Hematology: week 4 Blueprint Flashcards
(Cancer cell properties), autocrine stimulation, tumor cell markers, telomerase-1
Cancer Cell Properties:
Avoid immune destruction
Enable replicative immortality
Activate invasion and metastasis
Induce angiogenesis
Resist cell death
Deregulate cellular energetics
Sustain proliferative signaling
Evade growth suppressors
Possess genome instability and mutation
Mediate a tumor-associated inflammatory response
Cancer cell properties, (autocrine stimulation), tumor cell markers, telomerase
The ability of cancer cells to produce and to respond to their own growth factors.
All cells need signals to tell them what to do: do I grow, duplicate, stop growing. Cancer cells do not need growth signals. Cancer cells ignore the normal inhibitory signals to tell it to stop growing. Invading cell death, invasion of cell death, they prevent the cells of apoptosis.
Activate special proteins called transcription factors inside the cell nucleus. It facilitates turning the gene on.
Secretion of growth factors (autocrine stimulation)
Increase of growth factor receptors
Mutation of the signal from cell surface receptor in the “on” position
Mutation in the Ras intracellular signaling protein
Inactivation of retinoblastoma protein (Rb) tumor suppressor
Activation of protein kinases that drive the cell cycle
Mutation in the TP53 gene (tumor-suppressor gene)
TP53 gene produces protein 53 it is able when the cell is distress to knock into arrest or triggers apoptosis, if the damage is severe enough. It is activated by the Rb gene which is second way it can be inhibited.
Suppression of normal apoptosis
Lung, Breast and colon cancer
Cancer cell properties, autocrine stimulation, (tumor cell markers), telomerase
Tumor Cell Markers: substances produced by benign or malignant cells. Found on or in a tumor cell, in the blood, in the spinal fluid, or in urine. (Hormones, enzymes, genes, antigens, antibodies). If a tumor marker has biologic activity, symptoms will be expressed and paraneoplastic syndrome occurs.
These markers are used to:
Screen and identify individuals at high risk for cancer
Diagnose specific types of tumors
Follow the clinical course of cancer
Liver and germ cell tumors
Secrete a protein known as alpha fetoprotein (AFP) into the blood. Liked to hepatic carcinomas
CEA: cancer of the stomach
Prostate tumors
Secrete prostate-specific antigen (PSA) into the blood.
PSA has a low specificity and low sensitivity; best way would be to remove the cancer and biopsy
If a tumor marker, itself, has biologic activity:
Symptoms are expressed.
A phenomenon known as a paraneoplastic syndrome occurs.
Tumor markers are used to
-screen and identify individuals at high risk for cancer.
-diagnose specific types of tumors.
-follow the clinical course of cancer.
Cancer cell properties, autocrine stimulation, tumor cell markers, (telomerase)
also called terminal transferase, is a ribonucleoprotein that adds a species-dependent telomere repeat sequence to the 3’ end of telomeres. A telomere is a region of repetitive sequences at each end of the chromosomes of most eukaryotes.
What does a telomerase do?
Maintain telomere length
Affects DNA replication
Affects cellular apoptosis
Affects tumorigenesis
Affects resistance to therapy of cancer cells
Telomeres: Are protective caps on each chromosome that are held in place by a telomerase.
Telomeres become smaller and smaller with each cell division. Then apoptosis is triggered when it can not divide anymore and cell death occurs.
In tumors, they provide their own telomeres or telomerase: INDEFINITE DIVISION/IMMORTALITY. 85-95% of cancers provide their own telomerase. New cancer growth is repeated.
Cancer cells can activate telomeres, leading to continued division.
Cancer stem cells are a subpopulation of tumor cells that have replication immortality. They arise from tissue resident stem cells or develop from transformed differentiated cells.
What is Angiogenisis?
Growth of new vessels
AKA: neovascularization
In tumors: it feeds the tumor o2/nutrients
Benign Vs Maligant
Growth: Slow
Well-defined capsule
Non-invasive
Well Differentiated
Low mitotic index
DOES NOT METs
malignant
Rapid growth
no capsule
invasive
poorly differentiated: Anaplasia
High mitotic index
can metastasize
Apoptosis (normal cell death)
The loss of apoptotic control allows cancer cells to survive longer and gives more time for the accumulation of mutations which can increase invasiveness during tumor progression, stimulate angiogenesis, deregulate cell proliferation and interfere with differentiation
Cancer Invasion and Metastasis
Epithelial-mesenchymal
transition (EMT) produces
which result?
- Increased resistance to
apoptosis - Adherence to basement
membranes - Decreased migratory
capacity - Promotion of
angiogenesis
ANS: 1
* Carcinomas undergo a process of epithelial- mesenchymal transition (EMT) during which many epithelial-like characteristics are lost (e.g., polarity, adhesion to basement membrane) resulting in increased migratory capacity and increased resistance to apoptosis.
- Carcinomas undergo a process of epithelial- mesenchymal transition (EMT) during which
many epithelial-like characteristics are lost (e.g., polarity, adhesion to basement membrane).
- Carcinomas undergo a process of epithelial- mesenchymal transition (EMT) during which
- Carcinomas undergo a process of epithelial-mesenchymal transition (EMT) during which
many epithelial-like characteristics are lost (e.g., polarity, adhesion to basement membrane) resulting in increased migratory capacity.
- Carcinomas undergo a process of epithelial-mesenchymal transition (EMT) during which
- TAMs secrete cellular growth factors (for example TGF-ß and fibroblast growth factor
[FGF-2]) that favor tumor cell proliferation, angiogenesis, and tissue remodeling, similar to
their activities in wound healing
- TAMs secrete cellular growth factors (for example TGF-ß and fibroblast growth factor
Can Cancer cells perform glycolysis?
YES!:
Reverse Warburg effect: ca cells generate large amts of ATP
Cancer complications
(acute treatment caused) Nausea, vomiting, diarrhea, hypersensitivity reactions
Febrile neutropenia
Cachexia (wasting)
Tumor lysis
Paraneoplastic Syndrome
Malignant Tumors & Metastasis
Metastasis
Metastasis: Is the spread of cancer cells from the site of the original tumor to distant tissues and organs through the body. It is the main cause of death from cancer. Spreading to different sites.
Key steps of metastasis:
Invasion
Intravasation (movement of cancer cells through the lumen of the vasculature)
Circulation
Extravasation
Colonization
Is a complex process that requires cells to have many new abilities.
Spread
Survive
Proliferate in distant locations
Destination must be receptive to growth of cancer
Malignant Tumors & Metastasis-2
Invasion
Invasion: Local spread into local or surrounding tissue
Is a prerequisite for metastasis and the first step in the metastatic process.
Cancer often spreads first to regional lymph nodes through the lymphatic system and then to distant organs through the bloodstream.
Invasion then requires that the cancer attach to specific receptors and survive in the specific environment.
Invading cancer cells require a permissive environment before metastasis this environment process involves secretory factors and extracellular vesicles that cause vascular leakage, ECM remodeling, and immunosuppression in the secondary sites, thus promoting the ability of cancer cells to successfully establish metastasis.
Cancer cells secrete protease.
Proteases digest the extracellular matrix and basement membranes.
Create pathways through which cells can move.
Metastatic cells must be able to withstand the physiologic stresses of travel in the blood and lymphatic circulation.
Metastatic cells must then survive in a new environment.
Liver and lung are great sites for metastatic cancer because the cancer cell will embed in the first capillary bed which they encounter which is after lymphatic spread or hematogenous spread which is the liver or the lung.
Risk Factors for Cancers
*Lifestyle choices, such as smoking, alcohol intake, and diet
*Obesity of lack of physical exercise
*Certain mold, bacterial, and viral infections, parasites, and predisposing sexual practices
*Chronic inflammatory diseases: (GI, pancr, thyroid, prostate, bladder, Pleura, skin)
(UC, HEP B/C, H. pylori
*Environmental exposure (sunlight, natural and medical ionizing radiation, non-ionizing radiation; and/or air, water, and soil carcinogens, or those in household, pharmaceutical and recreational drugs, personal care products.
*Occupational exposures to chemical and physical carcinogens
*Certain prescribed drugs and other hormones, and illicit medications
*Socioeconomic, racial, geographic, and ethnic factors that affect exposures, risk, and detection and treatment.
Environmental factors of cancers:
Tobacco, Diet, Xenobiotic chemicals, Obesity & Etoh
Environmental–Lifestyle Factors
Tobacco use -MC
* Is linked to cancers of the lung, mouth, lips, nasal cavity and sinuses, larynx, pharynx, esophagus,
pancreas, kidney, uterus, cervix, colon and rectum, liver, and acute leukemia.
* Secondhand smoke: Environmental tobacco smoke (ETS) increases the risk for lung cancer.
Diet
* Nutrigenomics: Is the study of nutrition on the phenotypic variability of individuals, based on genomic differences.
* Primary dietary potential donors of DNA methylation include:
* Folate, choline, B vitamins.
* ex link between a compound called polyphenols in dark chocolate and cancer. These polyphenols have been shown to cause a change in gene expression and potentially decrease one’s risk of free radical damage, which can lead to cancer.
* Dietary factors
* Altered micro-ribonucleic acid (miRNA): Predisposes an individual to cancer.
* Suppress cancer stem cell renewal: Decreases the risk of cancer.
- Consuming kiwi fruits, cooked carrots, or supplemental coenzyme Q10 improves DNA repair.
* Decreases the chance of cancer. - Xenobiotic chemicals
* Toxic, mutagenic, and carcinogenic chemicals in food
* Activated by phase I activation enzymes
* Primary substance: Cytochrome P-450 family
* Defense mechanisms
* Phase II detoxification enzymes (liver) and antioxidants
* Glutathione-S-transferases (GSTs): Enzyme housekeepers that metabolize environmental carcinogens and reactive oxygen species (ROS)
* If GSTs are lacking, then the risk for cancer is higher
* Diets high in red meats and processed meats: Colorectal cancer
Obesity
* Is associated with endometrial, colorectal, kidney, esophageal, breast (postmenopausal), pancreatic,
and several other cancers.
* Correlates with the body mass index (BMI) .
* Energy expenditure involves resting metabolic rate, thermic food effects, and physical activity.
* Causes a poorer outcome for some cancers.
Increases insulin resistance–producing hyperinsulinemia.
* Insulin promotes insulin-like growth factor 1.
* Adipose tissue secretes adipokines.
* Circadian disruptions may affect cancer growth.
Alcohol consumption
* Is classified as a human carcinogen.
* Increases the risk for oral cavity, pharynx, larynx, esophageal, liver, colorectal, and breast cancers.
* A combination of cigarette smoking and alcohol consumption increases a person’s risk for
malignant tumors.
Other environmental risks for cancer: 2
Air pollution (in/out), Ionizing radiation, UV rad, and electromagnetic rad.
Air pollution
* Air pollution is linked to lung cancer.
* Outdoor pollution: Smog and particle pollution
* Smog: Increases daily mortality.
* Particle pollution: Causes pulmonary inflammation, oxidative stress and oxidation of DNA, nonfatal heart attacks, irregular heartbeat, and decreased lung function.
- Indoor pollution
* Is considered worse than outdoor pollution.
* Cigarette smoke, radon: Lung cancer
Ionizing radiation
* Is emitted from x-ray machines, radioisotopes, and other radioactive sources.
* Is associated with acute leukemias; increased frequencies of thyroid and breast carcinomas; lung,
stomach, colon, esophageal, and urinary tract cancers, and multiple myeloma.
* Enters cells and randomly deposits energy in tissues.
* Oncogene activation
* Tumor-suppressor genes deactivation
* Chromosomal aberrations and DNA damage
* Cell transformation
* Nontargeted/bystander effects
Effects
* Damage to organs with high proliferative cells (skin, GI systems)
* Alters tumor microenvironment (immune system cells)
* Long-term risk of developing other cancers (leukemia)/diseases
Ultraviolet radiation
* Causes basal cell carcinoma, squamous cell carcinoma, and melanoma.
* Skin cancer is the most commonly diagnosed malignancy in US.
* Principal source is sunlight.
* Ultraviolet A (UVA) and ultraviolet B (UVB)
Electromagnetic radiation
* Is energy in the form of transverse magnetic and electric waves.
* Microwaves, radar, mobile and cellular telephones, mobile telephone base stations, appliances, power
frequency radiation associated with electricity and radio waves, fluorescent lights, computers, and
other electric equipment
* Question: Is electromagnetic radiation carcinogenic, especially for brain tumors (gliomas)?
* Conflicting research exists.
other Enviornmental Causes of Cancer-3
**Infection, STD, occupational
Infection: Is an important contributor to cancer.
* Human papillomavirus (HPV): Cervical cancer
* Hepatitis B and C together: Liver cancer
* Helicobacter pylori: Stomach cancers
* Epstein-Barr virus (EBV): Cancers of the nasopharynx and stomach, Hodgkin disease, and non-Hodgkin lymphoma
* Human herpes virus type 8: Kaposi sarcoma
* Human T-cell lymphotropic virus type 1: Leukemia and lymphoma
Sexual and reproductive behaviors and HPVs
* HPV is the most common sexually transmitted virus.
* HPV types 16 and 18 cause the majority of cancers.
* Are associated with cervical and anal cancers.
* Cause almost one-half of vaginal, vulvar, and penile cancers.
* Are recently associated with cancers of the oropharynx (soft palate, base of the tongue, tonsils).
* HPV infects epithelial cells.
* Mutations lead to cancer.
Chemicals and occupational hazards
- Substantial number of occupational carcinogenic agents exists. * Asbestos: Mesothelioma and lung cancer
* Dyes, rubber, paint, aromatic amines: Bladder cancer
* Explosives, rubber cement, and dyeing industries: Leukemia
* Heavy metals
* Diesel exhaust
- Many other chemicals and occupational hazards exist.
Viruses associated with human Cancer?
Human papillomavirus (HPV)
* Epstein-Barr virus (EBV)
* Kaposi sarcoma herpesvirus (KSHV or HHV8)
* Human T-cell lymphotropic virus type I (HTLV-1)
* Hepatitis B (HBV)
* Hepatitis C (HCV)
* Cervical cancer
* Hepatocellular carcinoma
Infection: Is an important contributor to cancer.
* Human papillomavirus (HPV): Cervical cancer
* Hepatitis B and C together: Liver cancer
* Helicobacter pylori: Stomach cancers
* Epstein-Barr virus (EBV): Cancers of the nasopharynx and stomach, Hodgkin disease, and
non-Hodgkin lymphoma
* Human herpes virus type 8: Kaposi sarcoma
* Human T-cell lymphotropic virus type 1: Leukemia and lymphoma
Tumor Markers-tell me about them (lecture)
substances produces by both malig & benign cells
-found: in/on tumor, in blood/spinal fluid or urine
ex: Hormones, enzymes, genes, antigens, and antibodies.
Liver/germ cell =alpha fetoprotein (AFP)
Prostate=prostate specific antigen (PSA)
If marker itself has biologic activity=
paraneoplastic syndrome
What is paraneoplastic syndrome? (more)
tumor marker w/ biologic activity
can affect every system
Paraneoplastic syndromes are a group of rare disorders that occur when the immune system has a reaction to a cancerous tumor (neoplasm)
ex: neuropathies, GBS, cushings
MC: Lung, liver, renal, leukemias, breast,
Positive risk factor for cancer
Physical activity
* Decreases the risk of cancer.
* Decreases insulin and insulin-like growth factors.
* Decreases obesity.
* Decreases inflammatory mediators.
* Decreases circulating sex/metabolic hormones
* Improves immune function.
* Reduces the risk for breast, colon, and endometrial cancers, independent of weight changes.
* After a cancer diagnosis, physical activity is associated with improved cancer-specific and overall survival with early-stage breast, prostate, and colorectal cancers.
Colon cancer
Those with ulcerative colitis for 10 years or more have up to a 30-fold increase in developing colon cancer.
Inherited gene mutations like APC (familial adenomatous polyposis), MLH1, MSH2, MSH6 (Lynch syndrome) significantly increase the risk. These account for around 5-10% of colon cancer cases (100/40)% risk per ds
mutations of the APC gene
Tobacco use
Poor diet
ionizing radiation
inflammation in the GI tract
infections: ie: H. Pylori,
diets high in red meat, animal fats, low fiber, fruits/veggies
etio: >50 years, personal/family hx, race (usually dx’d later in ds)
tx: surgical removal w/ wide margins, FOLFOX regimen for >Stg 3, neoadjuvant w/ MAB’s,
Breast cancer- Mutation in the TP53 or APC gene
In breast cancer, production of the human epidermal growth factor receptor 2 (HER2) is upregulated and is hyperresponsive to low levels of EGF. Some breast cancers are treated by inhibitors of HER2 and other ECR receptors that block this pathway.
Chromosome translocation
* Large changes in chromosome structure
* Piece of one chromosome is translocated to another chromosome.
Affiliated with b cells cancers and lymphomas (breast cancer: example)
Genomic Instability
Results from epigenetic silencing (modulation of gene).
Mutations in caretaker genes that protect genome and DNA repair increase genomic instability and risk of cancer
BRCA 1 and BRCA 2 (breast cancer risk) – lead to ovary, prostrate, pancreas and bile duct cancers
Alcohol consumption
* Is classified as a human carcinogen.
* Increases the risk for oral cavity, pharynx, larynx, esophageal, liver, colorectal, and breast cancers.
Mutation in the TP53 gene (tumor-suppressor gene) (lung, breast, & colon cancer)
Mutations of the APC gene have close to a 100% lifetime risk of colon cancer: Colectomy.
- Women with BRCA1/2 mutations have a significantly increased risk of breast and ovarian cancer: Prophylactic mastectomy or bilateral salpingo-oophorectomy or both.
Naming cancers *Benign vs Malignant
Benign tumors
Are named according to the tissues from which they arise and include the suffix, -oma. Might not be cancer but can cause harm based on where they are located. Could press against another organ and move the organ and cause issues.
EX: Lipoma: Fat, Leiomyoma: Smooth muscle
Osteoma: Oste equals bone; oma benign tumor if the tumor was to change it would become osteocaroma
Some exceptions to the rule with “omas” like lymphoma
Cancer refers to a malignant tumor and not used for benign growths such as lipomas or hypertrophy of an organ.
Benign tumors are usually encapsulated with connective tissue and contain well-differentiated cells. Do not invade beyond their capsule.
A nurse practitioner learns
that an individual has
benign tumors. What does
this mean?
The tumors:
1. are poorly differentiated.
2. are encapsulated.
3. may develop anaplasia.
4. may spread to a distant
location
ANS: 2
* Benign tumors are usually
encapsulated and do not invade
the capsule that surrounds them.
- Benign tumors are typically well
differentiated; malignant cancer is
poorly differentiated.
- Benign tumors are typically well
- Benign tumors maintain some
normal tissue structure; malignant
cancer develops anaplasia.
- Benign tumors maintain some
- Benign tumors do not spread or metastasize to distant locations;
malignant cancer metastasizes.
- Benign tumors do not spread or metastasize to distant locations;
Naming cancers Benign vs *Malignant
Malignant tumors: loss of differentiation and absence of normal tissue organization.
Hallmarks of cancer: Anaplasia: loss of cellular differentiation. They are also Pleomorphic: marked with variability of size and shape
Can be harmful by cutting off blood supply to other organs.
Malignant tumors will always be carcinomas; named to their tissues to where they arise.
Are named according to the tissues from which they arise.
Malignant epithelial tumors: Carcinomas
Adenocarcinoma: Ducts or glands
Malignant connective tissue tumors: Sarcomas
Cancers of lymphatic tissue: Lymphomas
Cancers of blood-forming cells: Leukemias
Most deadly characteristic is their ability to spread beyond the tissue of origin: metastasis.
Name is associated with cell type: example carcinomas: epithelial tissue, ductal or glandular structures: adenocarcinomas.
TWO MAIN CHARACTERISTICS: INVASION AND METASTISIS
Grading vs Staging of cancers
No set standard is used for measuring, staging and grading. They are both interpretations that reflect the condition of what happens and the condition of the patient.
Staging (1-4) refers to what has happened to the tumor, and grading refers to how bad the tumor has become. Zeros in TNM system are good, and the greater the numerical values the worse the prognosis usually is.
1: confined to organ
2. Locally invasive
3: has advanced to regional structures
4. Spread to distant sites
ex: Distant metastasis has no way of being evaluated, so it is represented by M0 = there is no way to evaluate this. For example, breast cancer may be represented by T3 N2 M0. T3 reflects a relatively large tumor that has spread to nearing lymph nodes, but not to other parts of the body- there is no metastasis.
ex: prostate cancer represented by T2 N0 M0. This involves a tumor that is located only in the prostate, has no signs of lymphatic spread or metastatic spread. The result is a good prognosis for the patient.
Ensure you know how to APPLY the TNMO system
0-4 (higher the # =more advanced/spread
T=Primary tumor size & Spread
N= Describes spread to lymph nodes
M= degree of metastasis
A tumor that has
advanced to regional
structures is in which
Stage?
1. Stage 1
2. Stage 2
3. Stage 3
4. Stage 4
- ANS: 3
- A tumor that has advanced
to regional structures is in
Stage 3.
- A tumor in Stage 1 is
confined to its organ of origin. - A tumor in Stage 2 is locally
invasive. - A tumor in Stage 4 has
spread to distant site
Chromosome instability may result in the overexpression of
1.tumor-suppressor
genes.
2.heterozygosity.
3.oncogenes.
4.point mutations
ANS: 3
Chromosome instability (often referred to as CIN) also
appears to be increased in malignant cells.
Chromosome instability results in a high rate of
chromosome loss, as well as loss of heterozygosity
and chromosome amplification. Each of these events
can accelerate the loss of tumor-suppressor genes
and the overexpression of oncogenes.
* 1. Chromosome instability results in a high rate of
chromosome loss, as well as loss (not
overexpression) of heterozygosity and
chromosome amplification. Each of these events
can accelerate the loss (not overexpression) of
tumor-suppressor genes and the overexpression
of oncogenes.
* 2. Chromosome instability results in a high rate of
chromosome loss, as well as loss of
heterozygosity and chromosome amplification.
* 4. A point mutation in the ras gene converts it from
a regulated proto-oncogene to an unregulated
oncogene, an accelerator of cellular proliferation
Hallmarks of Cancer: (lecture)
- Self sufficiency in growth signals/overexpressed
- Evasion of cell death
- Genonme Instability:
evade host immune sys w/ both innate & adaptive - Limitless replication potential
- Angiogenesis
Diagnosing anemia, cellular compensation of anemia & Anemia of CKD
Anemia: reduction in the total number of erythrocytes in the circulating blood or in the quality or quantity of
hemoglobin
- Impaired erythrocyte production
- Acute or chronic blood loss
- Increased erythrocyte destruction
- Combination of the above
Classifications
- Etiologic factor (cause)
- Size
- Identified by terms that end in “-cytic” (size)
- Hemoglobin content
- Identified by terms that end in “-chromic” (color)
- Microcytic hypochromic
- Disorders of hemoglobin synthesis (iron deficiency)
- Macrocytic
- Macrocytic anemias arise from abnormalities that hinder maturation of erythroid precursors in bone marrow.
- Normocytic-normochromic
- Shape of red blood cells help determine cause
Anisocytosis
- Red blood cells (RBCs) are present in various sizes.
Poikilocytosis
- RBCs are present in various shapes.
Clinical manifestations
- Reduced oxygen-carrying capacity: hypoxia
- Reduced oxygen levels in the blood: hypoxemia
- Dyspnea, palpitations, dizziness, fatigue, pallor
- Neurological and GI changes
Tx: Transfusions, dietary correction, and administration of supplemental vitamins or iron
* Correction of the underlying condition
When onset of anemia is severe/acute, initial compensatory mechanism is peripheral blood vessel constriction, which diverts blood flow to essential vital organs. Decreased blood flow detected by the kidneys activates the renin-angiotensin response, causing salt and water retention in an attempt to increase blood volume. Emergency so long-term compensatory mechanisms do not develop.
Anemia of Chronic Ds
Pancytopenia
Reduction or absence of all three blood cell types (anemia, neutropenia, and thrombocytopenia).
Seen in aplastic anemia and leukemia
Granulocytosis
An increase in granulocytes (neutrophils, eosinophils, or basophils) begins when store blood cells are released. Aka neutrophilia.
Is evident in the first stages of infection or inflammation
If the need for neutrophils increases beyond the supply, then immature neutrophils (and other leukocytes) are released into the blood.
*Premature release of immature leukocytes is termed a shift-to-the-left. Bands, immature neutrophils.
- Leukemoid reaction
Causes
- Prolonged severe infection
- Decreased production
- Reduced survival
- Abnormal neutrophil distribution and sequestration
Sequela of cigarette smoking
Tobacco use
* Cigarette smoking is carcinogenic and the most important risk factor for cancer.
* Is linked to cancers of the lung, mouth, lips, nasal cavity and sinuses, larynx, pharynx, esophagus,
pancreas, kidney, uterus, cervix, colon and rectum, liver, and acute leukemia.
* Secondhand smoke: Environmental tobacco smoke (ETS) increases the risk for lung cancer.
- A combination of cigarette smoking and alcohol consumption increases a person’s risk for malignant tumors.
What is Oncogenesis?
when cancer tissues grow, genetic mechanism where normal cell transforms into a cancerous cell
oncogenes-hypergrowth
tumor suppressor genes
overexpressed–preventing apoptosis
Carcinoma in situ (CIS)
Are preinvasive epithelial malignant tumors of glandular or squamous origin.
Have not broken through the basement membrane or invaded the surrounding stroma.
Are not malignant.
Three prognoses:
Can remain stable for a long time.
Can progress to invasive and metastatic cancers.
Can regress and disappear.
