Hematology: week 4 Blueprint

Question 1

(Cancer cell properties), autocrine stimulation, tumor cell markers, telomerase-1

Answer 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

Question 2

Cancer cell properties, (autocrine stimulation), tumor cell markers, telomerase

Answer 2

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

Question 3

Cancer cell properties, autocrine stimulation, (tumor cell markers), telomerase

Answer 3

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.

Question 4

Cancer cell properties, autocrine stimulation, tumor cell markers, (telomerase)

Answer 4

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.

Question 5

What is Angiogenisis?

Answer 5

Growth of new vessels
AKA: neovascularization

In tumors: it feeds the tumor o2/nutrients

Question 6

Benign Vs Maligant

Growth: Slow
Well-defined capsule
Non-invasive
Well Differentiated
Low mitotic index
DOES NOT METs

Answer 6

malignant

Rapid growth
no capsule
invasive
poorly differentiated: Anaplasia
High mitotic index
can metastasize

Question 7

Apoptosis (normal cell death)

Answer 7

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

Question 8

Cancer Invasion and Metastasis
Epithelial-mesenchymal
transition (EMT) produces
which result?

1. Increased resistance to
   apoptosis
2. Adherence to basement
   membranes
3. Decreased migratory
   capacity
4. Promotion of
   angiogenesis

Answer 8

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.

• 2. Carcinomas undergo a process of epithelial- mesenchymal transition (EMT) during which
     many epithelial-like characteristics are lost (e.g., polarity, adhesion to basement membrane).
• 3. 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.
• 4. 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

Question 9

Can Cancer cells perform glycolysis?

Answer 9

YES!:
Reverse Warburg effect: ca cells generate large amts of ATP

Question 10

Cancer complications

Answer 10

(acute treatment caused) Nausea, vomiting, diarrhea, hypersensitivity reactions

Febrile neutropenia

Cachexia (wasting)

Tumor lysis

Paraneoplastic Syndrome

Question 11

Malignant Tumors & Metastasis

Metastasis

Answer 11

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

Question 12

Malignant Tumors & Metastasis-2
Invasion

Answer 12

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.

Question 13

Risk Factors for Cancers

Answer 13

*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.

Question 14

Environmental factors of cancers:
Tobacco, Diet, Xenobiotic chemicals, Obesity & Etoh

Answer 14

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.

Question 15

Other environmental risks for cancer: 2
Air pollution (in/out), Ionizing radiation, UV rad, and electromagnetic rad.

Answer 15

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.

Question 16

other Enviornmental Causes of Cancer-3
**Infection, STD, occupational

Answer 16

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.

Question 17

Viruses associated with human Cancer?

Answer 17

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

Question 18

Tumor Markers-tell me about them (lecture)

Answer 18

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

Question 19

What is paraneoplastic syndrome? (more)

Answer 19

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,

Question 20

Positive risk factor for cancer

Answer 20

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.

Question 21

Colon cancer

Answer 21

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,

Question 22

Breast cancer- Mutation in the TP53 or APC gene

Answer 22

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.

Question 23

Naming cancers *Benign vs Malignant

Answer 23

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.

Question 24

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

Answer 24

ANS: 2
* Benign tumors are usually
encapsulated and do not invade
the capsule that surrounds them.

• 1. Benign tumors are typically well
     differentiated; malignant cancer is
     poorly differentiated.
• 3. Benign tumors maintain some
     normal tissue structure; malignant
     cancer develops anaplasia.
• 4. Benign tumors do not spread or metastasize to distant locations;
     malignant cancer metastasizes.

Question 25

Naming cancers Benign vs *Malignant

Answer 25

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

Question 26

Grading vs Staging of cancers

Answer 26

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.

Question 27

Ensure you know how to APPLY the TNMO system

Answer 27

0-4 (higher the # =more advanced/spread

T=Primary tumor size & Spread

N= Describes spread to lymph nodes

M= degree of metastasis

Question 28

A tumor that has
advanced to regional
structures is in which
Stage?
1. Stage 1
2. Stage 2
3. Stage 3
4. Stage 4

Answer 28

• ANS: 3
• A tumor that has advanced
  to regional structures is in
  Stage 3.

1. A tumor in Stage 1 is
   confined to its organ of origin.
2. A tumor in Stage 2 is locally
   invasive.
3. A tumor in Stage 4 has
   spread to distant site

Question 29

Chromosome instability may result in the overexpression of
1.tumor-suppressor
genes.
2.heterozygosity.
3.oncogenes.
4.point mutations

Answer 29

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

Question 30

Hallmarks of Cancer: (lecture)

Answer 30

1. Self sufficiency in growth signals/overexpressed
2. Evasion of cell death
3. Genonme Instability:
   evade host immune sys w/ both innate & adaptive
4. Limitless replication potential
5. Angiogenesis

Question 31

Diagnosing anemia, cellular compensation of anemia & Anemia of CKD

Answer 31

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.

Question 32

Anemia of Chronic Ds

Answer 32

Question 33

Pancytopenia

Answer 33

Reduction or absence of all three blood cell types (anemia, neutropenia, and thrombocytopenia).

Seen in aplastic anemia and leukemia

Question 34

Granulocytosis

Answer 34

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

Question 35

Sequela of cigarette smoking

Answer 35

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.

Question 36

What is Oncogenesis?

Answer 36

when cancer tissues grow, genetic mechanism where normal cell transforms into a cancerous cell
oncogenes-hypergrowth
tumor suppressor genes
overexpressed–preventing apoptosis

Question 37

Carcinoma in situ (CIS)

Answer 37

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.