.
Laboratory results: Elevated total prostate-specific antigen (PSA) levels with a corresponding rise in the percentage of free PSA.
Treatment includes finasteride, a 5-alpha-reductase inhibitor; tamsulosin, a 1 blocker; and transurethral resection of the prostate (TURP) for severe instances.
Benign prostatic hyperplasia (BPH) is the most common cause of urinary tract blockage in men and is not considered a condition that leads to cancer.
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Pathology - Endometrial Carcinoma
Risk factors comprise unopposed estrogen use, obesity, diabetes, hypertension, nulliparity, and late menopause.
The highest occurrence is often observed between the ages of 55 and 65.
Endometrial carcinoma is the most prevalent gynecologic malignancy.
Usually occurs after endometrial hyperplasia.
Gross: Either a localized polypoid tumor or a widespread tumor affecting the entire uterine surface.
Adenocarcinoma is identified by distinct gland patterns formed by malignant stratified columnar epithelial cells, with the possibility of observing some squamous cells.
Manifests as postmenopausal vaginal bleeding, facilitating early detection; can result in cervical blockage with accumulation of pus (pyometra) or blood (hematometra), leading to lower abdomen pain.
Therapy
Complete removal of the uterus, fallopian tubes, and ovaries; treatment with radiation therapy and chemotherapy for symptom relief.
Endometrial hyperplasia is the abnormal growth of endometrial glands due to an excess of estrogen, which can be caused by conditions such as polycystic ovarian syndrome, estrogen-secreting ovarian tumors, or estrogen replacement treatment. It presents clinically with postmenopausal vaginal bleeding and can result in endometrial cancer based on the level of atypia.
Risk factors comprise unopposed estrogen use, obesity, diabetes, hypertension, nulliparity, and late menopause.
The highest occurrence is often observed between the ages of 55 and 65.
Endometrial carcinoma is the most prevalent gynecologic malignancy.
Usually occurs after endometrial hyperplasia.
Gross: Either a localized polypoid tumor or a widespread tumor affecting the entire uterine surface.
Adenocarcinoma is identified by distinct gland patterns formed by malignant stratified columnar epithelial cells, with the possibility of observing some squamous cells.
Manifests as postmenopausal vaginal bleeding, facilitating early detection; can result in cervical blockage with accumulation of pus (pyometra) or blood (hematometra), leading to lower abdomen pain.
Therapy
Complete removal of the uterus, fallopian tubes, and ovaries; treatment with radiation therapy and chemotherapy for symptom relief.
Endometrial hyperplasia is the abnormal growth of endometrial glands due to an excess of estrogen, which can be caused by conditions such as polycystic ovarian syndrome, estrogen-secreting ovarian tumors, or estrogen replacement treatment. It presents clinically with postmenopausal vaginal bleeding and can result in endometrial cancer based on the level of atypia.
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Pathology - Dysplasia, Carcinoma in Situ, and Squamous Cell Carcinoma of the Cervix
Linked to HPV types 16, 18, 31, and 33, early sexual debut, multiple sexual partners, HIV infection, and smoking.
Cervical dysplasia (CD): Concerns the squamocolumnar junction; identified by cells with hyperchromatic nuclei, irregular nuclear shapes, and minimal cytoplasm; epithelial proliferation starts at the basal layer and spreads outward; categorized as cervical intraepithelial neoplasia (CIN) grades I-III; CIN I displays abnormal undifferentiated cells solely in the lower third of the epithelium, while CIN III exhibits atypical cells throughout more than two-thirds of the epithelium.
Cervical carcinoma in situ (CIS) is characterized by dysplastic cells that spread over the whole epithelium but do not invade the basement membrane.
Symptoms and signs
Cervical cancer that has invaded surrounding tissues/ invasive cervical carcinoma (ICC). Gross: may present as exophytic, ulcerating, or infiltrating mass.
The microscopic findings typically show squamous cell carcinoma (SCC) with big cells and keratinization. It can also present as adenocarcinoma or undifferentiated carcinoma. The cancer originates from preexisting cervical intraepithelial neoplasia (CIN) at the squamocolumnar junction. Non-neoplastic epithelial cells generally exhibit koilocytosis, which is linked to HPV infection.
Therapies
Clinical ICC symptoms include irregular vaginal bleeding, postcoital spotting, pelvic pain, cervical ulceration and discharge, dysuria, and potential ureter obstruction causing renal failure.
Treatment: For CIN I, consider either expectant management or excision as 75% regress spontaneously. Treat CIN II-III by excision.
ICC: Hysterectomy, chemotherapy, and radiation for treatment; HPV vaccine for prevention.
Linked to HPV types 16, 18, 31, and 33, early sexual debut, multiple sexual partners, HIV infection, and smoking.
Cervical dysplasia (CD): Concerns the squamocolumnar junction; identified by cells with hyperchromatic nuclei, irregular nuclear shapes, and minimal cytoplasm; epithelial proliferation starts at the basal layer and spreads outward; categorized as cervical intraepithelial neoplasia (CIN) grades I-III; CIN I displays abnormal undifferentiated cells solely in the lower third of the epithelium, while CIN III exhibits atypical cells throughout more than two-thirds of the epithelium.
Cervical carcinoma in situ (CIS) is characterized by dysplastic cells that spread over the whole epithelium but do not invade the basement membrane.
Symptoms and signs
Cervical cancer that has invaded surrounding tissues/ invasive cervical carcinoma (ICC). Gross: may present as exophytic, ulcerating, or infiltrating mass.
The microscopic findings typically show squamous cell carcinoma (SCC) with big cells and keratinization. It can also present as adenocarcinoma or undifferentiated carcinoma. The cancer originates from preexisting cervical intraepithelial neoplasia (CIN) at the squamocolumnar junction. Non-neoplastic epithelial cells generally exhibit koilocytosis, which is linked to HPV infection.
Therapies
Clinical ICC symptoms include irregular vaginal bleeding, postcoital spotting, pelvic pain, cervical ulceration and discharge, dysuria, and potential ureter obstruction causing renal failure.
Treatment: For CIN I, consider either expectant management or excision as 75% regress spontaneously. Treat CIN II-III by excision.
ICC: Hysterectomy, chemotherapy, and radiation for treatment; HPV vaccine for prevention.
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Pathology - Zollinger-Ellison Syndrome
Gastrinoma is typically caused by a pancreatic islet cell tumor. While most gastrinomas occur sporadically, 25% are linked to Multiple Endocrine Neoplasia Type I (MEN I).
Gastrinoma can originate in the pancreas, duodenum, or adjacent tissues. They are frequently malignant and tend to spread to the liver, although they typically do not exhibit anaplasia histologically.
Gastrinomas release gastrin, which results in acid hypersecretion, leading to peptic ulcers and inactivation of pancreatic enzymes.
Peptic ulcer disease in the duodenum can lead to ulcer perforation, along with symptoms such as diarrhea, steatorrhea, and weight loss due to pancreatic enzyme inactivation.
Laboratory results: Elevated gastrin levels, reduced stomach acidity.
Excision of gastrinoma; regulation of stomach acid production with proton pump inhibitors.
Insulinoma is a pancreatic tumor that results in excessive release of insulin and elevated levels of C-peptide, a chemical produced during insulin manufacture. It is linked to the Whipple triad, which consists of episodic hyperinsulinemia and hypoglycemia, hypoglycemic CNS impairment, and the reversal of CNS dysfunction when hypoglycemia is resolved.
Gastrinoma is typically caused by a pancreatic islet cell tumor. While most gastrinomas occur sporadically, 25% are linked to Multiple Endocrine Neoplasia Type I (MEN I).
Gastrinoma can originate in the pancreas, duodenum, or adjacent tissues. They are frequently malignant and tend to spread to the liver, although they typically do not exhibit anaplasia histologically.
Gastrinomas release gastrin, which results in acid hypersecretion, leading to peptic ulcers and inactivation of pancreatic enzymes.
Peptic ulcer disease in the duodenum can lead to ulcer perforation, along with symptoms such as diarrhea, steatorrhea, and weight loss due to pancreatic enzyme inactivation.
Laboratory results: Elevated gastrin levels, reduced stomach acidity.
Excision of gastrinoma; regulation of stomach acid production with proton pump inhibitors.
Insulinoma is a pancreatic tumor that results in excessive release of insulin and elevated levels of C-peptide, a chemical produced during insulin manufacture. It is linked to the Whipple triad, which consists of episodic hyperinsulinemia and hypoglycemia, hypoglycemic CNS impairment, and the reversal of CNS dysfunction when hypoglycemia is resolved.
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Pathology - Fibrocystic Breast Disease
Resulting from a hormonal imbalance characterized by elevated estrogens and/or reduced progesterones.
The highest occurrence is often observed between the ages of 25 and 50.
Multiple histological variations: (1) Cystic lesions: numerous fluid-filled cysts are observed as blue (referred to as blue-dome cysts). The cysts are bordered by polygonal cells with eosinophilic granular cytoplasm resembling apocrine epithelium (known as apocrine metaplasia). Papillary projections of cystic epithelium may also be present.
Epithelial hyperplasia of the breast duct refers to a rise in the number of epithelial layers in the terminal duct lobules, leading to uneven lumens. Stromal fibrosis involves hyperplasia and fibrosis of the breast stroma.
Sclerosing adenosis is characterized by an elevated quantity of acini and fibrosis in the stromal tissue.
Clinical Symptoms and Signs
Manifests as diffuse breast pain, most severe during the premenstrual phase, with many palpable lesions that are often felt on both sides. There are no changes in the skin or nipple, and the masses tend to rapidly alter in size.
Perform biopsy to rule out malignancy. Once the disease is established, address symptoms by controlling pain with NSAIDs, oral contraceptives, and a supportive brassiere.
Fibrocystic disease is the predominant breast illness. Cystic fibrosis and stromal fibrosis do not pose a higher risk for cancer, although epithelial hyperplasia and sclerosing adenosis do have a slightly elevated risk.
Resulting from a hormonal imbalance characterized by elevated estrogens and/or reduced progesterones.
The highest occurrence is often observed between the ages of 25 and 50.
Multiple histological variations: (1) Cystic lesions: numerous fluid-filled cysts are observed as blue (referred to as blue-dome cysts). The cysts are bordered by polygonal cells with eosinophilic granular cytoplasm resembling apocrine epithelium (known as apocrine metaplasia). Papillary projections of cystic epithelium may also be present.
Epithelial hyperplasia of the breast duct refers to a rise in the number of epithelial layers in the terminal duct lobules, leading to uneven lumens. Stromal fibrosis involves hyperplasia and fibrosis of the breast stroma.
Sclerosing adenosis is characterized by an elevated quantity of acini and fibrosis in the stromal tissue.
Clinical Symptoms and Signs
Manifests as diffuse breast pain, most severe during the premenstrual phase, with many palpable lesions that are often felt on both sides. There are no changes in the skin or nipple, and the masses tend to rapidly alter in size.
Perform biopsy to rule out malignancy. Once the disease is established, address symptoms by controlling pain with NSAIDs, oral contraceptives, and a supportive brassiere.
Fibrocystic disease is the predominant breast illness. Cystic fibrosis and stromal fibrosis do not pose a higher risk for cancer, although epithelial hyperplasia and sclerosing adenosis do have a slightly elevated risk.
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Pathology - Benign Tumors of the Breast
Fibroadenoma (FA): Common in women under 40, more prevalent in African American women at a younger age.
Phyllodes tumor (PT) typically develops in individuals over the age of 50.
Intraductal papilloma (IP) typically affects women in their middle age.
FA: Gross: tiny, mobile, springy, hard mass with distinct, well-defined edges.
Microscopic description: fibroblastic stroma surrounds cystic and glandular areas; may decrease in size after menopause and show calcifications.
PT: Gross: substantial, bulky accumulation of connective tissue and cysts. Microscopic examination reveals cystic areas on the cut piece of stroma including leaflike extensions from cyst walls, resulting in a leaflike appearance on the breast surface. Approximately 5%-10% of these cases progress malignant transformation with atypia, known as cystosarcoma phyllodes.
IP: Gross: originating from significant lactiferous ducts. Microscopic description: increased development of ductal epithelial tissue in a papillary pattern; presence of apocrine metaplasia.
FA and PT: Enlarged mass becomes more sensitive during pregnancy or menstrual cycle; no changes in skin appearance; no swollen lymph nodes; no nipple retraction.
IP: Exhibits nipple discharge.
FA: No intervention or basic removal.
PT: Local excision with broad margin; may return post-resection. IP: Basic removal.
PT and IP are associated with a slightly elevated risk of breast cancer.
Fibroadenoma (FA): Common in women under 40, more prevalent in African American women at a younger age.
Phyllodes tumor (PT) typically develops in individuals over the age of 50.
Intraductal papilloma (IP) typically affects women in their middle age.
FA: Gross: tiny, mobile, springy, hard mass with distinct, well-defined edges.
Microscopic description: fibroblastic stroma surrounds cystic and glandular areas; may decrease in size after menopause and show calcifications.
PT: Gross: substantial, bulky accumulation of connective tissue and cysts. Microscopic examination reveals cystic areas on the cut piece of stroma including leaflike extensions from cyst walls, resulting in a leaflike appearance on the breast surface. Approximately 5%-10% of these cases progress malignant transformation with atypia, known as cystosarcoma phyllodes.
IP: Gross: originating from significant lactiferous ducts. Microscopic description: increased development of ductal epithelial tissue in a papillary pattern; presence of apocrine metaplasia.
FA and PT: Enlarged mass becomes more sensitive during pregnancy or menstrual cycle; no changes in skin appearance; no swollen lymph nodes; no nipple retraction.
IP: Exhibits nipple discharge.
FA: No intervention or basic removal.
PT: Local excision with broad margin; may return post-resection. IP: Basic removal.
PT and IP are associated with a slightly elevated risk of breast cancer.
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Pathology - Breast Cancer
Risk factors for breast cancer include a family history of first-degree relative with breast cancer at a young age, autosomal dominant inheritance of mutations in BRCA1 or BRCA2 gene, female gender, increased age, early first menarche, delayed first pregnancy, nulliparity, late menopause, radiation exposure, and exogenous estrogen use.
Incidence rises with advancing age.
Pathology
Infiltrating ductal carcinoma is characterized by tumor cells organized in cords, islands, or glands inside a dense fibrous stroma. It may develop from ductal carcinoma in situ (DCIS).
Intraductal comedocarcinoma is characterized by a cluster of tumor cells enclosed within a duct, with central necrosis, periductal fibrosis, and inflammation.
Inflammation: Lymphatic system affecting the skin above.
Paget disease is characterized by the invasion of giant cells with a visible halo of pale cytoplasm from ducts into the epidermis of the nipple. This condition always involves underlying ductal adenocarcinoma inside subareolar excretory channels.
Lobular infiltration: Frequently found in multiple and bilateral locations; cells align in a single file pattern with tumor cells surrounding the lobule in a target-like manner; presence of signet ring cells; may develop from lobular carcinoma in situ (LCIS) over an extended period.
Medullary: Dense cell sheets with prominent nucleoli in minimal connective tissue; presence of lymphocytic infiltration.
A painless, typically immobile, firm lump commonly located in the upper outer quadrant of the breast; skin and nipple changes; detectable axillary lymph nodes; bone discomfort if metastasis to bones occurs.
Treatment Notes
Infiltrating ductal carcinoma: Dense, immovable, fibrous lump.
Characterized by redness, swelling, heat, agony upon touch, and skin resembling an orange peel.
Paget's disease presents as pruritic, scaly, and painless eczematous lesions on the nipple.
Medullary: Soft mass with a fleshy consistency.
Lab results indicate that a paraneoplastic illness causing the release of PTH-related peptide can result in high levels of calcium in the blood.
Imaging: Mammogram showing microcalcifications or a spiculated, growing tumor.
Treatment options include surgery, radiation treatment, chemotherapy, hormonal therapy (tamoxifen or aromatase inhibitors) for patients with estrogen receptor-positive cancer cells, and monoclonal antibody therapy (trastuzumab) for individuals with HER2/neu expression.
Metastasis spreads to lymph nodes, lungs, liver, central nervous system (CNS), and bones.
Mucinous (colloid) refers to pools of extracellular mucin around tumor cell clusters with a gelatinous nature.
Among women, breast carcinoma ranks as the second leading cause of cancer-related mortality.
Clinical Symptoms
A painless, typically immobile, firm lump commonly located in the upper outer quadrant of the breast; skin and nipple retraction; detectable axillary lymph nodes; bone discomfort if metastasis to the bone occurs.
Infiltrating ductal cancer presents as a firm, fixed, fibrous mass.
Characterized by redness, swelling, heat, agony upon touch, and a skin texture like an orange peel.
Paget's disease presents as pruritic, scaly, and painless eczematous lesions on the nipple.
Medullary: Soft mass with a fleshy consistency.
Lab results indicate that a paraneoplastic condition causing the release of PTH-related peptide can result in hypercalcemia.
Imaging: Mammogram showing microcalcifications or spiculated, growing mass.
Therapies
Treatment options include surgery, radiation treatment, chemotherapy, hormonal therapy (tamoxifen or aromatase inhibitors) for patients with estrogen receptor-positive cancer cells, and monoclonal antibody therapy (trastuzumab) for individuals with HER2/neu expression.
Metastasis can spread to lymph nodes, lungs, liver, central nervous system (CNS), and bones.
Risk factors for breast cancer include a family history of first-degree relative with breast cancer at a young age, autosomal dominant inheritance of mutations in BRCA1 or BRCA2 gene, female gender, increased age, early first menarche, delayed first pregnancy, nulliparity, late menopause, radiation exposure, and exogenous estrogen use.
Incidence rises with advancing age.
Pathology
Infiltrating ductal carcinoma is characterized by tumor cells organized in cords, islands, or glands inside a dense fibrous stroma. It may develop from ductal carcinoma in situ (DCIS).
Intraductal comedocarcinoma is characterized by a cluster of tumor cells enclosed within a duct, with central necrosis, periductal fibrosis, and inflammation.
Inflammation: Lymphatic system affecting the skin above.
Paget disease is characterized by the invasion of giant cells with a visible halo of pale cytoplasm from ducts into the epidermis of the nipple. This condition always involves underlying ductal adenocarcinoma inside subareolar excretory channels.
Lobular infiltration: Frequently found in multiple and bilateral locations; cells align in a single file pattern with tumor cells surrounding the lobule in a target-like manner; presence of signet ring cells; may develop from lobular carcinoma in situ (LCIS) over an extended period.
Medullary: Dense cell sheets with prominent nucleoli in minimal connective tissue; presence of lymphocytic infiltration.
A painless, typically immobile, firm lump commonly located in the upper outer quadrant of the breast; skin and nipple changes; detectable axillary lymph nodes; bone discomfort if metastasis to bones occurs.
Treatment Notes
Infiltrating ductal carcinoma: Dense, immovable, fibrous lump.
Characterized by redness, swelling, heat, agony upon touch, and skin resembling an orange peel.
Paget's disease presents as pruritic, scaly, and painless eczematous lesions on the nipple.
Medullary: Soft mass with a fleshy consistency.
Lab results indicate that a paraneoplastic illness causing the release of PTH-related peptide can result in high levels of calcium in the blood.
Imaging: Mammogram showing microcalcifications or a spiculated, growing tumor.
Treatment options include surgery, radiation treatment, chemotherapy, hormonal therapy (tamoxifen or aromatase inhibitors) for patients with estrogen receptor-positive cancer cells, and monoclonal antibody therapy (trastuzumab) for individuals with HER2/neu expression.
Metastasis spreads to lymph nodes, lungs, liver, central nervous system (CNS), and bones.
Mucinous (colloid) refers to pools of extracellular mucin around tumor cell clusters with a gelatinous nature.
Among women, breast carcinoma ranks as the second leading cause of cancer-related mortality.
Clinical Symptoms
A painless, typically immobile, firm lump commonly located in the upper outer quadrant of the breast; skin and nipple retraction; detectable axillary lymph nodes; bone discomfort if metastasis to the bone occurs.
Infiltrating ductal cancer presents as a firm, fixed, fibrous mass.
Characterized by redness, swelling, heat, agony upon touch, and a skin texture like an orange peel.
Paget's disease presents as pruritic, scaly, and painless eczematous lesions on the nipple.
Medullary: Soft mass with a fleshy consistency.
Lab results indicate that a paraneoplastic condition causing the release of PTH-related peptide can result in hypercalcemia.
Imaging: Mammogram showing microcalcifications or spiculated, growing mass.
Therapies
Treatment options include surgery, radiation treatment, chemotherapy, hormonal therapy (tamoxifen or aromatase inhibitors) for patients with estrogen receptor-positive cancer cells, and monoclonal antibody therapy (trastuzumab) for individuals with HER2/neu expression.
Metastasis can spread to lymph nodes, lungs, liver, central nervous system (CNS), and bones.
