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Examination of irradiated neuroblastoma and neuroepithelial cell lines for the interrelationship between cell survival, micronucleation, apoptosis and DNA repairAkudugu, John Mbabuni 12 1900 (has links)
Thesis (Ph.D.)--Stellenbosch University, 2000. / ENGLISH ABSTRACT:
Predictive assays are of key importance in clinical radiotherapy, chemotherapy
and toxicology. Prior to exposing malignant tissues to irradiation or drugs in
the clinic, a good understanding of the damage response to the cytotoxic agent
is required. Such information is necessary for effective planning and treatment.
Regrettably however the methods which detect DNA damage, namely
micronucleus, apoptosis and DNA repair assays do not rank cells according to
their intrinsic survival response to cytotoxic agents. The application of
predictive assays based on micronuclei and apoptosis in the clinic therefore
remains unreliable. Using a panel of 7 neuroblastoma and 6 neuroepithelial
cell lines, it is shown that damage assays also do not rank cell lines according
to cell survival. However, radiosensitivity can be reconstructed from
micronuclei formation and apoptosis, and a new parameter, cell death due to
small deletions, chromosome aberrations and misrepair. The interrelationships
between radiation-induced micronuclei, apoptosis and repair is complex and
varies between cell lines. Micronuclei formation and apoptosis are
exponentially interrelated. This suggests that these cell inactivation pathways
are strongly correlated. Evidence exists to show that the expression of
apoptosis and micronuclei is influenced by the extent of DNA double-strand
break repair within the first 2 hours after irradiation. Cell lines which repair
more damage in the first 2 hours express more micronuclei and less apoptosis.
Micronuclei formation and apoptosis and are not significantly correlated with
the 20 hours slow repair component. There is however a strong correlation between 20 hours of repair and radiosensitivity, with the more radioresistant
cell lines being more repair proficient. This suggests that the 2 hours (fast)
DNA repair component is more error prone, and that cells lines repairing more
damage late after irradiation tend to show better survival. In conclusion,
micronuclei formation, apoptosis and DNA repair are strictly cell type specific
and are not suitable for predicting radiosensitivity in terms of cell survival.
However, these assays are very useful for studies on the influences of dose
modifying agents i.e. oxygen tension, radiation modality, pH, cytotoxic
sensitisers and radiation protectors which alter cellular responses and provide
insight into damage mechanisms. / AFRIKAANSE OPSOMMING: Toetse wat kliniese gevolge kan voorspel is van uiterse beking in
stralingsterapie, chemoterapie en toksikologie. Voordat kwaadaardige
weefsels aan bestraling of chemise middels blootgestel can word in die kliniek,
moet daar 'n goeie begrip van die skade weerstand wees van die selgiftige
middel. Hierdie inligting is noodsaaklik vir effektiewe beplanning en
behandeling. Ongelukkig stem die metodes wat ONS skade, apoptose en
ONS hersteltoetse, nie ooreen met die selle se inherente straling sensitiwiteit
nie. Die aanwending van voorspelbare toetse gebaseer op mikrokerne en
apoptose in die kliniek bly dus onbetroubaar. Deur gebruik te maak van 'n
paneel van 13 neurologiese sellyne, is daar bewys dat ONS skade toetse nie
sellyne rangskik volgens seloorlewing nie. Radiosensitiwiteit kan herbou word
deur 'n neiging om mikrokerne te vorm, apoptose, en sel sterftes weens klein
vermiste ONS volgordes, chromosoom aberrasies en verkeerd herstelde ONS.
Die verhouding tussen straling-geïnduseerde mikrokerne, apoptose en selgenees
is kompleks en varieer tussen sellyne. Die ontstaan van mikrokerne
en apoptose is eksponensiel verbind. Dit dui aan dat hierdie
seltraagheidsbane streng gekorreleer word. Daar is bewys dat die uitdrukking
van apoptose en mikrokerne deur die mate van herstel van die ONS
dubbelstring-breuke binne die eerste 2 ure na bestraling beïnvloed is. Daar is
gevind dat sellyne wat meer skade herstel binne die eerste 2 ure meer
mikrokerne en minder apoptose toon. Die ontstaan van mikrokerne en apoptose is nie betekenisvol gekorreleer met die 20-uur stadige herstel
komponent nie. Daar is inderdaad 'n sterk korrelasie tussen die 20-uur herstel
komponent en radiosensitiwiteit, en die meer radioweerstandbiedende sellyne
net In hoër herstel bekwaamheid. Dit laat mens dink dat die 2 uur (vinnige)
DNS herstel komponent meer geneig is om foutief te wees, en dat sellyne wat
meer skade, laat na bestraling herstel, beter oorlewing toon. Ten slotte, die
ontstaan van mikrokerne, apoptose en DNS herstel is strenggesproke seltipe
spesifiek en is nie toepaslik om radiosensitiviteit, in terme van seloorlewing, te
voorspel nie. Hierdie toetse is nuttig vir studies waar die invloed van
dosismodifiseringsagente, soos suurstof-spanning, straling-tipe, pH,
sitotoksieke sensiteerders en stralingsbeskermers, wat sellulêre gevoeligheid
verander en insig gee tot skade meganismes.
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The influence of pentoxifylline on damage responses in tumour cellsTheron, Catherina S 04 1900 (has links)
Thesis (PhD)--Stellenbosch University, 2000. / ENGLISH ABSTRACT: Pentoxifylline enhances the toxicity of radiation and has emerged as an
effective modulator of the radiation response of tumour cells. The molecular
mechanisms involved in the enhancement of radiotoxicity by pentoxifylline
have not yet been elucidated. Cell cycle blocks, DNA repair and programmed
cell death (apoptosis) are all pert of the cellular response to DNA damage and
as such must be considered as targets of the drug. In this study, the influence
of pentoxifylline on radiosensitisation, G2 block abrogation, DNA repair
inhibition and the induction of apoptosis have been investigated in 8e11 and
MeWo melanoma and 4197 and 4451 squamous cell carcinoma (SCC) cell
lines. The influence of pentoxifylline on radiation-induced apoptosis in Jurkat
J5 T-lymphocytic leukemia cells has also been assessed. Hela cervical
carcinoma cells were used to investigate the molecular events involved in the
abrogation of the G2 block by pentoxifylline. It is shown that pentoxifylline
preferentially sensitises the TP53 mutant MeWo and 4451 cell lines and
enhances radiotoxicity by factors of up to 14.5. In the MeWo melanoma, but
not in the 4451 SCC cell line, radiosensitisation is accompanied by inhibition
of DNA repair. No significant enhancement of radiation-induced apoptosis
was observed in MeWo melanoma and 4451 SCC cells. However, Jurkat J5
cells showed an increase in apoptosis after irradiation in the presence of the
drug. In irradiated Hela cervical carcinoma cells, pentoxifylline affects the
expression of the two components of the mitosis promoting factor (MPF),
namely cyclin 81 and p34cdC2, and rapidly restores cyclin 81/p34cdC2 ratios to
control levels. Analysis of cyclin 81 expression in whole cells and isolated nuclei furthermore reveals an influence of the drug on the subcellular
translocation of the MPF.
It is concluded that G2 block abrogation is not the only mechanism involved in
the radiosensitisation of tumour cells by pentoxifylline, but that DNA repair
inhibition plays a role in certain cell types. Although pentoxifylline induces
apoptosis in Jurkat J5 thymocytes, radiation-induced apoptosis plays no role
in the radiosensitisation of the two TP53 mutant melanoma and sec cell
lines. Abrogation of the G2 block by pentoxifylline, which sensitises tumour
cells to a second irradiation or chemotherapeutic challenge, involves a
modulation of the levels of cyclin 81 and p34cdC2, and the subcellular location
of the MPF. These results are of utmost importance for the clinical potential of
pentoxifylline as a dose modifier in cancer therapy. / AFRIKAANSE OPSOMMING: Pentoxifylline verhoog die toksisiteit van bestraling en het dus na vore getree
as 'n effektiewe modulator van die sellulêre stralingsrespons in kankerselle.
Die molekulêre meganismes betrokke by die verhoging van stralingstoksisiteit
deur pentoxifylline is egter nog nie duidelik nie. Blokkering van die
selsiklus, die herstel van ONS skade en geprogrammeerde seldood
(apoptose) vorm almal deel van die sellulêre respons ná bestraling en word as
sulks beskou as potensiële teikens van die middel. In hierdie studie is die
invloed van pentoxifylline op stralings-sensitiwiteit, G2 blok verwydering, die
vertraging van ONS herstel en die indusering van apoptose ondersoek in die
Be11 en MeWo melanoom en 4197 en 4451 plaveisel-sel karsinoom sellyne.
Die invloed van pentoxifylline op stralings-geïnduseerde apoptose in Jurkat J5
T-limfosiete is ook bestudeer. Hela servikale karsinoom selle is gebruik om
die molekulêre gebeurtenisse rondom die verwydering van die G2 blok deur
pentoxifylline te ondersoek. Dit word aangetoon dat pentoxifylline by voorkeur
die radiosensitiwiteit van die TP53 mutante MeWo en 4451 sellyne verhoog,
en stralingstoksisiteits verhogingsfaktore van tot 14.5 genereer. Hierdie effek
gaan gepaard met die vertraging van ONS herstel in die MeWo melanoom,
maar nie in die 4451 plaveisel-sel karsinoom sellyn nie. Die meting van
apoptose toon geen noemenswaardige verhoging van stralings-geïnduseerde
apoptose in MeWo melanoom óf in 4451 plaveisel-sel karsinoom selle nie.
Jurkat J5 T-limfosiete toon egter wel 'n verhoging in apoptose wanneer
bestraling in die teenwoordigheid van pentoxifylline gedoen word. In Hela
servikale karsinoom selle affekteer pentoxifylline die uitdrukking van die twee
komponente van die mitose promoverings faktor (MPF), naamlik siklien B1 en p34CdC2
, en restoreer die siklien 81/p34cdC2 verhoudings vinnig na normale
vlakke. Ontleding van die siklien 81 uitdrukking in heel selle en in geïsoleerde
selkerne toon verder dat die middelook die sub-sellulêre ligging van die MPF
affekteer.
Die gevolgtrekking word gemaak dat G2 blok verwydering nie die enigste
meganisme is waardeur pentoxifylline radiosensitiwiteit verhoog nie, maar dat
die vertraging van ONS herstel in sommige seltipes 'n rol speel. Alhoewel
pentoxifylline apoptose verhoog in T-limfosiete, speel dit nie 'n rol in die
verhoogde radiotoksisiteit wat waargeneem is in die TP53 mutante melanoom
en plaveisel-sel karsinoom sellyne nie. Verwydering van die G2 blok deur
pentoxifylline, wat selle meer sensitief kan maak vir 'n tweede stralings- of
chemoterapie aanslag, behels die modulasie van siklien 81 en p34cdc2 vlakke
en die sub-sellulêre ligging van die MPF. Hierdie resultate is van uiterste
belang vir die kliniese aanwending van pentoxifylline as 'n dosis-modifiseerder
in kankerterapie.
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Cell biological responses of prostatic tumour cell lines to irradiation and anticancer drugsSerafin, Antonio Mendes 12 1900 (has links)
Thesis (PhD)--Stellenbosch University, 2003. / ENGLISH ABSTRACT: The "classic" prostate cell lines, DU145, PC-3 and LNCaP, have served as a valuable
cell biological model for research into prostate cancer. However, their relevance may
be limited because they derive from metastatic, and not from primary normal and
tumour epithelium. The cell lines (1532T, 1535T, 1542T, 1542N and BPH-l) have
been derived from primary benign and malignant human tumour prostate epithelium
and may be more representative. Using these cell lines I have examined the role of
basic cell damage responses (repair, checkpoint activation, apoptosis and associated
signalling proteins, and the influence of androgen status) in cell inactivation, and its
relevance to treatment.
Numerous studies have suggested that loss of p53 function leads to resistance to
chemotherapeutic agents and irradiation. It is shown here that the p53-inactive cell
lines are, in fact, the most sensitive to chemotherapeutic agents such as etoposide,
vinblastine and estramustine, whilst the p53 wild-type cell line, LNCaP, is the most
radiosensitive. Notwithstanding the effects of p53 degradation by the HPV -16 E6
viral protein, the results on chemosensitivity raises the possibility that different
chemotherapeutic agents may have different p53-dependent effects in different
tumour cells.
Androgen deprivation is demonstrated to sensitise prostate cancer cells to
chemotherapeutic agents and it is shown that the hormone independent cell lines are
the most chemosensitive. The LNCaP cell line displayed an increased resistance to
apoptosis induced by etoposide and gamma irradiation, suggesting that androgens are
capable of protection against both these DNA damaging agents.
The major factors determining radiosensitivity in human tumour cell lines are known
to be DNA double-strand break (dsb) induction and repair. In the prostate cell lines I
find that cellular radiosensitivity correlates with the number of DNA double-strand
breaks measured within 2 hours of irradiation, and that the more radioresistant cell
lines show better repair competence. Conclusions as to the influence of androgen dependence on radiosensitivity and repair are not possible at this stage since only the
LNCaP cell line was androgen sensitive. The fact that the 2 hour repair period can
separate radiosensitive from radioresistant cells in 2 groups of human tumour cell
lines highlights the role of non-homologous end-joining repair. This has implications
for therapy, and is consistent with the clinical observation that prostate tumours can
be successfully controlled by low dose rate-brachytherapy.
To evaluate the role of apoptosis, cells were exposed to TD50 concentrations of
chemotherapeutic drugs, and 60Co y-irradiation. Apoptosis was found to be low,
overall, and ranged from 0.1% - 12.1%,3.0% - 6.0% and 0.1% - 8.5% for etoposide,
estramustine and vinblastine, respectively. The percentage of cells undergoing druginduced
apoptosis was, on average, higher in the tumour cell lines than in the normal
cell lines. Gamma irradiation-induced apoptosis levels ranged from 1.3% - 7%. The
LNCaP cell line yielded the lowest percentage of apoptotic cells after exposure. The
l532T cell line yielded the highest percentage of apoptotic cells after exposure.
Apoptotic propensity did not rank the cell lines according to their radiosensitivity.
Immunoblotting demonstrated that the apoptosis-associated proteins, bax and bcl-2,
are expressed at a basal level in all the cell lines tested, but no increase was detected
after exposure to TD50 doses of etoposide, vinblastine and estramustine. The ratio of
bax and bcl-2 also was not altered by DNA damage.
No evidence was found that a correlation may exist between reproductive cell death
and the expression of genes which control apoptosis. My results show that apoptosis
is not a major mechanism of drug- or radiation-induced cell death in prostate cell
lines.
In conclusion, loss of p53 function and loss of androgen dependence was not found to
be correlated with resistance of tumours to chemotherapeutic drugs. Cellular
radiosensitivity was found to be correlated with the number of DNA double-strand
breaks remaining after 2 hours of repair. The more radioresistant cell lines showed
better repair competence. Apoptosis and genes affecting apoptosis, such as p53 and
members of the bcl-2 family, do not seem to contribute significantly to the sensitivity
of prostate cancer cells to anticancer drugs and irradiation. / AFRIKAANSE OPSOMMING: Die klassieke prostaat sellyne, DU145, PC-3 en LNCaP, het 'n waardevolle bydrae
gemaak in die sel biologiese model in prostaat kanker. Die toepaslikheid daarvan
mag egter beperk wees, aangesien hierdie sellyne afkomstig is van metastatiese, en
nie van primêr normale en tumor epiteel nie. Die sellyne 1532T, 1535T, 1542T,
1542N en BPH-I is afkomstig van primêre benigne en maligne menslike prostaat
tumor epiteel en mag moontlik meer verteenwoordigend wees. Deur van hierdie
sellyne gebruik te maak, is die rolondersoek van die reaksie op basiese selskade
(d.w.s. herstel, beheerpunt aktivering, apoptose en verwante sein proteïene, en die
invloed van androgeen status) tydens die proses van sel inaktivering, asook die
toepaslikheid ten opsigte van behandeling.
Volgens verskeie studies lei die verlies aan p53 funksie tot weerstandigheid teen
chemoterapeutiese middels en bestraling. Die resultate van hierdie studie toon dat die
p53-onaktiewe sellyne egter die sensitiefste is vir chemoterapeutiese middels, soos
etoposied, vinblastien en estramustien, terwyl die p53 natuurlike-tipe sellyn, LNCaP,
die meeste radiosensitief is. Ten spyte van die invloed van p53 afbraak deur die
HPV -16 E6 virale proteïen, dui die resultate van chemosensitiwiteit op die
moontlikheid dat verskillende chemoterapeutiese middels verskillende p53-afhanklike
effekte op verskillende tumorselle mag hê.
Dit is bewys dat onttrekking van androgeen prostaat kankerselle sensitiseer teen
chemoterapeutiese middels en dat hormoon-onafhanklike sellyne die hoogste
chemosensitiwiteit vertoon. Die LNCaP sellyn vertoon 'n verhoogde weerstandigheid
teen apoptose wat deur etoposied en y-bestraling geïnduseer is, wat 'n aanduiding is
dat androgene beskerming kan bied teen beide hierdie DNA beskadigingsfaktore.
Die belangrikste faktore wat die radiosensitiwiteit in menslike tumorselle bepaal, IS
bekend dat dit die dubbelbande van DNA verbreek en herstel. Hierdie studie het
aangetoon dat in prostaat sellyne die sellulêre radiosensitiwiteit korreleer met die
aantal DNA dubbelband verbrekings binne 2 uur na bestraling, en dat die meer
radioweerstandige sellyne beter herstelvermoë vertoon. Gevolgtrekkings oor die invloed van androgeen se afhanklikheid van radiosensitiwiteit en herstel kan egter nie
op hierdie stadium gemaak word nie, aangesien slegs die LNCaP sellyn androgeenafhanklik
was. Die feit dat die 2 uur herstelperiode 'n skeiding kan maak tussen
radiosensitiewe en radioweerstandige selle in twee groepe menslike tumor sellyne,
onderstreep die rol van herstel van nie-homoloë endverbindings. Dit hou implikasies
in vir terapie, en stem ooreen met die kliniese waarnemings dat prostaat tumore
suksesvol gekontroleer kan word deur lae intensiteit dosis bragiterapie.
Ten einde die rol van apoptose te ondersoek, is selle blootgestel aan TD50
konsentrasies chemoterapeutiese middels, asook 60Co y-bestraling. Apoptose was oor
die algemeen laag, en het gestrek van 0.1% tot 12.1%,3.0% tot 6.0% en 0.1% tot
8.5% vir etoposied, estramustien en vinblastien onderskeidelik. Die persentasie selle
wat middel geïnduseerde apoptose ondergaan het, was gemiddeld hoër in tumor
sellyne as in normale sellyne. Die waardes van apoptose geïnduseer deur y-bestraling
het gewissel van 1.3% tot 7.0%. Die LNCaP sellyn het die laagste persentasie
apoptotiese selle na bestraling gelewer, terwyl die 1532 r sellyn die hoogste
persentasie gelewer het. Die volgorde van die radiosensitiwiteit van die sellyne was
nie waarneembaar in hulle geneigdheid tot apoptose nie. Immunoblots het aangetoon
dat die apoptose-geassosieerde proteïene, bax en bcl-2, uitgeskei word teen 'n
basisvlak in al die sellyne wat getoets is, maar dat geen verhoogde uitskeiding
waarneembaar was na blootstelling aan TD50 dosisse etoposied, vinblastien en
estramustien nie. Die verhouding van bax en bcl-2 is ook nie beïnvloed deur DNA
beskadiging nie.
Dit blyk daarom dus onwaarskynlik dat daar 'n korrelasie bestaan tussen
reproduktiewe seldood en die uitskeiding van gene wat apoptose beheer. Die resultate
dui daarop dat apoptose me 'n belangrike meganisme vir middel- of
bestralingsgeïnduseerde seldood in prostaat sellyne is nie.
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Breast cancer diagnosed in women with the Human Immune-Deficiency Virus (HIV)Langenhoven, Lizanne 12 1900 (has links)
Thesis (MMed)--Stellenbosch University, 2014. / ENGLISH ABSTRACT: Background: HIV is the defining pandemic of our era, with an estimated 5.9 million people
infected in South Africa according to World Health Organization (WHO) estimates for 2011.
The expression and treatment of non-AIDS defining cancers has become an important
consideration in this cohort, as antiretroviral therapy (ART) has prolonged survival in a
subgroup previously at risk of early mortality.
Study Design: A retrospective cohort study of all women seen at the Combined Breast
Cancer Clinic at Tygerberg Hospital between January 2010 and December 2011, stratified
into three subgroups based on HIV status.
Methods: Of the 816 patients screened, 586 met inclusion criteria; of which 31 (5.3%)
patients were HIV positive, 420 (71.7%) HIV negative, and 135 (23%) had an unknown HIV
status. The disease phenotype was described in each subgroup, as well as toxicities
associated with standard chemotherapy regimens, with an emphasis on completion rates of
systemic cytotoxic treatment. The insult of cytotoxic therapy to the CD4 count was described
for this cohort.
Results: Women with HIV had a statistically significant (p<0.001) younger age at
presentation of breast cancer with a median age of 42 years (range 39 – 45 years) in
comparison with the HIV-negative cohort with a median age of 54 years (range 53 – 55
years) .
No difference was detected in disease phenotype when stage at presentation (p=0.7874),
histological subtype (p=0.3375), grade of differentiation (p=0.8297), nodal involvement
(p=0.0998) or hormone-receptor positivity (p=0.6285) was considered. Completion rates for
systemic chemotherapy were excellent (>90%) regardless of HIV-status and no statistically
significant toxicity was observed. The median CD4 count at diagnosis was 477 cells/μL
(range 234 – 807 cells/μL), with a nadir value of 333 cells/μL (range 62 – 713 cells/μL),
representing a decrease of 30.2% during treatment. One case of suspected treatment-related
mortality was recorded.
Conclusion: This retrospective study confirmed that women infected with HIV had a younger
age at breast cancer diagnosis when compared to women with a negative HIV-status. No
difference in disease phenotype could be demonstrated for women with HIV, denoting the coexistence
of two common chronic diseases. Chemotherapy was tolerated well, but caused a
median decline in CD4-count of 30% during treatment. / AFRIKAANSE OPSOMMING: Agtergrond: Infeksie met die Menslike Immuungebrek-Virus (MIV) is die pandemie van ons
era, met ‘n geraamde 5.9 miljoen mense geïnfekteerd in Suid-Afrika volgens die Wêreld
Gesondheids-Organisasie (WGO) in 2011. Kankers wat nie met MIV geassosieer word nie,
het n belangrike oorweging in hierdie populasie-groep geword as gevolg van die gebruik van
anti-retrovirale terapie wat die lewensverwagting van mense met MIV verleng.
Navorsingsontwerp: ‘n Retrospektiewe kohort studie van alle vroue wat tydens die tydperk
Januarie 2010 en Desember 2011 by die Gekombineerde Borskanker Kliniek te Tygerberg
Hospitaal behandel was, verdeel in 3 groepe volgens hul retrovirale status.
Metodes: ‘n Totaal van 819 vroue was oorweeg vir insluiting in die studie, waarvan 586 aan
die insluitingskriteria voldoen het. Daar was 31 vroue met MIV (5.3%), 420 vroue het MIVnegatief
getoets (71.7%), en 135 (23%) vroue waarvan die MIV-status onbekend was. Die
fenotipe van borskanker was beskryf vir elke sub-groep, sowel as die toksiteite wat
geassosieer word met die gebruik van standaard chemoterapie-skedules, insluitend die effek
van chemoterapie op die CD4-telling.
Bevindinge: Vroue met MIV het op ‘n statisties noemenswaardige (p<0.001) jonger
ouderdom gepresenteer met borskanker (gemiddelde ouderdom 42 jaar, reikwydte 39 – 45
jaar) in vergelyking met vroue wat MIV-negatief was (gemiddelde ouderdom 54 jaar,
reikwydte 53 – 55 jaar). Geen verskil was waargeneem in die fenotipe van borskanker in
vroue met MIV vir die stadium by diagnose (p = 0.7874), histologiese tipe (p=0.3375), graad
van differensiasie (p = 0.8297), nodale betrekking (p = 0.0998) of hormoon-reseptor status
(p=0.6285) nie. Voltooing van sistemiese chemoterapie is bereik in meer as negentig persent
van gevalle onafhanklik van MIV-status. ‘n Gemiddelde CD4-telling van 477 selle/μL
(reikwydte 234 – 807 selle/ μL) met diagnose het ‘n gemiddelde afname van 30.2% tydens
behandeling getoon na ‘n gemiddelde waarde van 333 selle/ μL (reikwydte 62 – 713 selle/
μL).
Gevolgtrekkings: Hierdie retrospektiewe studie het bevind dat vroue met MIV op ‘n jonger
ouderdom met borskanker presenteer as vroue wat MIV-negatief is. Geen noemenswaardige
verskil was waargeneem in die fenotipe van borskanker in vroue met MIV nie, en dui daarop
dat borskanker en MIV twee algemene, maar onafhanklike entiteite is. Chemoterapie was
goed getolereer met ‘n gemiddelde afname in die CD4-telling van 30.2% tydens
chemoterapie.
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