Oncology

• Decisions for surgical prevention should be individualized, considering potential complications, lifestyle consequences, and other preventive options.
• The cell cycle is divided into four phases: S, G1, G2, and M.
• During the synthetic or S phase, the cell generates a single copy of its genetic material, whereas in the mitotic or M phase, the cellular components are partitioned between two daughter cells.
• Routine ongoing cancer screening is recommended for cancers of the thyroid, testicles, ovaries, lymph nodes, oral cavity, and skin, as well as health counseling about tobacco, sun exposure, diet and nutrition, risk actors, sexual practices, and environmental and occupational exposures.
• Surgical prevention is considered in high-risk settings like hereditary cancer syndromes (e.g., hereditary breast-ovarian cancer) and involves large ablative surgeries like bilateral risk-reducing mastectomy.
• The G1 and G2 phases represent gap phases during which the cells prepare themselves for completion of the S and M phases.
• Antimetabolites are cell-cycle specific agents that have their major activity in the S phase of the cell cycle.
• Tamoxifen in breast cancer reduces risk by half, especially in high-risk patients.
• There are six essential alterations in cell physiology that dictate malignant growth: self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evasion of apoptosis, potential or limitless replication, angiogenesis, and invasion and metastasis.
• Raloxifene is FDA-approved for breast cancer prevention, showing efficacy comparable to tamoxifen.
• Anticancer chemotherapy agents include alkylating agents, antitumor antibiotics, antimetabolites, and plant alkaloids.
• Breast self-examination involves inspecting and palpating the breasts.
• Celecoxib, a COX-2 inhibitor, is approved for reducing polyp burden in familial adenomatous polyposis (FAP) but has limitations.
• Cancer variants are somatic mutations that are present only in cancer cells and may result from exposure to environmental factors such as ultraviolet light, smoking, radiation, alcohol, or can be entirely random.
• Hereditary cancers are those where an individual carries a particular germline mutation in every cell, most of which are tumor-suppressor genes, and a few are oncogenes.
• Patients with mutations in the rb1 gene may present with Anisocoria, with impaired dilation.
• Factors suggesting the presence of a hereditary cancer include tumor development at a much younger age than usual, presence of bilateral disease, presence of multiple primary malignancies, and presentation of a cancer in the less affected sex.
• Genes associated with different well-known cancers include rb1 for Retinoblastoma, BRCA1 and BRCA2 for Hereditary Breast-Ovarian Syndrome, APC for Familial Adenomatous Polyposis, PTEN for Cowden, p53 for Li-Faumeni, and RET proto-oncogene for MEN-2.
• Clustering of the same cancer type in relatives and occurrence of cancer in association with other conditions such as mental retardation or pathognomonic skin lesions are also indicators of a hereditary cancer.
• Germline mutations are alterations in the DNA inherited from germ cells during conception, are passed from parents to offspring, and are usually not expressed in individuals carrying the mutation.
• Knudson’s “two hit” Hypothesis suggests that the “hit” may be a point mutation, chromosomal deletion referred to as allelic loss, or loss of heterozygosity.
• Somatic mutations include several classes of DNA changes such as substitution of one base by another, insertion or deletion of small and large segments of DNA, rearrangement of DNA, and copy number losses or gains.
• The rb1 gene, also known as the Retinoblastoma gene, is the first tumor suppressor to be cloned and its gene product, the Rb Protein, is a regulator of transcription that controls the cell cycle, differentiation and apoptosis in normal development.
• Prognostic markers are used to describe molecular markers that predict disease-free survival, giving information on prognosis or to supplement the projections on the clinical presentation of the cancer.
• Lung cancer screening involves low-dose CT (Chest) for current or former smokers aged 50 to 74 years in good health with at least a 30 pack-year history.
• Tumor markers are substances that can be detected in higher than normal amounts in the serum, urine, or tissues of patients with certain types of cancer, and can be used as prognostic or predictive markers.
• Colon cancer screening involves flexible sigmoidoscopy, guaiac-based fecal occult blood test, fecal immunochemical test, stool DNA, and double-contrast barium enema, starting at age 50 years, every 5 years.
• Cervical cancer screening involves Pap smear test and HPV DNA test, starting at age 21 years, every 3 years for women aged 21 to 29 years, and every 5 years for women aged 30 to 65 years.
• Endometrial cancer screening involves no testing at the time of menopause, but women at average risk should be informed about the risks and symptoms of endometrial cancer and strongly encouraged to report any unexpected bleeding or spotting to their physicians.
• Prostate cancer screening involves digital rectal exam and Prostate Specific Antigen, with men at average risk receiving screening information beginning at age 50 years and men in higher risk groups receiving screening information before age 50 years.
• Cancer screening for breast cancer involves mammography for women aged 40 to 54 years and biennial mammography for women aged 55 years or older or with a life expectancy of more than 10 years.
• Predictive markers are used in the context of predicting response to certain therapies.
• Definitive diagnosis of solid tumors involves biopsy (tissue diagnosis), which determines tumor histology and grade, assists in definitive therapeutic planning, and is an exception to cancers that are not easily accessible such as GLIOMA.
• The initiating events are usually genetic and occur as deletions of tumor-suppressor genes or amplification or mutation of oncogenes.
• Field effect refers to normal appearing cells that have an increased malignant potential.
• Gene Expression is a multistep process that starts with: Transcription of gene into mRNA followed by Translation into functional proteins.
• Malignant tumor formation requires mutations in at least four (4) or five (5) genes.
• Cancer is thought to be a disease of clonal progression as tumors arise from a single cell and accumulate mutations that confer on the tumor an increasingly aggressive behavior.
• Benign Tumor requires fewer changes.
• The neoplastic process is initiated by mutations in the adenomatous polyposis coli (APC) or b-catenin genes.