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Endometriosis Part 1-Cancer Cytogenetic-Lecture Handout, Exercises of Cancer Cytogenetics

Sree Chitra Tirunal Institute of Medical Sciences and Technology Cancer Cytogenetics

This lecture handout was designed and distributed by Prof. Akhilesh Kulkarni at Sree Chitra Thirunal Institute of Medical Sciences and Technology. This is part of Cancer Cytogenetic course. It includes: Endometriosis, Peritonial, Mesothelium, Endomaterial, Syclic, Metaplasia, Coelomic, Lungs, Embryonic, Pleura

Typology: Exercises

2011/2012

Uploaded on 08/01/2012

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I

N SUMMARY HST 071

E

NDOMETRIOSIS

E

NDOMETRIOSIS

• A

ttachment of endometrial cells to the peritonea l surface

• I

nvasion of these ce

l

ls into the mesothelium

• R

ecruitment of inflammatory cells

• A

ngiogenesis around the nascent implant

• E

ndometrial cellular proliferation

• M

onkeys are only animal (cyclic)

• N

o cases reported prior to puberty

• O

ften seen in teenage years

• S

hort cycle and longer f

l

ows have tw

• E

arly menarche

• D

elayed childbearing

• M

enstrual outflow obstruction

• I

mplantation (Sampson's theory)

ice the risk of endometriosis

• V

iable endometrial tissue is refluxed through the fallopian tubes during menstruation

• I

mplants on peritoneal surf

a

ce or pelvic organs

R

etrograde menstruation

• O

ccurs through the fallopian tubes

• R

efluxed endometrial cells are

v

iable

• R

efluxed endometrial cells are able to

a

dhere to peritoneum

C

oelomic Metaplasia

• O

vary & Mullerian ducts derive from coelomic mesotheli

u

m

• G

erminal epithelium attempts to recapitulate endometrium

• O

nly explains ovarian endometriosis

• P

eritoneal mesothelium is

t

otipotential

• D

evelops from metaplasia of cells that line the pelvic peritoneum

• I

nfectious, hormonal, or other inductive stimuli may r

e

sult in metaplasia

D

issemination

• D

isseminated tissue can cause metaplasia

• I

njection into ear vein of rabbit causes endometriosis of lungs

• L

aparotomy scar

• E

pisiotomies

• C

esarean sections

• T

ransplantation confirmed in animal experiments

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IN SUMMARY

HST 07 1

ENDOMETRIOSIS

Attachment of endometrial cells to the peritoneal surface
Invasion of these cells into the mesothelium
Recruitment of inflammatory cells
Angiogenesis around the nascent implant
Endometrial cellular proliferation
Monkeys are only animal (cyclic)
No cases reported prior to puberty
Often seen in teenage years
Short cycle and longer flows have tw
Early menarche
Delayed childbearing
Menstrual outflow obstruction
Implantation (Sampson's theory) ice the risk of endometriosis
Viable endometrial tissue is refluxed through the fallopian tubes during menstruation
Implants on peritoneal surface or pelvic organs Retrograde menstruation
Occurs through the fallopian tubes
Refluxed endometrial cells are viable
Refluxed endometrial cells are able to adhere to peritoneum Coelomic Metaplasia
Ovary & Mullerian ducts derive from coelomic mesothelium
Germinal epithelium attempts to recapitulate endometrium
Only explains ovarian endometriosis
Peritoneal mesothelium is totipotential
Develops from metaplasia of cells that line the pelvic peritoneum
Infectious, hormonal, or other inductive stimuli may result in metaplasia Dissemination
Disseminated tissue can cause metaplasia
Injection into ear vein of rabbit causes endometriosis of lungs
Laparotomy scar
Episiotomies
Cesarean sections
Transplantation confirmed in animal experiments

ENDOMETRIOSIS

Embryonic rest theory

Cell rests of Mullerian origin
Lymphatic and hematogenous dissemination of endometrial cells
Evidence suggests that endometrial cells can metastasize
Pleura, umbilicus, retroperitoneal space, lower extremity, vagina, and cervix - are anatomically possible
Endometrial tissue in uterine veins in women with adenomyosis
Induced pulmonary endometriosis by injecting endometrial tissue intravenously in rabbits
Lymph node endometriosis was found to be present in 6.7% autopsies Found In
Bone
Muscle
Brain
Nerve
Lung parenchyma
Vertebral space
Extremities Genetics
Much more common in patients with a FH
Maternal inheritance pattern
7% in first degree relatives
More severe in women with a + first degree re
6/8 monozygotic twins had endometriosis
3.8% of non-monozygous sisters
Polygenic/multifactorial
No HLA system seems involved
Perhaps different diseases Adherence lative
Endometrial fragments obtained in either phase of the cycle – adhere to the epithelial side of the amnion but only at locations where the amniotic epithelium was damaged or absent
Cultured peritoneal explants adhered to peritoneal explants only at locations where the mesothelium was absent or damaged and the basement membrane was exposed
Intact mesothelium constitutes a defense barrier
Occasionally there is attachment to intact mesothelium Integrins
Intracellular adhesion molecule- 1
Vascular cell adhesion molecule- 1
Integrin-blocking antibodies do not interfere with endometrial stromal or epithelial cell adherence to mesothelium Hyaluronic Acid
Peritoneal mesothelium produces hyaluronic acid
Hyaluronic acid is expressed along the cell membrane and contributes to the pericellular matrix
Major component of the extracellular matrix ground substance
CD44 is the principal receptor for hyaluronic acid
Involved in binding of gastric cancer and ovarian cancer cells to mesothelium
Endometrial stromal end epithelial cells express CD
Hyaluronidase pretreatment of mesothelial cells decreases the binding of endometrial stromal and epithelial cells to mesothelium

ENDOMETRIOSIS

Contributes to pain and infertility

Cytokines
Prostaglandins
Dyspareunia
Chronic pelvic pain
Inflammation --> Infertility
adhesion formation
scarring
disrupt fallopian tube patency
impair folliculogenesis
fertilization
embryo implantation Hormonal Dependence
Endometriosis is an estrogen-dependent disorder
Aberrant estrogen synthesis and metabolism –
Aromatase catalyzes the synthesis of estrone and estradiol testosterone, respectively
Expressed by many human cell types
Ovarian granulosa cells
Placental syncytiotrophoblasts
Adipose cells
Skin fibroblasts from androstenedione and
Estrogen produced by aromatase activity in the cytoplasm of leiomyoma smooth muscle cells or endometriotic stromal cells
Disease-free endometrium and myometrium lack aromatase expression Aromatase
Cultured stromal cells derived from endometriotic implants and incubated with a CAMP analog display extraordinarily high levels of aromatase
Growth factors, cytokines - possible inducers of aromatase
Prostaglandin E2 was identified as the most potent inducer
Estrogen - up-regulates prostaglandin E2 formation
Stimulates cyclo-oxygenase type 2 enzyme in endometrial stromal cells
Positive feedback loop for continuous local estrogen and prostaglandin E2 production
Possible genetic defect in aromatase expression in endo
Androstenedione of adrenal and ovarian origins – premenopausal women
Adrenal androstenedione in postmenopausal women
Estrone - weakly estrogenic
Must be converted to estradiol
17 α-hydroxysteroid dehydrogenase (17α-HSD) type 1 is expressed in endometriosis
In contrast 17α-HSD type 2 inactivates estradiol by catalyzing its conversion to estrone in eutopic endometrial glandular cells during the luteal phase
Progesterone induces the activity of 17α-HSD
Inactivation of estradiol to estrone one of the anti-estrogenic properties of progesterone
17 α-HSD type 2 is absent from endometriotic glandular cells

Endometriosis Part 1-Cancer Cytogenetic-Lecture Handout, Exercises of Cancer Cytogenetics

Related documents

Partial preview of the text

Download Endometriosis Part 1-Cancer Cytogenetic-Lecture Handout and more Exercises Cancer Cytogenetics in PDF only on Docsity!

IN SUMMARY

HST 07 1

ENDOMETRIOSIS

ENDOMETRIOSIS

ENDOMETRIOSIS

ENDOMETRIOSIS

ENDOMETRIOSIS

FUDAMENTAL QUESTIONS

1. What are the three theories of the development of endometriosis?

2. Where is endometriosis most commonly found?

3. What clinical impact does endometriosis have on the woman?

4. What treatment modalities are available for endometriosis?

5. Other than steroid hormones, what causes endometriosis to grow and

proliferate?

6. Discuss in some detail, the steroidal environment that alters endometriotic

development?

7. Describe the histology of endometriosis?